Abstract
Left ventricular remodeling (LVR) is a strong predictor of cardiovascular events after myocardial infarction (MI). Although several factors have been shown to influence LVR, interindividual variability exists. Some studies have suggested that gene polymorphisms may be associated with LVR, but these studies were limited by either a retrospective design or the inclusion of limited patient numbers. The present study was designed to prospectively assess the impact of gene polymorphisms on LVR. We included 266 patients with inaugural anterior MI. Systematic echocardiographic follow-ups were performed at 3 months and at 1 year after MI. The polymorphisms were selected using a candidate gene approach based on LVR pathophysiology. We analyzed 14 polymorphisms in 3 different systems: the renin-angiotensin-aldosterone system (ACE I/D, RAT1 1166A/C, angiotensinogen M235T, CYP11B2 -344C/T), the adrenergic system (beta1AR Ser49Gly, beta1AR Gly389Arg, beta2AR Gly16Arg, beta2AR Gln27Glu, beta2AR Thr164Ile, alpha2cAR Del322-325), and the metalloproteinase (MMP) system (-1607 1G/2G MMP-1, -1306 C/T MMP-2, -1171 5A/6A MMP-3, -1562 C/T MMP-9). Left ventricular remodeling was documented by a progressive increase in end-diastolic volume from 56.5 +/- 14.9 mL/m2 at baseline to 62.8 +/- 18.8 mL/m2 at 1 year (P < .0001). End-diastolic volume at baseline, 3 months, or 1 year did not differ significantly among genotypes for any polymorphism. The change in end-diastolic volume from baseline to 1 year was also similar among genotypes for all polymorphisms. Left ventricular remodeling after MI is not associated with common polymorphisms in the renin-angiotensin-aldosterone, adrenergic, or MMP systems.
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