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Showing posts with label Myocardial Ischemia. Show all posts
Showing posts with label Myocardial Ischemia. Show all posts

Wednesday, November 14, 2007

ARBs could reduce effort myocardial ischemia

ARBs could reduce effort myocardial ischemia


By Caroline Price - MedwireNews


13 November 2007


Am J Cardiol 2007; 100: 1517-1521


MedWire News: Treatment with the angiotensin receptor blocker (ARB) losartan decreased electrocardiographic measures of ischemia in patients with stable coronary artery disease (CAD), suggesting a possible role for this class of drugs in effort myocardial ischemia, report US researchers.


"Our results showed that losartan 100 mg is able to decrease transient exercise-induced myocardial ischemia by decreasing time to onset of 1-mm ST segment depression, ST-segment depression at peak exercise, and time to recovery of ST-segment depression and increasing exercise duration and maximal workload," report Giancarlo Longobardi (Scientific Institute of Telese Terme, Italy).


The researchers randomly assigned 28 CAD patients to receive losartan 100 mg or placebo for 28 days, followed by 1 week of placebo in both groups and then cross-over to the alternative regimen for a further 28 days.


All patients had reproducible positive exercise test results at the beginning of the study and were normotensive and in sinus rhythm. None of the patients had evidence of left ventricular hypertrophy or conduction defects, or a history of myocardial infarction.


Patients underwent an exercise stress test at the end of each phase of the study.


The results, published in the American Journal of Cardiology, showed that patients' systolic blood pressure (SBP) levels were significantly decreased with losartan compared with placebo (p<0.05). SBP and rate-pressure product were lower after losartan treatment than after placebo at submaximal exercise (both p<0.005), at 1-mm ST depression (p<0.001 and p<0.02, respectively), and at peak exercise (p<0.001 and p<0.005, respectively).


Patients had significantly delayed time to 1-mm ST-depression onset after losartan treatment compared with placebo treatment (479 vs 475 seconds, p<0.01) as well as decreased ST-segment depression at peak exercise (1.3 vs 1.0, p<0.05) and time to recovery of ST-segment depression (120 vs 177, p<0.01).


Furthermore, losartan treatment significantly increased exercise duration (603 vs 565 seconds, p<0.001) and maximal workload (4208 vs 3742 kg, p<0.001) during exercise stress testing compared with placebo.


The team speculates that the mechanism of action, similar to that of nitrates, is likely related to vasodilation in conductive arteries, with a relative decrease in afterload, and vasodilator effects on epicardial and resistance vessels in the coronary circulation.


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Friday, October 26, 2007

Resolution of Asymptomatic Myocardial Ischemia in Patients With Type 2 Diabetes in the Detection of Ischemia in Asymptomatic Diabetics (DIAD) Study

Resolution of Asymptomatic Myocardial Ischemia in Patients With Type 2 Diabetes in the Detection of Ischemia in Asymptomatic Diabetics (DIAD) Study

Diabetes Care 2007 30: 2892-2898

Frans J. Th. Wackers, MD, Deborah A. Chyun, PHD, Lawrence H. Young, MD, Gary V. Heller, MD, Ami E. Iskandrian, MD, Janice A. Davey, MSN, Eugene J. Barrett, MD, Raymond Taillefer, MD, Steven D. Wittlin, MD, Neil Filipchuk, MD, Robert E. Ratner, MD, Silvio E. Inzucchi, MD for the Detection of Ischemia in Asymptomatic Diabetics (DIAD) Investigators



ABSTRACT


OBJECTIVE
The porrpose of this study was to assess whether the prevalence of inducible myocardial ischemia increases over time in patients with type 2 diabetes.


RESEARCH DESIGN AND METHODS
Participants enrolled in the Detection of Ischemia in Asymptomatic Diabetics (DIAD) study underwent repeat adenosine-stress myocardial perfusion imaging 3 years after initial evaluation. Patients with intervening cardiac events or revascularization and those who were unable or unwilling to repeat stress imaging were excluded.


RESULTS
Of the initial 522 DIAD patients, 358 had repeat stress imaging (DIAD-2), of whom 71 (20%) had ischemia at enrollment (DIAD-1). Of 287 patients with normal DIAD-1 studies, 259 (90%) remained normal in DIAD-2, whereas 28 (10%) developed new ischemia in DIAD-2. Of the 71 patients with abnormal DIAD-1 studies, 56 (79%) demonstrated resolution of ischemia, whereas 15 (21%) remained abnormal. During this 3-year interval, medical treatment was intensified, with more patients using statins, aspirin, and ACE inhibitors than at baseline. Patients with resolution of ischemia had significantly greater increases in these medications than patients who developed new ischemia (P = 0.04).


CONCLUSIONS
Thus, the majority of asymptomatic patients with type 2 diabetes demonstrated resolution of ischemia upon repeat stress imaging after 3 years. This resolution was associated with more intensive treatment of cardiovascular risk factors.