Title: Association of Early Follow-Up After Acute Myocardial Infarction With Higher Rates of Medication
Date Posted: 3/10/2008
Author(s): Daugherty SL, Ho PM, Spertus JA, et al.
Citation: Arch Intern Med 2008;168:485-491.
Study Question: What is the relationship between early outpatient follow-up after acute myocardial infarction (AMI) and use of evidence-based therapies?
Methods: A total of 1,516 patients hospitalized with AMI participated in the multicenter Prospective Registry Evaluating Outcomes After Myocardial Infarction: Events and Recovery registry. Early follow-up was defined as patient-reported visits with a primary care physician or cardiologist within 1 month after discharge. The primary outcomes were use of aspirin, beta-blockers, angiotensin-converting enzyme inhibitors, and statins in eligible patients at 6 months. Multivariable analyses assessed the association between early follow-up and medication use at 6 months, adjusting for patient and clinical characteristics. Secondary analyses compared medication use at 6 months for patients receiving collaborative follow-up from a single provider versus those receiving follow-up from both provider types.
Results: Among the cohort, 34% reported no outpatient follow-up during the month following discharge. Rates of medication prescription among appropriate candidates were similar at hospital discharge for both follow-up groups. Compared with those not receiving early follow-up, those receiving early follow-up were more likely to be prescribed beta-blockers (80.1% vs. 71.3%; p = 0.001), aspirin (82.9% vs. 77.1%; p = 0.01), or statins (75.9% vs. 68.6%; p = 0.005) at 6 months. In multivariable analyses, a persistent relationship remained between early follow-up and beta-blocker use (risk ratio [RR], 1.08; 95% confidence interval [CI], 1.02-1.15). In secondary analyses, statin use was higher in patients receiving collaborative follow-up (RR, 1.11; 95% CI, 1.01-1.22).
Conclusions: Early outpatient follow-up and collaborative follow-up after AMI are associated with higher rates of evidence-based medication use. Although further studies should assess whether this relationship is causal, these results support current guideline recommendations for follow-up after AMI.
Perspective: This prospective observational study demonstrated a modest advantage of early follow-up post-MI, but which could infer a significant clinical outcome benefit. I suspect it underestimates the value of the cardiologist assessment and opportunity for referral to cardiac rehabilitation, smoking cessation, and education. Our experience is that early follow-up by a nurse practitioner can be effective as well. Melvyn Rubenfire, M.D., F.A.C.C.
Showing posts with label Acute Myocardial Infarction. Show all posts
Showing posts with label Acute Myocardial Infarction. Show all posts
Tuesday, March 11, 2008
Saturday, March 1, 2008
Medwire - 29.02.08
Minority of CHD patients do recommended exercise
29 February 2008
Study findings reveal that patients with coronary heart disease often do not comply with physical activity recommendations, and are less likely to do so than individuals without CHD.
Information, reassurance, and support aid post-CABG recovery
29 February 2008
The results of a small, qualitative UK survey show that patients undergoing coronary bypass grafting surgery who may feel anxious or depressed about their recovery can be helped if they remain optimistic and are given information, reassurance, and support from the healthcare team and their social network.
Persistent hyperglycemia in AMI predicts in-hospital mortality
29 February 2008
Persistent hyperglycemia determined by multiple glucose assessments during hospitalization for acute myocardial infarction better predicts mortality than hyperglycemia on admission, research shows.
29 February 2008
Study findings reveal that patients with coronary heart disease often do not comply with physical activity recommendations, and are less likely to do so than individuals without CHD.
Information, reassurance, and support aid post-CABG recovery
29 February 2008
The results of a small, qualitative UK survey show that patients undergoing coronary bypass grafting surgery who may feel anxious or depressed about their recovery can be helped if they remain optimistic and are given information, reassurance, and support from the healthcare team and their social network.
Persistent hyperglycemia in AMI predicts in-hospital mortality
29 February 2008
Persistent hyperglycemia determined by multiple glucose assessments during hospitalization for acute myocardial infarction better predicts mortality than hyperglycemia on admission, research shows.
Wednesday, February 6, 2008
Incidence of Death and Acute Myocardial Infarction Associated With Stopping Clopidogrel After Acute Coronary Syndrome
Incidence of Death and Acute Myocardial Infarction Associated With Stopping Clopidogrel After Acute Coronary Syndrome
P. Michael Ho, MD, PhD; Eric D. Peterson, MD, MPH; Li Wang, MS; David J. Magid, MD, MPH; Stephan D. Fihn, MD, MPH; Greg C. Larsen, MD; Robert A. Jesse, MD, PhD; John S. Rumsfeld, MD, PhD
JAMA. 2008;299(5):532-539.
Context
It is unknown whether patients are at increased short-term risk for adverse events following clopidogrel cessation.
Objective
To assess the rates of adverse events after stopping treatment with clopidogrel in a national sample of patients with acute coronary syndrome (ACS).
Design, Setting, and Patients
Retrospective cohort study of 3137 patients with ACS discharged from 127 Veterans Affairs hospitals between October 1, 2003, and March 31, 2005, with posthospital treatment with clopidogrel.
Main Outcome Measure
Rate of all-cause mortality or acute myocardial infarction (AMI) after stopping treatment with clopidogrel.
Results
Mean (SD) follow-up after stopping treatment with clopidogrel was 196 (152) days for medically treated patients with ACS without stents (n = 1568) and 203 (148) days for patients with ACS treated with percutaneous coronary intervention (PCI) (n = 1569). Among medically treated patients, mean (SD) duration of clopidogrel treatment was 302 (151) days and death or AMI occurred in 17.1% (n = 268) of patients, with 60.8% (n = 163) of events occurring during 0 to 90 days, 21.3% (n = 57) during 91 to 180 days, and 9.7% (n = 26) during 181 to 270 days after stopping treatment with clopidogrel. In multivariable analysis including adjustment for duration of clopidogrel treatment, the first 90-day interval after stopping treatment with clopidogrel was associated with a significantly higher risk of adverse events (incidence rate ratio [IRR], 1.98; 95% confidence interval [CI], 1.46-2.69 vs the interval of 91-180 days). Similarly, among PCI-treated patients with ACS, mean (SD) duration of clopidogrel treatment was 278 (169) days and death or AMI occurred in 7.9% (n = 124) of patients, with 58.9% (n = 73) of events occurring during 0 to 90 days, 23.4% (n = 29) during 91 to 180 days, and 6.5% (n = 8) during 181 to 270 days after stopping clopidogrel treatment. In multivariable analysis including adjustment for duration of clopidogrel treatment, the first 90-day interval after stopping clopidogrel treatment was associated with a significantly higher risk of adverse events (IRR, 1.82; 95% CI, 1.17-2.83).
Conclusions
'
P. Michael Ho, MD, PhD; Eric D. Peterson, MD, MPH; Li Wang, MS; David J. Magid, MD, MPH; Stephan D. Fihn, MD, MPH; Greg C. Larsen, MD; Robert A. Jesse, MD, PhD; John S. Rumsfeld, MD, PhD
JAMA. 2008;299(5):532-539.
