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Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

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Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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Cardiomyopathy II: Dilated Cardiomyopathy01:30

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Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
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Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure
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Cardiomyocyte nuclear remodeling after mechanical unloading.

Jun Luo1, Stephen D Farris1, Deri Helterline1

  • 1Department of Medicine, University of Washington School of Medicine, Seattle, Washington, United States.

American Journal of Physiology. Heart and Circulatory Physiology
|May 19, 2023
PubMed
Summary

Mechanical unloading of failing hearts reduces cardiomyocyte DNA content without increasing cell proliferation. This suggests a reversal of hypertrophic remodeling, not cell division, in heart failure recovery.

Keywords:
cardiac hypertrophycardiomyocyteheart failureploidy

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Area of Science:

  • Cardiovascular Biology
  • Cellular Biology
  • Heart Failure Pathophysiology

Background:

  • Cardiomyocytes (heart muscle cells) can increase DNA content under stress.
  • Mechanical unloading via left ventricular assist devices (LVADs) has been linked to decreased DNA content and increased proliferation markers in cardiomyocytes.
  • Cardiac recovery leading to LVAD explantation is infrequent, limiting studies on long-term effects.

Purpose of the Study:

  • To investigate if changes in cardiomyocyte DNA content during mechanical unloading occur independently of cardiomyocyte proliferation.
  • To quantify nuclear number, cell size, DNA content, and cell-cycling markers in cardiomyocytes from unloaded and loaded hearts.

Main Methods:

  • Utilized a novel imaging flow cytometry technique.
  • Compared human subjects undergoing LVAD implantation versus primary heart transplantation.
  • Quantified cardiomyocyte nuclear number, cell size, DNA content, and cell-cycle markers (Ki67, H3P).

Main Results:

  • Cardiomyocyte size was 15% smaller in unloaded hearts compared to loaded controls.
  • No significant differences were observed in mono-, bi-, or multinucleated cells.
  • DNA content per nucleus significantly decreased in unloaded hearts.
  • Cell-cycle markers Ki67 and phospho-histone H3 were not elevated in unloaded samples.

Conclusions:

  • Mechanical unloading of failing hearts is associated with decreased cardiomyocyte DNA content per nucleus.
  • These changes occur independently of the cell's nucleation state.
  • The findings suggest a regression of hypertrophic nuclear remodeling rather than cardiomyocyte proliferation during unloading.