Background: Renin -angiotensin-system activity, a principal factor determining ventricular remodelling after myocardial infarction (MI), is dependant on local angiotensin II concentration and angiotensin AT 1 receptor (AT 1 R) density. The latter is regulated by systemic factors acting independently from angiotensin II concentration. Objective: To test the hypothesis that AT 1 R density at the onset of MI determines post-MI ventricular remodelling. Methods: In 48 patients with first acute MI who did not undergo reperfusion therapy, angiotensin AT 1 R density on blood platelets (reflecting cardiovascular AT 1 R density) was assessed 13 T 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. Results: Predischarge LVESVI and LVEDVI positively and EF negatively correlated with AT 1 R density. Patients with AT 1 R density below median had significantly lower LVESVI (33.2 T 2.4 mL/m 2 ), LVEDVI (70.0 T 2.8 mL/m 2 ) and higher EF (52.8 T 2.3%) than patients with AT 1 R density above median (LVESVI = 44.9 T 2.6, LVEDVI = 81.3 T 3.9 mL/m 2 and EF = 44.9 T 2.6%, all p < 0.01). In multivariate analysis, only AT 1 R density and infarct size were independent predictors of early post-MI ventricular dilation. Conclusions: High density of AT 1 R at the onset of MI is a predictor of early left ventricular remodelling.

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