Context
It is unknown whether patients are at increased short-term risk for adverse events following clopidogrel cessation.
Objective
To assess the rates of adverse events after stopping treatment with clopidogrel in a national sample of patients with acute coronary syndrome (ACS).
Design, Setting, and Patients
Retrospective cohort study of 3137 patients with ACS discharged from 127 Veterans Affairs hospitals between October 1, 2003, and March 31, 2005, with posthospital treatment with clopidogrel.
Main Outcome Measure
Rate of all-cause mortality or acute myocardial infarction (AMI) after stopping treatment with clopidogrel.
Results
Mean (SD) follow-up after stopping treatment with clopidogrel was 196 (152) days for medically treated patients with ACS without stents (n = 1568) and 203 (148) days for patients with ACS treated with percutaneous coronary intervention (PCI) (n = 1569). Among medically treated patients, mean (SD) duration of clopidogrel treatment was 302 (151) days and death or AMI occurred in 17.1% (n = 268) of patients, with 60.8% (n = 163) of events occurring during 0 to 90 days, 21.3% (n = 57) during 91 to 180 days, and 9.7% (n = 26) during 181 to 270 days after stopping treatment with clopidogrel. In multivariable analysis including adjustment for duration of clopidogrel treatment, the first 90-day interval after stopping treatment with clopidogrel was associated with a significantly higher risk of adverse events (incidence rate ratio [IRR], 1.98; 95% confidence interval [CI], 1.46-2.69 vs the interval of 91-180 days). Similarly, among PCI-treated patients with ACS, mean (SD) duration of clopidogrel treatment was 278 (169) days and death or AMI occurred in 7.9% (n = 124) of patients, with 58.9% (n = 73) of events occurring during 0 to 90 days, 23.4% (n = 29) during 91 to 180 days, and 6.5% (n = 8) during 181 to 270 days after stopping clopidogrel treatment. In multivariable analysis including adjustment for duration of clopidogrel treatment, the first 90-day interval after stopping clopidogrel treatment was associated with a significantly higher risk of adverse events (IRR, 1.82; 95% CI, 1.17-2.83).
Conclusions
'
Monday, January 28, 2008
ACE inhibitor prevents cardiac rupture after acute MI
Causes of death in patients with acute myocardial infarction treated with angiotensin-converting enzyme inhibitors: Findings from the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto (GISSI)–3 trial
American Heart Journal
Volume 155, Issue 2, Pages 388-394 (February 2008)
Giovanni Pedrazzini, MD, Eugenio Santoro, MS, Roberto Latini, MD, Laurie Fromm, PharmD, Maria Grazia Franzosi, BiolScD, Tiziano Mocetti, MD, Lidia Staszewsky, MD, Simona Barlera, MS, Gianni Tognoni, MD, Aldo P. Maggioni, MD
Background
The causes of death occurring in clinical trials of myocardial infarction (MI) are scarcely reported in the literature. The present analysis is aimed to describe the inhospital causes of death in patients with acute MI stratified to angiotensin converting enzyme (ACE) inhibitor treatment/no treatment, as described in the GISSI-3 trial. Furthermore, the 5-year survival analysis of GISSI-3 patients is reported.
Methods and Results
An independent committee assigned the definition of causes of death of GISSI-3 based on clinical and/or anatomical data. Univariate and multivariable analyses were performed to identify the predictors of early and late deaths. Kaplan-Meier mortality curves were used to describe the effects of ACE-I treatment on mortality on a median follow-up period of 56 months.
Patients receiving lisinopril had fewer inhospital cardiac deaths than patients allocated to the no-lisinopril group (4.7% vs 5.3%, P = .052), corresponding to a 12% relative risk reduction. The risk of dying from cardiac rupture was reduced by 39% by lisinopril treatment. The improvement in survival associated with the lisinopril treatment was mainly due to a reduction in cardiac rupture, electromechanical dissociation, and pump failure occurring early (within 4 days) from the onset of MI symptoms.
The beneficial effects of lisinopril observed at 6 weeks (8 fewer deaths per 1000 treated patients) were maintained up to nearly 5 years (10 fewer deaths per 1000).
Conclusions
Early administration of ACE inhibitors in unselected patients with acute MI should be considered standard therapy to reduce early deaths, specifically those due to cardiac rupture. The early beneficial effect persisted up to nearly 5 years.
American Heart Journal
Volume 155, Issue 2, Pages 388-394 (February 2008)
Giovanni Pedrazzini, MD, Eugenio Santoro, MS, Roberto Latini, MD, Laurie Fromm, PharmD, Maria Grazia Franzosi, BiolScD, Tiziano Mocetti, MD, Lidia Staszewsky, MD, Simona Barlera, MS, Gianni Tognoni, MD, Aldo P. Maggioni, MD
Background
The causes of death occurring in clinical trials of myocardial infarction (MI) are scarcely reported in the literature. The present analysis is aimed to describe the inhospital causes of death in patients with acute MI stratified to angiotensin converting enzyme (ACE) inhibitor treatment/no treatment, as described in the GISSI-3 trial. Furthermore, the 5-year survival analysis of GISSI-3 patients is reported.
Methods and Results
An independent committee assigned the definition of causes of death of GISSI-3 based on clinical and/or anatomical data. Univariate and multivariable analyses were performed to identify the predictors of early and late deaths. Kaplan-Meier mortality curves were used to describe the effects of ACE-I treatment on mortality on a median follow-up period of 56 months.
Patients receiving lisinopril had fewer inhospital cardiac deaths than patients allocated to the no-lisinopril group (4.7% vs 5.3%, P = .052), corresponding to a 12% relative risk reduction. The risk of dying from cardiac rupture was reduced by 39% by lisinopril treatment. The improvement in survival associated with the lisinopril treatment was mainly due to a reduction in cardiac rupture, electromechanical dissociation, and pump failure occurring early (within 4 days) from the onset of MI symptoms.
The beneficial effects of lisinopril observed at 6 weeks (8 fewer deaths per 1000 treated patients) were maintained up to nearly 5 years (10 fewer deaths per 1000).
Conclusions
Early administration of ACE inhibitors in unselected patients with acute MI should be considered standard therapy to reduce early deaths, specifically those due to cardiac rupture. The early beneficial effect persisted up to nearly 5 years.
