Background: Progressive left ventricular dilatation (PLVD) occurs after myocardial infarction
(MI), and this may take place in the area of primary percutaneous coronary intervention
(PCI). The factors predicting PLVD after primary PCI still need to be clarified. The aim of the
study was to assess the prevalence and to define the baseline clinical and echocardiographic
predictors of PLVD in patients with STEMI treated by primary PCI.
Methods: Of the 90 patients initially selected for the study 88 (29 women and 59 men, mean
age 67.1 ± 5.6 years) with first ST-elevation myocardial infarction (STEMI) treated with
primary PCI were examined. Echocardiographic examination was performed in all patients at
discharge (M1) and after 6 months (M2). The following factors influencing PLVD were
evaluated: type of infarct-related artery (IRA), infarct size expressed as wall motion score index
(WMSI) ≥ 1.5, left ventricular end-diastolic volume index (LVEDVI) ≥ 80 ml/m2, ejection
fraction (EF) ≤ 45%, restrictive pattern of transmitral flow, time to reperfusion, left ventricular
mass index (LVMI) ≥ 125 g/m2 and coronary risk factors.
Results: The overall prevalence of PLVD (according to the criterion of 20% LVEDVI increase
from M1 to M2) was 24%. Univariate regression analysis revealed that the following were the
significant baseline M1 predictors of adverse PLVD: left anterior descending as IRA (relative risk:
rr = 2.3, p < 0.05), WMSI ≥ 1.5 (rr = 4.29, p < 0.005), EF ≤ 45% (rr = 2.89, p < 0.005) and
a restrictive pattern of transmitral flow (rr = 2.4, p < 0.01). Multivariate logistic analysis
showed that the only independent determinant of PLVD was WMSI ≥ 1.5.
Conclusions: Both regional and global left ventricular systolic dysfunction indices as well as
severe left ventricular diastolic abnormalities but not left ventricular dilatation at discharge
are significant predictors of adverse cardiac remodelling after STEMI in patients treated with
primary PCI. However the only independent determinant of PLVD was WMSI ≥ 1.5 expressing
the infarct size. (Cardiol J 2007; 14: 238-245
