Role of aldosterone in mid‐ and long‐term left ventricular remodelling after acute myocardial infarction: The REMI study

Author:

Monzo Luca1ORCID,Huttin Olivier1,Ferreira João Pedro12,Lamiral Zohra1,Bozec Erwan1,Beaumont Marine3,Micard Emilien3,Baudry Guillaume1,Marie Pierre‐Yves4,Eschalier Romain56,Rossignol Patrick17,Zannad Faiez1,Girerd Nicolas1

Affiliation:

1. Université de Lorraine, Centre d'Investigations Cliniques Plurithématique 1433 and Inserm U1116, CHRU Nancy, FCRIN INI‐CRCT (Cardiovascular and Renal Clinical Trialists) Nancy France

2. Cardiovascular Research and Development Center, Department of Surgery and Physiology, Faculty of Medicine University of Porto Porto Portugal

3. Centre d'Investigations Cliniques IADI U947 Centre Hospitalier Universitaire de Nancy Vandoeuvre les Nancy France

4. CHRU‐Nancy, Université de Lorraine, Nuclear Medicine & Nancyclotep Imaging Platform Nancy France

5. Cardiology Department CHU Clermont‐Ferrand Clermont‐Ferrand France

6. Université Clermont Auvergne, CHU Clermont‐Ferrand, CNRS, SIGMA Clermont, Institut Pascal Clermont‐Ferrand France

7. Department of Medicine and Nephrology‐Hemodialysis Princess Grace Hospital, and Monaco Private Hemodialysis Centre La Colle Monaco

Abstract

AbstractAimsWhether aldosterone levels after myocardial infarction (MI) are associated with mid‐ 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 resultsPlasma aldosterone was measured in 119 patients successfully treated by primary percutaneous coronary angioplasty for a first acute ST‐elevation 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. In the multivariable model, higher post‐MI aldosterone concentration was significantly associated with more pronounced increase in LV end‐diastolic volume index (TTE: β ± standard error [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 patients with a LV ejection fraction (LVEF) >40%. The association between baseline plasma aldosterone and adverse LV remodelling did not persist at the 3–9‐year follow‐up evaluation.ConclusionAldosterone concentration in the acute phase was associated with adverse LV remodelling in the medium 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).

Funder

Ministère de la Santé et des Services sociaux

Publisher

Wiley

Subject

Cardiology and Cardiovascular Medicine

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