Article ID Journal Published Year Pages File Type
2985472 The Journal of Thoracic and Cardiovascular Surgery 2009 10 Pages PDF
Abstract
In experimental infant left ventricular hypertrophy, myocyte apoptosis is initiated in the face of normalized wall stress and preserved contractility. The ongoing rate of apoptosis causes a measurable decrease in myocyte number that is coincident with the onset of ventricular dysfunction. It thus appears that pressure overload, even at its earliest stages, is not well tolerated by the developing ventricle.
Related Topics
Health Sciences Medicine and Dentistry Cardiology and Cardiovascular Medicine
Authors
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