Republished: Pathogenesis and diagnosis of myocarditis
- 1Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, Minnesota, USA
- 2Department of Environmental Health Sciences, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, Maryland, USA
- Correspondence to Dr Leslie T Cooper, Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA;
Contributors We certify that this manuscript has not been published or is being considered for publication elsewhere.
- Received 30 January 2012
- Accepted 14 February 2012
Acute myocarditis is an inflammatory disease of the heart muscle that may progress to dilated cardiomyopathy and chronic heart failure. A number of factors including the sex hormone testosterone, components of innate immunity, and profibrotic cytokines have been identified in animal models as important pathogenic mechanisms that increase inflammation and susceptibility to chronic dilated cardiomyopathy. The clinical presentation of acute myocarditis is non-specific and mimics more common causes of heart failure and arrhythmias. Suspected myocarditis is currently confirmed using advanced non-invasive imaging and histopathologic examination of heart tissue. However, the diverse presentations of myocarditis and the lack of widely available, safe, and accurate non-invasive diagnostic tests remain major obstacles to early diagnosis and population based research. Recent advances in the understanding of disease pathogenesis described in this review should lead to more accurate diagnostic algorithms and non-invasive tests.
- dilated cardiomyopathy
- cardiac magnetic resonance
- heart biopsy
- cardiac function
- endomyocardial fibrosis
- arrhythmic right ventricular dysplasia
- cardiomyopathy restrictive
- cardiomyopathy dilated
This is a reprint of a paper that first appeared in Heart, 2012, Volume 98, pages 835–40.
Funding Dr Fairweather is supported by funding from the National Institutes of Health (R01 HL087033). Dr Cooper is supported by funding from the National Institutes of Health (R01 HL56267, Co-PI).
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.