An Initial Strategy of Intensive Medical Therapy Is Comparable to That of Coronary Revascularization for Suppression of Scintigraphic Ischemia in High-Risk But Stable Survivors of Acute Myocardial Infarction

ObjectivesThe purpose of this study was to determine the relative benefit of intensive medical therapy compared with coronary revascularization for suppressing scintigraphic ischemia.BackgroundAlthough medical therapies can reduce myocardial ischemia and improve patient survival after acute myocardial infarction, the relative benefit of medical therapy versus coronary revascularization for reducing ischemia is unknown.MethodsA prospective randomized trial in 205 stable survivors of acute myocardial infarction was made to define the relative efficacy of an intensive medical therapy strategy versus coronary revascularization for suppressing scintigraphic ischemia as assessed by serial gated adenosine Tc-99m sestamibi myocardial perfusion tomography. All patients at baseline had large total (≥20%) and ischemic (≥10%) adenosine-induced left ventricular perfusion defects and an ejection fraction ≥35%. Imaging was performed during 1 to 10 days of hospital admission and repeated in an identical fashion after optimization of therapy. Patients randomized to either strategy had similar baseline demographic and scintigraphic characteristics.ResultsBoth intensive medical therapy and coronary revascularization induced significant but comparable reductions in total (−16.2 ± 10% vs. −17.8 ± 12%; p = NS) and ischemic (−15 ± 9% vs. −16.2 ± 9%; p = NS) perfusion defect sizes. Likewise, a similar percentage of patients randomized to medical therapy versus coronary revascularization had suppression of adenosine-induced ischemia (80% vs. 81%; p = NS).ConclusionsSequential adenosine sestamibi myocardial perfusion tomography can effectively monitor changes in scintigraphic ischemia after anti-ischemic medical or coronary revascularization therapy. A strategy of intensive medical therapy is comparable to coronary revascularization for suppressing ischemia in stable patients after acute infarction who have preserved LV function

Association of Angiotensin I-Converting Enzyme Gene Polymorphism With Myocardial Ischemia and Patency of Infarct-Related Artery in Patients With Acute Myocardial Infarction

AbstractObjectives. We determined the influence of angiotensin I-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism on the extent of myocardial ischemia in patients with acute myocardial infarction.Background. The I/D polymorphism, which in part controls plasma and tissue expression of ACE, has been implicated in predisposition to myocardial infarction and ventricular remodeling.Methods. I/D genotyping, predischarge adenosine–thallium-201 perfusion tomography and radionuclide angiography were performed in 113 patients (72 men, 41 women) with a diagnosis of acute myocardial infarction. A subgroup of 96 patients also underwent coronary angiography.Results. Genotypes DD, ID and II were present in 27, 56 and 30 patients, respectively. There was no significant difference in the baseline characteristics of patients, total creatine kinase, peak MB fraction, Killip class, mean ejection fraction or the number of diseased vessels in patients with the DD, ID or II genotype. However, the size of the total and the reversible perfusion defects was greater in those with DD than in those with ID or II genotype (total defect size [mean ± SD] 33.7 ± 22.5%, 29.5 ± 19.2% and 22.2 ± 16.0%, respectively [p = 0.022]; reversible defect size 18.0 ± 16.0%, 12.1 ± 11.6% and 8.2 ± 7.8%, respectively [p = 0.006]). Occlusion of the infarct-related artery was also more common in patients with DD genotype (odds ratio 3.9, 95% confidence interval 1.4 to 11.0). Multivariate analysis showed that the I/D genotype was an independent predictor of perfusion defect size and patency of the infarct-related artery (p = 0.001).Conclusions. DD genotype was associated with a larger ischemic defect and occlusion of the infarct-related artery. Patients with DD genotype, having a larger ischemic defect, are expected to be at a greater risk for subsequent cardiovascular events.(J Am Coll Cardiol 1997;29:1468–73