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Pathophysiology of Heart Failure

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...

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Simultaneous Electrical and Mechanical Stimulation to Enhance Cells' Cardiomyogenic Potential

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Aging Effects on Cardiac Progenitor Cell Physiology.

Marcello Rota¹, Polina Goichberg¹, Piero Anversa¹

¹Departments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Comprehensive Physiology

|October 2, 2015

Summary

This summary is machine-generated.

Cardiac aging involves changes in cardiac progenitor cells (CPCs), not just aging myocytes. These stem cell alterations contribute to heart failure, but functional CPCs offer potential for stem cell therapy.

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Area of Science:

Cardiovascular Biology
Gerontology
Stem Cell Biology

Background:

The heart was traditionally viewed as a postmitotic organ with a fixed number of myocytes.
This perspective suggested cardiac cell age matched organismal age, implying homogeneous myocyte populations.

Purpose of the Study:

To re-evaluate cardiac aging mechanisms in light of cardiac progenitor cell (CPC) discovery.
To investigate the role of CPC alterations in the development of age-related heart dysfunction (myopathy).

Main Methods:

Review of existing literature on cardiac aging and stem cell biology.
Analysis of proposed mechanisms of CPC dysfunction, including self-renewal, differentiation, and telomere shortening.

Main Results:

Cardiac aging may stem from progressive alterations in CPCs, impacting differentiated cell populations.
CPC changes include reduced self-renewal, biased differentiation, impaired migration, and senescence.
Telomere shortening in CPCs is linked to myocardial aging and chronic heart failure.

Conclusions:

Cardiac progenitor cell dysfunction is a critical factor in human aging myopathy.
Functionally competent CPCs persist even in failing hearts.
Stem cell therapy presents a novel therapeutic avenue for age-related heart disease.