Similar outcome after thrombolysis or primary angioplasty in STEMI
Comparison of Left Ventricular Ejection Fraction and Inducible Ventricular Tachycardia in ST-Elevation Myocardial Infarction Treated by Primary Angioplasty Versus Thrombolysis
American Journal of Cardiology
Volume 101, Issue 2, Pages 153-157 (15 January 2008)
James J.H. Chong, MDa, Anand N. Ganesan, MD, PhD, Vicki Eippera, Pramesh Kovoor, MD, PhD
Electrophysiologic studies predict the risk for sudden death after myocardial infarction (MI). Although primary angioplasty has become the preferred method of treatment for ST-elevation MI, intravenous thrombolysis remains the first-line treatment in 30% to 70% of cases worldwide. Rates of ventricular tachyarrhythmias may vary according to type of reperfusion treatment. This study was undertaken to examine the hypothesis that the left ventricular ejection fraction (LVEF) and rates of inducible ventricular tachycardia may be more favorable in treatment with primary angioplasty rather than thrombolysis. Consecutive patients receiving primary angioplasty (n = 225) or thrombolysis (n = 195) for ST-elevation MI were included. The mean LVEF was 48 ± 12% for the primary angioplasty group and 46 ± 13% for the thrombolysis group (p = 0.30). The proportion of patients with LVEFs <40% was 30% in the primary angioplasty group and 30% in the thrombolysis group (p = 0.98). Patients with LVEFs <40% underwent electrophysiologic studies. Ventricular tachycardia was inducible in 23 of 66 primary angioplasty patients (34.8%) compared with 21 of 55 (38.1%) thrombolysis patients (p = 0.69). Implantable cardiac defibrillators were inserted in 30 patients, of whom 8 (27%) had appropriate device activations. The mean time from MI to first spontaneous activation was 387 ± 458 days.
In conclusion, patients treated with thrombolysis or primary angioplasty for ST-elevation MIs had similar resultant LVEFs and rates of inducible ventricular tachycardia. There was a surprisingly high rate of spontaneous defibrillator activations, often occurring late after MI.
American Journal of Cardiology
Volume 101, Issue 2, Pages 153-157 (15 January 2008)
James J.H. Chong, MDa, Anand N. Ganesan, MD, PhD, Vicki Eippera, Pramesh Kovoor, MD, PhD
Electrophysiologic studies predict the risk for sudden death after myocardial infarction (MI). Although primary angioplasty has become the preferred method of treatment for ST-elevation MI, intravenous thrombolysis remains the first-line treatment in 30% to 70% of cases worldwide. Rates of ventricular tachyarrhythmias may vary according to type of reperfusion treatment. This study was undertaken to examine the hypothesis that the left ventricular ejection fraction (LVEF) and rates of inducible ventricular tachycardia may be more favorable in treatment with primary angioplasty rather than thrombolysis. Consecutive patients receiving primary angioplasty (n = 225) or thrombolysis (n = 195) for ST-elevation MI were included. The mean LVEF was 48 ± 12% for the primary angioplasty group and 46 ± 13% for the thrombolysis group (p = 0.30). The proportion of patients with LVEFs <40% was 30% in the primary angioplasty group and 30% in the thrombolysis group (p = 0.98). Patients with LVEFs <40% underwent electrophysiologic studies. Ventricular tachycardia was inducible in 23 of 66 primary angioplasty patients (34.8%) compared with 21 of 55 (38.1%) thrombolysis patients (p = 0.69). Implantable cardiac defibrillators were inserted in 30 patients, of whom 8 (27%) had appropriate device activations. The mean time from MI to first spontaneous activation was 387 ± 458 days.
In conclusion, patients treated with thrombolysis or primary angioplasty for ST-elevation MIs had similar resultant LVEFs and rates of inducible ventricular tachycardia. There was a surprisingly high rate of spontaneous defibrillator activations, often occurring late after MI.
Tuesday, January 22, 2008
Initial Aspirin Dose and Outcome Among ST-Elevation Myocardial Infarction Patients Treated With Fibrinolytic Therapy
Commentaries:
Increased dose increased bleeding. What´s the mre convenient dose of Aspirin?
Initial Aspirin Dose and Outcome Among ST-Elevation Myocardial Infarction Patients Treated With Fibrinolytic Therapy
Circulation
Volume 117, Issue 2; January 15, 2008
Jeffrey S. Berger, MD, MS; Amanda Stebbins, MS; Christopher B. Granger, MD; Eric M. Ohman, MD; Paul W. Armstrong, MD; Frans Van de Werf, MD, PhD; Harvey D. White, DSc; R. John Simes, MD; Robert A. Harrington, MD; Robert M. Califf, MD; Eric D. Peterson, MD, MPH
Background— Although treatment with immediate aspirin reduces morbidity and mortality in ST-elevation myocardial infarction, the optimal dose is unclear. We therefore compared the acute mortality and bleeding risks associated with the initial use of 162 versus 325 mg aspirin in fibrinolytic-treated ST-elevation myocardial infarction patients.
Methods and Results— Using combined data from the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO I) and Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO III) trials (n=48 422 ST-elevation myocardial infarction patients), we compared the association between initial aspirin dose of 162 versus 325 mg and 24-hour and 7-day mortality, as well as rates of in-hospital moderate/severe bleeding. Results were adjusted for previously identified mortality and bleeding risk factors. Overall, 24.4% of patients (n=11 828) received an initial aspirin dose of 325 mg, and 75.6% (n=36 594) received 162 mg. The 24-hour mortality rates were 2.9% versus 2.8% (P=0.894) for those receiving an initial aspirin dose of 325 versus 162 mg. Mortality rates at 7 and 30 days were 5.2% versus 4.9% (P=0.118) and 7.1% versus 6.5% (P=0.017) among patients receiving the 325 versus 162 mg aspirin. After adjustment, aspirin dose was not associated with 24-hour (odds ratio [OR], 1.01; 95% CI, 0.82 to 1.25), 7-day (OR, 1.00; 95% CI, 0.87 to 1.17), or 30-day (OR, 0.99; 95% CI, 0.87 to 1.12) mortality rates. No significant difference was noted for myocardial infarction or the composite of death or myocardial infarction between groups. In-hospital moderate/severe bleeding occurred in 9.3% of those treated with 325 mg versus 12.2% among those receiving 162 mg (P<0.001). After adjustment, 325 mg was associated with a significant increase in moderate/severe bleeding (OR, 1.14; 95% CI, 1.05 to 1.24; P=0.003).
Conclusion— These data suggest that an initial dose of 162 mg aspirin may be as effective as and perhaps safer than 325 mg for the acute treatment of ST-elevation myocardial infarction.
Increased dose increased bleeding. What´s the mre convenient dose of Aspirin?
Initial Aspirin Dose and Outcome Among ST-Elevation Myocardial Infarction Patients Treated With Fibrinolytic Therapy
Circulation
Volume 117, Issue 2; January 15, 2008
Jeffrey S. Berger, MD, MS; Amanda Stebbins, MS; Christopher B. Granger, MD; Eric M. Ohman, MD; Paul W. Armstrong, MD; Frans Van de Werf, MD, PhD; Harvey D. White, DSc; R. John Simes, MD; Robert A. Harrington, MD; Robert M. Califf, MD; Eric D. Peterson, MD, MPH
Background— Although treatment with immediate aspirin reduces morbidity and mortality in ST-elevation myocardial infarction, the optimal dose is unclear. We therefore compared the acute mortality and bleeding risks associated with the initial use of 162 versus 325 mg aspirin in fibrinolytic-treated ST-elevation myocardial infarction patients.
