Updated Guidelines Help Patients Reduce Risk Of Cardiac Event Before Surgery
30 Sep 2007
People with heart disease should take special precautions before undergoing any kind of surgery, even noncardiac surgery, to reduce their risk of a cardiac event, according to new joint guidelines from the American College of Cardiology and the American Heart Association.
The American College of Cardiology/American Heart Association 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery will be published online ahead of print in the October 23, 2007, issues of Circulation: Journal of the American Heart Association and the Journal of the American College of Cardiology.
The guidelines -- an update of those published in 2002 -- provide a framework for considering a person's risk of a cardiac event in the "perioperative" (during or immediately after) period of noncardiac surgery.
According to the recommendations, patients should not stop taking cholesterol-lowering drugs before surgery. In addition, the guidelines say that many people with heart disease can safely undergo noncardiac surgery without first "fixing" their heart disease with an artery-opening procedure or coronary bypass grafting. The guidelines also address how best to treat those people who need a heart procedure before noncardiac surgery, have coronary stents or require anti-clotting medication.
"In the past we had to go on indefinite evidence, but now there are a number of studies published to help us direct best practices," said Lee A. Fleisher, M.D., chair of the guideline writing committee. "Statin use wasn't even addressed in the previous guidelines. New trials have shown us that patients should continue taking them."
In the case of non-emergency or elective procedures, the guidelines say that intervention (such as bypass surgery or angioplasty) is rarely necessary to lower the risk of surgery unless a patient would need the intervention anyway. If the noncardiac surgery is an emergency, heart testing should be forgone and a patient should go straight to an operating room.
The guidelines recommend that patients undergo evaluation and treatment before noncardiac surgery only for "active" cardiac conditions such as unstable coronary syndromes (severe angina), decompensated heart failure, significant heart rhythm disturbances (arrhythmias) or severe heart valve disease.
"Previously, to have someone ready for surgery, many people needed diagnostic tests to look at the extent of heart disease," said Fleisher, chair of the Department of Anesthesiology and Critical Care at the Hospital of the University of Pennsylvania. "We would do a lot of screening, and we might fix their heart disease to get them ready for the noncardiac surgery. We know now that surgical outcomes are the same in many people whether or not we fix the heart disease first."
The difference in whether heart procedures reduce the risk of surgery is whether a person's heart disease is either severe or symptomatic -- both of which would require treatment regardless of the impending surgery. "Several trials now show that in people without symptomatic heart disease, fixing the heart first doesn't make much of a difference in how well they do in surgery," Fleisher said.
Thus, the surgical setting shouldn't be the only catalyst for a heart procedure. Fleisher said angioplasty with stenting might even increase the risk of perioperative heart problems. The risk of heart attack increases in the four to six weeks immediately after receiving a stent, so patients are prescribed anti-clotting medication during this period. This risk, and the duration of anti-clotting therapy, is up to one year for patients who received a coated or drug-eluting stent.
Due to the risks of excessive bleeding common to any surgery, patients were previously advised to stop taking their anti-clotting drugs prior to surgery. "We now know that the antiplatelet medication is very important after stent placement, and we advocate stopping it for as little time as possible," Fleisher said.
For patients who need non-urgent or elective noncardiac surgery, and who need to undergo an artery-opening procedure beforehand, the guidelines recommend angioplasty using a bare metal stent followed by four to six weeks of anti-clotting therapy.
For patients who already have a drug-eluting coronary stent and need to undergo urgent noncardiac surgery that requires stopping the prescription anti-clotting drug, the guidelines recommend continuing aspirin therapy if possible, and restarting the prescription medicine as soon as possible.
The guidelines recommend coronary artery bypass grafting or angioplasty before a noncardiac surgery for patients with severe or symptomatic heart disease, such as having two or more blood vessels blocked, unstable angina or heart attack symptoms.
"In general," according to the guidelines, "indications for further cardiac testing and treatments are the same as in the non-operative setting, but their timing is dependent on several factors." These factors include the urgency of noncardiac surgery, the patient's specific risk factors and the type of surgery (whether it's a lower-risk or higher-risk procedure). Preoperative testing should be limited to those circumstances in which test
Sunday, September 30, 2007
Saturday, September 29, 2007
Antihypertensive Treatment May Help Maintain Memory
Antihypertensive Treatment May Help Maintain Memory
Caroline Cassels
Medscape Medical News 2007. © 2007 Medscape
September 27, 2007 — New research indicates antihypertensive treatment leads to increased, joint activation of brain areas responsible for memory performance — a finding that suggests such treatment may help patients maintain cognition and memory.
A study led by J. Richard Jennings, PhD, from the University of Pittsburgh, in Pennsylvania, and presented at the American Heart Association (AHA) 61st Annual Fall Conference of the Council for High Blood Pressure Research, showed patients had a 2-fold increase in the joint activation of these areas of the brain after a year of treatment with either the angiotensin-converting enzyme lisinopril or beta blocker atenolol.
While there is an established link between hypertension and mild cognitive deficits, the mechanism has not been clear. Previous research by Dr. Jennings's team used brain imaging to examine the correlation among the activation of the prefrontal areas, parietal areas, and amygdala/hippocampus in hypertensives compared with controls and found it was higher in individuals with high blood pressure.
Increased Correlation
"In the first study, we found that in hypertensive individuals the correlation between levels of activation of these areas of the brain was 0.61. Our next question was, If we successfully treated these individuals [for hypertension], would this finding be reversed and would their brain function look more like normotensives?" Dr. Jennings told Medscape Neurology & Neurosurgery.
"To our surprise, we found that rather than decreasing, the correlation increased to 0.90. Thus, these areas of the brain were nearly always activated at the same level, suggesting there was less specificity, which means that instead of each area doing its own specific job, they were all working at the same time to try to solve the [memory] task," he added.
The study included 28 never-medicated hypertensives, randomized to receive treatment with lisinopril or atenolol for 1 year. All patients underwent psychological and physiological tests, magnetic resonance structural imaging, and positron emission tomography.
Pretreatment correlation of parietal and prefrontal change was 0.61 vs 0.94 after treatment. According to the investigators, similar differences were observed for all areas, with an average pretreatment correlation of 0.66 vs an average posttreatment correlation of 0.91.
Mental Fatigue?
These findings, said Dr. Jennings, suggest hypertensive patients' brains adapt to maintain their intellectual function and that antihypertensive treatment appears to maintain or even augment this adjustment.
At this point, said Dr. Jennings, it is not clear whether there is a "cost" associated with the brain's adaptation to hypertension. "It could mean that [in patients with hypertension] the brain has to work harder, and this could result in mental fatigue, but at this point we just don't know," he said.
This question, he added, will be the focus of future research. In addition, he said, the investigators also want to look at different types of antihypertensive treatments to determine whether they have effects similar to the 2 agents studied in the current work.
According to AHA president Daniel Jones, MD, this study provides reassurance to individuals concerned about potential adverse cognitive effects of antihypertensive treatment. "Treating hypertension is beneficial not only for extending life, but also for improving quality of life," he said in a statement.
The study was funded by the National Heart, Lung, and Blood Institute of the National Institutes of Health.
American Heart Association 61st Annual Fall Conference of the Council for High Blood Pressure Research: Abstract P105. Presented September 27, 2007.
Caroline Cassels
Medscape Medical News 2007. © 2007 Medscape
September 27, 2007 — New research indicates antihypertensive treatment leads to increased, joint activation of brain areas responsible for memory performance — a finding that suggests such treatment may help patients maintain cognition and memory.
A study led by J. Richard Jennings, PhD, from the University of Pittsburgh, in Pennsylvania, and presented at the American Heart Association (AHA) 61st Annual Fall Conference of the Council for High Blood Pressure Research, showed patients had a 2-fold increase in the joint activation of these areas of the brain after a year of treatment with either the angiotensin-converting enzyme lisinopril or beta blocker atenolol.
While there is an established link between hypertension and mild cognitive deficits, the mechanism has not been clear. Previous research by Dr. Jennings's team used brain imaging to examine the correlation among the activation of the prefrontal areas, parietal areas, and amygdala/hippocampus in hypertensives compared with controls and found it was higher in individuals with high blood pressure.
Increased Correlation
"In the first study, we found that in hypertensive individuals the correlation between levels of activation of these areas of the brain was 0.61. Our next question was, If we successfully treated these individuals [for hypertension], would this finding be reversed and would their brain function look more like normotensives?" Dr. Jennings told Medscape Neurology & Neurosurgery.
"To our surprise, we found that rather than decreasing, the correlation increased to 0.90. Thus, these areas of the brain were nearly always activated at the same level, suggesting there was less specificity, which means that instead of each area doing its own specific job, they were all working at the same time to try to solve the [memory] task," he added.
The study included 28 never-medicated hypertensives, randomized to receive treatment with lisinopril or atenolol for 1 year. All patients underwent psychological and physiological tests, magnetic resonance structural imaging, and positron emission tomography.
Pretreatment correlation of parietal and prefrontal change was 0.61 vs 0.94 after treatment. According to the investigators, similar differences were observed for all areas, with an average pretreatment correlation of 0.66 vs an average posttreatment correlation of 0.91.
Mental Fatigue?
These findings, said Dr. Jennings, suggest hypertensive patients' brains adapt to maintain their intellectual function and that antihypertensive treatment appears to maintain or even augment this adjustment.
At this point, said Dr. Jennings, it is not clear whether there is a "cost" associated with the brain's adaptation to hypertension. "It could mean that [in patients with hypertension] the brain has to work harder, and this could result in mental fatigue, but at this point we just don't know," he said.
This question, he added, will be the focus of future research. In addition, he said, the investigators also want to look at different types of antihypertensive treatments to determine whether they have effects similar to the 2 agents studied in the current work.
According to AHA president Daniel Jones, MD, this study provides reassurance to individuals concerned about potential adverse cognitive effects of antihypertensive treatment. "Treating hypertension is beneficial not only for extending life, but also for improving quality of life," he said in a statement.
The study was funded by the National Heart, Lung, and Blood Institute of the National Institutes of Health.
American Heart Association 61st Annual Fall Conference of the Council for High Blood Pressure Research: Abstract P105. Presented September 27, 2007.
Friday, September 28, 2007
Ensuring drug safety: lessons from the thiazolidinediones
Ensuring drug safety: lessons from the thiazolidinediones
Editorial
The Lancet, Current Issue, Volume 370, Number 9593, 29 September 2007
In today's Lancet, Rodrigo Lago and colleagues add to the ongoing analysis of the safety of thiazolidinediones for control of hyperglycaemia. Initial concerns about the cardiovascular risks of one of the thiazolidinediones, rosiglitazone, erupted in a firestorm of controversy when a meta-analysis by Nissen and Wolski was published online in the New England Journal of Medicine in May. Nissen and Wolski found that rosiglitazone (Avandia, GSK) was associated with a significantly increased risk of myocardial infarction, and a risk of death from cardiovascular causes that was of borderline statistical significance. The authors acknowledged that their analysis was limited by the public availability of trial results and a lack of access to patient-level data, and that the pooled studies were not designed to assess cardiovascular outcomes. But they concluded that the risks of rosiglitazone use in diabetes should be carefully considered by both doctors and their patients.
Response to these findings was swift. An editorial that accompanied the paper, while acknowledging the findings' “fragility”, called for urgent regulatory action; GSK vigorously defended its product, saying that studies show Avandia's cardiovascular profile to be comparable to other oral antidiabetes agents; and this journal counselled against a rush to judgment, advising patience until the final results of RECORD, a phase III trial designed to assess cardiovascular outcomes, were available. Media coverage was extensive. A US Congressional hearing was hastily called, as was a Food and Drug Administration (FDA) Advisory Committee meeting. The Congressional hearing was a spectacular display of partisan agendas and bipartisan ignorance. The FDA meeting resulted in a 22 to 1 vote to keep Avandia on the market, and to add a “black box” warning on the label of the risks of the drug's use in patients with congestive heart failure. If this sequence of events sounds familiar, it is because a nearly identical path was trodden when the safety of selective cyclo-oxygenase 2 (COX-2) inhibitors was called into question. Then, as now, the question was about the drugs' cardiovascular effects.
Other analyses of the thiazolidinedione have followed the NEJM paper, including two papers that appeared in JAMA on Sept 12, one on the risk of cardiovascular events with pioglitazone, the only other available agent in the thiazolidinedione class (Actos, Takeda), and one assessing long-term cardiovascular risk with rosiglitazone. Here, both drugs were associated with an increased risk of heart failure, though without an associated increase in mortality. This is the same conclusion reached by Lago and colleagues: patients taking thiazolidinediones seem to have a higher risk of congestive heart failure, but do not have a higher risk of death from cardiovascular causes.
Is there then a bottom line to all these bits of evidence? What should doctors and patients do? Is there in fact enough good evidence on which to decide anything? It seems that the jury is still out for the thiazolidinediones as a class. But there are many interim take-home messages. Some of these are highlighted by Comments in today's issue. First, it must be remembered that meta-analysis is a technique with important limitations. And the studies on which the thiazolidinedione meta-analyses are based have thus far all involved surrogate markers; the studies were not designed to assess cardiovascular outcomes, but rather improved glycaemic control. This outcome, as Victor Montori and colleagues note, is not a patient-centred one. The current clinical emphasis on glucose control (as measured by HbA1c) skirts the outcomes that matter most to patients—microvascular and macrovascular complications, quality of life, and survival.
These commentators highlight issues that must be taken into account in the ongoing debate about thiazolidinediones. Future trials ought to be designed with these issues firmly in mind. Further, it is no secret that the regulatory system is also in urgent need of repair. Manufacturers must do—in a timely fashion—postmarketing studies that assess the long-term safety of their drugs, and regulatory agencies must hold manufacturers' feet to the fire to ensure that these are performed, performed properly, thoroughly evaluated, and made available to guide decisions about prescribing. Agencies like the US FDA must have the resources and authority to close what is now a potentially dangerous gap. Unless limitations on the understanding, analysis, and communication of drug safety issues are addressed, the thiazolidinediones might simply become the latest in a series of preventable drug disasters.
The Lancet
Editorial
The Lancet, Current Issue, Volume 370, Number 9593, 29 September 2007
In today's Lancet, Rodrigo Lago and colleagues add to the ongoing analysis of the safety of thiazolidinediones for control of hyperglycaemia. Initial concerns about the cardiovascular risks of one of the thiazolidinediones, rosiglitazone, erupted in a firestorm of controversy when a meta-analysis by Nissen and Wolski was published online in the New England Journal of Medicine in May. Nissen and Wolski found that rosiglitazone (Avandia, GSK) was associated with a significantly increased risk of myocardial infarction, and a risk of death from cardiovascular causes that was of borderline statistical significance. The authors acknowledged that their analysis was limited by the public availability of trial results and a lack of access to patient-level data, and that the pooled studies were not designed to assess cardiovascular outcomes. But they concluded that the risks of rosiglitazone use in diabetes should be carefully considered by both doctors and their patients.
Response to these findings was swift. An editorial that accompanied the paper, while acknowledging the findings' “fragility”, called for urgent regulatory action; GSK vigorously defended its product, saying that studies show Avandia's cardiovascular profile to be comparable to other oral antidiabetes agents; and this journal counselled against a rush to judgment, advising patience until the final results of RECORD, a phase III trial designed to assess cardiovascular outcomes, were available. Media coverage was extensive. A US Congressional hearing was hastily called, as was a Food and Drug Administration (FDA) Advisory Committee meeting. The Congressional hearing was a spectacular display of partisan agendas and bipartisan ignorance. The FDA meeting resulted in a 22 to 1 vote to keep Avandia on the market, and to add a “black box” warning on the label of the risks of the drug's use in patients with congestive heart failure. If this sequence of events sounds familiar, it is because a nearly identical path was trodden when the safety of selective cyclo-oxygenase 2 (COX-2) inhibitors was called into question. Then, as now, the question was about the drugs' cardiovascular effects.
