Plasma Galectin-3 predicts deleterious vascular dysfunction affecting post-myocardial infarction patients: An explanatory study.

Olivier Huttin,Pierre-Yves Marie,Zohra Lamiral,Patrick Rossignol,Emilien Micard,Nicolas Girerd,Freddy Odille,Faïez Zannad,Batric Popovic,Damien Mandry

doi:10.1371/journal.pone.0232572

Abstract

In a previous analysis of a post-myocardial infarction (MI) cohort, abnormally high systemic vascular resistances (SVR) were shown to be frequently revealed by MRI during the healing period, independently of MI severity, giving evidence of vascular dysfunction and limiting further recovery of cardiac function. The present ancillary and exploratory analysis of the same cohort was aimed at characterizing those patients suffering from high SVR remotely from MI with a large a panel of cardiovascular MRI parameters and blood biomarkers. MRI and blood sampling were performed 2-4 days after a reperfused MI and 6 months thereafter in 121 patients. SVR were monitored with a phase-contrast MRI sequence and patients with abnormally high SVR at 6-months were characterized through MRI parameters and blood biomarkers, including Galectin-3, an indicator of cardiovascular inflammation and fibrosis after MI. SVR were normal at 6-months in 90 patients (SVR-) and abnormally high in 31 among whom 21 already had high SVR at the acute phase (SVR++) while 10 did not (SVR+). When compared with SVR-, both SVR+ and SVR++ exhibited lower recovery in cardiac function from baseline to 6-months, while baseline levels of Galectin-3 were significantly different in both SVR+ (median: 14.4 (interquartile range: 12.3-16.7) ng.mL-1) and SVR++ (13.0 (11.7-19.4) ng.mL-1) compared to SVR- (11.7 (9.8-13.5) ng.mL-1, both p < 0.05). Plasma Galectin-3 was an independent baseline predictor of high SVR at 6-months (p = 0.002), together with the baseline levels of SVR and left ventricular end-diastolic volume, whereas indices of MI severity and left ventricular function were not. In conclusion, plasma Galectin-3 predicts a deleterious vascular dysfunction affecting post-MI patients, an observation that could lead to consider new therapeutic targets if confirmed through dedicated prospective studies.

Highlights

IntroductionIn the previous “REMI” (relation between aldosterone and cardiac REmodeling after Myocardial Infarction) cohort, a lower recovery in cardiac function was documented in patients for whom systemic vascular resistances (SVR) were abnormally high during the post-myocardial infarction (MI) healing period, independently of MI severity and in spite of the commonly prescribed vasodilator regimens (Angiotensin Converting Enzyme Inhibitors (ACEI) or Angiotensin Receptor Blockers (ARBs)) [1]
In the previous “REMI” cohort, a lower recovery in cardiac function was documented in patients for whom systemic vascular resistances (SVR) were abnormally high during the post-myocardial infarction (MI) healing period, independently of MI severity and in spite of the commonly prescribed vasodilator regimens (Angiotensin Converting Enzyme Inhibitors (ACEI) or Angiotensin Receptor Blockers (ARBs)) [1]
When compared with SVR, both SVR+ and SVR++ exhibited lower recovery in cardiac function from baseline to 6-months, while baseline levels of Galectin-3 were significantly different in both SVR+ (median: 14.4 ng.mL-1) and SVR++ (13.0 (11.7–19.4) ng.mL-1) compared to SVR- (11.7 (9.8–13.5) ng.mL-1, both p < 0.05)

Summary

Introduction

In the previous “REMI” (relation between aldosterone and cardiac REmodeling after Myocardial Infarction) cohort, a lower recovery in cardiac function was documented in patients for whom systemic vascular resistances (SVR) were abnormally high during the post-myocardial infarction (MI) healing period, independently of MI severity and in spite of the commonly prescribed vasodilator regimens (Angiotensin Converting Enzyme Inhibitors (ACEI) or Angiotensin Receptor Blockers (ARBs)) [1] Such patients with high SVR may be difficult to detect after MI, as well as in the more general setting of heart failure, hypertension being frequently masked by decreases in cardiac contractility and stroke volume [1,2]. This analysis should consider certain hemodynamic factors, especially the fact that higher SVR are required for maintaining a sufficiently high blood pressure (BP) in patients presenting the lowest stroke volumes [3,5,10,11]

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