Methods and Results— Using combined data from the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO I) and Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO III) trials (n=48 422 ST-elevation myocardial infarction patients), we compared the association between initial aspirin dose of 162 versus 325 mg and 24-hour and 7-day mortality, as well as rates of in-hospital moderate/severe bleeding. Results were adjusted for previously identified mortality and bleeding risk factors. Overall, 24.4% of patients (n=11 828) received an initial aspirin dose of 325 mg, and 75.6% (n=36 594) received 162 mg. The 24-hour mortality rates were 2.9% versus 2.8% (P=0.894) for those receiving an initial aspirin dose of 325 versus 162 mg. Mortality rates at 7 and 30 days were 5.2% versus 4.9% (P=0.118) and 7.1% versus 6.5% (P=0.017) among patients receiving the 325 versus 162 mg aspirin. After adjustment, aspirin dose was not associated with 24-hour (odds ratio [OR], 1.01; 95% CI, 0.82 to 1.25), 7-day (OR, 1.00; 95% CI, 0.87 to 1.17), or 30-day (OR, 0.99; 95% CI, 0.87 to 1.12) mortality rates. No significant difference was noted for myocardial infarction or the composite of death or myocardial infarction between groups. In-hospital moderate/severe bleeding occurred in 9.3% of those treated with 325 mg versus 12.2% among those receiving 162 mg (P<0.001). After adjustment, 325 mg was associated with a significant increase in moderate/severe bleeding (OR, 1.14; 95% CI, 1.05 to 1.24; P=0.003).
Conclusion— These data suggest that an initial dose of 162 mg aspirin may be as effective as and perhaps safer than 325 mg for the acute treatment of ST-elevation myocardial infarction.
Monday, January 21, 2008
Amiodarone use after acute myocardial infarction complicated by heart failure and/or left ventricular dysfunction - Mortality
Commentaries:
Obsertvationl study; need to be validate with prospective studies.
Amiodarone use after acute myocardial infarction complicated by heart failure and/or left ventricular dysfunction may be associated with excess mortality
American Heart Journal
Volume 155, Issue 1, Pages 87-93 (January 2008)
Kevin L. Thomas, MDa, Sana M. Al-Khatib, MHS, MDa, Yuliya Lokhnygina, PhDa, Scott D. Solomon, MDb, Lars Kober, MDc, John J.V. McMurray, MDd, Robert M. Califf, MDa, Eric J. Velazquez, MDa
Background
We sought to assess the association of amiodarone use with mortality during consecutive periods in patients with post–acute myocardial infarction with left ventricular systolic dysfunction and/or HF treated with a contemporary medical regimen.
Methods
This study used data from VALIANT, a randomized comparison of valsartan, captopril, or both in patients with acute myocardial infarction with HF and/or left ventricular systolic dysfunction. We compared baseline characteristics of 825 patients treated with amiodarone at randomization with 13 875 patients not treated with amiodarone. Using Cox models, we examined the association of amiodarone use with subsequent mortality during consecutive periods after randomization (days 1-16, 17-45, 46-198, and 199-1096).
Results
Patients treated with amiodarone were older, had higher Killip class, and were more likely to have a history of diabetes mellitus and hypertension. Adjusting for baseline predictors of mortality, we found that amiodarone use was associated with a significant increase in mortality during 3 of the 4 periods: hazard ratio 1.5, 95% CI (1.1-2.0), P = .02, for days 1 to 16; 2.1 (1.5-2.9), P < .001, for days 17 to 45; 1.1 (0.83-1.46), P = .51, for days 46 to 198; and 1.4 (1.2-1.6), P < .001, for days 199 to 1096. Conclusion
In this study, amiodarone use was associated with excess early and late all-cause and cardiovascular mortality. These observational findings are in contrast to earlier randomized trials of amiodarone and need to be validated prospectively.
Obsertvationl study; need to be validate with prospective studies.
Amiodarone use after acute myocardial infarction complicated by heart failure and/or left ventricular dysfunction may be associated with excess mortality
American Heart Journal
Volume 155, Issue 1, Pages 87-93 (January 2008)
Kevin L. Thomas, MDa, Sana M. Al-Khatib, MHS, MDa, Yuliya Lokhnygina, PhDa, Scott D. Solomon, MDb, Lars Kober, MDc, John J.V. McMurray, MDd, Robert M. Califf, MDa, Eric J. Velazquez, MDa
Background
We sought to assess the association of amiodarone use with mortality during consecutive periods in patients with post–acute myocardial infarction with left ventricular systolic dysfunction and/or HF treated with a contemporary medical regimen.
Methods
This study used data from VALIANT, a randomized comparison of valsartan, captopril, or both in patients with acute myocardial infarction with HF and/or left ventricular systolic dysfunction. We compared baseline characteristics of 825 patients treated with amiodarone at randomization with 13 875 patients not treated with amiodarone. Using Cox models, we examined the association of amiodarone use with subsequent mortality during consecutive periods after randomization (days 1-16, 17-45, 46-198, and 199-1096).
Results
Patients treated with amiodarone were older, had higher Killip class, and were more likely to have a history of diabetes mellitus and hypertension. Adjusting for baseline predictors of mortality, we found that amiodarone use was associated with a significant increase in mortality during 3 of the 4 periods: hazard ratio 1.5, 95% CI (1.1-2.0), P = .02, for days 1 to 16; 2.1 (1.5-2.9), P < .001, for days 17 to 45; 1.1 (0.83-1.46), P = .51, for days 46 to 198; and 1.4 (1.2-1.6), P < .001, for days 199 to 1096. Conclusion
In this study, amiodarone use was associated with excess early and late all-cause and cardiovascular mortality. These observational findings are in contrast to earlier randomized trials of amiodarone and need to be validated prospectively.
Saturday, January 12, 2008
Alcohol and long-term prognosis after a first acute myocardial infarction: the SHEEP study
Alcohol and long-term prognosis after a first acute myocardial infarction: the SHEEP study
Eur Heart J 2008 29: 45-53.
Context: Few studies have investigated the relation between alcohol consumption, former drinking, and prognosis after an acute myocardial infarction (AMI), particularly for non-fatal outcomes.
Objective: To investigate the prognostic importance of drinking habits among patients surviving a first AMI.
Design, settings, and patients: A total of 1346 consecutive patients between 45–70 years with a first non-fatal AMI underwent a standardized clinical examination and were followed for over 8 years.
Main outcome measures: Total and cardiac mortality and hospitalization for non-fatal cardiovascular disease in relation to individual alcoholic beverage consumption at the time of AMI and 5 years before inclusion, assessed by a standardized questionnaire administered during hospitalization.
