Echocardiographic diastolic function evolution in patients with an anterior Q‐wave myocardial infarction: insights from the REVE‐2 study

AIMS: Myocardial fibrosis plays a key role in the development of adverse left ventricular remodelling after myocardial infarction (MI). This study aimed to determine whether the circulating levels of BNP, collagen peptides, and galectin‐3 are associated with diastolic function evolution (both deterioration and improvement) at 1 year after an anterior MI. METHODS AND RESULTS: The REVE‐2 is a prospective multicentre study including 246 patients with a first anterior Q‐wave MI. Echocardiographic assessment was performed at hospital discharge and ±1 year after MI. BNP, galectin‐3, and collagen peptides were measured ±1 month after MI. Left ventricular diastolic dysfunction (DD) was defined according to the presence of at least two criteria of echocardiographic parameters: septal e′ < 8 cm/s, lateral e′ < 10 cm/s, and left atrial volume ≥ 34 mL/m(2). At baseline, 87 (35.4%) patients had normal diastolic function and 159 (64.6%) patients had DD. Follow‐up of 61 patients among the 87 patients with normal diastolic function at baseline showed that 22 patients (36%) developed DD at 1 year post‐MI. The circulating levels of amino‐terminal propeptide of type III procollagen > 6 mg/L [odds ratio (OR) = 5.29; 95% confidence interval (CI) = 1.05–26.66; P = 0.044], galectin‐3 > 13 μg/L (OR = 5.99; 95% CI = 1.18–30.45; P = 0.031), and BNP > 82 ng/L (OR = 10.25; 95% CI = 2.36–44.50; P = 0.002) quantified at 1 month post‐MI were independently associated with 1 year DD. Follow‐up of the 137 patients with DD at baseline among the 159 patients showed that 36 patients (26%) had a normalized diastolic function at 1 year post‐MI. Patients with a BNP > 82 ng/L were less likely to improve diastolic function (OR = 0.06; 95% CI = 0.01–0.28; P = 0.0003). CONCLUSIONS: The present study suggests that circulating levels of amino‐terminal propeptide of type III procollagen, galectin‐3, and BNP may be independently associated with new‐onset DD in post‐MI patients.