Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2978603 | The Journal of Thoracic and Cardiovascular Surgery | 2016 | 14 Pages |
Abstract
Despite well-preserved preoperative LV ejection fraction, severe oxidative stress and disruption of cardiomyocyte desmin-mitochondrial sarcomeric architecture may explain postoperative LV functional decline and further supports the move toward earlier surgical intervention.
Keywords
PBSleft ventricular end-diastolicLVESLVEDLVEFVDAC4-hydroxynonenal4-HNEBSAbovine serum albuminMRITemLeft ventricularMagnetic resonance imagingPhosphate buffered salineCardiomyocyteMitochondriaTransmission electron microscopyheart failuremitral regurgitationvoltage-dependent anion channelleft ventricular ejection fraction
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Authors
Mustafa I. MD, Jason L. MD, PhD, Namakkal S. PhD, Shama PhD, Nithya PhD, Silvio MD, Himanshu MD, Steven G. MD, Thomas S. PhD, Pamela Cox MS, Inmaculada PhD, James F. PhD, James E. MD, David C. MD, Louis J. MD,