LEFT-VENTRICULAR REMODELING IN THE YEAR AFTER MYOCARDIAL-INFARCTION - AN ECHOCARDIOGRAPHIC, HEMODYNAMIC, AND RADIONUCLIDE ANGIOGRAPHIC STUDY

Background: The factors that influence infarct expansion early after myocardial infarction have been identified; however, there is less information about late-phase left ventricular enlargement. This study was designed to identify the clinical, haemodynamic, echocardiographic, and radionuclide angiographic criteria that predict the progress of left ventricular dilation after discharge for a first-anterior myocardial infarction. Methods: Sixty-seven patients with first Q-wave acute anterior myocardial infarction not treated with thrombolytic agents underwent baseline echocardiographic, haemodynamic, and radionuclide angiographic evaluation 4-7 days after the onset of symptoms. The echocardiographic and radionuclide evaluations were repeated after 1 year in the 55 patients who completed the follow-up. By multivariate stepwise linear regression analysis, left ventricular end-diastolic volume after 1 year and change from baseline were modelled as a function of baseline left ventricular end-diastolic volume and other potential predictors. Results: A model including left ventricular end-diastolic pressure, global wall motion score, baseline left ventricular end-diastolic volume, and a Thrombolysis in Myocardial Infarction (TIMI) score of 0-1 was able to predict 84% of the left ventricular end-diastolic volume at the follow-up; a TIMI score of G-1, the transverse end-diastolic diameter, global wall motion score, and the number of coronary vessels with 70% stenosis accounted for 81% of the variation in left ventricular end-diastolic volume from baseline, while the transverse end-diastolic diameter was inversely related to this parameter. Conclusions: The results of this study demonstrate that after an anterior myocardial infarction, the patency of the infarct-related artery is the major determinant of late left ventricular dilation, while left ventricular end-diastolic pressure influences early left ventricular dilation and baseline end-diastolic volume. Therefore, to improve left ventricular remodelling, it appears necessary to increase the patency of the infarct-related artery and improve the diastolic loading of the left ventricle at an early stage in the infarction. The inverse relationship between baseline left ventricular transverse diameter and the change in left ventricular volume after discharge indicates that the higher the baseline left ventricular volume, the less it changed during the follow-up. The global wall motion score appears to be a non-invasive parameter that is useful for identifying patients with a high risk of progressive left ventricular dilation.