Key result
Depletion of normal cardiocytes strongly correlates with cardiomyopathy and fibrosis progression in LVAD patients.
Why the study?
Cardiocyte myofibrillolysis and interstitial fibrosis are histopathological changes in cardiomyopathies leading to heart failure, but their relationship in LVAD apical samples needed evaluation.
Are there differences in myocardial fibrosis and myofibrillolysis between patients with advanced cardiomyopathy requiring LVAD and healthy controls?
Case-Control (n=46)
Double-blind
No
Are there differences in myocardial fibrosis and myofibrillolysis between patients with advanced cardiomyopathy requiring LVAD and healthy controls?
Effect estimate: Spearman R = -0.955
p-value: p=<0.00001
Progression of cardiomyopathy and fibrosis appears to depend more on the loss of normal cardiocytes rather than just their degeneration.
Cardiocyte depletion may drive fibrosis in advanced cardiomyopathy; hypothesis-generating and should not yet change LVAD practice.
INTRODUCTION: Cardiocyte myofibrillolysis and interstitial fibrosis belong to histopathological changes in cardiomyopathies, leading to heart failure. AIM: To evaluate these changes in apical resection during left ventricular assist device (LVAD) implantation. MATERIAL AND METHODS: The studied group consisted of 40 patients with cardiomyopathy, and apical samples excised during left ventricular assist device implantation were studied (CM/VAD group, mean: 48.1 ±10 y/o). A control group consisted of 6 apical samples from healthy heart graft donors (mean: 29 ±2.3 years old). Area fraction (AF) was calculated for: fibrosis, cardiocytes with myofibrillolysis (MFL), non-myofibrillolytic cardiocytes (non-MFL). RESULTS: Single lymphocytes were seen in 18 (45%) cases in the CM/VAD group. Cardiomyopathy grade evaluated semiquantitatively in CM/VAD was: slight (25% of a group), moderate (35.5%), advanced (35.5%). CM/VAD cases showed nearly ten times higher fibrosis than the control group. The MFL cells occupied nearly a five times larger area in CM/VAD than in the control group, whereas non-MFL cells were found in the control group, as a predominant pattern. The linear regression calculated between fibrosis AF and types of cardiocytes indicated the depletion of cardiomyocytes with fibrosis increase. The control group presented insignificant dependency between fibrosis and MFL cells, suggesting the lack of replacement fibrosis. Significant negative dependence between fibrosis and non-MFL cardiocytes suggested remodeling in controls. Correlation analysis showed a strong relation between depletion of normal cardiocytes and progression of fibrosis. CONCLUSIONS: Progression of cardiomyopathy and fibrosis depends on the loss of cardiocytes rather than degeneration of these cells.
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Pacholewicz et al. (2019) conducted a case-control in Advanced heart failure / Cardiomyopathy (n=46). Advanced heart failure vs. Healthy heart donors was evaluated on Correlation between cardiomyopathy grade and non-myofibrillolytic cardiocyte area fraction (Spearman R = -0.955, p=<0.00001). Progression of cardiomyopathy and fibrosis in patients requiring LVAD strongly correlated with the depletion of normal non-myofibrillolytic cardiocytes (Spearman R = -0.955, p < 0.00001).
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