Influence of angiotensin II receptors blocking on overall left ventricle's performance of patients with acute myocardial infarction of limited extent. Echocardiographic assessment.

INTRODUCTION: Recent studies documented the beneficial effect of angiotensin-receptor blockers (ARBs) on patients (pts) with acute myocardial infarction (AMI) combined with left ventricle (LV) systolic dysfunction. The present study intended to assess the impact of the ARB irbesartan, on the overall LV performance in pts with uncomplicated AMI of limited extent. METHODS: Forty consecutive pts with first inferior AMI (AMI-I) and preserved LV-systolic function were enrolled. They were allocated into two groups: (a) 20 pts received the conventional treatment of AMI-I and placebo (CT) and (b) 20 pts administered irbesartan additionally to the conventional treatment (IR). Twenty four healthy individuals of matching age and sex were recruited as control group (CG). Complete echocardiographic examination, Tei index of overall LV function and systolic blood pressure (SBP) were measured on the 8th post-infarct day. RESULTS: The Tei index of IR group (0.53+/-0.03) was significantly lower compared to that of CT group (0.78+/-0.05) (p<0.001) and was similar to that of CG (0.45+/-0.03)(p=NS). Irbesartan induced a considerable decrease in both isovolumic relaxation (115+/-7 ms vs 140+/-7 ms; p<0.01) and contraction time (52+/-2 ms vs 64+/-3 ms; p<0.01) and a significant increase in ejection time (279+/-6 ms vs 256+/-8 ms; p<0.05). SBP in pts of IR group was similar to that of CT group (112+/-3 mmHg vs 113+/-4 mmHg; p=NS). CONCLUSIONS: Therapy with Irbesartan improves overall LV function of pts with AMI-I. Irbesartan leads to acceleration of the LV relaxation, which possibly indirectly ameliorates LV systolic performance too. This beneficial influence is possible attributed to a direct tissue effect of the drug and not to its hemodynamic action.

Influence of perindopril on left ventricular global performance during the early phase of inferior acute myocardial infarction: assessment by Tei index.

UNLABELLED: The beneficial effect of angiotensin-converting enzyme inhibitors (ACE inhibitors) on left ventricular (LV) function in patients with acute myocardial infarction (AMI) is widely known. However, controversy exists about their efficacy on patients with small infarcts and preserved LV systolic function. The aim of the present study was to detect the influence of the ACE-I perindopril on the global LV performance in patients with pure inferior AMI (AMI-I) using a Doppler-derived index (DI) that combines systolic and diastolic time intervals (Tei index). Our study included 40 patients with first AMI-I, mean age 60 years +/- 9.06 years (SD) and 24 age- and gender-matched normal patients who constituted the control group (COG). Patients were randomized into two groups to receive the conventional treatment of AMI-I (GCT) or the above therapy plus P (GP). Complete Doppler echocardiography (systolic and diastolic parameters), DI, and systolic blood pressure (SBP) were measured on the 8.07 +/- 1.16(SD) post-infarct day. The same examination was performed to COG. The DI was significantly lower in healthy patients(0.45 +/- 0.23)compared with the value in patients of either GP(0.56 +/- 0.03; P = 0.023)or GCT(0.78 +/- 0.05; P = 0.000). Moreover DI was higher in patients of GCT compared with that of GP(P = 0.000). In addition, perindopril administration decreased isovolumic relaxation time(IRT; 120.00 +/- 4.23 vs. 139.00 +/- 6.74; P = 0.006)and increased significantly ejection time (ET;274.25 +/- 7.35 vs. 253.50 +/- 7.68; P = 0.042). SBP in patients of GP was similar to that of GCT(120.5 +/- 2.85 mmHg vs. 112.5 +/- 3.49 mmHg; P = NS). CONCLUSIONS: Global LV function (DI) is impaired in patients with AMI-I. Administration of perindopril has a favorable impact on LV performance in patients with AMI-I, achieved through improvement of the diastolic function (IRT), which indirectly improves LV systolic function (ET, DI). This beneficial influence of perindopril is the result of the direct tissue effect of the drug and not its hemodynamic action.