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Published on: February 10, 2023
Depressed Myocardial Contractility: Can It Be Rescued?
1Division of Cardiovascular Diseases, University of Tennessee Health Science Center, Memphis, TN.
Systolic heart failure may not cause irreversible myocardial contractility depression. Thyroid hormone signaling and cardiomyocyte rescue can improve heart function and contractile mass in advanced heart failure patients.
Area of Science:
- Cardiology
- Molecular Biology
- Cellular Biology
Background:
- Current understanding posits irreversible myocardial contractility depression in advanced systolic heart failure.
- Continuous flow ventricular assist devices (CF-VADs) have shown improved ventricular function, challenging this dogma.
- This suggests potential for reversing myocardial dysfunction.
Purpose of the Study:
- To explore cellular and molecular mechanisms underlying the reversal of depressed myocardial contractility.
- To identify signaling pathways that can restore cardiac function in advanced heart failure.
Main Methods:
- Investigation of cardiomyocyte thyroid hormone signaling pathways.
- Analysis of the reexpression of fetal gene programs in cardiomyocytes.
- Assessment of the rescue of atrophic myocytes and impact on fibrotic microdomains.
Main Results:
- Thyroid hormone signaling promotes the reexpression of a fetal gene program, enhancing cardiomyocyte efficiency.
- This signaling pathway aids in rescuing atrophic myocytes, potentially increasing contractile mass.
- Evidence suggests a mechanism for reversing myocardial depression beyond current therapeutic limitations.
Conclusions:
- Myocardial contractility depression in advanced systolic heart failure may be reversible.
- Thyroid hormone signaling is a key mechanism for restoring cardiomyocyte function and efficiency.
- Targeting these pathways offers novel therapeutic strategies for heart failure treatment.
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