Objectives: Acute myocardial infarction induces diastolic dysfunction as a result of the alteration of left ventricular relaxation and stiffness caused by ischemia and fibrosis. This study analyzes the association of infarct size with the diastolic filling pattern and the evolution of the latter during the first postinfarction year.
Patients and methods: The study group consisted of 68 patients with a first acute myocardial infarction treated with thrombolytic agents. A Doppler echocardiography was performed at 8 +/- 2, 32 +/- 7 and 370 +/- 23 days after infarction. Five measurements of the ratio between E and A waves peak velocities (E/A ratio) and of the E deceleration time (EDT, ms) were averaged in each echocardiographic study. The patients were divided according to infarct size into a large infarct group (creatine kinase > 1,000 U/ml; 1,913 +/- 883; n = 26) and a small infarct group (creatine kinase < 1,000 U/ml; 556 +/- 227; n = 42).
Results: The large infarct group exhibited a greater E/A ratio and shorter EDT than the small infarct group in the first week (E/A ratio: 1.4 +/- 0.7 vs 0.8 +/- 0.3; p = 0.0001; EDT: 159 +/- 49 vs 192 +/- 56; p = 0.02) and at one month (E/A ratio: 1.2 +/- 0.7 vs 0.9 +/- 0.3; p = 0.01; EDT: 170 +/- 55 vs 207 +/- 40; p = 0.004); however no differences were observed between either group at one year in either E/A ratio (0.8 +/- 0.2 vs 0.9 +/- 0.4; NS) or EDT (207 +/- 44 vs 219 +/- 54; NS). In the large infarct group, E/A ratio decreased and EDT increased at one year compared to the first week (E/A ratio: p = 0.0004; EDT: p = 0.0001) and the first month (E/A: p = 0.02; EDT: p = 0.003); in contrast, in the small infarct group there were no significant differences in E/A ratio nor EDT during the first year postinfarction.
Conclusions: In the first month postinfarction, large infarcts exhibit a greater E/A ratio and shorter EDT than small infarcts. The evolution of large infarcts is characterized by an attenuation of this pattern, with a progressive reduction of E/A ratio and prolongation of EDT during the first year post-infarction.