The clinical value of mitral A-wave deceleration time in the prediction of a long-term adverse outcome in patients with myocardial infarction.

INTRODUCTION: Mitral A-wave deceleration time (Adt) is a promising Doppler parameter for the evaluation of left ventricular (LV) diastolic function. The aim of the present study was to investigate the long-term prognostic value of Adt in relation to the development of heart failure and cardiac death in the setting of the first acute myocardial infarction (MI). METHODS: Conventional Doppler echocardiographic study and Adt measurements were performed in 105 patients (age 60 +/- 10 years, 77 men) 8.07 +/- 0.96 days post MI. Patients were divided into three groups according to Adt duration: group 1 with Adt > or =70 ms, group 2 with 70 ms < Adt <115 ms, and group 3 with Adt > or =115 ms. RESULTS: Patients of groups 1 (Adt: 64 +/- 5 ms, n=11) and 3 (Adt: 123 +/- 8 ms, n=38) presented characteristics of restrictive physiology or impaired relaxation, respectively, while patients of group 2 (Adt: 92 +/- 9 ms, n=56) had near to normal LV filling characteristics. Patients were followed up for a mean of 44.7 months. Heart failure was found in 4 patients (36%) in group 1 and 6 (16%) in group 3, whereas the patients in group 2 were free of heart failure. Cardiac death occurred in 4 patients (36%) in group 1, 3 (7.9%) in group 3 and 2 (3.6%) in group 2. Kaplan-Meier survival curves indicated that patients with Adt < or =70 ms or Adt > or =115 ms had more frequent cardiac events and a significantly shorter event-free survival period in comparison with those with 70 ms < Adt < 115 ms (p = 0.0017). Cox analysis showed that Adt < or =70 ms (p = 0.002), Adt > or =115 ms (p = 0.02), restrictive LV filling pattern (p = 0.003), anterior wall MI (p = 0.02), ejection fraction (p = 0.03), age (p = 0.04), and treatment with angiotensin converting enzyme inhibitors (p = 0.009) were independent predictors of outcome. CONCLUSIONS: Adt appears to be a strong and independent predictor of heart failure or cardiac death following a MI. A shortened Adt < or =70 ms is associated with higher rates of both cardiac death and heart failure, while a prolonged Adt > or =115 ms is associated with heart failure only.

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.