Results: We recorded 267 deaths, and 145 deaths from cardiac causes, during the follow-up period. After adjustment for several potential confounders, hazard ratios for total and cardiac mortality were 0.77 (0.51–1.15) and 0.61 (0.36–1.02) for those drinking >0–<5 g per day, 0.77 (0.50–1.18) and 0.62 (0.36–1.07) for those drinking 5–20 g per day, and 0.89 (0.56–1.40) and 0.69 (0.38–1.25) for those drinking over 20 g per day. Risk of hospitalization for recurrent non-fatal AMI, stroke, or heart failure generally showed a similar pattern to that of total and cardiac mortality. Recent quitters at the time of AMI had a hazard ratio of 4.55 (2.03–10.20) for total mortality. Measures of insulin sensitivity appeared to be the strongest mediators of this association.
Conclusions: Moderate alcohol drinking might have beneficial effects on several aspects of long-term prognosis after an AMI. Our findings also highlight that former drinkers should be examined separately from long-term abstainers. The potential mechanisms that underlie this association still need to be elucidated.
Eur Heart J 2008 29: 45-53.
Context: Few studies have investigated the relation between alcohol consumption, former drinking, and prognosis after an acute myocardial infarction (AMI), particularly for non-fatal outcomes.
Objective: To investigate the prognostic importance of drinking habits among patients surviving a first AMI.
Design, settings, and patients: A total of 1346 consecutive patients between 45–70 years with a first non-fatal AMI underwent a standardized clinical examination and were followed for over 8 years.
Main outcome measures: Total and cardiac mortality and hospitalization for non-fatal cardiovascular disease in relation to individual alcoholic beverage consumption at the time of AMI and 5 years before inclusion, assessed by a standardized questionnaire administered during hospitalization.
Results: We recorded 267 deaths, and 145 deaths from cardiac causes, during the follow-up period. After adjustment for several potential confounders, hazard ratios for total and cardiac mortality were 0.77 (0.51–1.15) and 0.61 (0.36–1.02) for those drinking >0–<5 g per day, 0.77 (0.50–1.18) and 0.62 (0.36–1.07) for those drinking 5–20 g per day, and 0.89 (0.56–1.40) and 0.69 (0.38–1.25) for those drinking over 20 g per day. Risk of hospitalization for recurrent non-fatal AMI, stroke, or heart failure generally showed a similar pattern to that of total and cardiac mortality. Recent quitters at the time of AMI had a hazard ratio of 4.55 (2.03–10.20) for total mortality. Measures of insulin sensitivity appeared to be the strongest mediators of this association.
Conclusions: Moderate alcohol drinking might have beneficial effects on several aspects of long-term prognosis after an AMI. Our findings also highlight that former drinkers should be examined separately from long-term abstainers. The potential mechanisms that underlie this association still need to be elucidated.
Wednesday, January 2, 2008
Coffee Consumption and Risk of Cardiovascular Events After Acute Myocardial Infarction
Coffee Consumption and Risk of Cardiovascular Events After Acute Myocardial Infarction
Results From the GISSI (Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico)-Prevenzione Trial
Circulation. 2007;116:2944-2951
Background— The relation between coffee consumption and cardiovascular disease has been studied extensively, but results are still debated. In addition, little evidence is available on patients with established coronary heart disease.
Methods and Results— Prospectively ascertained information among 11 231 Italian patients (9584 males and 1647 females) with recent (3 months) myocardial infarction enrolled in the GISSI (Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico)-Prevenzione trial was used. Usual dietary habits were assessed at baseline and updated at 0.5 and 1.5 years. Coffee consumption was categorized as never/almost never, <2>4 cups per day. Medication use and fasting glucose were assessed at 0.5, 1, 1.5, 2.5, and 3.5 years. Risk was evaluated with Cox proportional hazards with time-varying covariates. The main outcome measure was the cumulative incidence of cardiovascular events (cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke). A total of 1167 cardiovascular events occurred during 36 961 person-years of follow-up. After multivariable adjustment for potential confounders in the time-dependent analysis, the relative risk of cardiovascular events across categories of coffee consumption was 1.02 (95% CI 0.87 to 1.20) for <2>4 cups per day compared with abstainers (P for trend=0.18). Ultimately, coffee consumption did not change the risk of coronary heart disease events, stroke, and sudden death.
Conclusions— No association between moderate coffee intake and cardiovascular events was observed in post–myocardial infarction patients
Results From the GISSI (Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico)-Prevenzione Trial
Circulation. 2007;116:2944-2951
Background— The relation between coffee consumption and cardiovascular disease has been studied extensively, but results are still debated. In addition, little evidence is available on patients with established coronary heart disease.
Methods and Results— Prospectively ascertained information among 11 231 Italian patients (9584 males and 1647 females) with recent (3 months) myocardial infarction enrolled in the GISSI (Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico)-Prevenzione trial was used. Usual dietary habits were assessed at baseline and updated at 0.5 and 1.5 years. Coffee consumption was categorized as never/almost never, <2>4 cups per day. Medication use and fasting glucose were assessed at 0.5, 1, 1.5, 2.5, and 3.5 years. Risk was evaluated with Cox proportional hazards with time-varying covariates. The main outcome measure was the cumulative incidence of cardiovascular events (cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke). A total of 1167 cardiovascular events occurred during 36 961 person-years of follow-up. After multivariable adjustment for potential confounders in the time-dependent analysis, the relative risk of cardiovascular events across categories of coffee consumption was 1.02 (95% CI 0.87 to 1.20) for <2>4 cups per day compared with abstainers (P for trend=0.18). Ultimately, coffee consumption did not change the risk of coronary heart disease events, stroke, and sudden death.
Conclusions— No association between moderate coffee intake and cardiovascular events was observed in post–myocardial infarction patients
Thursday, December 20, 2007
Rationale and design of the Trial of Routine ANgioplasty and Stenting After Fibrinolysis to Enhance Reperfusion in Acute Myocardial Infarction (TRANSF
Rationale and design of the Trial of Routine ANgioplasty and Stenting After Fibrinolysis to Enhance Reperfusion in Acute Myocardial Infarction (TRANSFER-AMI).
Am Heart J. 2008 Jan;155(1):19-25. Epub 2007 Oct 25.
BACKGROUND: Most patients with ST-elevation myocardial infarction present to hospitals without percutaneous coronary intervention (PCI) facilities and receive fibrinolysis. The role of routine early PCI after fibrinolysis, using stents and contemporary pharmacotherapy, has not been studied in a large adequately powered randomized trial.
OBJECTIVE: To compare a pharmacoinvasive strategy of transfer for routine PCI within 6 hours after fibrinolysis with standard treatment after fibrinolysis (including predefined criteria for rescue PCI and delayed cardiac catheterization for patients who do not require rescue PCI).
METHODS: A total of 1200 patients with high-risk ST-elevation myocardial infarction
presenting to non-PCI centers will be randomized to a pharmacoinvasive strategy (transfer for routine PCI within 6 hours of fibrinolysis) or to standard treatment after fibrinolysis. The primary end point is the 30-day composite of death, reinfarction, recurrent ischemia, heart failure, or shock.
RESULTS: More than 900 patients have been enrolled as of April 2007. An interim safety analysis of the first 536 patients demonstrated no safety concerns. Enrolment is expected to be completed in late 2007.