Other analyses of the thiazolidinedione have followed the NEJM paper, including two papers that appeared in JAMA on Sept 12, one on the risk of cardiovascular events with pioglitazone, the only other available agent in the thiazolidinedione class (Actos, Takeda), and one assessing long-term cardiovascular risk with rosiglitazone. Here, both drugs were associated with an increased risk of heart failure, though without an associated increase in mortality. This is the same conclusion reached by Lago and colleagues: patients taking thiazolidinediones seem to have a higher risk of congestive heart failure, but do not have a higher risk of death from cardiovascular causes.
Is there then a bottom line to all these bits of evidence? What should doctors and patients do? Is there in fact enough good evidence on which to decide anything? It seems that the jury is still out for the thiazolidinediones as a class. But there are many interim take-home messages. Some of these are highlighted by Comments in today's issue. First, it must be remembered that meta-analysis is a technique with important limitations. And the studies on which the thiazolidinedione meta-analyses are based have thus far all involved surrogate markers; the studies were not designed to assess cardiovascular outcomes, but rather improved glycaemic control. This outcome, as Victor Montori and colleagues note, is not a patient-centred one. The current clinical emphasis on glucose control (as measured by HbA1c) skirts the outcomes that matter most to patients—microvascular and macrovascular complications, quality of life, and survival.
These commentators highlight issues that must be taken into account in the ongoing debate about thiazolidinediones. Future trials ought to be designed with these issues firmly in mind. Further, it is no secret that the regulatory system is also in urgent need of repair. Manufacturers must do—in a timely fashion—postmarketing studies that assess the long-term safety of their drugs, and regulatory agencies must hold manufacturers' feet to the fire to ensure that these are performed, performed properly, thoroughly evaluated, and made available to guide decisions about prescribing. Agencies like the US FDA must have the resources and authority to close what is now a potentially dangerous gap. Unless limitations on the understanding, analysis, and communication of drug safety issues are addressed, the thiazolidinediones might simply become the latest in a series of preventable drug disasters.
The Lancet
Thursday, September 27, 2007
ECG does not rule out LV hypertrophy
ECG does not rule out LV hypertrophy
By Caroline Price
07 September 2007
Br Med J 2007; Advance online publication
MedWire News: Electrocardiographic criteria should not be used to rule out left ventricular (LV) hypertrophy in patients with hypertension, say clinicians in an advance online publication by the British Medical Journal.
Matthias Egger (Universities of Bern, Switzerland, and Bristol, UK) and colleagues conclude this after conducting a systematic review of studies testing the accuracy of six different electrocardiographic indexes.
Accurate and early diagnosis of LV hypertrophy is an important component of the care of hypertension patients, in whom it leads to a five- to 10-fold increase in cardiovascular risk, explain the researchers, but the appropriate diagnostic work-up of suspected LV hypertrophy remains unclear.
Egger and co-workers set out to clarify the accuracy of commonly used electrocardiographic indexes, focusing on their ability to rule out LV hypertrophy in patients with arterial hypertension.
"As the electrocardiogram (ECG) will mainly be used to rule out the diagnosis of LV hypertrophy, we were particularly interested in the sensitivity and the likelihood ratio of a negative ECG result," they note.
The team searched electronic databases, reference lists of relevant studies and reviews, and discussions with experts for observational studies that evaluated the accuracy of electrocardiographic indexes for LV hypertrophy diagnosis, and established the presence of LV hypertrophy using echocardiography.
This yielded 21 observational studies, involving a total of 5608 patients, 10 of which were conducted in primary care and 11 in secondary care.
The median prevalence of LV hypertrophy was 33% in primary care settings, and 65% in secondary care.
The researchers focused their analysis on data for the six most commonly used indexes: the Sokolow-Lyon voltage index; the Cornell voltage and Cornell product indexes; the Gubner index; and the Romhilt-Estes score with two different thresholds.
The results showed that the median sensitivity ranged from 10.5% for the Gubner index to 21% for the Sokolow-Lyon index.
The median negative likelihood ratio was similar across these different indexes, ranging from 0.85 for the Romhilt-Estes score (with a threshold for positive test of ≥4 points) to 0.91 for the Gubner index.
Using the median likelihood ratio from the Romhilt-Estes score (four points) in primary care, a negative ECG result would reduce the typical pre-test probability of 33% to 31%, Egger et al report.
In secondary care, the typical pre-test probability of 65% would be reduced to 63%.
"Irrespective of the index used, the ECG is a poor screening tool to exclude LV hypertrophy in hypertensive patients in primary and secondary care settings," the authors write.
Journal
By Caroline Price
07 September 2007
Br Med J 2007; Advance online publication
MedWire News: Electrocardiographic criteria should not be used to rule out left ventricular (LV) hypertrophy in patients with hypertension, say clinicians in an advance online publication by the British Medical Journal.
Matthias Egger (Universities of Bern, Switzerland, and Bristol, UK) and colleagues conclude this after conducting a systematic review of studies testing the accuracy of six different electrocardiographic indexes.
Accurate and early diagnosis of LV hypertrophy is an important component of the care of hypertension patients, in whom it leads to a five- to 10-fold increase in cardiovascular risk, explain the researchers, but the appropriate diagnostic work-up of suspected LV hypertrophy remains unclear.
Egger and co-workers set out to clarify the accuracy of commonly used electrocardiographic indexes, focusing on their ability to rule out LV hypertrophy in patients with arterial hypertension.
"As the electrocardiogram (ECG) will mainly be used to rule out the diagnosis of LV hypertrophy, we were particularly interested in the sensitivity and the likelihood ratio of a negative ECG result," they note.
The team searched electronic databases, reference lists of relevant studies and reviews, and discussions with experts for observational studies that evaluated the accuracy of electrocardiographic indexes for LV hypertrophy diagnosis, and established the presence of LV hypertrophy using echocardiography.
This yielded 21 observational studies, involving a total of 5608 patients, 10 of which were conducted in primary care and 11 in secondary care.
The median prevalence of LV hypertrophy was 33% in primary care settings, and 65% in secondary care.
The researchers focused their analysis on data for the six most commonly used indexes: the Sokolow-Lyon voltage index; the Cornell voltage and Cornell product indexes; the Gubner index; and the Romhilt-Estes score with two different thresholds.
The results showed that the median sensitivity ranged from 10.5% for the Gubner index to 21% for the Sokolow-Lyon index.
The median negative likelihood ratio was similar across these different indexes, ranging from 0.85 for the Romhilt-Estes score (with a threshold for positive test of ≥4 points) to 0.91 for the Gubner index.
Using the median likelihood ratio from the Romhilt-Estes score (four points) in primary care, a negative ECG result would reduce the typical pre-test probability of 33% to 31%, Egger et al report.
In secondary care, the typical pre-test probability of 65% would be reduced to 63%.
"Irrespective of the index used, the ECG is a poor screening tool to exclude LV hypertrophy in hypertensive patients in primary and secondary care settings," the authors write.
Journal
HDL Levels Remain Predictive of Heart Risk Even in the Face of Very Low LDL
HDL Levels Remain Predictive of Heart Risk Even in the Face of Very Low LDL
HDL levels retain their prognostic value in patients treated with statins — even among those who achieve very low LDL levels — researchers report in the New England Journal of Medicine.
A post hoc analysis from the industry-funded Treating to New Targets study examined the predictive value of HDL levels on nearly 10,000 adults with coronary heart disease after 3 months of atorvastatin treatment.
After multivariate adjustment, the 5-year risk for major cardiovascular events was reduced by 25% among patients in the highest quintile of HDL cholesterol compared with those in the lowest quintile. Even among patients who had achieved LDL levels below 70 mg/dL, risk remained significantly reduced (by 39%) in the highest HDL quintile.
Writing in Journal Watch General Medicine, Allan S. Brett concludes: "Whether patients with both low LDL and low HDL would benefit from additional drug therapies to raise HDL cholesterol is unclear. "
NEJM article (Free abstract; full text requires subscription)
Related Journal Watch link(s):
Previous Physician's First Watch coverage of Treating to New Targets study (Free)
Journal Watch General Medicine summary (Free)
Journal Watch Cardiology summary (Free)
HDL levels retain their prognostic value in patients treated with statins — even among those who achieve very low LDL levels — researchers report in the New England Journal of Medicine.
A post hoc analysis from the industry-funded Treating to New Targets study examined the predictive value of HDL levels on nearly 10,000 adults with coronary heart disease after 3 months of atorvastatin treatment.
After multivariate adjustment, the 5-year risk for major cardiovascular events was reduced by 25% among patients in the highest quintile of HDL cholesterol compared with those in the lowest quintile. Even among patients who had achieved LDL levels below 70 mg/dL, risk remained significantly reduced (by 39%) in the highest HDL quintile.
Writing in Journal Watch General Medicine, Allan S. Brett concludes: "Whether patients with both low LDL and low HDL would benefit from additional drug therapies to raise HDL cholesterol is unclear. "
NEJM article (Free abstract; full text requires subscription)
Related Journal Watch link(s):
Previous Physician's First Watch coverage of Treating to New Targets study (Free)
Journal Watch General Medicine summary (Free)
Journal Watch Cardiology summary (Free)
Wednesday, September 26, 2007
Anger and stress increase risk for hypertension and CHD in men
Anger and stress increase risk for hypertension and CHD in men
By Sara Carrillo de Albornoz
26 September 2007
Ann Fam Med 2007; 5: 403-411
MedWire News: Prehypertensive men with high levels of trait anger and stress are at high risk for hypertension and coronary heart disease (CHD), research shows.
Marty Player and colleagues from the Medical University of South Carolina in Charleston, USA, examined data from the prospective population-based Atherosclerosis risk in communities (ARIC) study on 2334 men and women aged 45-64 years who had prehypertension but were free of heart disease or stroke.
They then investigated whether psychosocial factors were associated with progression from prehypertension to hypertension and to CHD during the follow-up period from 1987 to 1998.
The researchers measured trait anger - a stable personality trait characterized by the frequency, intensity, and duration of anger - using the Spielberger trait anger scale. Psychological stress was assessed using the Maastricht questionnaire.
After adjusting for age, gender, ethnic background, and cardiovascular risk factors, patients with high levels of trait anger were significantly more likely to progress from prehypertension to hypertension than patients with low/moderate levels (odds ratio [OR]=1.53).
High trait anger scores were also significantly associated with CHD risk (OR=1.71), compared with low trait anger scores.
Nevertheless, stratification by gender revealed that high trait anger was only a risk factor for hypertension and CHD in men, at ORs of 1.71 and 1.92, respectively.
Both men and women with high levels of stress were significantly more likely to develop CHD than those with low/moderate levels (OR=1.68). However, long-term stress did not significantly increase the likelihood of prehypertension progressing to hypertension.
Player et al conclude in the Annals of Family Medicine: "This study adds to the growing evidence of the role of psychological factors in the development of cardiovascular disease."
They add: "Further studies may help determine whether treatment of anger by counseling, medication, or other means will have a beneficial effect on slowing progression from prehypertension to CHD."
Free full text
By Sara Carrillo de Albornoz
26 September 2007
Ann Fam Med 2007; 5: 403-411
MedWire News: Prehypertensive men with high levels of trait anger and stress are at high risk for hypertension and coronary heart disease (CHD), research shows.
Marty Player and colleagues from the Medical University of South Carolina in Charleston, USA, examined data from the prospective population-based Atherosclerosis risk in communities (ARIC) study on 2334 men and women aged 45-64 years who had prehypertension but were free of heart disease or stroke.
They then investigated whether psychosocial factors were associated with progression from prehypertension to hypertension and to CHD during the follow-up period from 1987 to 1998.
The researchers measured trait anger - a stable personality trait characterized by the frequency, intensity, and duration of anger - using the Spielberger trait anger scale. Psychological stress was assessed using the Maastricht questionnaire.
After adjusting for age, gender, ethnic background, and cardiovascular risk factors, patients with high levels of trait anger were significantly more likely to progress from prehypertension to hypertension than patients with low/moderate levels (odds ratio [OR]=1.53).
High trait anger scores were also significantly associated with CHD risk (OR=1.71), compared with low trait anger scores.
Nevertheless, stratification by gender revealed that high trait anger was only a risk factor for hypertension and CHD in men, at ORs of 1.71 and 1.92, respectively.
Both men and women with high levels of stress were significantly more likely to develop CHD than those with low/moderate levels (OR=1.68). However, long-term stress did not significantly increase the likelihood of prehypertension progressing to hypertension.
Player et al conclude in the Annals of Family Medicine: "This study adds to the growing evidence of the role of psychological factors in the development of cardiovascular disease."
They add: "Further studies may help determine whether treatment of anger by counseling, medication, or other means will have a beneficial effect on slowing progression from prehypertension to CHD."
Free full text
Tuesday, September 25, 2007
Colorectal Tumor Risk Greater For People With Coronary Artery Disease
Colorectal Tumor Risk Greater For People With Coronary Artery Disease
25 Sep 2007
People with coronary artery disease have nearly twice the risk of developing colorectal tumor cancers, compared to people without the disease - the link is even stronger for people with coronary artery disease (CAD) who also smoke(d) or have metabolic syndrome, says a report in the Journal of the American Medical Association (JAMA).
Approximately one in every twenty people worldwide will develop colorectal cancer; it is the second most common cancer. CAD is the foremost cause of death in industrialized countries, write the authors as background to the article. Precancerous tumors or cancer (colorectal neoplasm) or CAD share similar risk factors, therefore their co-occurrence may be linked.
Annie On On Chan, M.D., Ph.D., of the University of Hong Kong, China, and team wanted to see how close the link between colorectal cancer and colorectal neoplasms was in patients who had recently been diagnosed with CAD.
The study participants, all from Hong Kong, were recruited for screening colonoscopy after undergoing coronary angiography for suspected CAD during the period November 2004 to June 2006. They defined CAD as a narrowing of 50% or more in any one of the major coronary arteries - otherwise, the subjects were considered CAD-negative. 206 were CAD-positive, while 208 were CAD negative. A control group of 207, matched for age and sex was recruited from the general population.
Below is what the researchers found:
CAD-Positive Group
-- prevalence of colorectal neoplasms - 34%
-- prevalence of advanced lesions - 18.4%
-- prevalence of cancer - 4.4% (half were early stage)
CAD-Negative Group
-- prevalence of colorectal neoplasms - 18.8%
-- prevalence of advanced lesions - 8.7%
-- prevalence of cancer - 0.5%
Control Group
-- prevalence of colorectal neoplasms - 20.8%
-- prevalence of advanced lesions - 5.8%
-- prevalence of cancer - 1.4%
It was also found that a history of smoking and/or metabolic syndrome were significant independent predictive factors for the positive link between advanced lesions and CAD.
The authors wrote "Both colorectal neoplasm and CAD probably develop through the mechanism of chronic inflammation. Inflammation is now recognized as being pivotal in the pathogenesis of atherosclerosis and, hence, CAD. Colorectal cancer is also thought to progress through the pathway of inflammation." JAMA2007;298(12):1412-1419
25 Sep 2007
People with coronary artery disease have nearly twice the risk of developing colorectal tumor cancers, compared to people without the disease - the link is even stronger for people with coronary artery disease (CAD) who also smoke(d) or have metabolic syndrome, says a report in the Journal of the American Medical Association (JAMA).
Approximately one in every twenty people worldwide will develop colorectal cancer; it is the second most common cancer. CAD is the foremost cause of death in industrialized countries, write the authors as background to the article. Precancerous tumors or cancer (colorectal neoplasm) or CAD share similar risk factors, therefore their co-occurrence may be linked.
