Author + information
- Received August 12, 2019
- Revision received May 18, 2020
- Accepted May 18, 2020
- Published online August 24, 2020.
- Cheavar A. Blair, PhDa,
- Elizabeth A. Brundage, BSb,
- Katherine L. Thompson, PhDc,
- Arnold Stromberg, PhDc,
- Maya Guglin, MD, PhDd,
- Brandon J. Biesiadecki, PhDb and
- Kenneth S. Campbell, PhDa,d,∗ ()
- aDepartment of Physiology, University of Kentucky, Lexington, Kentucky
- bDepartment of Physiology and Cell Biology and The Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio
- cDepartment of Statistics, University of Kentucky, Lexington, Kentucky
- dDivision of Cardiovascular Medicine, University of Kentucky, Lexington, Kentucky
- ↵∗Address for correspondence:
Dr. Kenneth S. Campbell, Department of Physiology, University of Kentucky, Medical Science Building MS-508, 800 Rose Street, Lexington, Kentucky 40536-0298.
• Contractile assays were performed using multicellular preparations isolated from the left and right ventricles of organ donors and patients with heart failure.
• Heart failure reduced maximum force and power by approximately 30% in the myocardium from both ventricles.
• Heart failure increased the Ca2+ sensitivity of contraction, but the effect was bigger in right ventricular tissue than in left ventricular samples.
• The changes in Ca2+ sensitivity may reflect ventricle-specific post-translational modifications to sarcomeric proteins.
This study measured how heart failure affects the contractile properties of the human myocardium from the left and right ventricles. The data showed that maximum force and maximum power were reduced by approximately 30% in multicellular preparations from both ventricles, possibly because of ventricular remodeling (e.g., cellular disarray and/or excess fibrosis). Heart failure increased the calcium (Ca2+) sensitivity of contraction in both ventricles, but the effect was bigger in right ventricular samples. The changes in Ca2+ sensitivity were associated with ventricle-specific changes in the phosphorylation of troponin I, which indicated that adrenergic stimulation might induce different effects in the left and right ventricles.
Dr. Biesiadecki was supported by the National Institutes of Health (HL114940). Dr. Campbell was supported by the American Heart Association (GRNT25460003, TPA34860008), the National Institutes of Health (TR033173, HL133359, and HL146676. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Basic to Translational Science author instructions page.
- Received August 12, 2019.
- Revision received May 18, 2020.
- Accepted May 18, 2020.
- 2020 The Authors