HIGHLIGHTS
SUMMARY
Hypertrophic obstructive cardiomyopathy is one of the most frequent genetic diseases of the heart muscle. The shear stress on the mitral valve apparatus in this process may activate molecular mechanisms that induce early degeneration of the valvular tissue, additionally altering the mitral valve function. The authors have previously reported an increase in local ROS at the level of the diseased mitral valve harvested during surgical replacement from a young patient with primary severe mitral regurgitation; interestingly, the magnitude of oxidative was mitigated after treating the sample with an angiotensin II type 1 (AT1) receptor . . .
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