Annie On On Chan, M.D., Ph.D., of the University of Hong Kong, China, and team wanted to see how close the link between colorectal cancer and colorectal neoplasms was in patients who had recently been diagnosed with CAD.
The study participants, all from Hong Kong, were recruited for screening colonoscopy after undergoing coronary angiography for suspected CAD during the period November 2004 to June 2006. They defined CAD as a narrowing of 50% or more in any one of the major coronary arteries - otherwise, the subjects were considered CAD-negative. 206 were CAD-positive, while 208 were CAD negative. A control group of 207, matched for age and sex was recruited from the general population.
Below is what the researchers found:
CAD-Positive Group
-- prevalence of colorectal neoplasms - 34%
-- prevalence of advanced lesions - 18.4%
-- prevalence of cancer - 4.4% (half were early stage)
CAD-Negative Group
-- prevalence of colorectal neoplasms - 18.8%
-- prevalence of advanced lesions - 8.7%
-- prevalence of cancer - 0.5%
Control Group
-- prevalence of colorectal neoplasms - 20.8%
-- prevalence of advanced lesions - 5.8%
-- prevalence of cancer - 1.4%
It was also found that a history of smoking and/or metabolic syndrome were significant independent predictive factors for the positive link between advanced lesions and CAD.
The authors wrote "Both colorectal neoplasm and CAD probably develop through the mechanism of chronic inflammation. Inflammation is now recognized as being pivotal in the pathogenesis of atherosclerosis and, hence, CAD. Colorectal cancer is also thought to progress through the pathway of inflammation." JAMA2007;298(12):1412-1419
Too Little Or Too Much Sleep Increases Risk Of Death
Too Little Or Too Much Sleep Increases Risk Of Death
25 Sep 2007
Researchers from the University of Warwick, and University College London, have found that lack of sleep can more than double the risk of death from cardiovascular disease.
However they have also found that a point comes when too much sleep can also more than double the risk of death.
In research presented to the British Sleep Society, Professor Francesco Cappuccio from the University of Warwick's Warwick Medical School showed the results of a study of how sleep patterns affected the mortality of 10,308 civil servants in the "Whitehall II study". Amongst other things the data they used provided information on the mortality rates and sleep patterns on the same group of civil servants at two points in their life (1985-8 and those still alive in 1992-3).
The researchers took into account other possible factors such age, sex, marital status, employment grade, smoking status, physical activity, alcohol consumption, self-rated health, body mass index, blood pressure, cholesterol, other physical illness etc. Once they had adjusted for those factors they were able to isolate the effect that changes in sleep patterns over 5 years had on mortality rates 11-17 years later.
Taking those who had not made any change in their sleeping habits between 1985-8 and 1992-3 as their baseline (7 hours per night being the figure normally recommended as an appropriate period of sleep for an adult) they were able to see what difference having reduced the amount of sleep over time made to mortality rates by 2004.
Those who had cut their sleeping from 7h to 5 hours or less faced a 1.7 fold increased risk in mortality from all causes, and twice the increased risk of death from a cardiovascular problem in particular.
Professor Francesco Cappuccio from the University of Warwick's Warwick Medical School said to the British Sleep Society:
"Fewer hours sleep and greater levels of sleep disturbance have become widespread in industrialised societies. This change, largely the result of sleep curtailment to create more time for leisure and shift-work, has meant that reports of fatigue, tiredness and excessive daytime sleepiness are more common than a few decades ago. Sleep represents the daily process of physiological restitution and recovery, and lack of sleep has far-reaching effects."
Curiously the researchers also found that too much sleep also increased mortality. They found that those individuals who showed an increase in sleep duration to 8 hours or more a night were more than twice as likely to die as those who had not changed their habit, however, predominantly from non-cardiovascular diseases.
Professor Francesco Cappuccio says:
"Short sleep has been shown to be a risk factor for weight gain, hypertension and Type 2 diabetes sometimes leading to mortality but in contrast to the short sleep-mortality association it appears that no potential mechanisms by which long sleep could be associated with increased mortality have yet been investigated. Some candidate causes for this include depression, low socioeconomic status and cancer-related fatigue."
"In terms of prevention, our findings indicate that consistently sleeping around 7 hours per night is optimal for health and a sustained reduction may predispose to ill-health."
The research paper entitled: "A prospective study of change in sleep duration; associations with mortality in the Whitehall II cohort" will be published in the Journal SLEEP and the full list of the authors is: Jane E. Ferrie, Martin J. Shipley, Francesco P. Cappuccio, Eric Brunner, Michelle A. Miller, Meena Kumari, and Michael G. Marmot
Monday, September 24, 2007
Primary Angioplasty compared with Thrombolysis - Acute Myocardial Infarction
Assessing the effectiveness of primary angioplasty compared with thrombolysis and its relationship to time delay: a Bayesian evidence synthesis
Heart 2007;93:1244-1250
Christian Asseburg, Yolanda Bravo Vergel, Stephen Palmer, Elisabeth Fenwick, Mark de Belder, Keith R Abrams, Mark Sculpher
ABSTRACT
Background: Meta-analyses of trials have shown greater benefits from angioplasty than thrombolysis after an acute myocardial infarction, but the time delay in initiating angioplasty needs to be considered.
Objective: To extend earlier meta-analyses by considering 1- and 6-month outcome data for both forms of reperfusion. To use Bayesian statistical methods to quantify the uncertainty associated with the estimated relationships.
Methods: A systematic review and meta-analysis published in 2003 was updated. Data on key clinical outcomes and the difference between time-to-balloon and time-to-needle were independently extracted by two researchers. Bayesian statistical methods were used to synthesise evidence despite differences between reported follow-up times and outcomes. Outcomes are presented as absolute probabilities of specific events and odds ratios (ORs; with 95% credible intervals (CrI)) as a function of the additional time delay associated with angioplasty.
Results: 22 studies were included in the meta-analysis, with 3760 and 3758 patients randomised to primary angioplasty and thrombolysis, respectively. The mean (SE) angioplasty-related time delay (over and above time to thrombolysis) was 54.3 (2.2) minutes. For this delay, mean event probabilities were lower for primary angioplasty for all outcomes. Mortality within 1 month was 4.5% after angioplasty and 6.4% after thrombolysis (OR = 0.68 (95% CrI 0.46 to 1.01)). For non-fatal reinfarction, OR = 0.32 (95% CrI 0.20 to 0.51); for non-fatal stroke OR = 0.24 (95% CrI 0.11 to 0.50). For all outcomes, the benefit of angioplasty decreased with longer delay from initiation.
Conclusions: The benefit of primary angioplasty, over thrombolysis, depends on the former’s additional time delay. For delays of 30–90 minutes, angioplasty is superior for 1-month fatal and non-fatal outcomes. For delays of around 90 minutes thrombolysis may be the preferred option as assessed by 6-month mortality; there is considerable uncertainty for longer time delays.
Heart 2007;93:1244-1250
Christian Asseburg, Yolanda Bravo Vergel, Stephen Palmer, Elisabeth Fenwick, Mark de Belder, Keith R Abrams, Mark Sculpher
ABSTRACT
Background: Meta-analyses of trials have shown greater benefits from angioplasty than thrombolysis after an acute myocardial infarction, but the time delay in initiating angioplasty needs to be considered.
Objective: To extend earlier meta-analyses by considering 1- and 6-month outcome data for both forms of reperfusion. To use Bayesian statistical methods to quantify the uncertainty associated with the estimated relationships.
Methods: A systematic review and meta-analysis published in 2003 was updated. Data on key clinical outcomes and the difference between time-to-balloon and time-to-needle were independently extracted by two researchers. Bayesian statistical methods were used to synthesise evidence despite differences between reported follow-up times and outcomes. Outcomes are presented as absolute probabilities of specific events and odds ratios (ORs; with 95% credible intervals (CrI)) as a function of the additional time delay associated with angioplasty.
Results: 22 studies were included in the meta-analysis, with 3760 and 3758 patients randomised to primary angioplasty and thrombolysis, respectively. The mean (SE) angioplasty-related time delay (over and above time to thrombolysis) was 54.3 (2.2) minutes. For this delay, mean event probabilities were lower for primary angioplasty for all outcomes. Mortality within 1 month was 4.5% after angioplasty and 6.4% after thrombolysis (OR = 0.68 (95% CrI 0.46 to 1.01)). For non-fatal reinfarction, OR = 0.32 (95% CrI 0.20 to 0.51); for non-fatal stroke OR = 0.24 (95% CrI 0.11 to 0.50). For all outcomes, the benefit of angioplasty decreased with longer delay from initiation.
Conclusions: The benefit of primary angioplasty, over thrombolysis, depends on the former’s additional time delay. For delays of 30–90 minutes, angioplasty is superior for 1-month fatal and non-fatal outcomes. For delays of around 90 minutes thrombolysis may be the preferred option as assessed by 6-month mortality; there is considerable uncertainty for longer time delays.
Wednesday, September 19, 2007
ESC Congress - News - 2007 - Plaque erosion: an underestimated mechanism of vulnerable plaque.
Plaque erosion: an underestimated mechanism of vulnerable plaque.
Dr. A LafontParis, FranceVice-Chairman of the ESC working group on Interventional Cardiology and Coronary Pathophysiology
Vulnerable plaque has been classically related to plaque rupture, yet autopsy studies have detected that plaque erosion (i.e., endothelial abrasion) was detected in 25-40% of patients with sudden coronary death in the absence of plaque rupture. This finding is worrisome since there are neither diagnostic nor therapeutic strategies targeted against plaque erosion. Moreover, it appears that plaque erosion represents an entity which is distinct from plaque rupture.
Major improvements have been made to try to understand the mechanism(s) which may lead to acute coronary occlusion (1-4). Initially, plaque rupture was defined as the mechanism responsible for the evolution from vulnerable plaque to acute occlusion. Although plaque rupture remains a major cause of plaque complications, other mechanisms have emerged, i.e., plaque erosion, and much less frequently, calcified nodules protruding in the artery lumen (5-7). The fact that coronary thrombosis may occur without plaque rupture is a revolution that needs to be taken into account in the definition of vulnerability.
Recently, the Becker group studied the histology of 11 patients less than 35 years of age who presented sudden cardiac death (
This shows that thrombus formation occurred at least several weeks prior to death in the case of plaque erosion (89%) whereas the thrombus was fresh in the two cases of plaque rupture at the culprit plaque level. This study is particularly interesting because of the profile of the population at risk which is characterized by its very young age (30.9+/-4): indeed, this population had distinct features which are in contrast with the population at risk of plaque rupture. These very young patients with plaque erosion were most frequently smokers (44%) and female (44%), high cholesterol being present in only 11% of the patients. Moreover, this study confirms the work of the Virmani group: in a young population, plaque erosion is the principal lesion responsible for sudden coronary death. This clearly defines plaque erosion as an entity which may be independent of plaque rupture. There is a need to define new strategies for the detection and treatment of plaque erosion. Indeed, there is a lack of experimental models, as well as human biological markers, or even in vivo imaging techniques able to detect it. Eventually, more care should be paid to this population at risk whose clinical symptoms may not receive sufficient attention in emergency units.
1. *Davies MJ, Thomas A. A thrombosis and acute coronary-artery lesions in sudden cardiac ischemic death. N Eng J Med, 1984; 310: 1137-40.
2. Lafont A, Libby P. The smooth muscle cell: sinner or saint in restenosis and the acute coronary syndromes? J Am Coll Cardiol. 1998 ;32(1):283-5
3. *Libby P. Molecular bases of the acute coronary syndromes. Circulation. 1995 1;91(11):2844-50
4. *Falk E. Why do plaques rupture? Circulation. 1992 ;86(6 Supp
5. *Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000 May;20(5):1262-75.
6. *Burke AP, Farb A, Malcom GT, Liang YH, Smialek J, Virmani R. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. N Engl J Med. 1997 1;336(18):1276-82.
7. Kolodgie FD, Narula J, Burke AP, Haider N, Farb A, Hui-Liang Y, Smialek J, Virmani R. Localization of apoptotic macrophages at the site of plaque rupture in sudden coronary death. Am J Pathol. 2000 ;157(4):1259-68.
8. Henriques de Gouveia R, van der Wal AC, van der Loos CM, Becker AE. Sudden unexpected death in young adults. Discrepancies between initiation of acute plaque complications and the onset of acute coronary death. Eur Heart J. 2002;23(18):1433-40.
Dr. A LafontParis, FranceVice-Chairman of the ESC working group on Interventional Cardiology and Coronary Pathophysiology
Vulnerable plaque has been classically related to plaque rupture, yet autopsy studies have detected that plaque erosion (i.e., endothelial abrasion) was detected in 25-40% of patients with sudden coronary death in the absence of plaque rupture. This finding is worrisome since there are neither diagnostic nor therapeutic strategies targeted against plaque erosion. Moreover, it appears that plaque erosion represents an entity which is distinct from plaque rupture.
Major improvements have been made to try to understand the mechanism(s) which may lead to acute coronary occlusion (1-4). Initially, plaque rupture was defined as the mechanism responsible for the evolution from vulnerable plaque to acute occlusion. Although plaque rupture remains a major cause of plaque complications, other mechanisms have emerged, i.e., plaque erosion, and much less frequently, calcified nodules protruding in the artery lumen (5-7). The fact that coronary thrombosis may occur without plaque rupture is a revolution that needs to be taken into account in the definition of vulnerability.
Recently, the Becker group studied the histology of 11 patients less than 35 years of age who presented sudden cardiac death (
This shows that thrombus formation occurred at least several weeks prior to death in the case of plaque erosion (89%) whereas the thrombus was fresh in the two cases of plaque rupture at the culprit plaque level. This study is particularly interesting because of the profile of the population at risk which is characterized by its very young age (30.9+/-4): indeed, this population had distinct features which are in contrast with the population at risk of plaque rupture. These very young patients with plaque erosion were most frequently smokers (44%) and female (44%), high cholesterol being present in only 11% of the patients. Moreover, this study confirms the work of the Virmani group: in a young population, plaque erosion is the principal lesion responsible for sudden coronary death. This clearly defines plaque erosion as an entity which may be independent of plaque rupture. There is a need to define new strategies for the detection and treatment of plaque erosion. Indeed, there is a lack of experimental models, as well as human biological markers, or even in vivo imaging techniques able to detect it. Eventually, more care should be paid to this population at risk whose clinical symptoms may not receive sufficient attention in emergency units.
1. *Davies MJ, Thomas A. A thrombosis and acute coronary-artery lesions in sudden cardiac ischemic death. N Eng J Med, 1984; 310: 1137-40.
2. Lafont A, Libby P. The smooth muscle cell: sinner or saint in restenosis and the acute coronary syndromes? J Am Coll Cardiol. 1998 ;32(1):283-5
3. *Libby P. Molecular bases of the acute coronary syndromes. Circulation. 1995 1;91(11):2844-50
4. *Falk E. Why do plaques rupture? Circulation. 1992 ;86(6 Supp
5. *Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000 May;20(5):1262-75.
6. *Burke AP, Farb A, Malcom GT, Liang YH, Smialek J, Virmani R. Coronary risk factors and plaque morphology in men with coronary disease who died suddenly. N Engl J Med. 1997 1;336(18):1276-82.
7. Kolodgie FD, Narula J, Burke AP, Haider N, Farb A, Hui-Liang Y, Smialek J, Virmani R. Localization of apoptotic macrophages at the site of plaque rupture in sudden coronary death. Am J Pathol. 2000 ;157(4):1259-68.
8. Henriques de Gouveia R, van der Wal AC, van der Loos CM, Becker AE. Sudden unexpected death in young adults. Discrepancies between initiation of acute plaque complications and the onset of acute coronary death. Eur Heart J. 2002;23(18):1433-40.
ESC Congress - News - 2007 - anti-coagulation therapy in venous thrombo-embolism
Intensity and duration of oral anti-coagulation therapy in venous thrombo-embolism
J. F. Lassen and Prof. S.D. Kristensen
Aarhus, Denmark
Member and Vice-chairman and of the working group on Thrombosis
After initial medium-intensity warfarin therapy for 6 months (INR 2.0-3.0), long-term, low-intensity warfarin therapy (INR 1.5-2.0) is superior to placebo in patients with idiopathic venous thrombo-embolism.
Anti-coagulation (AC) therapy with heparins followed by oral vitamin K-antagonists is recommended after deep venous thrombosis (DVT) and pulmonary embolism. The bleeding risk is related to the duration and intensity of AC therapy. A target INR of 2.0-3.0 is as effective as high-intensity AC therapy with target INR of 3.0-4.5 and causes less bleeding (1). This intensity of AC therapy is usually recommended after DVT or pulmonary embolism.
Recommended duration of therapy is: 1) in patients with reversible or time-limited risk factors: 3 months of AC therapy, 2) first episode of idiopathic venous thrombo-embolism: at least 6 months 3) recurrent idiopathic venous thrombo-embolism or long-term risk factors: 12 months or life-long (2). In case persistent DVT and verified on a duplex scan after e.g. 6 months of therapy, one might consider prolonged AC therapy. Initiation of AC therapy with a loading dose is often used. However, this approach does not necessarily bring the therapy more quickly into the therapeutic range.
Recently, Ridker and co-workers assessed the effects of low intensity warfarin (target INR 1.5-2.0) in patients with idiopathic venous thrombo-embolism (3). The 508 patients were all treated with full-dose AC therapy for at least 6 months (median 6.5 month) and then randomised to low-intensity warfarin or placebo and followed for up to 4.3 years (median 2.1 years). In the placebo group, 37 developed recurrent venous thrombo-embolism (7.2 per 100 person-years) as compared with 14 in the low-intensity warfarin group (2.6 per 100 person-year) – a risk reduction of 64% (p<0.001). Major bleeding occurred in two patients in the placebo vs. five patients in the low intensity warfarin group (p=0.25). Low intensity warfarin was associated with a 48% reduction in the composite end point recurrent venous thrombo-embolism, major haemorrhage or death.
Preliminary data from Kearon et al shows that initial low-intensity warfarin (target INR 1.5-1.9) is significantly less effective than conventional-intensity warfarin (target INR 2.0-3.0) (4).
Therefore, it seems appropriate to wait for the publication of more trials. While waiting for such trials initial therapy with target INR 2.0-3.0 for at least 6 months followed by low intensity AC therapy might be an option in some patients. Also, new drugs like oral thrombin inhibitors should be tested in this setting.
1) Hull R, Hirsh J, Gent M et al. Different intensities of oral anti-coagulant therapy in the treatment of deep proximal-vein thrombosis. N Engl J Med 1982; 307: 1676-81.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6755255&dopt=Abstract
2) Hirsh J, Dalen JE, Anderson DR et al. Oral anticoagulants: mechanism of action, clinical effectiveness and optimal therapeutic range. Chest 2001; 119: Suppl:8S-21S.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11157640&dopt=Abstract
3) Ridker PM, Goldhaber SZ, Danielson E et al. Long-term, low-intensity warfarin therapy for the prevention of recurrent venous thrombo-embolism. N Engl J Med 2003; 348: 1425-34.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12601075&dopt=Abstract
4) Kearon C, Ginsberg JS, Kovacs M et al. Low-intensity (INR 1.5-1.9) versus conventional-intensity (INR 2.0-3.0) anticoagulation for extended treatment of unprovoked VTE: a randomized double blind trial. Blood 2002; 100: 150a (abstract).http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12565715&dopt=Abstract
J. F. Lassen and Prof. S.D. Kristensen
Aarhus, Denmark
Member and Vice-chairman and of the working group on Thrombosis
After initial medium-intensity warfarin therapy for 6 months (INR 2.0-3.0), long-term, low-intensity warfarin therapy (INR 1.5-2.0) is superior to placebo in patients with idiopathic venous thrombo-embolism.
Anti-coagulation (AC) therapy with heparins followed by oral vitamin K-antagonists is recommended after deep venous thrombosis (DVT) and pulmonary embolism. The bleeding risk is related to the duration and intensity of AC therapy. A target INR of 2.0-3.0 is as effective as high-intensity AC therapy with target INR of 3.0-4.5 and causes less bleeding (1). This intensity of AC therapy is usually recommended after DVT or pulmonary embolism.
Recommended duration of therapy is: 1) in patients with reversible or time-limited risk factors: 3 months of AC therapy, 2) first episode of idiopathic venous thrombo-embolism: at least 6 months 3) recurrent idiopathic venous thrombo-embolism or long-term risk factors: 12 months or life-long (2). In case persistent DVT and verified on a duplex scan after e.g. 6 months of therapy, one might consider prolonged AC therapy. Initiation of AC therapy with a loading dose is often used. However, this approach does not necessarily bring the therapy more quickly into the therapeutic range.
Recently, Ridker and co-workers assessed the effects of low intensity warfarin (target INR 1.5-2.0) in patients with idiopathic venous thrombo-embolism (3). The 508 patients were all treated with full-dose AC therapy for at least 6 months (median 6.5 month) and then randomised to low-intensity warfarin or placebo and followed for up to 4.3 years (median 2.1 years). In the placebo group, 37 developed recurrent venous thrombo-embolism (7.2 per 100 person-years) as compared with 14 in the low-intensity warfarin group (2.6 per 100 person-year) – a risk reduction of 64% (p<0.001). Major bleeding occurred in two patients in the placebo vs. five patients in the low intensity warfarin group (p=0.25). Low intensity warfarin was associated with a 48% reduction in the composite end point recurrent venous thrombo-embolism, major haemorrhage or death.
Preliminary data from Kearon et al shows that initial low-intensity warfarin (target INR 1.5-1.9) is significantly less effective than conventional-intensity warfarin (target INR 2.0-3.0) (4).
Therefore, it seems appropriate to wait for the publication of more trials. While waiting for such trials initial therapy with target INR 2.0-3.0 for at least 6 months followed by low intensity AC therapy might be an option in some patients. Also, new drugs like oral thrombin inhibitors should be tested in this setting.
1) Hull R, Hirsh J, Gent M et al. Different intensities of oral anti-coagulant therapy in the treatment of deep proximal-vein thrombosis. N Engl J Med 1982; 307: 1676-81.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6755255&dopt=Abstract
2) Hirsh J, Dalen JE, Anderson DR et al. Oral anticoagulants: mechanism of action, clinical effectiveness and optimal therapeutic range. Chest 2001; 119: Suppl:8S-21S.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11157640&dopt=Abstract
3) Ridker PM, Goldhaber SZ, Danielson E et al. Long-term, low-intensity warfarin therapy for the prevention of recurrent venous thrombo-embolism. N Engl J Med 2003; 348: 1425-34.http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12601075&dopt=Abstract
4) Kearon C, Ginsberg JS, Kovacs M et al. Low-intensity (INR 1.5-1.9) versus conventional-intensity (INR 2.0-3.0) anticoagulation for extended treatment of unprovoked VTE: a randomized double blind trial. Blood 2002; 100: 150a (abstract).http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12565715&dopt=Abstract
ESC Congress - News - 2007 - CORONARY REVASCULARIZATION
Burning questions in coronary revascularisation Symposium
In this interesting session the role of surgical revascularisation was discussed. The number of CABG procedures has considerably decreased in the last ten years, with a concomitant increase in PCI procedures.
Despite this trend, surgical revascularisation still plays an important role. Looking accurately in the results reported by the randomised trials comparing CABG versus PCI in multivessel disease, most of the enrolled patients have two vessel disease and normal ejection fraction. This selection bias eliminates or reduces the group of patients with triple vessel disease, left main stenosis or low ejection fraction, who benefit most from CABG.
On the basis of the data from the literature, surgical revascularisation still remains the treatment of choice for patients with triple vessel disease, left main stenosis and low ejection fraction.
The advantage of surgical revascularisation is more pronounced in patients treated by complete arterial revascularisation. The results reported in the literature for different type of grafts show that the use of bilateral internal mammary artery have an important impact on long term survival and freedom from reoperation.
The use of technical solutions like the Y graft offer the possibility to revascularise all the coronaries with the use of two mammary grafts, giving patients the best option for a durable operation. The role of complete versus incomplete myocardial revascularisation has been analysed, and data currently available are inconclusive on this topic. New data are necessary to answer to this question.
Finally an accurate analysis was done about the role of previous PCI on the results of patients treated by CABG. This revision of the literature clearly shows that patients previously treated by PCI have higher mortality and worse long term results after CABG. The reason of this finding is not clear but is probably related to the activation of an inflammatory process by the PCI procedure.
ESC Congress - News - 2007 - HYPERTENSION
Hypertension: New insights and implications for management
Prof. G. Y. H. LipBirmingham, United KingdomNucleus member of the Working Group on Hypertension and the Heart
There is a dose-response relationship between an increasing blood pressure and an increasing risk of stroke and coronary heart disease . The treatment of hypertension results in a 30-35% reduction in strokes and a 20% reduction in heart attacks . It is therefore crucial to detect, treat and control high blood pressure, and if management of hypertension is inadequate or inappropriate this could even be considered as negligent. It is no longer a question of ‘do we treat’ hypertension, but more a question of ‘who to treat’ and ‘how to treat’ hypertension.
Who to treat?
Hypertension can be defined pragmatically as that level of blood pressure above which the use of antihypertensive treatment does more good than harm. Indeed, hypertensive patients do not make up a homogeneous population and hypertension per se is not a condition that can be regarded in isolation. All major hypertension management guidelines recommend the use of risk stratification, in the context of a patient’s total cardiovascular risk , . Indeed, risk factors such as diabetes mellitus, hyperlipidaemia, smoking, age and gender need to be taken into account, as these risk factors are cumulative to the overall cardiovascular risk burden. All risk factors must therefore be managed in a holistic manner, in a ‘package of care’ that includes treating high risk groups, with non-pharmacological and pharmacological measures.
How to treat?
Until recently, the thiazide diuretics and beta-blockers have been regarded as the mainstay of hypertension treatment. However, there is an increasing recognition that beta-blockers are ineffective as first-line agents in the elderly and in Afro-Caribbean patients - whether beta-blockers are even effective in reducing endpoints in hypertension, especially in the elderly has been extensively debated , . On the other hand, thiazides are cheap and effective agents, but the lowest possible dose should be used, as there is no dose-response antihypertensive effect, whilst higher doses of thiazides are associated with increasing metabolic effects .
Many randomised controlled trials have also compared the newer antihypertensive agents, such as the alpha blockers, calcium antagonists, ACE inhibitors and angiotensin receptor antagonists to the ‘old’ drugs, thiazides and beta-blockers. The largest was the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) in ‘high-risk’ hypertensive patients who were initially randomised to a diuretic (chlorthalidone) versus each of three ‘alternative’ (newer) antihypertensive drugs: an alpha-adrenergic blocker (doxazosin), an ACE-inhibitor (lisinopril), and a CCB (amlodipine) . The doxazosin arm was stopped early due to an excess of cardiovascular events, especially heart failure. For the thiazide, ACE inhibitor, and dihydropyridine calcium antagonist arms of the study, the incidence of the primary endpoints of fatal coronary heart disease (CHD) and non-fatal myocardial infarction (MI), was essentially identical, although there was an apparent excess of stroke endpoints in the lisinopril arm, and more heart failure with lisinopril and amlodipine compared to thiazide. The merits (or otherwise!) of the ALLHAT trial have recently been extensively discussed.
Recent recognition of the value of lipid lowering therapy in hypertension is provided by the MRC/BHF Heart Protection Study (HPS) , which studied patients at ‘high risk’ of death due to coronary heart disease (41% were hypertensive), where the use of simvastatin 40mg/day reduced all cause mortality (12.9% versus placebo, 14.7%). There were also significant decreases in non fatal myocardial infarctions, fatal or non fatal strokes and coronary or non coronary revascularisations. These data from the HPS were complemented by the lipid-lowering arm data from the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) study . In the latter, atorvastatin 10mg daily was associated with a significant reduction in the primary end point of fatal myocardial infarction and nonfatal coronary heart disease events (by 36%), together with significant reductions in the secondary end points of stroke (by 27%), all cardiovascular events and procedures (by 21%), and total coronary events (by 29%). Risk reductions in CHD events in both HPS and ASCOT were unrelated to baseline cholesterol levels and were consistent across the whole range of cholesterol. The merits and issues with regard to using lipid lowering in hypertension have recently been discussed .
Implications for management
The recent trials have proven the value of a holistic approach to cardiovascular risk management in hypertensive patients with additional risk factors, by the addition of statin therapy, irrespective of serum cholesterol level. It is clear that we have to move away from treating individual risk factors such as hypertension or hyperlipidaemia in isolation, and all risk factors need a complete, comprehensive ‘package of care’ of cardiovascular risk management.
The data from ALLHAT also would advise some degree of caution with the use of alpha-blockers in hypertensives at risk of heart failure. Most trials also confirm the need for combination therapy to achieve adequate blood pressure control – generally <140/85mmHg in non-diabetics and <130/80mmHg in diabetes – and as an average, half of all hypertensives will require two or more drugs, whilst a third will require three or more drugs to achieve adequate blood pressure control. It therefore makes sense to use antihypertensive agents that are synergistic in action to each other, as well as minimising adverse effects (if any) from each other.
Prof. G. Y. H. LipBirmingham, United KingdomNucleus member of the Working Group on Hypertension and the Heart
There is a dose-response relationship between an increasing blood pressure and an increasing risk of stroke and coronary heart disease . The treatment of hypertension results in a 30-35% reduction in strokes and a 20% reduction in heart attacks . It is therefore crucial to detect, treat and control high blood pressure, and if management of hypertension is inadequate or inappropriate this could even be considered as negligent. It is no longer a question of ‘do we treat’ hypertension, but more a question of ‘who to treat’ and ‘how to treat’ hypertension.
Who to treat?
Hypertension can be defined pragmatically as that level of blood pressure above which the use of antihypertensive treatment does more good than harm. Indeed, hypertensive patients do not make up a homogeneous population and hypertension per se is not a condition that can be regarded in isolation. All major hypertension management guidelines recommend the use of risk stratification, in the context of a patient’s total cardiovascular risk , . Indeed, risk factors such as diabetes mellitus, hyperlipidaemia, smoking, age and gender need to be taken into account, as these risk factors are cumulative to the overall cardiovascular risk burden. All risk factors must therefore be managed in a holistic manner, in a ‘package of care’ that includes treating high risk groups, with non-pharmacological and pharmacological measures.
How to treat?
Until recently, the thiazide diuretics and beta-blockers have been regarded as the mainstay of hypertension treatment. However, there is an increasing recognition that beta-blockers are ineffective as first-line agents in the elderly and in Afro-Caribbean patients - whether beta-blockers are even effective in reducing endpoints in hypertension, especially in the elderly has been extensively debated , . On the other hand, thiazides are cheap and effective agents, but the lowest possible dose should be used, as there is no dose-response antihypertensive effect, whilst higher doses of thiazides are associated with increasing metabolic effects .
Many randomised controlled trials have also compared the newer antihypertensive agents, such as the alpha blockers, calcium antagonists, ACE inhibitors and angiotensin receptor antagonists to the ‘old’ drugs, thiazides and beta-blockers. The largest was the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) in ‘high-risk’ hypertensive patients who were initially randomised to a diuretic (chlorthalidone) versus each of three ‘alternative’ (newer) antihypertensive drugs: an alpha-adrenergic blocker (doxazosin), an ACE-inhibitor (lisinopril), and a CCB (amlodipine) . The doxazosin arm was stopped early due to an excess of cardiovascular events, especially heart failure. For the thiazide, ACE inhibitor, and dihydropyridine calcium antagonist arms of the study, the incidence of the primary endpoints of fatal coronary heart disease (CHD) and non-fatal myocardial infarction (MI), was essentially identical, although there was an apparent excess of stroke endpoints in the lisinopril arm, and more heart failure with lisinopril and amlodipine compared to thiazide. The merits (or otherwise!) of the ALLHAT trial have recently been extensively discussed.
Recent recognition of the value of lipid lowering therapy in hypertension is provided by the MRC/BHF Heart Protection Study (HPS) , which studied patients at ‘high risk’ of death due to coronary heart disease (41% were hypertensive), where the use of simvastatin 40mg/day reduced all cause mortality (12.9% versus placebo, 14.7%). There were also significant decreases in non fatal myocardial infarctions, fatal or non fatal strokes and coronary or non coronary revascularisations. These data from the HPS were complemented by the lipid-lowering arm data from the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) study . In the latter, atorvastatin 10mg daily was associated with a significant reduction in the primary end point of fatal myocardial infarction and nonfatal coronary heart disease events (by 36%), together with significant reductions in the secondary end points of stroke (by 27%), all cardiovascular events and procedures (by 21%), and total coronary events (by 29%). Risk reductions in CHD events in both HPS and ASCOT were unrelated to baseline cholesterol levels and were consistent across the whole range of cholesterol. The merits and issues with regard to using lipid lowering in hypertension have recently been discussed .
Implications for management
The recent trials have proven the value of a holistic approach to cardiovascular risk management in hypertensive patients with additional risk factors, by the addition of statin therapy, irrespective of serum cholesterol level. It is clear that we have to move away from treating individual risk factors such as hypertension or hyperlipidaemia in isolation, and all risk factors need a complete, comprehensive ‘package of care’ of cardiovascular risk management.
The data from ALLHAT also would advise some degree of caution with the use of alpha-blockers in hypertensives at risk of heart failure. Most trials also confirm the need for combination therapy to achieve adequate blood pressure control – generally <140/85mmHg in non-diabetics and <130/80mmHg in diabetes – and as an average, half of all hypertensives will require two or more drugs, whilst a third will require three or more drugs to achieve adequate blood pressure control. It therefore makes sense to use antihypertensive agents that are synergistic in action to each other, as well as minimising adverse effects (if any) from each other.
Atrial Fibrillation: Rhythm or rate control
Atrial Fibrillation: Rhythm or rate control
Prof. J.Y. Le HeuzeyParis, FranceNucleus member of the Working Group on Arrythmias
Therapy for AF is often directed toward the maintenance of sinus rhythm obtained after a cardioversion or by antiarrhythmic agents. The objectives of this rhythm control strategy include relief of symptoms, better exercise tolerance, prevention of embolism and avoidance of cardiomyopathy which together lead to a better quality of life and better survival.
An accepted strategy is to control the ventricular response rate of AF with the depression of conduction across the AV node by pharmacological agents or ablation of the atrioventricular junction and pacemaker implantation. The rationale for using a rate-control strategy is that most symptoms in AF may be caused by an irregular ventricular rate which may be treated by rate-control drugs. Additionally, effective rate-control drugs may prevent tachycardia-induced cardiomyopathy and the adverse effects of drugs.
Strategy trials
Three recent randomized trials compared rhythm and rate control in atrial fibrillation.
In the PIAF trial (1), the two strategies yielded similar clinical results regarding symptoms but exercise tolerance was better in the rhythm-control group.
In the AFFIRM trial (2), 4060 patients with recurrent AF were randomized to one of the two strategies. In this study, there was no survival benefits with the rhythm-control strategy (mortality at 5 years, 23.8% versus 21.3% in the rhythm and rate control group, respectively, p=0.08). The number of hospitalizations [1374 (80.1%) versus 1220 (73.0%), p <0.001] and the proportion of adverse drug effects were greater in the rhythm-control group, especially prolongation of the QT interval, torsade de pointes and bradycardia.
The third randomized trial, Rate control vs electrical cardioversion for persistent atrial fibrillation, RACE (3), compared the two strategies in 522 patients with recurrent persistent AF. The primary end-point was a composite of death from cardiovascular causes, heart failure, bleeding, thrombo-embolic complications, implantation of a pacemaker, and severe adverse effects of drugs.
The primary end-point occurred in 17.2% of the patients in the rate-control group and in 22.6% of the patients in the rhythm-control group which represents a trend in favour of rate control.
These studies show that rate-control is not inferior to rhythm-control strategy and may be an appropriate first choice therapy in patients with recurrent AF. It must be emphasized that most of these studies included patients with structural heart diseases and risk factors of recurrence and thrombo-embolism. Their results cannot be extrapolated to other patients, especially the young patients without underlying cardiopathy.
Management strategies
Patients without symptoms who have experienced at least one cardioversion to restore sinus rhythm can remain in AF with rate-control therapy and prevention of thrombo-embolism.
For patients with disabling symptoms during AF, a drug limiting cardiac rate during the episode can be used. An anti-arrhythmic drug therapy is generally used to maintain the sinus rhythm after the termination of AF.
For patients without heart disease, the first-line therapy includes one of the following drugs : flecainide, propafanone, or sotalol. Second-line therapy includes amiodarone or dofetilide. Third-line therapy includes disopyramide, procainamide, quinidine and non-pharmacological options.
For adrenergic AF, beta-blockers and sotalol are the initial drugs of choice.
For patients experiencing heart failure, solely amiodarone can be used.
For patients with coronary artery disease, sotalol represents the initial drug. In case of recurrence, amiodarone can be used.
In case of hypertension, the choice of antiarrhythmic drugs depends on the importance of left ventricular hypertrophy (LVH). If LVH is <>
Antithrombotic strategies
It has been demonstrated for many years that anticoagulants might be used in permanent atrial fibrillation (AFASAK, BAATAF, SPAF, CAFA, SPINAF…). The AFFIRM trial has clearly demonstrated that this anticoagulation might be pursued in patients for whom the rhythm control strategy is chosen. Even if the sinus rhythm is restored, patients with high risk of thrombo-embolic events must be continuously treated by anticoagulants (age > 65 years, history of stroke or TIA, diabetes, left atrial enlargement, congestive heart failure…).
Conclusion
Atrial fibrillation is characterized by frequent recurrences. Different strategies could be used to maintain sinus rhythm. Rate control is not inferior to rhythm control for the prevention of morbidity and mortality and may be an appropriate strategy in patients with numerous risk factors of recurrence and/or asymptomatic AF episodes. In other patients, especially young patients without structural heart disease and with symptomatic episodes of AF, rhythm control remains the first strategy.
Prof. J.Y. Le HeuzeyParis, FranceNucleus member of the Working Group on Arrythmias
Therapy for AF is often directed toward the maintenance of sinus rhythm obtained after a cardioversion or by antiarrhythmic agents. The objectives of this rhythm control strategy include relief of symptoms, better exercise tolerance, prevention of embolism and avoidance of cardiomyopathy which together lead to a better quality of life and better survival.
An accepted strategy is to control the ventricular response rate of AF with the depression of conduction across the AV node by pharmacological agents or ablation of the atrioventricular junction and pacemaker implantation. The rationale for using a rate-control strategy is that most symptoms in AF may be caused by an irregular ventricular rate which may be treated by rate-control drugs. Additionally, effective rate-control drugs may prevent tachycardia-induced cardiomyopathy and the adverse effects of drugs.
Strategy trials
Three recent randomized trials compared rhythm and rate control in atrial fibrillation.
In the PIAF trial (1), the two strategies yielded similar clinical results regarding symptoms but exercise tolerance was better in the rhythm-control group.
In the AFFIRM trial (2), 4060 patients with recurrent AF were randomized to one of the two strategies. In this study, there was no survival benefits with the rhythm-control strategy (mortality at 5 years, 23.8% versus 21.3% in the rhythm and rate control group, respectively, p=0.08). The number of hospitalizations [1374 (80.1%) versus 1220 (73.0%), p <0.001] and the proportion of adverse drug effects were greater in the rhythm-control group, especially prolongation of the QT interval, torsade de pointes and bradycardia.
The third randomized trial, Rate control vs electrical cardioversion for persistent atrial fibrillation, RACE (3), compared the two strategies in 522 patients with recurrent persistent AF. The primary end-point was a composite of death from cardiovascular causes, heart failure, bleeding, thrombo-embolic complications, implantation of a pacemaker, and severe adverse effects of drugs.
The primary end-point occurred in 17.2% of the patients in the rate-control group and in 22.6% of the patients in the rhythm-control group which represents a trend in favour of rate control.
These studies show that rate-control is not inferior to rhythm-control strategy and may be an appropriate first choice therapy in patients with recurrent AF. It must be emphasized that most of these studies included patients with structural heart diseases and risk factors of recurrence and thrombo-embolism. Their results cannot be extrapolated to other patients, especially the young patients without underlying cardiopathy.
Management strategies
Patients without symptoms who have experienced at least one cardioversion to restore sinus rhythm can remain in AF with rate-control therapy and prevention of thrombo-embolism.
For patients with disabling symptoms during AF, a drug limiting cardiac rate during the episode can be used. An anti-arrhythmic drug therapy is generally used to maintain the sinus rhythm after the termination of AF.
For patients without heart disease, the first-line therapy includes one of the following drugs : flecainide, propafanone, or sotalol. Second-line therapy includes amiodarone or dofetilide. Third-line therapy includes disopyramide, procainamide, quinidine and non-pharmacological options.
For adrenergic AF, beta-blockers and sotalol are the initial drugs of choice.
For patients experiencing heart failure, solely amiodarone can be used.
For patients with coronary artery disease, sotalol represents the initial drug. In case of recurrence, amiodarone can be used.
In case of hypertension, the choice of antiarrhythmic drugs depends on the importance of left ventricular hypertrophy (LVH). If LVH is <>
Antithrombotic strategies
It has been demonstrated for many years that anticoagulants might be used in permanent atrial fibrillation (AFASAK, BAATAF, SPAF, CAFA, SPINAF…). The AFFIRM trial has clearly demonstrated that this anticoagulation might be pursued in patients for whom the rhythm control strategy is chosen. Even if the sinus rhythm is restored, patients with high risk of thrombo-embolic events must be continuously treated by anticoagulants (age > 65 years, history of stroke or TIA, diabetes, left atrial enlargement, congestive heart failure…).
Conclusion
Atrial fibrillation is characterized by frequent recurrences. Different strategies could be used to maintain sinus rhythm. Rate control is not inferior to rhythm control for the prevention of morbidity and mortality and may be an appropriate strategy in patients with numerous risk factors of recurrence and/or asymptomatic AF episodes. In other patients, especially young patients without structural heart disease and with symptomatic episodes of AF, rhythm control remains the first strategy.
ESC Congress - News - 2007 - ENDOCARDITIS
ESC Congress - 2007
Date : 3 September 2007
Reported by : Boudoulas, Harisios (Greece)
Challenges in endocarditis Symposium
Infective endocarditis is a serious and often fatal disease with multiple cardiac and extracardiac manifestations. As a general rule, endocarditis affects patients with underlying valvular heart disease (especially prosthetic valves) and congenital heart disease. Patients with intracardiac catheters, e.g. pacemakers, defibrillators, are also prone to endocarditis. The disease is common in IV drug abusers and patients with compromised immune systems. Criteria and guidelines have been established for the diagnosis and management of endocarditis; these guidelines however cannot replace clinilca judgement, clinical experience and common sense. Endocarditis should be suspected in any patient with unusual symptoms, fever, “Not feeling well”, especially if a heart murmur is present.
Patients with endocarditis or suspected endocarditis should be managed in a large medical center where a cardiologist, a cardiac surgeon, and an infectious disease physician should be involved in the patient’s care. Blood cultures should be obtained in all patients, and therapy with antibiotics should be based on the isolated microorganism and sensitivity tests. It should be emphasised that up to 30% of blood cultures could be negative if they are obtained after the initiation of antibiotic therapy.
A transoesophageal echocardiogram (TEE) should be performed in all patients with endocarditis. Size and precise location of vegetations, aortic root abscess (10-30% of patients) can be only defined with TEE. Surgery, if it is indicated (heart failure, embolic events, large size vegetations) should be performed without delay.
Extracardiac manifestations of endocarditis, such as skin lesions, neurologic phenomena, renal and other organ involvement are not uncommon. Clinical manifestations of endocarditis in developing countries may be quite different. As a general rule, the diagnosis is delayed (more than a month) and the presence of other infectious diseases, e.g. malaria, may alter the clinical picture and the course of the disease.
Patients with valvular heart disease, congenital heart disease and intracardiac catheters should maintain the best oral hygiene to prevent endocarditis.
Conclusions:
Endocarditis is a serious and often fatal disease with multiple cardiac and extracardiac manifestations. The management of endocarditis should be based primarily on good clinical judgement and common sense. Patients with endocarditis should be managed in a large medical center. A cardiologist, cardiac surgeon and infectious diseases specialist should be involved in the patient’s care. Blood cultures should be obtained in all patients with suspected endocarditis prior to therapy with antibiotics. Optimal oral hygiene can help prevent the development of infective endocarditis
Date : 3 September 2007
Reported by : Boudoulas, Harisios (Greece)
Challenges in endocarditis Symposium
Infective endocarditis is a serious and often fatal disease with multiple cardiac and extracardiac manifestations. As a general rule, endocarditis affects patients with underlying valvular heart disease (especially prosthetic valves) and congenital heart disease. Patients with intracardiac catheters, e.g. pacemakers, defibrillators, are also prone to endocarditis. The disease is common in IV drug abusers and patients with compromised immune systems. Criteria and guidelines have been established for the diagnosis and management of endocarditis; these guidelines however cannot replace clinilca judgement, clinical experience and common sense. Endocarditis should be suspected in any patient with unusual symptoms, fever, “Not feeling well”, especially if a heart murmur is present.
Patients with endocarditis or suspected endocarditis should be managed in a large medical center where a cardiologist, a cardiac surgeon, and an infectious disease physician should be involved in the patient’s care. Blood cultures should be obtained in all patients, and therapy with antibiotics should be based on the isolated microorganism and sensitivity tests. It should be emphasised that up to 30% of blood cultures could be negative if they are obtained after the initiation of antibiotic therapy.
A transoesophageal echocardiogram (TEE) should be performed in all patients with endocarditis. Size and precise location of vegetations, aortic root abscess (10-30% of patients) can be only defined with TEE. Surgery, if it is indicated (heart failure, embolic events, large size vegetations) should be performed without delay.
Extracardiac manifestations of endocarditis, such as skin lesions, neurologic phenomena, renal and other organ involvement are not uncommon. Clinical manifestations of endocarditis in developing countries may be quite different. As a general rule, the diagnosis is delayed (more than a month) and the presence of other infectious diseases, e.g. malaria, may alter the clinical picture and the course of the disease.
Patients with valvular heart disease, congenital heart disease and intracardiac catheters should maintain the best oral hygiene to prevent endocarditis.
Conclusions:
Endocarditis is a serious and often fatal disease with multiple cardiac and extracardiac manifestations. The management of endocarditis should be based primarily on good clinical judgement and common sense. Patients with endocarditis should be managed in a large medical center. A cardiologist, cardiac surgeon and infectious diseases specialist should be involved in the patient’s care. Blood cultures should be obtained in all patients with suspected endocarditis prior to therapy with antibiotics. Optimal oral hygiene can help prevent the development of infective endocarditis
Frequent Nocturnal Hemodialysis Reduces LV Mass
Frequent Nocturnal Hemodialysis Reduces LV Mass
Patients undergoing hemodialysis 6 nights a week show a greater reduction in left ventricular mass than those on a conventional treatment schedule.