CONCLUSIONS: This study will provide important data on whether routine early PCI within 6 hours after fibrinolysis is safe and superior to the standard treatment of fibrinolysis with rescue PCI or delayed cardiac catheterization.
Ref:
http://www.cardiosource.com/guidelines/PCI_Focused_Update.pdf
Am Heart J. 2008 Jan;155(1):19-25. Epub 2007 Oct 25.
BACKGROUND: Most patients with ST-elevation myocardial infarction present to hospitals without percutaneous coronary intervention (PCI) facilities and receive fibrinolysis. The role of routine early PCI after fibrinolysis, using stents and contemporary pharmacotherapy, has not been studied in a large adequately powered randomized trial.
OBJECTIVE: To compare a pharmacoinvasive strategy of transfer for routine PCI within 6 hours after fibrinolysis with standard treatment after fibrinolysis (including predefined criteria for rescue PCI and delayed cardiac catheterization for patients who do not require rescue PCI).
METHODS: A total of 1200 patients with high-risk ST-elevation myocardial infarction
presenting to non-PCI centers will be randomized to a pharmacoinvasive strategy (transfer for routine PCI within 6 hours of fibrinolysis) or to standard treatment after fibrinolysis. The primary end point is the 30-day composite of death, reinfarction, recurrent ischemia, heart failure, or shock.
RESULTS: More than 900 patients have been enrolled as of April 2007. An interim safety analysis of the first 536 patients demonstrated no safety concerns. Enrolment is expected to be completed in late 2007.
CONCLUSIONS: This study will provide important data on whether routine early PCI within 6 hours after fibrinolysis is safe and superior to the standard treatment of fibrinolysis with rescue PCI or delayed cardiac catheterization.
Ref:
http://www.cardiosource.com/guidelines/PCI_Focused_Update.pdf
Tuesday, December 11, 2007
Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction
Title: 2007 Focused Update of the 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
Source: Developed in Collaboration With the Canadian Cardiovascular Society
Date Posted: 12/10/2007
Author(s): Antman EM, Hand M, Armstrong PW, et al., for the 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee.
Citation: J Am Coll Cardiol. 2008;51:[Epub ahead of print].
Perspective: The following are 10 points to remember about these updated guidelines:
1. Patients routinely taking nonsteroidal anti-inflammatory drugs (except for aspirin), both nonselective as well as cyclooxygenase-2 selective agents, before ST-elevation myocardial infarction (STEMI) should have those agents discontinued at the time of presentation with STEMI because of the increased risk of mortality, reinfarction, hypertension, heart failure, and myocardial rupture associated with their use.
2. Oral beta-blocker therapy should be initiated in the first 24 hours for patients who do not have any of the following: a) signs of heart failure, b) evidence of a low output state, c) increased risk for cardiogenic shock, or d) other relative contraindications to beta blockade (PR interval >0.24 seconds, second- or third-degree heart block, active asthma, or reactive airway disease).
3. STEMI patients presenting to a hospital with PCI capability should be treated with primary percutaneous coronary intervention (PCI) within 90 minutes of first medical contact as a systems goal.
4. STEMI patients presenting to a hospital without PCI capability and who cannot be transferred to a PCI center and undergo PCI within 90 minutes of first medical contact should be treated with fibrinolytic therapy within 30 minutes of hospital presentation as a systems goal unless fibrinolytic therapy is contraindicated.
5. A strategy of coronary angiography with intent to perform PCI (or emergency coronary artery bypass graft surgery) is recommended for patients who have received fibrinolytic therapy and have any of the following: a) cardiogenic shock in patients <75 years who are suitable candidates for revascularization, b) severe congestive heart failure and/or pulmonary edema (Killip class III), or c) hemodynamically compromising ventricular arrhythmias.
6. Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours and preferably for the duration of the index hospitalization, up to 8 days (regimens other than unfractionated heparin [UFH] are recommended if anticoagulant therapy is given for more than 48 hours because of the risk of heparin-induced thrombocytopenia with prolonged UFH treatment). Anticoagulant regimens with established efficacy include:a) UFH (initial intravenous [IV] bolus 60 U/kg [maximum 4000 U]) followed by an IV infusion of 12 U/kg/h (maximum 1000 U/h) initially, adjusted to maintain the activated partial thromboplastin time at 1.5-2.0 times control (~50-70 seconds).b) Enoxaparin (provided the serum creatinine is <2.5 mg/dl in men and 2.0 mg/dl in women): for patients <75 years of age, an initial 30 mg IV bolus is given, followed 15 minutes later by subcutaneous injections of 1.0 mg/kg every 12 hours; for patients at least 75 years of age, the initial IV bolus is eliminated and the subcutaneous dose is reduced to 0.75 mg/kg every 12 hours. Regardless of age, if the creatinine clearance (using the Cockroft-Gault formula) during the course of treatment is estimated to be <30 ml/min, the subcutaneous regimen is 1.0 mg/kg every 24 hours. Maintenance dosing with enoxaparin should be continued for the duration of the index hospitalization, up to 8 days.c) Fondaparinux (provided the serum creatinine is <3.0 mg/dl): initial dose 2.5 mg IV; subsequently subcutaneous injections of 2.5 mg once daily. Maintenance dosing with fondaparinux should be continued for the duration of the index hospitalization, up to 8 days.
7. Clopidogrel 75 mg per day orally should be added to aspirin in patients with STEMI regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. Treatment with clopidogrel should continue for at least 14 days.
8. Every tobacco user and family members who smoke should be advised to quit at every visit.
9. For all post-PCI STEMI stented patients without aspirin resistance, allergy, or increased risk of bleeding, aspirin 162-325 mg daily should be given for at least 1 month after bare-metal stent (BMS) implantation, 3 months after sirolimus-eluting stent implantation, and 6 months after paclitaxel-eluting stent implantation, after which long-term aspirin use should be continued indefinitely at a dose of 75-162 mg daily.
10. For all post-PCI patients who receive a drug-eluting stent, clopidogrel 75 mg daily should be given for at least 12 months if patients are not at high risk of bleeding. For post-PCI patients receiving a BMS, clopidogrel should be given for a minimum of 1 month and ideally up to 12 months (unless the patient is at increased risk of bleeding; then it should be given for a minimum of 2 weeks). Debabrata Mukherjee, M.D., F.A.C.C.
Source: Developed in Collaboration With the Canadian Cardiovascular Society
Date Posted: 12/10/2007
Author(s): Antman EM, Hand M, Armstrong PW, et al., for the 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee.
Citation: J Am Coll Cardiol. 2008;51:[Epub ahead of print].
Perspective: The following are 10 points to remember about these updated guidelines:
1. Patients routinely taking nonsteroidal anti-inflammatory drugs (except for aspirin), both nonselective as well as cyclooxygenase-2 selective agents, before ST-elevation myocardial infarction (STEMI) should have those agents discontinued at the time of presentation with STEMI because of the increased risk of mortality, reinfarction, hypertension, heart failure, and myocardial rupture associated with their use.
