Myocarditis is inflammation of the myocardium, the muscular tissue of the heart. The history of myocarditis dates back to the 19th century. Today, it is recognized as a potentially serious inflammatory disease that can result from infections, immune reactions, medications and other causes.
Early descriptions: before myocarditis had a name
Physicians had recognized inflammation and structural abnormalities of the heart long before myocarditis became a clearly defined disease.
A major milestone came in 1837, when German physician Joseph Friedrich Sobernheim used the term “myocarditis.” The word literally refers to inflammation of the heart muscle. At this stage, however, myocarditis was not a precisely defined disease and was often used broadly for different forms of heart inflammation.
Fiedler and the definition of a distinct disease
The understanding of myocarditis changed substantially in 1899. German pathologist Carl Ludwig Alfred Fiedler described what he called “acute isolated interstitial myocarditis.” His observations were based on microscopic examination of heart tissue and helped establish myocarditis as a distinct pathological condition rather than simply a general description of an inflamed heart.
Fiedler’s work was particularly important because earlier pathological studies tended to focus on people who had died from severe disease. Consequently, doctors knew considerably more about the appearance of myocarditis at autopsy than about how the disease developed in living patients.
The 1940s: understanding different forms
By the 1940s, researchers were beginning to recognize that myocarditis did not behave in exactly the same way in every patient.
In 1948, Burch and Ray described clinical manifestations of myocarditis and recognized differences between acute and chronic forms. The connection between inflammation of the myocardium and subsequent heart failure and dilated cardiomyopathy gradually became an important area of research.
The 1960s: diagnosis in living patients
One of the biggest breakthroughs came in the 1960s, with the development and increasing use of endomyocardial biopsy (EMB).
For the first time, doctors could obtain a small sample of heart muscle from a living patient and examine it under a microscope. This allowed researchers to compare pathological findings with symptoms, heart function and clinical outcomes.
The technique subsequently became an important reference method for confirming myocarditis, although researchers later discovered that biopsy could miss disease because inflammation may occur in patches rather than uniformly throughout the heart. This problem is known as sampling error.
1960s-1980s: viruses enter the picture
During the second half of the 20th century, evidence increasingly connected myocarditis with viral infections. Research into Coxsackie B viruses was particularly influential. By the 1960s and 1970s, studies were investigating how viral infections could produce inflammation and injury in the heart.
1986-1987: the Dallas criteria
Another important milestone occurred in the 1980s. In 1986, the Dallas criteria were proposed to standardize the microscopic diagnosis of myocarditis. They required evidence of an inflammatory cellular infiltrate, with or without associated damage to heart-muscle cells. The criteria were formally published in 1987.
The Dallas criteria remained an important reference for more than 20 years, but they had significant limitations. Interpretation could vary between pathologists, and biopsies could miss inflammation because of its patchy distribution.
1990s-2000s: from biopsy to cardiac MRI
By the 1990s, researchers increasingly recognized myocarditis as a possible cause of acute heart failure, arrhythmias and dilated cardiomyopathy. At the same time, advances in molecular techniques helped researchers investigate infectious and immune mechanisms in greater detail.
The next major transformation came with cardiac magnetic resonance (CMR). In 2009, the Lake Louise Criteria provided a standardized approach for using CMR to identify myocardial inflammation. The criteria used three major imaging features involving edema, hyperemia/capillary leakage and non-ischaemic tissue injury; the original framework considered CMR supportive of myocarditis when at least 2 of 3 criteria were present.
This was important because CMR could assess inflammation without removing heart tissue. CMR subsequently became a major non-invasive tool in the evaluation of suspected myocarditis.
Myocarditis today
Modern medicine now recognizes that myocarditis has multiple causes. Viral infections remain important, but bacterial infections, autoimmune diseases, medications, toxins and other inflammatory triggers can also cause the condition.
The COVID-19 pandemic brought myocarditis back into widespread public attention. Myocarditis can occur following SARS-CoV-2 infection, while rare cases have also been reported following mRNA COVID-19 vaccination. WHO notes that reported post-vaccination cases were generally mild and that most reported patients recovered.
Today, diagnosis may combine symptoms, ECG and blood tests, echocardiography, CMR and, in selected cases, endomyocardial biopsy. The disease is now understood as a spectrum ranging from mild inflammation to severe myocardial injury, arrhythmias and heart failure.
References
Feldman AM, McNamara D. Myocarditis. N Engl J Med. 2000;343:1388–1398. NEJM article
Story telling of myocarditis. International Journal of Cardiology. 2019. ScienceDirect article
Dec GW. Introduction to Clinical Myocarditis. Springer, pp. 257–281.
Aretz HT, et al. Myocarditis: A histopathologic definition and classification. Am J Cardiovasc Pathol. 1987;1:3–14.
Friedrich MG, et al. Cardiovascular Magnetic Resonance in Myocarditis: A JACC White Paper. J Am Coll Cardiol. 2009.
WHO. Q&A on Myocarditis and COVID-19 Vaccines. 2021.
