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

Author:

Weir Robin A.P.1,Petrie Colin J.1,Murphy C. Aengus1,Clements Suzanne1,Steedman Tracey1,Miller Ashley M.1,McInnes Iain B.1,Squire Iain B.1,Ng Leong L.1,Dargie Henry J.1,McMurray John J.V.1

Affiliation:

1. From the Cardiology Department, Hairmyres Hospital, Lanarkshire, United Kingdom (R.A.P.W.); Cardiology Department, Monklands Hospital, Lanarkshire, United Kingdom (C.J.P., C.A.M.); Cardiology Department, Western Infirmary, Glasgow, Scotland, United Kingdom (S.C., T.S., H.J.D.); Division of Immunology, Infection and Inflammation, Glasgow Biomedical Research Centre, University of Glasgow, Scotland, United Kingdom (A.M.M., I.B.M.); Department of Cardiovascular Sciences, Leicester Royal Infirmary,...

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 end-systolic 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.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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