Author + information
- Received December 13, 2018
- Revision received April 5, 2019
- Accepted April 11, 2019
- Published online November 4, 2019.
- aUPMC Cardiovascular Magnetic Resonance Center, Pittsburgh, Pennsylvania
- bHeart and Vascular Institute, UPMC, Pittsburgh, Pennsylvania
- cDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania
- dClinical and Translational Science Institute, University of Pittsburgh, Pittsburgh, Pennsylvania
- eDepartment of Medicine, University of Mississippi, Jackson, Mississippi
- fProgram of Cardiovascular Diseases, Centre for Applied Medical Research, University of Navarra, and Instituto de Investigación Sanitaria de Navarra, IDISNA, Pamplona, Spain
- gCIBERCV, Carlos III Institute of Health, Madrid, Spain
- hDepartments of Nephrology, and Cardiology and Cardiac Surgery, University of Navarra Clinic, Pamplona, Spain
- ↵∗Address for correspondence:
Dr. Erik B. Schelbert, Cardiovascular Magnetic Resonance Center, Heart and Vascular Institute, UPMC, University of Pittsburgh School of Medicine, 200 Lothrop Street, PUH E E354.2, Pittsburgh, Pennsylvania 15213.
• Interstitial heart disease, whether from MF or CA, indicates excess protein in the interstitium, which promotes HF and excess cardiac morbidity and mortality.
• Rather than conceptualizing myocardium as a homogenous tissue, ECV permits quantification of the extent of MF or CA and the extent to which it responds to interventions.
• Abundant data support the concept that interstitial heart disease from excess interstitial protein, especially MF, represents a promising therapeutic target worthy of further investigation with interventional trials.
Interstitial heart disease, whether primarily from myocardial fibrosis or cardiac amyloidosis, indicates excess protein accumulation in the interstitium and constitutes a major source of heart failure with excess cardiac morbidity and mortality. Myocardial fibrosis (defined as excess myocardial collagen concentration that distorts myocardial architecture) is prevalent and causes cardiac symptoms and ultimately adverse cardiac events, such as heart failure, arrhythmia, and death. Conversely, cardiac amyloidosis is far less prevalent than myocardial fibrosis but represents a more extreme form of interstitial heart disease with marked interstitial expansion, profound architectural distortion, and then rapid clinical decline. Myocardial extracellular volume measures fundamentally advance the understanding of myocardium and specifically highlights the role of the interstitium. Rather than conceptualizing myocardium as a homogenous tissue, dichotomizing the myocardium into its interstitial (including the microvasculature) and cardiomyocyte phenotypes promotes additional understanding of heart failure pathophysiology that may spur the development of more effective therapies.
- cardiovascular magnetic resonance
- extracellular matrix
- extracellular volume
- myocardial fibrosis
Dr. Schelbert has served on Advisory Boards for Bayer and Merck; and has received contrast material donated for research purposes from Bracco Diagnostics. Dr. Bulter has received research support from the National Institutes of Health, Patient Centered Outcomes Research, and the European Union; has served on the Speaker Bureau for Novartis, Janssen, and NovoNordisk; and has served as a consultant for Abbott, Adrenomed, Amgen, Array, AstraZeneca, Bayer, BerlinCures, Boehringer Ingelheim, Bristol-Myers Squibb, Cardiocell, CVRx, G3 Pharmaceutical, Innolife, Janssen, Lantheus, LinaNova, Luitpold, Medscape, Medtronic, Merck, Novartis, NovoNordisk, Relypsa, Roche, Sanofi, StealthPeptide, SC Pharma, V-Wave Limited, Vifor, and ZS Pharma. Dr. Diez has reported he has no relationships relevant to the contents of this paper to disclose.
- Received December 13, 2018.
- Revision received April 5, 2019.
- Accepted April 11, 2019.
- 2019 American College of Cardiology Foundation
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