Writing in JAMA, Canadian researchers report randomizing some 50 patients to a schedule of either 6 nights a week of home hemodialysis or conventional 3-days-a-week treatment. After 6 months, those on frequent nocturnal dialysis showed a nearly 18-g decrease in left ventricular mass, while those on conventional treatment showed a 1.8-g increase.
An editorialist comments that proving a survival benefit will be elusive, given the difficulty in recruiting patients, but he says the study succeeded in "clearly demonstrating reduced [left ventricular hypertrophy] with nocturnal hemodialysis."
JAMA article (Free)
JAMA editorial (Subscription required)
Patients undergoing hemodialysis 6 nights a week show a greater reduction in left ventricular mass than those on a conventional treatment schedule.
Writing in JAMA, Canadian researchers report randomizing some 50 patients to a schedule of either 6 nights a week of home hemodialysis or conventional 3-days-a-week treatment. After 6 months, those on frequent nocturnal dialysis showed a nearly 18-g decrease in left ventricular mass, while those on conventional treatment showed a 1.8-g increase.
An editorialist comments that proving a survival benefit will be elusive, given the difficulty in recruiting patients, but he says the study succeeded in "clearly demonstrating reduced [left ventricular hypertrophy] with nocturnal hemodialysis."
JAMA article (Free)
JAMA editorial (Subscription required)
Tuesday, September 18, 2007
Prescribing Amiodarone
Prescribing Amiodarone
An Evidence-Based Review of Clinical Indications
Patricia Vassallo, MD; Richard G. Trohman, MD
JAMA. 2007;298:1312-1322.
Context Although amiodarone is approved by the US Food and Drug Administration only for refractory ventricular arrhythmias, it is one of the most frequently prescribed antiarrhythmic medications in the United States.
Objective To evaluate and synthesize evidence regarding optimal use of amiodarone for various arrhythmias.
Evidence Acquisition Systematic search of MEDLINE to identify peer-reviewed clinical trials, randomized controlled trials, meta-analyses, and other studies with clinical pertinence. The search was limited to human-participant, English-language reports published between 1970 and 2007. Amiodarone was searched using the terms adverse effects, atrial fibrillation, atrial flutter, congestive heart failure, electrical storm, hypertrophic cardiomyopathy, implantable cardioverter-defibrillator, surgery, ventricular arrhythmia, ventricular fibrillation, and Wolff-Parkinson-White. Bibliographies of identified articles and guidelines from official societies were reviewed for additional references. Ninety-two identified studies met inclusion criteria and were included in the review.
Evidence Synthesis Amiodarone may have clinical value in patients with left ventricular dysfunction and heart failure as first-line treatment for atrial fibrillation, though other agents are available. Amiodarone is useful in acute management of sustained ventricular tachyarrythmias, regardless of hemodynamic stability. The only role for prophylactic amiodarone is in the perioperative period of cardiac surgery. Amiodarone may be effective as an adjunct to implantable cardioverter-defibrillator therapy to reduce number of shocks. However, amiodarone has a number of serious adverse effects, including corneal microdeposits (>90%), optic neuropathy/neuritis (1%-2%), blue-gray skin discoloration (4%-9%), photosensitivity (25%-75%), hypothyroidism (6%), hyperthyroidism (0.9%-2%), pulmonary toxicity (1%-17%), peripheral neuropathy (0.3% annually), and hepatotoxicity (elevated enzyme levels, 15%-30%; hepatitis and cirrhosis, <3% [0.6% annually]).
Conclusion Amiodarone should be used with close follow-up in patients who are likely to derive the most benefit, namely those with atrial fibrillation and left ventricular dysfunction, those with acute sustained ventricular arrhythmias, those about to undergo cardiac surgery, and those with implantable cardioverter-defibrillators and symptomatic shocks.
Author Affiliations: Department of Medicine, Section of Cardiology, Electrophysiology, Arrhythmia, and Pacemaker Service, Rush University Medical Center, Chicago, Illinois.
An Evidence-Based Review of Clinical Indications
Patricia Vassallo, MD; Richard G. Trohman, MD
JAMA. 2007;298:1312-1322.
Context Although amiodarone is approved by the US Food and Drug Administration only for refractory ventricular arrhythmias, it is one of the most frequently prescribed antiarrhythmic medications in the United States.
Objective To evaluate and synthesize evidence regarding optimal use of amiodarone for various arrhythmias.
Evidence Acquisition Systematic search of MEDLINE to identify peer-reviewed clinical trials, randomized controlled trials, meta-analyses, and other studies with clinical pertinence. The search was limited to human-participant, English-language reports published between 1970 and 2007. Amiodarone was searched using the terms adverse effects, atrial fibrillation, atrial flutter, congestive heart failure, electrical storm, hypertrophic cardiomyopathy, implantable cardioverter-defibrillator, surgery, ventricular arrhythmia, ventricular fibrillation, and Wolff-Parkinson-White. Bibliographies of identified articles and guidelines from official societies were reviewed for additional references. Ninety-two identified studies met inclusion criteria and were included in the review.
Evidence Synthesis Amiodarone may have clinical value in patients with left ventricular dysfunction and heart failure as first-line treatment for atrial fibrillation, though other agents are available. Amiodarone is useful in acute management of sustained ventricular tachyarrythmias, regardless of hemodynamic stability. The only role for prophylactic amiodarone is in the perioperative period of cardiac surgery. Amiodarone may be effective as an adjunct to implantable cardioverter-defibrillator therapy to reduce number of shocks. However, amiodarone has a number of serious adverse effects, including corneal microdeposits (>90%), optic neuropathy/neuritis (1%-2%), blue-gray skin discoloration (4%-9%), photosensitivity (25%-75%), hypothyroidism (6%), hyperthyroidism (0.9%-2%), pulmonary toxicity (1%-17%), peripheral neuropathy (0.3% annually), and hepatotoxicity (elevated enzyme levels, 15%-30%; hepatitis and cirrhosis, <3% [0.6% annually]).
Conclusion Amiodarone should be used with close follow-up in patients who are likely to derive the most benefit, namely those with atrial fibrillation and left ventricular dysfunction, those with acute sustained ventricular arrhythmias, those about to undergo cardiac surgery, and those with implantable cardioverter-defibrillators and symptomatic shocks.
Author Affiliations: Department of Medicine, Section of Cardiology, Electrophysiology, Arrhythmia, and Pacemaker Service, Rush University Medical Center, Chicago, Illinois.
Screening, diagnosis & monitoring of depression/distress in CHF patients
Screening, diagnosis & monitoring of depression/distress in CHF patients
Journal: Heart Failure Reviews
Wednesday, August 01, 2007
Mark W. Ketterer and Walter Knysz
Abstract
Objective and validated measures of depression/distress (anxiety and anger) are available and readily usable at the bedside or in clinic.
Foremost among these is the Patient’s Health Questionnaire—an adaptation of DSM IV criteria for Major Depressive Disorder that permits administration and scoring by nursing or physician personnel, and quantification of the intensity of depression. A score of 10 or greater indicates a need for evaluation/treatment.
Because of patient denial/minimization/alexithymia, PHQ negatives should undergo further screening by having a spouse or friend complete a depression/distress rating scale.
The only standardized, normed, and validated spouse/friend scale presently available is the Ketterer Stress Symptom Frequency Checklist, which is available by internet.
Journal: Heart Failure Reviews
Wednesday, August 01, 2007
Mark W. Ketterer and Walter Knysz
Abstract
Objective and validated measures of depression/distress (anxiety and anger) are available and readily usable at the bedside or in clinic.
Foremost among these is the Patient’s Health Questionnaire—an adaptation of DSM IV criteria for Major Depressive Disorder that permits administration and scoring by nursing or physician personnel, and quantification of the intensity of depression. A score of 10 or greater indicates a need for evaluation/treatment.
Because of patient denial/minimization/alexithymia, PHQ negatives should undergo further screening by having a spouse or friend complete a depression/distress rating scale.
The only standardized, normed, and validated spouse/friend scale presently available is the Ketterer Stress Symptom Frequency Checklist, which is available by internet.
Cardiovascular Effects of Haloperidol
FDA Issues Warning on Cardiovascular Effects of Haloperidol
The FDA is warning clinicians about the risks for cardiovascular side effects and sudden death from haloperidol.
The agency says there are "at least 28 case reports" of QT prolongation and Torsades de Pointes in the literature associated with the antipsychotic drug, "especially when given intravenously"; some cases have been fatal. A 2005 postmarketing study conducted for the Italian drug authority, but only recently submitted to the FDA by Johnson & Johnson, found 13 additional cases. The FDA notes that the drug is often used intravenously off-label, especially in intensive care units, to treat severe agitation.
Label warnings will be strengthened, the FDA says, and it recommends ECG monitoring if the drug is used intravenously. The FDA urges particular caution in patients with other QT-prolonging conditions, such as electrolyte imbalance (especially hypokalemia and hypomagnesemia).
FDA alert (Free)
The FDA is warning clinicians about the risks for cardiovascular side effects and sudden death from haloperidol.
The agency says there are "at least 28 case reports" of QT prolongation and Torsades de Pointes in the literature associated with the antipsychotic drug, "especially when given intravenously"; some cases have been fatal. A 2005 postmarketing study conducted for the Italian drug authority, but only recently submitted to the FDA by Johnson & Johnson, found 13 additional cases. The FDA notes that the drug is often used intravenously off-label, especially in intensive care units, to treat severe agitation.
Label warnings will be strengthened, the FDA says, and it recommends ECG monitoring if the drug is used intravenously. The FDA urges particular caution in patients with other QT-prolonging conditions, such as electrolyte imbalance (especially hypokalemia and hypomagnesemia).
FDA alert (Free)
Aerobic, Resistance Training Improve Glycemic Control in Type 2 Diabetes
Aerobic, Resistance Training Improve Glycemic Control in Type 2 Diabetes
Both aerobic and resistance training help lower hemoglobin A1c levels in patients with type 2 diabetes — and a combination of the two is even more beneficial — researchers report in Annals of Internal Medicine.
Some 250 inactive diabetes patients were randomized to one of four groups: aerobic training, resistance training, both, or no exercise. The active-treatment groups exercised 3 times weekly for 22 weeks.
Adjusted absolute HbA1c levels fell significantly with aerobic training (-0.51 percentage point vs. no exercise) and resistance training (-0.38); the combination-exercise group saw additional reductions (-0.46 vs. aerobic training, -0.59 vs. resistance training). Changes in blood pressure and lipids did not differ among the groups.
The authors cite research showing a 15% to 20% reduction in major cardiovascular events with a 1-percentage-point decrease in HbA1c. Editorialists note limitations of the current study but conclude: "Failing to prescribe exercise to patients with diabetes is simply unacceptable practice."
Annals of Internal Medicine article (Free)
Annals of Internal Medicine editorial (Subscription required)
Both aerobic and resistance training help lower hemoglobin A1c levels in patients with type 2 diabetes — and a combination of the two is even more beneficial — researchers report in Annals of Internal Medicine.
Some 250 inactive diabetes patients were randomized to one of four groups: aerobic training, resistance training, both, or no exercise. The active-treatment groups exercised 3 times weekly for 22 weeks.
Adjusted absolute HbA1c levels fell significantly with aerobic training (-0.51 percentage point vs. no exercise) and resistance training (-0.38); the combination-exercise group saw additional reductions (-0.46 vs. aerobic training, -0.59 vs. resistance training). Changes in blood pressure and lipids did not differ among the groups.
The authors cite research showing a 15% to 20% reduction in major cardiovascular events with a 1-percentage-point decrease in HbA1c. Editorialists note limitations of the current study but conclude: "Failing to prescribe exercise to patients with diabetes is simply unacceptable practice."
Annals of Internal Medicine article (Free)
Annals of Internal Medicine editorial (Subscription required)
Monday, September 17, 2007
Most American Women Don't Know Their Cholesterol Level
Most American Women Don't Know Their Cholesterol Level
Medical News today
17 Sep 2007
80 per cent of women in the US between 18 and 44 don't know their cholesterol level, despite the fact that cholesterol is a major risk factor for the biggest killer of American women, heart disease.
Most women don't understand about cholesterol, concluded a recent survey by the Society for Women's Health Research (SWHR), an advocacy organization based in Washington DC.
President and CEO of the SWHR, Phyllis Greenberger, said:
"Heart disease is a serious threat to women. That fact that only one in five women surveyed knew their cholesterol level shows how much work remains to be done."
"You can't wait until mid-life or later to monitor or manage your cholesterol, which is a major risk factor for heart disease in both women and men," she explained.
A spokeswoman for the American Heart Association, Dr Mary Ann Bauman, who is an internal medicine specialist said:
"For the most part, women do not believe that heart disease risk pertains to them."
"They are often aware of the risk factors, but underestimate their own personal risk," she added.
Bauman suggested the reason was women tended to ignore themselves and focused on looking after others.
She added that despite many public health campaigns, women were still more concerned about other diseases such as breast cancer.
"Most women do not have a fear of heart disease, so it is easy to ignore the risks or warning signs," said Bauman.
Over 50 per cent of the women surveyed aged between 18 and 44 were concerned about cholesterol in general but only one in 5 knew what her personal cholesterol count was. 25 per cent did not even know how cholesterol is tested.
High cholesterol raises the risk of angina, stroke, heart disease and heart attack.
About half of American adults have high cholesterol, according to statistics from the National Heart, Lung, and Blood Institute's (NHLBI) National Cholesterol Education Program.
A person's cholesterol count is made up of three things: low density lipoprotein (LDL or "bad" cholesterol), high density lipoproteins (HDL or "good" cholesterol) and triglycerides, a type of blood fat.
According to the American Heart Association, you should aim for a "desirable" total cholesterol count that is under 200 mg per decilitre or less than 5.2 millimoles per litre.
High LDL increases risk of heart disease and stroke because it promotes deposits of plaque that make blood vessels narrower. An optimum LDL count should be no higher than 100.
Low HDL is linked to increased risk of cardiovascular disease, and an optimum level for women says the SWHR is 50 and above.
Some risk factors for heart disease are controllable and some are uncontrollable, like family history, age and being post menopausal.
Apart from cholesterol, the controllable risk factors for heart disease include: smoking, high blood pressure, obesity, diabetes and a sedentary lifestyle.
Bauman said the good news is there are several ways a woman can control cholesterol and reduce her risk of heart disease:
Take regular exercise.
Maintain a healthy weight.
Eat lots of fruit and vegetables.
Keep to a diet low in saturated fats and cholesterol.
Go for regular health screening, and check cholesterol every 5 years say the AHA and the NHLBI.
Giving up smoking and tobacco also reduces heart disease risk.
People with a family history of heart disease or high cholesterol should probably start regular health screening earlier than the recommended age of 20. Bauman said that lifestyle changes at a young age make a difference later in life:
"I think of heart disease as a disease of adolescence which manifests itself in adulthood," said Bauman.
"We must start early!" she urged.
Click here for Society for Women's Health Research (SWHR).
Medical News today
17 Sep 2007
80 per cent of women in the US between 18 and 44 don't know their cholesterol level, despite the fact that cholesterol is a major risk factor for the biggest killer of American women, heart disease.
Most women don't understand about cholesterol, concluded a recent survey by the Society for Women's Health Research (SWHR), an advocacy organization based in Washington DC.
President and CEO of the SWHR, Phyllis Greenberger, said:
"Heart disease is a serious threat to women. That fact that only one in five women surveyed knew their cholesterol level shows how much work remains to be done."
"You can't wait until mid-life or later to monitor or manage your cholesterol, which is a major risk factor for heart disease in both women and men," she explained.
A spokeswoman for the American Heart Association, Dr Mary Ann Bauman, who is an internal medicine specialist said:
"For the most part, women do not believe that heart disease risk pertains to them."
"They are often aware of the risk factors, but underestimate their own personal risk," she added.
Bauman suggested the reason was women tended to ignore themselves and focused on looking after others.
