Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2985472 | The Journal of Thoracic and Cardiovascular Surgery | 2009 | 10 Pages |
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.
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Authors
Yeong-Hoon MD, Douglas B. PhD, Adrian M. MBBS, Steven D. MD, Christof MD, Koh MD, Ingeborg MD, Pedro J. MD, Francis X. MD,