Galectin-3 and Cardiac Function in Survivors of Acute Myocardial Infarction

Abstract

Background-Galectin-3 is a biomarker associated with inflammation and fibrosis that predicts adverse outcome and relates to biomarkers of extracellular matrix turnover in patients with heart failure, particularly when left ventricular (LV) systolic function is preserved. Whether galectin-3 is related to LV remodeling after acute myocardial infarction is unknown. Methods and Results-Circulating galectin-3 and various extracellular matrix biomarkers were measured in 100 patients (age, 58.9±12.0 years; 77% men) admitted with acute myocardial infarction and LV dysfunction, at baseline (mean 46 hours) and at 24 weeks, with cardiac MRI at each time-point. LV remodeling was defined as change in LV endsystolic volume index. Relationships among galectin-3, biomarkers, and LV remodeling were analyzed across the entire cohort, then according to median baseline LV ejection fraction. Galectin-3 levels were elevated in 22 patients (22%) at baseline and increased significantly over time from 14.7±5.5 to 16.3±6.6 ng/mL (P=0.007). Baseline galectin-3 did not correlate with any LV parameters at baseline or change in any parameter over time. Galectin-3 was positively associated with remodeling in patients with supramedian baseline LV ejection fraction (ie, >49.2%; r=0.40; P=0.01) but not when LV ejection fraction was ≤49.2%. Galectin-3 correlated significantly with matrix metalloproteinase-3 and monocyte chemoattractant protein-1 at baseline, biomarkers that have been shown to relate to LV remodeling in this cohort. Conclusions-Galectin-3 correlated significantly with certain biomarkers involved in extracellular matrix turnover, although no definite relationship was identified with LV remodeling. Whether galectin-3 plays a pathological role in remodeling remains unclear but merits further study. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT00132093. (Circ Heart Fail.2013;6:492-498.)

Galectin-3 in acute coronary syndrome

“…Nevertheless, a clinical study by Weir et al did not confirm such association. They found no favorable effects of eplerenone on plasma Gal-3 levels over 24 weeks in patients after AMI [34]. A possible explanation for the conflicting findings of clinical and experimental studies lies in the observation that myocardial and serum concentrations of Gal-3 do not always correlate [60].…”

“…Firstly, the most common finding among such investigations is that circulating Gal-3 levels are elevated in ACS/AMI, being released during the acute phase of AMI [31,[33][34][35][36][37][38][39]. Indeed, Gal-3 could be part of a survival mechanism of the injured myocardium to cope with the ischemic insult [14].…”

“…Indeed, LVR represents an important predictor of mortality and HF after MI [45]. Weir et al first explored the relationship between Gal-3 and LVR concluding that elevated baseline plasma Gal-3 levels are associated with lower left ventricular ejection fraction (LVEF), a wellknown indicator of poor outcome being associated to adverse LVR, at 24-weeks follow-up, but no at baseline, in patients with MI [34]. In the same year, Tsai et al showed a significant inverse correlation between Gal-3 and LVEF in STEMI patients treated by pPCI [33].…”

Left Ventricular Remodeling after Acute Myocardial Infarction and Biomarkers

“…Though, Weir et al had demonstrated that higher galectin-3 concentrations at baseline were significantly associated with lower LVEF at 24-week follow-up, although there was no significant relationship between galectin-3 and remodeling per se [32].…”

Long-term Sequelae from Acute Kidney Injury: Potential Mechanisms for the Observed Poor Renal Outcomes

“…There has been intense interest in the setting of chronic heart failure in which galectin-3 has been shown to have an emerging role in the prediction, diagnosis and prognosis of this condition, presumably due to its pathogenic role in cardiac fibrosis [54][55][56][57][58][59][60][61][62]. Heart failure studies also demonstrated that galectin-3 levels were inversely correlated to GFR [57,[63][64][65].…”