2. Oral beta-blocker therapy should be initiated in the first 24 hours for patients who do not have any of the following: a) signs of heart failure, b) evidence of a low output state, c) increased risk for cardiogenic shock, or d) other relative contraindications to beta blockade (PR interval >0.24 seconds, second- or third-degree heart block, active asthma, or reactive airway disease).
3. STEMI patients presenting to a hospital with PCI capability should be treated with primary percutaneous coronary intervention (PCI) within 90 minutes of first medical contact as a systems goal.
4. STEMI patients presenting to a hospital without PCI capability and who cannot be transferred to a PCI center and undergo PCI within 90 minutes of first medical contact should be treated with fibrinolytic therapy within 30 minutes of hospital presentation as a systems goal unless fibrinolytic therapy is contraindicated.
5. A strategy of coronary angiography with intent to perform PCI (or emergency coronary artery bypass graft surgery) is recommended for patients who have received fibrinolytic therapy and have any of the following: a) cardiogenic shock in patients <75 years who are suitable candidates for revascularization, b) severe congestive heart failure and/or pulmonary edema (Killip class III), or c) hemodynamically compromising ventricular arrhythmias.
6. Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours and preferably for the duration of the index hospitalization, up to 8 days (regimens other than unfractionated heparin [UFH] are recommended if anticoagulant therapy is given for more than 48 hours because of the risk of heparin-induced thrombocytopenia with prolonged UFH treatment). Anticoagulant regimens with established efficacy include:a) UFH (initial intravenous [IV] bolus 60 U/kg [maximum 4000 U]) followed by an IV infusion of 12 U/kg/h (maximum 1000 U/h) initially, adjusted to maintain the activated partial thromboplastin time at 1.5-2.0 times control (~50-70 seconds).b) Enoxaparin (provided the serum creatinine is <2.5 mg/dl in men and 2.0 mg/dl in women): for patients <75 years of age, an initial 30 mg IV bolus is given, followed 15 minutes later by subcutaneous injections of 1.0 mg/kg every 12 hours; for patients at least 75 years of age, the initial IV bolus is eliminated and the subcutaneous dose is reduced to 0.75 mg/kg every 12 hours. Regardless of age, if the creatinine clearance (using the Cockroft-Gault formula) during the course of treatment is estimated to be <30 ml/min, the subcutaneous regimen is 1.0 mg/kg every 24 hours. Maintenance dosing with enoxaparin should be continued for the duration of the index hospitalization, up to 8 days.c) Fondaparinux (provided the serum creatinine is <3.0 mg/dl): initial dose 2.5 mg IV; subsequently subcutaneous injections of 2.5 mg once daily. Maintenance dosing with fondaparinux should be continued for the duration of the index hospitalization, up to 8 days.
7. Clopidogrel 75 mg per day orally should be added to aspirin in patients with STEMI regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. Treatment with clopidogrel should continue for at least 14 days.
8. Every tobacco user and family members who smoke should be advised to quit at every visit.
9. For all post-PCI STEMI stented patients without aspirin resistance, allergy, or increased risk of bleeding, aspirin 162-325 mg daily should be given for at least 1 month after bare-metal stent (BMS) implantation, 3 months after sirolimus-eluting stent implantation, and 6 months after paclitaxel-eluting stent implantation, after which long-term aspirin use should be continued indefinitely at a dose of 75-162 mg daily.
10. For all post-PCI patients who receive a drug-eluting stent, clopidogrel 75 mg daily should be given for at least 12 months if patients are not at high risk of bleeding. For post-PCI patients receiving a BMS, clopidogrel should be given for a minimum of 1 month and ideally up to 12 months (unless the patient is at increased risk of bleeding; then it should be given for a minimum of 2 weeks). Debabrata Mukherjee, M.D., F.A.C.C.
Tuesday, November 27, 2007
Glucose-Insulin-Potassium Therapy in Patients With ST-Segment Elevation Myocardial
Title: Glucose-Insulin-Potassium Therapy in Patients With ST-Segment Elevation Myocardial
InfarctionTopic: General CardiologyDate Posted: 11/27/2007
Author(s): Diaz R, Goyal A, Mehta S, et al.Citation: JAMA. 2007;298:2399-2405.
Clinical Trial: No
Study Question: What is the impact of glucose-insulin-potassium (GIK) therapy on outcome of patients presenting with ST-segment elevation myocardial infarction (STEMI)?
Methods: The authors present primary outcome data on 2,748 patients randomized in the OASIS-6 GIK study to GIK versus no infusion. They also present a pooled analysis of the OASIS-6 GIK study and the CREATE-ECLA GIK trial (n = 22,943 patients).
Results: In the OASIS-6 GIK trial, there was no difference in the 6-month mortality (10.8% vs. 10.4%; hazard ratio [HR], 1.04; 95% confidence interval [CI], 0.83-1.31; p = 0.72); heart failure (11.1% vs. 13.5%; HR, 0.83; 95% CI, 0.67-1.02; p = 0.08); or composite of heart failure or mortality (17.5% vs. 19.2%; HR, 0.91; 95% CI, 0.76-1.08; p = 0.27) among patients randomized to GIK compared with controls. Within the pooled trial cohort, there was higher mortality in the GIK group at 3 days (6.2% vs. 5.5%; HR, 1.13; 95% CI, 1.02-1.26; p = 0.03), but there was no difference in the 30-day mortality (9.7% vs. 9.3%; HR, 1.04; 95% CI, 0.96-1.13; p = 0.33). GIK therapy was associated with an increase in glucose and potassium levels, along with a positive volume state in some patients. Patients with one or more of these metabolic derangements after GIK were more likely to have an adverse clinical outcome.
Conclusions: GIK does not provide any clinical benefit in patients with STEMI.
Perspective: Prior preclinical studies and meta-analysis had suggested impressive benefits of GIK in patients with STEMI. While some of the small, randomized trials had suggested impressive survival benefits, a possible increase in mortality in others (e.g., Pol-GIK trial) was dismissed as possibly related to chance. The results of the CREATE-ECLA GIK trial and the current analysis clearly establish the lack of benefit (and possible early harm) of GIK: Another beautiful hypothesis slain by an ugly randomized controlled trial (with apologies to Thomas Huxley). Hitinder S. Gurm, M.B.B.S., F.A.C.C.
InfarctionTopic: General CardiologyDate Posted: 11/27/2007
Author(s): Diaz R, Goyal A, Mehta S, et al.Citation: JAMA. 2007;298:2399-2405.
Clinical Trial: No
Study Question: What is the impact of glucose-insulin-potassium (GIK) therapy on outcome of patients presenting with ST-segment elevation myocardial infarction (STEMI)?
Methods: The authors present primary outcome data on 2,748 patients randomized in the OASIS-6 GIK study to GIK versus no infusion. They also present a pooled analysis of the OASIS-6 GIK study and the CREATE-ECLA GIK trial (n = 22,943 patients).
