Galectin-3 and mineralocorticoid receptor antagonist use in patients with chronic heart failure due to left ventricular systolic dysfunction.
BACKGROUND
Galectin-3 is a prognostic heart failure biomarker associated with aldosterone-induced myocardial fibrosis; mineralocorticoid receptor antagonists (MRAs) may reduce such fibrosis. We sought to examine outcomes of patients with heart failure with reduced ejection fraction (HFrEF) as a function of galectin-3 and MRA therapy.


METHODS
A total of 151 patients with chronic HFrEF were categorized by baseline galectin-3 and subsequent MRA therapy trends with regard to cardiovascular (CV) events, left ventricular remodeling, safety, and quality of life, over a mean of 10 months.


RESULTS
Although galectin-3 >20 ng/mL was associated with doubling in adjusted risk for CV events, regardless of MRA treatment, there was no difference in CV event rates with regard to MRA use patterns, independent of galectin-3 concentrations. Specifically, in patients with elevated galectin-3 treated with intensified MRA therapy, a significant difference was not detected in CV event rates (P = .79) or the cumulative number of such events (P = .76). Adjusted analysis revealed no difference in time to first CV event if MRA was added/intensified in those with elevated galectin-3 (hazard ratio 0.99, 95% CI 0.97-1.02, P = .74); similarly, cumulative MRA dose was not a specific predictor of benefit. In those with elevated galectin-3, MRA therapy did not affect left ventricular remodeling indices or quality of life at follow-up; these patients had the highest rates of treatment-related adverse events with intensified MRA use. Regardless of MRA use, elevated galectin-3 was associated with more significant renal dysfunction.


CONCLUSIONS
Among patients with chronic HFrEF and elevated galectin-3 concentrations, we found no specific benefit from addition or intensification of MRA therapy.
Division of Cardiology, Massachusetts General Hospital, Boston, MA.
Parul U
PU
Gandhi
Beth Israel Deaconess Medical Center, Boston, MA.
Shweta R
SR
Motiwala
Division of Cardiology, Massachusetts General Hospital, Boston, MA.
Arianna M
AM
Belcher
Division of Cardiology, Massachusetts General Hospital, Boston, MA.
Hanna K
HK
Gaggin
Division of Cardiology, Massachusetts General Hospital, Boston, MA.
Rory B
RB
Weiner
Division of Cardiology, Massachusetts General Hospital, Boston, MA.
Aaron L
AL
Baggish
Duke University Medical Center, Durham, NC.
Mona
M
Fiuzat
Department of Cardiology Maastricht University Medical Center, Maastricht, The Netherlands.
Hans-Peter
HP
Brunner-La Rocca
Division of Cardiology, Massachusetts General Hospital, Boston, MA. Electronic address: jjanuzzi@partners.org.
James L
JL
Januzzi
D000328:Adult; D000368:Aged; D005260:Female; D037502:Galectin 3 / Q000627:therapeutic use*; D006333:Heart Failure / Q000097:blood* / Q000209:etiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use*; D013318:Stroke Volume; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000150:complications*
D037502:Galectin 3; D000451:Mineralocorticoid Receptor Antagonists