Disruption of desmin-mitochondrial architecture in patients with regurgitant mitral valves and preserved ventricular function.

摘要: Abstract Objective Recent studies have demonstrated improved outcomes in patients receiving early surgery for degenerative mitral regurgitation (MR) rather than adhering to conventional guidelines surgical intervention. However, providing a mechanistic basis these findings are limited. Methods Left ventricular (LV) myocardium from 22 undergoing valve repair American Heart Association class I indications was evaluated desmin, the voltage-dependent anion channel, α-B-crystallin, and α, β-unsaturated aldehyde 4-hydroxynonenal by fluorescence microscopy. The same 6 normal control LV autopsy specimens. Cardiomyocyte ultrastructure examined transmission electron Magnetic resonance imaging with tissue tagging performed 55 subjects 22 MR before 6 months after repair. Results end-diastolic volume 1.5-fold ( P  = .004) hearts versus showed improvement surgery. ejection fraction decreased 65% ± 7% 52% ± 9%  = .002) Hearts MR had 53% decrease desmin Conclusions Despite well-preserved preoperative fraction, severe oxidative stress disruption of cardiomyocyte desmin-mitochondrial sarcomeric architecture may explain postoperative functional decline further supports move toward earlier