Results: In the OASIS-6 GIK trial, there was no difference in the 6-month mortality (10.8% vs. 10.4%; hazard ratio [HR], 1.04; 95% confidence interval [CI], 0.83-1.31; p = 0.72); heart failure (11.1% vs. 13.5%; HR, 0.83; 95% CI, 0.67-1.02; p = 0.08); or composite of heart failure or mortality (17.5% vs. 19.2%; HR, 0.91; 95% CI, 0.76-1.08; p = 0.27) among patients randomized to GIK compared with controls. Within the pooled trial cohort, there was higher mortality in the GIK group at 3 days (6.2% vs. 5.5%; HR, 1.13; 95% CI, 1.02-1.26; p = 0.03), but there was no difference in the 30-day mortality (9.7% vs. 9.3%; HR, 1.04; 95% CI, 0.96-1.13; p = 0.33). GIK therapy was associated with an increase in glucose and potassium levels, along with a positive volume state in some patients. Patients with one or more of these metabolic derangements after GIK were more likely to have an adverse clinical outcome.
Conclusions: GIK does not provide any clinical benefit in patients with STEMI.
Perspective: Prior preclinical studies and meta-analysis had suggested impressive benefits of GIK in patients with STEMI. While some of the small, randomized trials had suggested impressive survival benefits, a possible increase in mortality in others (e.g., Pol-GIK trial) was dismissed as possibly related to chance. The results of the CREATE-ECLA GIK trial and the current analysis clearly establish the lack of benefit (and possible early harm) of GIK: Another beautiful hypothesis slain by an ugly randomized controlled trial (with apologies to Thomas Huxley). Hitinder S. Gurm, M.B.B.S., F.A.C.C.
Monday, October 29, 2007
Acute Noncardiac Conditions and In-Hospital Mortality in Patients With Acute Myocardial Infarction
Acute Noncardiac Conditions and In-Hospital Mortality in Patients With Acute Myocardial Infarction
Judith H. Lichtman, John A. Spertus, Kimberly J. Reid, Martha J. Radford, John S. Rumsfeld, Norrina B. Allen, Frederick A. Masoudi, William S. Weintraub, and Harlan M. Krumholz
Circulation. 2007;116:1925-1930; published online before print October 8 2007, doi:10.1161/CIRCULATIONAHA.107.722090
Background— Acute myocardial infarction may be accompanied by acute, severe, concomitant, noncardiac conditions, but their prevalence and prognostic importance is not well defined. We sought to evaluate the prevalence of acute, severe, noncardiac conditions present at the time of hospital admission with acute myocardial infarction and to assess the association of these conditions with in-hospital mortality.
Methods and Results— A total of 3907 patients admitted with an acute myocardial infarction were prospectively enrolled in 19 US centers between January 2003 and June 2004. Acute noncardiac conditions present at admission with imminent threat to life were identified from medical record review within 24 hours of admission. Using multivariable analyses, we evaluated the relationship between these conditions and in-hospital mortality. We documented a concomitant acute, severe, noncardiac condition in 6.8% (n=267) of the study sample. The most common concomitant conditions were severe pneumonia (potentially requiring intubation; 18.4%), severe gastrointestinal bleeding/anemia (15.7%), stroke (9.7%), and sepsis (9.4%). These patients were less likely to be ideal for or to receive evidence-based therapies at the time of admission. The in-hospital mortality was 21.3% (57 of 267) for patients with concomitant conditions versus 2.7% (100 of 3640) for those without these conditions. The presence of an acute noncardiac condition was associated with an increased risk of in-hospital mortality after adjustment for demographic and clinical characteristics and disease severity (odds ratio, 5.0; 95% confidence interval, 3.3 to 7.7).
Conclusions— Concomitant, acute, noncardiac conditions are common and associated with a marked increase in the risk of in-hospital mortality.
Judith H. Lichtman, John A. Spertus, Kimberly J. Reid, Martha J. Radford, John S. Rumsfeld, Norrina B. Allen, Frederick A. Masoudi, William S. Weintraub, and Harlan M. Krumholz
Circulation. 2007;116:1925-1930; published online before print October 8 2007, doi:10.1161/CIRCULATIONAHA.107.722090
Background— Acute myocardial infarction may be accompanied by acute, severe, concomitant, noncardiac conditions, but their prevalence and prognostic importance is not well defined. We sought to evaluate the prevalence of acute, severe, noncardiac conditions present at the time of hospital admission with acute myocardial infarction and to assess the association of these conditions with in-hospital mortality.
Methods and Results— A total of 3907 patients admitted with an acute myocardial infarction were prospectively enrolled in 19 US centers between January 2003 and June 2004. Acute noncardiac conditions present at admission with imminent threat to life were identified from medical record review within 24 hours of admission. Using multivariable analyses, we evaluated the relationship between these conditions and in-hospital mortality. We documented a concomitant acute, severe, noncardiac condition in 6.8% (n=267) of the study sample. The most common concomitant conditions were severe pneumonia (potentially requiring intubation; 18.4%), severe gastrointestinal bleeding/anemia (15.7%), stroke (9.7%), and sepsis (9.4%). These patients were less likely to be ideal for or to receive evidence-based therapies at the time of admission. The in-hospital mortality was 21.3% (57 of 267) for patients with concomitant conditions versus 2.7% (100 of 3640) for those without these conditions. The presence of an acute noncardiac condition was associated with an increased risk of in-hospital mortality after adjustment for demographic and clinical characteristics and disease severity (odds ratio, 5.0; 95% confidence interval, 3.3 to 7.7).
Conclusions— Concomitant, acute, noncardiac conditions are common and associated with a marked increase in the risk of in-hospital mortality.
Tuesday, October 9, 2007
The Case for Early Statin Therapy After AMI
The Case for Early Statin Therapy After AMI
A Japanese study suggests that initiating standard statin therapy immediately after patients suffer an acute myocardial infarction (AMI) appears to decrease long-term mortality and subsequent cardiac events. Among AMI patients, the researchers found that male patients older than 60 and patients with high LDL cholesterol levels (155 mg/dL or greater) appeared to benefit most from early statin therapy. Early statin therapy strongly correlated with a lower risk of cardiovascular death, less recurrence of AMI, and less heart failure. “The hazard ratio for statin therapy was 0.64 throughout the study.” The study was published in the June 1, 2007 American Journal of Cardiology.
An abstract of the study is available at www.sciencedirect.com/
A Japanese study suggests that initiating standard statin therapy immediately after patients suffer an acute myocardial infarction (AMI) appears to decrease long-term mortality and subsequent cardiac events. Among AMI patients, the researchers found that male patients older than 60 and patients with high LDL cholesterol levels (155 mg/dL or greater) appeared to benefit most from early statin therapy. Early statin therapy strongly correlated with a lower risk of cardiovascular death, less recurrence of AMI, and less heart failure. “The hazard ratio for statin therapy was 0.64 throughout the study.” The study was published in the June 1, 2007 American Journal of Cardiology.
An abstract of the study is available at www.sciencedirect.com/
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.
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