She added that despite many public health campaigns, women were still more concerned about other diseases such as breast cancer.
"Most women do not have a fear of heart disease, so it is easy to ignore the risks or warning signs," said Bauman.
Over 50 per cent of the women surveyed aged between 18 and 44 were concerned about cholesterol in general but only one in 5 knew what her personal cholesterol count was. 25 per cent did not even know how cholesterol is tested.
High cholesterol raises the risk of angina, stroke, heart disease and heart attack.
About half of American adults have high cholesterol, according to statistics from the National Heart, Lung, and Blood Institute's (NHLBI) National Cholesterol Education Program.
A person's cholesterol count is made up of three things: low density lipoprotein (LDL or "bad" cholesterol), high density lipoproteins (HDL or "good" cholesterol) and triglycerides, a type of blood fat.
According to the American Heart Association, you should aim for a "desirable" total cholesterol count that is under 200 mg per decilitre or less than 5.2 millimoles per litre.
High LDL increases risk of heart disease and stroke because it promotes deposits of plaque that make blood vessels narrower. An optimum LDL count should be no higher than 100.
Low HDL is linked to increased risk of cardiovascular disease, and an optimum level for women says the SWHR is 50 and above.
Some risk factors for heart disease are controllable and some are uncontrollable, like family history, age and being post menopausal.
Apart from cholesterol, the controllable risk factors for heart disease include: smoking, high blood pressure, obesity, diabetes and a sedentary lifestyle.
Bauman said the good news is there are several ways a woman can control cholesterol and reduce her risk of heart disease:
Take regular exercise.
Maintain a healthy weight.
Eat lots of fruit and vegetables.
Keep to a diet low in saturated fats and cholesterol.
Go for regular health screening, and check cholesterol every 5 years say the AHA and the NHLBI.
Giving up smoking and tobacco also reduces heart disease risk.
People with a family history of heart disease or high cholesterol should probably start regular health screening earlier than the recommended age of 20. Bauman said that lifestyle changes at a young age make a difference later in life:
"I think of heart disease as a disease of adolescence which manifests itself in adulthood," said Bauman.
"We must start early!" she urged.
Click here for Society for Women's Health Research (SWHR).
New Risk Score Improves CVD Assessments in Women
New Risk Score Improves CVD Assessments in Women
Physician’s Weekly
Roger S. Blumenthal, MD
Despite an impressive 50-plus year history of identifying women at risk for cardiovascular disease (CVD) and strokes, the Framingham risk assessment model has sometimes fallen short in its accuracy in predicting risk. This has left many physicians wondering if they can do a better job of predicting CVD events.
Wanted: Greater Accuracy
The Framingham model examines five risk factors to assess CVD: age, blood pressure, smoking, cholesterol, and diabetes. Usually, these traditional determinants have worked well as prognosticators of risk, but they can sometimes be inconsistent with regard to accuracy, particularly among women who are classified as being at “low or intermediate risk.” This is an important note because about 70% of all future heart attacks and strokes will occur among women at this risk level. Complicating the matter is millions of women are unaware of their true CVD risk and unprepared to make lifestyle modifications.
Assessing the Reynolds Risk Score
A new CVD assessment model called the Reynolds Risk Score (RRS) has been developed and may overcome some of the shortcomings of the Framingham model. The RRS appears to be a markedly more accurate assessment tool because it addresses the predictive challenges by adding two new risk factors: parental family history of heart attack prior to age 60 and blood level of C-reactive protein (CRP). In a study published in the February 14, 2007 JAMA, Paul Ridker, MD, and colleagues demonstrated improved accuracy of predicting risk in women by using the RRS. The RRS reclassified 25% to 40% of women previously categorized under the Framingham model as intermediate risk into higher or lower risk groups. Their study also tested 35 biomarkers in nearly 25,000 women who participated in the Women’s Health Study, a 10-year research project, allowing clinicians to get a better picture of the patient’s heart health.
The RRS is a web-based tool (available online at www.reynoldsriskscore.org) that asks patients seven questions; a calculator then computes an individual’s 10-year CVD risk levels.
The RRS website also contains a long-term, risk-aging measure that allows doctors and patients to view risks at different stages in life (eg, ages 45, 55, 65, and 75) in order to provide a futuristic sense of what might happen if patients fail to address any problematic risk factors. While the RRS is specifically designed for women, several study groups have already demonstrated that the same concepts—particularly adding family history and CRP—works well for men too.
Superior Risk Assessment May Motivate Patients
Providing patients with better CVD risk assessments can give patients a better understanding of their true risk. Physicians can seize the teachable moment and encourage patients to follow better diet and exercise habits and to stop smoking. Physicians can then prescribe preventive aspirin and lipid lowering medication when appropriate. Many patients are at higher or lower CVD risk than we previously thought, but using the RRS tool may empower physicians to reduce the prescription interventions in some patients and ensure that patients in need of these therapies will receive them. Ideally, the RRS is designed to give patients a better means of taking ownership of their own CVD risk.
Roger S. Blumenthal, MD has indicated to Physician’s Weekly that he receives clinical research support from Merck, Pfizer, Schering-Plough and GE Healthcare.
Physician’s Weekly
Roger S. Blumenthal, MD
Despite an impressive 50-plus year history of identifying women at risk for cardiovascular disease (CVD) and strokes, the Framingham risk assessment model has sometimes fallen short in its accuracy in predicting risk. This has left many physicians wondering if they can do a better job of predicting CVD events.
Wanted: Greater Accuracy
The Framingham model examines five risk factors to assess CVD: age, blood pressure, smoking, cholesterol, and diabetes. Usually, these traditional determinants have worked well as prognosticators of risk, but they can sometimes be inconsistent with regard to accuracy, particularly among women who are classified as being at “low or intermediate risk.” This is an important note because about 70% of all future heart attacks and strokes will occur among women at this risk level. Complicating the matter is millions of women are unaware of their true CVD risk and unprepared to make lifestyle modifications.
Assessing the Reynolds Risk Score
A new CVD assessment model called the Reynolds Risk Score (RRS) has been developed and may overcome some of the shortcomings of the Framingham model. The RRS appears to be a markedly more accurate assessment tool because it addresses the predictive challenges by adding two new risk factors: parental family history of heart attack prior to age 60 and blood level of C-reactive protein (CRP). In a study published in the February 14, 2007 JAMA, Paul Ridker, MD, and colleagues demonstrated improved accuracy of predicting risk in women by using the RRS. The RRS reclassified 25% to 40% of women previously categorized under the Framingham model as intermediate risk into higher or lower risk groups. Their study also tested 35 biomarkers in nearly 25,000 women who participated in the Women’s Health Study, a 10-year research project, allowing clinicians to get a better picture of the patient’s heart health.
The RRS is a web-based tool (available online at www.reynoldsriskscore.org) that asks patients seven questions; a calculator then computes an individual’s 10-year CVD risk levels.
The RRS website also contains a long-term, risk-aging measure that allows doctors and patients to view risks at different stages in life (eg, ages 45, 55, 65, and 75) in order to provide a futuristic sense of what might happen if patients fail to address any problematic risk factors. While the RRS is specifically designed for women, several study groups have already demonstrated that the same concepts—particularly adding family history and CRP—works well for men too.
Superior Risk Assessment May Motivate Patients
Providing patients with better CVD risk assessments can give patients a better understanding of their true risk. Physicians can seize the teachable moment and encourage patients to follow better diet and exercise habits and to stop smoking. Physicians can then prescribe preventive aspirin and lipid lowering medication when appropriate. Many patients are at higher or lower CVD risk than we previously thought, but using the RRS tool may empower physicians to reduce the prescription interventions in some patients and ensure that patients in need of these therapies will receive them. Ideally, the RRS is designed to give patients a better means of taking ownership of their own CVD risk.
Roger S. Blumenthal, MD has indicated to Physician’s Weekly that he receives clinical research support from Merck, Pfizer, Schering-Plough and GE Healthcare.
A Nasal Cannula Can Be Used to Treat Obstructive Sleep Apnea
A Nasal Cannula Can Be Used to Treat Obstructive Sleep Apnea
American Journal of Respiratory and Critical Care Medicine Vol 176. pp. 194-200, (2007)
Brian M. McGinley1, Susheel P. Patil1, Jason P. Kirkness1, Philip L. Smith1, Alan R. Schwartz1 and Hartmut Schneider1
1 Johns Hopkins Sleep Disorders Center, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland
Correspondence and requests for reprints should be addressed to Hartmut Schneider, M.D., Ph.D., Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Room 4B47, Baltimore, MD 21224. E-mail: hschneid@jhmi.edu
Rationale: Obstructive sleep apnea syndrome is due to upper airway obstruction and is associated with increased morbidity. Although continuous positive airway pressure efficaciously treats obstructive apneas and hypopneas, treatment is impeded by low adherence rates.
Objectives: To assess the efficacy on obstructive sleep apnea of a minimally intrusive method for delivering warm and humidified air through an open nasal cannula.
Methods: Eleven subjects (age, 49.7 ± 5.0 yr; body mass index, 30.5 ± 4.3 kg/m2), with obstructive apnea–hypopnea syndrome ranging from mild to severe (5 to 60 events/h), were administered warm and humidified air at 20 L/minute through an open nasal cannula.
Measurements and Main Results: Measurements were based on standard sleep-disordered breathing and arousal indices. In a subset of patients pharyngeal pressure and ventilation were assessed to determine the mechanism of action of treatment with nasal insufflation. Treatment with nasal insufflation reduced the mean apnea–hypopnea index from 28 ± 5 to 10 ± 3 events per hour (p < 0.01), and reduced the respiratory arousal index from 18 ± 2 to 8 ± 2 events per hour (p < 0.01). Treatment with nasal insufflation reduced the apnea–hypopnea index to fewer than 10 events per hour in 8 of 11 subjects, and to fewer than 5 events per hour in 4 subjects. The mechanism of action appears to be through an increase in end-expiratory pharyngeal pressure, which alleviated upper airway obstruction and improved ventilation.
Conclusions: Our findings demonstrate clinical proof of concept that a nasal cannula for insufflating high airflows can be used to treat a diverse group of patients with obstructive sleep apnea.
AT A GLANCE COMMENTARY
Scientific Knowledge on the SubjectHigh levels of continuous positive airway pressure (CPAP) are needed to alleviate obstructive apneas; low compliance with CPAP impedes its therapeutic effectiveness; and, because hypopneas can be treated with low levels of CPAP, nasal insufflation of air might effectively treat mild obstructive sleep apnea.
What This Study Adds to the FieldNasal insufflation can provide distinct clinical advantages over CPAP for a substantial proportion of the patient population with sleep apnea.
American Journal of Respiratory and Critical Care Medicine Vol 176. pp. 194-200, (2007)
Brian M. McGinley1, Susheel P. Patil1, Jason P. Kirkness1, Philip L. Smith1, Alan R. Schwartz1 and Hartmut Schneider1
1 Johns Hopkins Sleep Disorders Center, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland
Correspondence and requests for reprints should be addressed to Hartmut Schneider, M.D., Ph.D., Johns Hopkins Asthma and Allergy Center, 5501 Hopkins Bayview Circle, Room 4B47, Baltimore, MD 21224. E-mail: hschneid@jhmi.edu
Rationale: Obstructive sleep apnea syndrome is due to upper airway obstruction and is associated with increased morbidity. Although continuous positive airway pressure efficaciously treats obstructive apneas and hypopneas, treatment is impeded by low adherence rates.
Objectives: To assess the efficacy on obstructive sleep apnea of a minimally intrusive method for delivering warm and humidified air through an open nasal cannula.
Methods: Eleven subjects (age, 49.7 ± 5.0 yr; body mass index, 30.5 ± 4.3 kg/m2), with obstructive apnea–hypopnea syndrome ranging from mild to severe (5 to 60 events/h), were administered warm and humidified air at 20 L/minute through an open nasal cannula.
Measurements and Main Results: Measurements were based on standard sleep-disordered breathing and arousal indices. In a subset of patients pharyngeal pressure and ventilation were assessed to determine the mechanism of action of treatment with nasal insufflation. Treatment with nasal insufflation reduced the mean apnea–hypopnea index from 28 ± 5 to 10 ± 3 events per hour (p < 0.01), and reduced the respiratory arousal index from 18 ± 2 to 8 ± 2 events per hour (p < 0.01). Treatment with nasal insufflation reduced the apnea–hypopnea index to fewer than 10 events per hour in 8 of 11 subjects, and to fewer than 5 events per hour in 4 subjects. The mechanism of action appears to be through an increase in end-expiratory pharyngeal pressure, which alleviated upper airway obstruction and improved ventilation.
Conclusions: Our findings demonstrate clinical proof of concept that a nasal cannula for insufflating high airflows can be used to treat a diverse group of patients with obstructive sleep apnea.
AT A GLANCE COMMENTARY
Scientific Knowledge on the SubjectHigh levels of continuous positive airway pressure (CPAP) are needed to alleviate obstructive apneas; low compliance with CPAP impedes its therapeutic effectiveness; and, because hypopneas can be treated with low levels of CPAP, nasal insufflation of air might effectively treat mild obstructive sleep apnea.
What This Study Adds to the FieldNasal insufflation can provide distinct clinical advantages over CPAP for a substantial proportion of the patient population with sleep apnea.
Friday, September 14, 2007
Can You Believe What Scientists Publish?
Can You Believe What Scientists Publish?
The Wall styreet Journal - Health Blog
Posted by Jacob Goldstein
Most published research is wrong, says epidemiologist John Ioannidis (pictured), author of the cult-classic paper Why Most Research Findings Are False.
The gist of his idea is that scientists are eager to find relationships between all sorts of variables — certain genes and the risk of a given disease, for example. And scientific journals are eager to publish research that reports these relationships.
But, while there are some true relationships in the world, there are also many unrelated variables that may falsely appear to be connected, WSJ’s Science Journal reports. For example, just because a person has a certain gene and gets a particular disease, doesn’t mean that the gene caused the disease.
“He has done systematic looks at the published literature and empirically shown us what we know deep inside our hearts,” Muin Khoury, director of the National Office of Public Health Genomics at the U.S. Centers for Disease Control and Prevention, told WSJ. “We need to pay more attention to the replication of published scientific results.”
Earlier this year, the Health Blog spoke with Ioannidis, who struck us then as the Pink Floyd of science. Like the moody rockers’ album “Dark Side of the Moon,” Ioannidis’s paper has proved an unexpected and surprisingly durable hit, setting records for downloads.
He explained why replication, not discovery is the real heart of truth:
You have millions of potential discoveries, but what is really true out of that? That’s the big question. The only way to get credibility is to go for repeated replication, again and again, with many different teams. Replication is more important than discovery.
Should scientists and scientific publishers be more vigilant about the findings they produce and publish? Go to Robert Lee Hotz’s forum to discuss.
The Wall styreet Journal - Health Blog
Posted by Jacob Goldstein
Most published research is wrong, says epidemiologist John Ioannidis (pictured), author of the cult-classic paper Why Most Research Findings Are False.
The gist of his idea is that scientists are eager to find relationships between all sorts of variables — certain genes and the risk of a given disease, for example. And scientific journals are eager to publish research that reports these relationships.
But, while there are some true relationships in the world, there are also many unrelated variables that may falsely appear to be connected, WSJ’s Science Journal reports. For example, just because a person has a certain gene and gets a particular disease, doesn’t mean that the gene caused the disease.
“He has done systematic looks at the published literature and empirically shown us what we know deep inside our hearts,” Muin Khoury, director of the National Office of Public Health Genomics at the U.S. Centers for Disease Control and Prevention, told WSJ. “We need to pay more attention to the replication of published scientific results.”
