Cardiac myocyte nuclear size and ploidy status decrease after mechanical support

“…11 A decrease in cardiomyocyte nuclear size and chromatin density after unloading with DNA cytometry and morphometry was reported in 2 patients. 12 In the present study, we have addressed the possibility of myocardial regeneration by investigating the plasticity and dynamics of cardiomyocyte DNA content and ploidy, as well as nuclear size and number of nuclei before and after mechanical support by LVAD. We show that there are dramatic changes in mean cardiomyocyte DNA content per nucleus and per individual cardiomyocyte and in the nuclear size and number of nuclei after hemodynamic unloading, suggesting that changes in nuclear size and ploidy are crucially involved in reverse cardiac remodeling.…”

Section: Editorial See P 957 Clinical Perspective On P 996mentioning

confidence: 99%

Hemodynamic Support by Left Ventricular Assist Devices Reduces Cardiomyocyte DNA Content in the Failing Human Heart

et al. 2010

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Background-Whether adult cardiomyocytes have the capacity to regenerate in response to injury and, if so, to what extent are still issues of intense debate. In human heart failure, cardiomyocytes harbor a polyploid genome. A unique opportunity to study the mechanism of polyploidization is provided through the setting of hemodynamic support by left ventricular assist devices. Hence, the cardiomyocyte DNA content, nuclear morphology, and number of nuclei per cell were assessed before and after left ventricular assist device support. Methods and Results-In 23 paired myocardial samples, cardiomyocyte ploidy was investigated by DNA image cytometry, flow cytometry, and in situ hybridization. Nuclear cross-sectional area and perimeters were measured morphometrically, and the binucleated cardiomyocytes were counted. The median of the cardiomyocyte DNA content and the number of polyploid cardiomyocytes both declined significantly from 6.79 c to 4.7 c and 40.2% to 23%, whereas a significant increase in diploid cardiomyocytes from 33.4% to 50.3% and in binucleated cardiomyocytes from 4.5% to 10% after unloading was observed. Conclusions-The decrease in polyploidy and increase in diploidy after left ventricular assist device suggest a numeric increase in diploid cardiomyocytes (eg, through cell cycle progression with completion of mitosis or by increased stem cells). The cardiac regeneration that follows may serve as a morphological correlate of the recovery observed in some patients after unloading. (Circulation. 2010;121:989-996.)

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“…In patients with end-stage cardiomyopathy, LVAD support appears to reverse disruption of the amino terminus of dystrophin in many cases [21]. It also leads to decreases in the nuclear size and DNA content of cardiac myocytes, which suggests a reversal of nuclear hypertrophy and polyploidization [22]. Collectively, these findings indicate that even the failing and structurally damaged heart has the potential to reverse key morphological features of hypertrophy and failure.…”

Section: Myocyte Morphologymentioning

confidence: 99%

Reverse Remodeling of the Failing Human Heart with Mechanical Unloading

Razeghi¹,

Myers²,

Frazier³

et al. 2002

Cardiology

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Anecdotal and clinical evidence suggests that mechanical unloading may restore cardiac function by inducing changes in the biological properties of the failing heart. This challenges the notion that the progression of end-stage heart failure is an irreversible process ending in either death of the patient or transplantation. Although it is still not clear how mechanical unloading of the failing heart improves cardiac function, the process likely involves adaptive responses of cardiac myocytes on the cellular, extracellular, and subcellular levels.

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Cardiac myocyte nuclear size and ploidy status decrease after mechanical support

Cited by 29 publications

References 14 publications

The 1,4,5-inositol trisphosphate pathway is a key component in Fas-mediated hypertrophy in neonatal rat ventricular myocytes

The 1,4,5-inositol trisphosphate pathway is a key component in Fas-mediated hypertrophy in neonatal rat ventricular myocytes

Hemodynamic Support by Left Ventricular Assist Devices Reduces Cardiomyocyte DNA Content in the Failing Human Heart

Reverse Remodeling of the Failing Human Heart with Mechanical Unloading

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