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Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction
Published on: February 13, 2021
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Skeletal muscle abnormalities in heart failure with preserved ejection fraction
Matthew Anderson Md1, Clifton Forrest Parrott1, Mark J Haykowsky Ph D2
1Cardiovascular Medicine Section, Department of Internal Medicine, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC, 27157-1045, USA.
Heart Failure Reviews
|March 30, 2022
Summary
Heart failure with preserved ejection fraction (HFpEF) involves skeletal muscle abnormalities causing exercise intolerance. Targeting these muscle issues may improve HFpEF patient outcomes and quality of life.
Area of Science:
- Cardiology
- Exercise Physiology
- Skeletal Muscle Biology
Background:
- Heart failure with preserved ejection fraction (HFpEF) accounts for nearly half of the heart failure burden.
- Exercise intolerance and reduced quality of life are primary symptoms in HFpEF patients.
Purpose of the Study:
- To investigate the intrinsic skeletal muscle abnormalities in HFpEF.
- To understand the link between skeletal muscle dysfunction and exercise intolerance in HFpEF.
- To explore potential therapeutic targets within skeletal muscle for HFpEF.
Main Methods:
- Review of recent studies on skeletal muscle characteristics in HFpEF patients.
- Analysis of skeletal muscle mass, fiber type, capillary density, fat infiltration, and gene expression.
- Assessment of mitochondrial function and energy metabolism during exercise and recovery.
- Evaluation of nitric oxide bioavailability in HFpEF microvasculature.
Main Results:
- HFpEF patients exhibit decreased muscle mass, reduced oxidative fibers, and impaired capillary-to-fiber ratios.
- Abnormal fat infiltration, increased atrophy gene expression, and reduced mitochondrial content are observed.
- Mitochondria show rapid depletion and delayed repletion of high-energy phosphates during exercise.
- Impaired nitric oxide bioavailability affects microvasculature, potentially hindering oxygen transport and extraction.
Conclusions:
- Skeletal muscle abnormalities are intrinsic to HFpEF and contribute significantly to exercise intolerance.
- Exercise training improves exercise tolerance primarily through peripheral skeletal muscle adaptations.
- Targeting specific skeletal muscle abnormalities offers a promising strategy to improve clinical outcomes in HFpEF.
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