Earlier this year, the Health Blog spoke with Ioannidis, who struck us then as the Pink Floyd of science. Like the moody rockers’ album “Dark Side of the Moon,” Ioannidis’s paper has proved an unexpected and surprisingly durable hit, setting records for downloads.
He explained why replication, not discovery is the real heart of truth:
You have millions of potential discoveries, but what is really true out of that? That’s the big question. The only way to get credibility is to go for repeated replication, again and again, with many different teams. Replication is more important than discovery.
Should scientists and scientific publishers be more vigilant about the findings they produce and publish? Go to Robert Lee Hotz’s forum to discuss.
GRACE - increased medical therapy use in AMI patients
GRACE shows 'encouraging' increased medical therapy use in AMI patients
By Caroline Price
14 September 2007
Arch Intern Med 2007; 167: 1766-1773
MedWire News: Use of both single and combination medical therapy in patients hospitalized with acute myocardial infarction (AMI) increased from 2000 through 2005, suggest results from the Global Registry of Acute Coronary Events (GRACE).
Robert Goldberg (Brown University, Providence, Rhode Island, USA) and colleagues explored use of four effective cardiac medications, namely aspirin, beta blockers, angiotensin converting enzyme (ACE) inhibitors, and lipid-lowering agents at discharge in 26,413 adult men and women without contraindications to any of the drugs.
Increases were seen in singular use of three out of the four therapies, particularly that of statins, which increased from 45% of patients in 2000 to 85% in 2005. ACE inhibitor use increased from 63% to 77%, and beta blocker use from 83% to 91%.
There was little or no increase in aspirin over time, since this therapy was already being used in most AMI hospital survivors (around 95%).
There were marked increases in the use of multiple medications, particularly in use of all four combined, which increased from 23% of patients in the first half of 2000 to 58% in the second half of 2005.
Virtually identical trends were seen in the use of single and combination therapy in ST-elevation myocardial infarction (STEMI) and non-STEMI patients.
Further analysis revealed that patients of advancing age (=65 years), women, and those with a history of heart failure or stroke, who were hospitalized in participating centers in Argentina and Brazil, or developed atrial fibrillation during hospitalization, were more likely to be discharged receiving one, two, or three instead of all four medications.
Similar factors were associated with underuse of all four medications when STEMI or non-STEMI patients were studied separately, and with use of relatively few compared with three medications, the authors say in the Archives of Internal Medicine.
However, they conclude: "Despite these encouraging trends, gaps in the use of combination medical therapies continue to exist. Closing this gap will require novel and concerted efforts."
They say increased understanding and minimization of drug interactions, increased use of combination tablets, and education about the differences between "polypharmacy" and effective combination therapy are needed to this end.
LINNK:
Free abstract
By Caroline Price
14 September 2007
Arch Intern Med 2007; 167: 1766-1773
MedWire News: Use of both single and combination medical therapy in patients hospitalized with acute myocardial infarction (AMI) increased from 2000 through 2005, suggest results from the Global Registry of Acute Coronary Events (GRACE).
Robert Goldberg (Brown University, Providence, Rhode Island, USA) and colleagues explored use of four effective cardiac medications, namely aspirin, beta blockers, angiotensin converting enzyme (ACE) inhibitors, and lipid-lowering agents at discharge in 26,413 adult men and women without contraindications to any of the drugs.
Increases were seen in singular use of three out of the four therapies, particularly that of statins, which increased from 45% of patients in 2000 to 85% in 2005. ACE inhibitor use increased from 63% to 77%, and beta blocker use from 83% to 91%.
There was little or no increase in aspirin over time, since this therapy was already being used in most AMI hospital survivors (around 95%).
There were marked increases in the use of multiple medications, particularly in use of all four combined, which increased from 23% of patients in the first half of 2000 to 58% in the second half of 2005.
Virtually identical trends were seen in the use of single and combination therapy in ST-elevation myocardial infarction (STEMI) and non-STEMI patients.
Further analysis revealed that patients of advancing age (=65 years), women, and those with a history of heart failure or stroke, who were hospitalized in participating centers in Argentina and Brazil, or developed atrial fibrillation during hospitalization, were more likely to be discharged receiving one, two, or three instead of all four medications.
Similar factors were associated with underuse of all four medications when STEMI or non-STEMI patients were studied separately, and with use of relatively few compared with three medications, the authors say in the Archives of Internal Medicine.
However, they conclude: "Despite these encouraging trends, gaps in the use of combination medical therapies continue to exist. Closing this gap will require novel and concerted efforts."
They say increased understanding and minimization of drug interactions, increased use of combination tablets, and education about the differences between "polypharmacy" and effective combination therapy are needed to this end.
LINNK:
Free abstract
Thursday, September 13, 2007
Meta-analyses contrast CV effects of pioglitazone and rosiglitazone
Latest meta-analyses contrast CV effects of pioglitazone and rosiglitazone
12 September 2007
MedWire News: Two separate meta-analyses of the thiazolidinediones pioglitazone and rosiglitazone published in the Journal of the American Medical Association point to contrasting effects of these glucose-lowering drugs on ischemic cardiovascular disease.
The latest meta-analysis in a series that has provoked much controversy indicates that, in line with some previous reports, rosiglitazone increases the risk for myocardial infarction (MI) by around 40%.
Meanwhile, the meta-analysis of pioglitazone shows that patients taking the drug have almost a 20% lower risk for death, MI, or stroke than those on alternative glucose-lowering medication.
Sonal Singh (Wake University School of Medicine, Winston-Salem, North Carolina, USA) and colleagues systematically reviewed the long-term cardiovascular risks associated with rosiglitazone. Unlike the initial meta-analysis by Steven Nissen and Kathy Wolski, and subsequent re-analyses of that study, Singh and colleagues included only studies of at least 12 months' duration.
Four studies, involving 6421 Type 2 diabetic patients treated with rosiglitazone and 7870 receiving control therapy, and with between 1 and 4 years of follow-up, met all inclusion criteria. The analysis of the pooled data from the four trials showed that rosiglitazone was associated with an increased risk for MI compared with control therapy, at a relative risk (RR) of 1.42 (p=0.02), and for heart failure compared with active control therapy or placebo, at a RR of 2.09 (p<0.001).
However, rosiglitazone did not increase the risk for cardiovascular mortality (RR=0.90) or all-cause mortality (RR=0.99) compared with control treatment.
There was no evidence for heterogeneity among the trials for any of these endpoints, the authors note.
They write: "These data suggest a reversal of the benefit-to-harm balance for rosiglitazone present at the time of approval. Thus, currently there appear to be much safer treatment alternatives."
Singh et al urge physicians not to wait for regulatory action, but to avoid using rosiglitazone in patients at risk for cardiovascular events.
For the second meta-analysis, Michael Lincoff (Cleveland Clinic, Ohio, USA) and colleagues included the complete set of patient-level, time-to-event data from all 19 randomized controlled trials of pioglitazone to date. These involved a total of 16,390 patients.
The primary outcome of death, MI, or stroke was significantly less frequent in the pioglitazone-treated patients, at 4.4% compared with 5.7% in those receiving control therapy (hazard ratio [HR]=0.82, p=0.005).
However, the increased risk for heart failure associated with pioglitazone was underlined, with serious heart failure reported in 2.3% of patients who received pioglitazone compared with 1.8% of control patients (HR=1.41).
The authors say that their findings, following inconclusive results of the PROactive trial, "provide reasonably strong evidence that [pioglitazone] does, in fact, reduce the risk of cardiovascular ischemic endpoints among patients with Type 2 diabetes."
LINK:
JAMA 2007; 298: 1180-1188, 1189-1195
12 September 2007
MedWire News: Two separate meta-analyses of the thiazolidinediones pioglitazone and rosiglitazone published in the Journal of the American Medical Association point to contrasting effects of these glucose-lowering drugs on ischemic cardiovascular disease.
The latest meta-analysis in a series that has provoked much controversy indicates that, in line with some previous reports, rosiglitazone increases the risk for myocardial infarction (MI) by around 40%.
Meanwhile, the meta-analysis of pioglitazone shows that patients taking the drug have almost a 20% lower risk for death, MI, or stroke than those on alternative glucose-lowering medication.
Sonal Singh (Wake University School of Medicine, Winston-Salem, North Carolina, USA) and colleagues systematically reviewed the long-term cardiovascular risks associated with rosiglitazone. Unlike the initial meta-analysis by Steven Nissen and Kathy Wolski, and subsequent re-analyses of that study, Singh and colleagues included only studies of at least 12 months' duration.
Four studies, involving 6421 Type 2 diabetic patients treated with rosiglitazone and 7870 receiving control therapy, and with between 1 and 4 years of follow-up, met all inclusion criteria. The analysis of the pooled data from the four trials showed that rosiglitazone was associated with an increased risk for MI compared with control therapy, at a relative risk (RR) of 1.42 (p=0.02), and for heart failure compared with active control therapy or placebo, at a RR of 2.09 (p<0.001).
However, rosiglitazone did not increase the risk for cardiovascular mortality (RR=0.90) or all-cause mortality (RR=0.99) compared with control treatment.
There was no evidence for heterogeneity among the trials for any of these endpoints, the authors note.
They write: "These data suggest a reversal of the benefit-to-harm balance for rosiglitazone present at the time of approval. Thus, currently there appear to be much safer treatment alternatives."
Singh et al urge physicians not to wait for regulatory action, but to avoid using rosiglitazone in patients at risk for cardiovascular events.
For the second meta-analysis, Michael Lincoff (Cleveland Clinic, Ohio, USA) and colleagues included the complete set of patient-level, time-to-event data from all 19 randomized controlled trials of pioglitazone to date. These involved a total of 16,390 patients.
The primary outcome of death, MI, or stroke was significantly less frequent in the pioglitazone-treated patients, at 4.4% compared with 5.7% in those receiving control therapy (hazard ratio [HR]=0.82, p=0.005).
However, the increased risk for heart failure associated with pioglitazone was underlined, with serious heart failure reported in 2.3% of patients who received pioglitazone compared with 1.8% of control patients (HR=1.41).
The authors say that their findings, following inconclusive results of the PROactive trial, "provide reasonably strong evidence that [pioglitazone] does, in fact, reduce the risk of cardiovascular ischemic endpoints among patients with Type 2 diabetes."
LINK:
JAMA 2007; 298: 1180-1188, 1189-1195
Wednesday, September 12, 2007
Pioglitazone and Rosiglitazone: Different Effects on Heart Disease
Pioglitazone and Rosiglitazone: Different Effects on Heart Disease
Physician's First Watch for September 12, 2007
Two new meta-analyses in JAMA confirm the increased risk for heart failure associated with pioglitazone and rosiglitazone, but they show disparate results for other cardiovascular outcomes.
In an analysis of data from 19 randomized controlled trials involving some 16,000 patients with type 2 diabetes, those randomized to pioglitazone showed an 18% reduced risk for the composite of death, MI, and stroke. There was also a nonsignificant reduction in risk for MI alone. The drug manufacturer contributed all data.
Another research group analyzed four long-term, randomized controlled trials of rosiglitazone in which cardiovascular safety was a prespecified endpoint; some 14,000 patients were included. Overall, rosiglitazone increased the risk for MI by 42%.
Editorialists note that the increased risk for MI observed with rosiglitazone is similar to the risk reported in a recent, much publicized meta-analysis. They add that "with many other available oral agents for diabetes, the potential benefit of [thiazolidinediones] requires reevaluation."
JAMA article on pioglitazone (Free abstract; full text requires subscription)
JAMA article on rosiglitazone (Free abstract; full text requires subscription)
JAMA editorial (Subscription required)
Physician's First Watch for September 12, 2007
Two new meta-analyses in JAMA confirm the increased risk for heart failure associated with pioglitazone and rosiglitazone, but they show disparate results for other cardiovascular outcomes.
In an analysis of data from 19 randomized controlled trials involving some 16,000 patients with type 2 diabetes, those randomized to pioglitazone showed an 18% reduced risk for the composite of death, MI, and stroke. There was also a nonsignificant reduction in risk for MI alone. The drug manufacturer contributed all data.
Another research group analyzed four long-term, randomized controlled trials of rosiglitazone in which cardiovascular safety was a prespecified endpoint; some 14,000 patients were included. Overall, rosiglitazone increased the risk for MI by 42%.
Editorialists note that the increased risk for MI observed with rosiglitazone is similar to the risk reported in a recent, much publicized meta-analysis. They add that "with many other available oral agents for diabetes, the potential benefit of [thiazolidinediones] requires reevaluation."
JAMA article on pioglitazone (Free abstract; full text requires subscription)
JAMA article on rosiglitazone (Free abstract; full text requires subscription)
JAMA editorial (Subscription required)
Tuesday, September 11, 2007
Weight gain increases likelihood of hospital admission among HF patients
Weight gain increases likelihood of hospital admission among HF patients
Circulation 2007; Advance online publication
MedWire News: Weight gain in heart failure (HF) patients puts them at increased risk for hospitalization, suggests a study.
"We found that even small amounts of weight gain - as small as just over two pounds - predict hospitalization," said lead author Sarwat Chaudhry (Yale University School of Medicine, New Haven, Connecticut, USA).
Increases in body weight associated with hospitalization began at least a week before admission.
Chaudhry commented: "We found that weight gain starts well before hospitalization, giving doctors and patients at least a few days to take steps to avoid the need for hospitalization."
Chaudhry's team conducted a nested case-control study among HF patients who weighed themselves every day as part of a home monitoring system. The researchers compared the pre-hospitalization records of 134 hospitalized HF patients with the records of 134 HF patients who did not require hospitalization.
Patterns in daily weight change were similar between the groups until a month before hospitalization, when those who were subsequently hospitalized started to gain more weight.
Within the week before hospitalization, changes in daily weight started to diverge more noticeably, whereas the weight of those not hospitalized remained fairly stable. Compared with patients who gained an average of 2 lbs (1kg) or less, those who gained on average 2-5 lbs were 2.8 times as likely to be hospitalized.
Meanwhile those who gained 5-10 lbs had 4.5 times the odds of being hospitalized, while those who gained more than 10 lbs had 7.7 times the odds.
"Our data suggest that a simple bathroom scale could empower patients in managing their own disease and alert their physicians to early signs of HF decompensation.
"Ultimately, our data may help change the standard of care to prevent patients form being hospitalized, improve their quality of life, and save precious healthcare resources."
Circulation 2007; Advance online publication
MedWire News: Weight gain in heart failure (HF) patients puts them at increased risk for hospitalization, suggests a study.
"We found that even small amounts of weight gain - as small as just over two pounds - predict hospitalization," said lead author Sarwat Chaudhry (Yale University School of Medicine, New Haven, Connecticut, USA).
Increases in body weight associated with hospitalization began at least a week before admission.
Chaudhry commented: "We found that weight gain starts well before hospitalization, giving doctors and patients at least a few days to take steps to avoid the need for hospitalization."
Chaudhry's team conducted a nested case-control study among HF patients who weighed themselves every day as part of a home monitoring system. The researchers compared the pre-hospitalization records of 134 hospitalized HF patients with the records of 134 HF patients who did not require hospitalization.
Patterns in daily weight change were similar between the groups until a month before hospitalization, when those who were subsequently hospitalized started to gain more weight.
Within the week before hospitalization, changes in daily weight started to diverge more noticeably, whereas the weight of those not hospitalized remained fairly stable. Compared with patients who gained an average of 2 lbs (1kg) or less, those who gained on average 2-5 lbs were 2.8 times as likely to be hospitalized.
Meanwhile those who gained 5-10 lbs had 4.5 times the odds of being hospitalized, while those who gained more than 10 lbs had 7.7 times the odds.
"Our data suggest that a simple bathroom scale could empower patients in managing their own disease and alert their physicians to early signs of HF decompensation.
"Ultimately, our data may help change the standard of care to prevent patients form being hospitalized, improve their quality of life, and save precious healthcare resources."
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