Cited by 720Cardiomyopathy and Myosin StudiesViral Infections and Immunology ResearchCardiovascular Effects of Exercise

Dilated cardiomyopathy

Open access
Schultheiss, Heinz-Peter, Fairweather, DeLisa, Caforio, Alida L. P., Escher, Felicitas, Hershberger, Ray E., Lipshultz, Steven E., Liu, Peter P., Matsumori, Akira +3 more·2019·Nature Reviews Disease Primers

Abstract

Dilated cardiomyopathy (DCM) is a clinical diagnosis characterized by left ventricular or biventricular dilation and impaired contraction that is not explained by abnormal loading conditions (for example, hypertension and valvular heart disease) or coronary artery disease. Mutations in several genes can cause DCM, including genes encoding structural components of the sarcomere and desmosome. Nongenetic forms of DCM can result from different aetiologies, including inflammation of the myocardium due to an infection (mostly viral); exposure to drugs, toxins or allergens; and systemic endocrine or autoimmune diseases. The heterogeneous aetiology and clinical presentation of DCM make a correct and timely diagnosis challenging. Echocardiography and other imaging techniques are required to assess ventricular dysfunction and adverse myocardial remodelling, and immunological and histological analyses of an endomyocardial biopsy sample are indicated when inflammation or infection is suspected. As DCM eventually leads to impaired contractility, standard approaches to prevent or treat heart failure are the first-line treatment for patients with DCM. Cardiac resynchronization therapy and implantable cardioverter-defibrillators may be required to prevent life-threatening arrhythmias. In addition, identifying the probable cause of DCM helps tailor specific therapies to improve prognosis. An improved aetiology-driven personalized approach to clinical care will benefit patients with DCM, as will new diagnostic tools, such as serum biomarkers, that enable early diagnosis and treatment.

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  • cMRI cannot identify specific cellular components of inflammation and may be less accurate in early stages of myocarditis because fibrosis typically develops weeks after acute myocarditis.

    “cMRI cannot identify specific cellular components of inflammation and may be less accurate in the early stages of myocarditis because fibrosis typically develops weeks after acute myocarditis. 128-130”

    From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [130]

    The Diagnosis section distinguishes MRI detection of oedema and fibrosis from biopsy-based immunohistochemistry, which characterizes specific immune cell types. It does not say MRI is less accurate in early myocarditis or that fibrosis typically develops weeks after acute myocarditis; its MRI figure instead shows oedema and late gadolinium enhancement in active myocarditis. The Inflammation section says fibrotic scar tissue develops over time but gives no weeks-long timeline. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

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Research works printed but not linked: 19

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Authors
Schultheiss, H.-P., Fairweather, D., Caforio, A. L. P., Escher, F., Hershberger, R. E., Lipshultz, S. E., Liu, P. P., Matsumori, A., Mazzanti, A., McMurray, J., & Priori, S. G.
Affiliations
  • Institut Kardiale Diagnostik und Therapie (DE)
  • Mayo Clinic (US)
  • University of Padua (IT)
  • German Centre for Cardiovascular Research (DE)
  • The Ohio State University (US)
  • Roswell Park Comprehensive Cancer Center (US)
  • University of Ottawa (CA)
  • Kyoto Medical Center (JP)
  • University of Pavia (IT)
  • British Heart Foundation (GB)
Corresponding author
  • Schultheiss, Heinz-Peter
  • Fairweather, DeLisa
Venue
Nature Reviews Disease Primers
Published
2019-05-09
Volume
5
Issue
1
Pages
32-32
ISSN
2056-676X (ISSN-L)
OpenAlex
W4211051044
Cited by
720
References
235
Citations by year
2026: 81 · 2025: 117 · 2024: 141 · 2023: 135 · 2022: 107 · 2021: 86 · 2020: 45 · 2019: 7
FWCI
11.10
Type
journal article
Language
en
Open access
Locations
  • Nature Reviews Disease Primers (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Research Bank (Australian Catholic University) (submittedVersion)
  • ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion, cc-by-sa)
  • Padua Research Archive (University of Padova) (submittedVersion)
Funders
  • American Heart Association (16GRNT30950007)
  • Deutsche Forschungsgemeinschaft
  • European Research Area Network on Cardiovascular Diseases (JTC2016-40-158)
  • National Institutes of Health (NIH-R01)
  • National Heart, Lung, and Blood Institute (R01HL111938)
  • National Institute of Allergy and Infectious Diseases (R21AI145356)
  • National Institute of Environmental Health Sciences (R21ES024414)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Effects of Exercise
Keywords
dilated cardiomyopathy, left ventricular dilatation, sarcomere gene mutations, viral myocarditis, drug-induced cardiomyopathy, autoimmune cardiomyopathy, endomyocardial biopsy, echocardiography, myocardial remodelling, heart failure, cardiac resynchronization therapy, implantable cardioverter-defibrillator, cardiac arrhythmias, serum biomarkers, personalized treatment
MeSH terms
Cardiomyopathy, Dilated, Echocardiography, Electrocardiography, Heart Failure, Humans, Inflammation, Magnetic Resonance Imaging, Prognosis, Quality of Life, Sex Factors, Autoimmunity, Cardiac Resynchronization Therapy

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