Key result
Homoarginine supplementation prevented left ventricular dilatation (P<0.01), preserved ejection fraction (P<0.05), and reduced myocardial fibrosis (P<0.001) in a mouse model of CAD.
Why the study?
Homoarginine is cardioprotective in ischemic heart failure, but the mechanism is unknown, prompting testing of whether it reduces calcification via TNAP inhibition in coronary artery disease.
Does homoarginine supplementation prevent left ventricular dilatation and preserve systolic function in a mouse model of coronary artery disease?
Population
Male WHC and WHC-endothelial TNAP mice starting at 6 weeks of age
Comparison
Homoarginine supplementation vs placebo
Design
Animal experimental study
Follow-up
4 to 5 weeks
Authors
Loading...
Does not support clinical use in CAD; leaves open whether homoarginine benefits translate beyond mouse models.
Does homoarginine supplementation prevent left ventricular dilatation and preserve systolic function in a mouse model of coronary artery disease?
p-value: p=<0.01
Homoarginine supplementation preserves systolic function and prevents left ventricular dilatation in a mouse model of coronary artery disease, likely through direct myocardial protection rather than inhibition of calcification.
Rodionov et al. (2019) studied Coronary artery disease. Homoarginine (hArg) supplementation vs. Placebo was evaluated on Left ventricular dilatation, ejection fraction, and myocardial fibrosis (p=<0.01). Homoarginine supplementation prevented left ventricular dilatation (P<0.01), preserved ejection fraction (P<0.05), and reduced myocardial fibrosis (P<0.001) in a mouse model of CAD.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: