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Role of aldosterone in the mid‐ and long‐term left ventricular remodelling after acute myocardial infarction: the REMI study
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Edité par CCSD ; European Society of Cardiology (Wiley) -
International audience. Abstract Aims Whether aldosterone levels after myocardial infarction (MI) are associated with medium and long‐term left ventricular (LV) remodelling in the era of systematic use of renin‐angiotensin system inhibitors is uncertain. We prospectively investigated the relationship between aldosterone levels and mid‐ and long‐term LV remodelling in patients with acute MI. Methods and results Plasma aldosterone was measured in 119 patients successfully treated by primary percutaneous coronary angioplasty for a first acute ST‐elevated MI (STEMI) 2‐4 days after the acute event. LV volumes were assessed by cardiac magnetic resonance (CMR) and transthoracic echocardiography (TTE) in the same timeframe and 6 months later. LV assessment was repeated by TTE 3‐9 years after MI (N=80). The median aldosterone level at baseline was 23.1 [16.8; 33.1] pg/mL. Higher post‐MI aldosterone concentration was significantly associated in multivariable model with more pronounced increase in LV end‐diastolic volume index (TTE: β ± SE: 0.113 ± 0.046, P =0.015; CMR: β ± SE: 0.098 ± 0.040, P =0.015) and LV end‐systolic volume index (TTE: β ± SE: 0.083 ± 0.030, P=0.008; CMR: β ± SE: 0.064 ± 0.032, P =0.048) at 6‐month follow‐up, regardless of the method of assessment. This result was consistent also in patient with a LV ejection fraction (LVEF) >40%. The association between baseline plasma aldosterone and adverse LV remodelling did not persist at the 3‐9 years follow‐up evaluation. Conclusion Aldosterone concentration in the acute phase was associated with adverse LV remodelling in the mid‐term, even in the subgroup of patients with LVEF >40%, suggesting a potential role of the mineralocorticoid system in post‐MI adverse remodelling. Plasma aldosterone was no longer associated with LV remodelling in the long‐term. ( NCT01109225) This article is protected by copyright. All rights reserved.
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