Angiotensin II AT1 receptor density on blood platelets predicts early left ventricular remodelling in non‐reperfused acute myocardial infarction in humans

Abstract

Renin-angiotensin-system activity, a principal factor determining ventricular remodelling after myocardial infarction (MI), is dependent on local angiotensin II concentration and angiotensin AT1 receptor (AT1R) density. The latter is regulated by systemic factors acting independently from angiotensin II concentration. To test the hypothesis that AT1R density at the onset of MI determines post-MI ventricular remodelling. In 48 patients with first acute MI who did not undergo reperfusion therapy, angiotensin AT1R density on blood platelets (reflecting cardiovascular AT1R density) was assessed 13+/-5 h after the onset of MI, using radioligand binding assay. Left ventricular end-systolic (LVESVI) and end-diastolic volume indices (LVEDVI) and ejection fraction (EF) were assessed by two-dimensional echocardiography as measures of ventricular remodelling. Predischarge LVESVI and LVEDVI positively and EF negatively correlated with AT1R density. Patients with AT1R density below median had significantly lower LVESVI (33.2+/-2.4 mL/m2), LVEDVI (70.0+/-2.8 mL/m2) and higher EF (52.8+/-2.3%) than patients with AT1R density above median (LVESVI = 44.9+/-2.6, LVEDVI = 81.3+/-3.9 mL/m2 and EF = 44.9+/-2.6%, all p<0.01). In multivariate analysis, only AT1R density and infarct size were independent predictors of early post-MI ventricular dilation. High density of AT1R at the onset of MI is a predictor of early left ventricular remodelling.