LEFT-VENTRICULAR DILATATION FOLLOWING MYOCARDIAL-INFARCTION

The aim of this prospective study was to investigate if left ventricul ar dilatation is confined to the early months following myocardial inf arction, or if it is a progressive process over several years. One hun dred patients (pts) who suffered from stable angina or had undergone m yocardial infarction, could be examined twice by coronary arteriograph y including ventriculography in an interval of 52 +/- 14 months. The p atients were retrospectively divided into three groups: 41 pts (group A) had coronary heart disease without prior myocardial infarction, in 29 pts (group B) the first examination was performed within (mean 2 +/ - 1 mo.) and in 30 pts (group C) beyond 6 months after myocardial infa rction (mean 32 +/- 24 mo.). The three groups were comparable concerni ng clinical data, but more pts with former myocardial infarction had m ulti-vessel disease (34 of 59 vs 16 of 41 pts) and depressed left vent ricular function. Left ventricular angiography was performed in RAO vi ew 300 after enddiastolic pressure (LVEDP) was registered. Left ventri cular enddiastolic and endsystolic volumes (EDVI and ESVI) were calcul ated by use of a modified Simpson's rule equation. In group A, EDVI an d LVEDP remained constant, whereas ESVI increased slightly but signifi cantly. Pts of group B and C had significantly higher volumes, which i ncreased significantly in both groups over a mean of 52 months. About half the pts suffered from ventricular dilatation independent of progr ession of underlying coronary sclerosis. Consecutively, left ventricul ar ejection fraction decreased and LVEDP rose significantly in both gr oups. Thus, left ventricular dilatation is not only confined to the ea rly months after myocardial infarction, but is a progressive process o ver several years, which is independent of progression of coronary hea rt disease. At risk were pts who had already increased volume indexes and reduced ventricular function at the initial catheterization.