Myocarditis

Classification and idiopathic Fiedler's myocarditis

There is still no universally accepted classification of inflammatory diseases of the heart muscle. In pathologic anatomy, it is customary to distinguish non-specific, granulomatous, giant-cell, secondary, and idiopathic forms.

Of particular interest is idiopathic Fiedler's myocarditis. This is a diagnosis of exclusion, as its exact etiology remains unknown. The influence of viral infections, medications, and allergic mechanisms is hypothesized. In 25% of patients, the pathology is combined with myositis, myasthenia gravis, or thymic tumors (thymomas).

The disease runs an acute course (with rapid fatal outcome) or is latent. Diffuse and granulomatous forms are distinguished. Microscopic examination of the myocardium reveals an infiltrate consisting of lymphocytes, plasma cells, occasional granulocytes, and giant cells, which likely have a myogenic origin. Over time, foci of necrosis develop in the center of these infiltrates. Subsequently, they undergo scarring, leading to the development of pronounced cardiosclerosis.

Bacterial and parasitic myocarditis

Bacterial lesions occur less frequently than viral ones. Their pathogenesis is dominated by the action of bacterial toxins or an allergic reaction to infection. Usually, the process starts 2–3 weeks after the onset of the underlying disease (tonsillitis, pulmonary tuberculosis, scarlet fever, salmonellosis, or meningococcal infection).

• Purulent myocarditis: develops against the background of septicopyemia or acute ulcerative endocarditis. The most striking morphological picture consists of multiple pinhead-sized abscesses containing staphylococci, streptococci, and sometimes pathogenic fungi. Complications depend on localization: subendocardial foci threaten abscess formation on the inner surface of the heart, while subepicardial foci threaten purulent pericarditis.
• Tuberculous myocarditis: a rare form characterized by the formation of multiple small tuberculous granulomas or large tubercles in the tissue.
• Parasitic myocarditis: occurs in protozoal infections. It is caused by Toxoplasma, Trypanosoma (Chagas myocarditis), Trichinella (interstitial eosinophilic variant), and Echinococcus. The parasite invades cardiomyocytes, multiplies, and destroys them. Cellular infiltrates of lymphocytes, neutrophils, and eosinophils form around the foci of myofibrillar necrosis. The process may transition into a latent form with sclerosis (while the parasites remain viable), lead to arrhythmias, or the formation of cardiac aneurysms.

Infectious-allergic and toxic lesions

The main link in the pathogenesis of infectious-allergic forms is prolonged contact with the pathogen, triggering a cell-mediated hypersensitivity reaction. Changes are localized predominantly in the right heart chambers, the apex, and the interventricular septum.

Morphologically, changes are observed in the stroma (most often perivascular), with accumulation of serous exudate and foci of myofibrillar necrosis. Infiltrates are diffuse or focal in nature, consisting of lymphocytes, plasma cells, and macrophages. In rheumatic fever, tuberculosis, and sarcoidosis, they acquire a granulomatous character. The most frequent form in this group is rheumatic myocarditis.

Sarcoid myocarditis affects the left side of the heart and the interventricular septum. Macroscopically, cardiomegaly, chamber dilation (especially of the left ventricle), and endocardial fibrosis are revealed. Microscopically, cardiomyocytes alternate (hypertrophied and atrophied), with perinuclear vacuoles visible within them. The stroma shows reticular cardiosclerosis and large scars. The main sign is granulomas composed of lymphocytes, histiocytes, and Langhans giant cells, located in scars and non-sclerotic myocardium.

Toxic myocarditis (diphtheritic and drug-induced) leads to reticular cardiosclerosis, parietal endocardial fibrosis, and pericardial fibrosis (up to constrictive pericarditis). The prognosis of the drug-induced form is serious due to the risk of transformation into restrictive cardiomyopathy.

Class and exam questions

What else to study on this topic

• Morphogenesis and stages of rheumatic heart disease
• Diphtheritic myocarditis: mechanism of action of the exotoxin
• Chagas myocarditis: features of the lesion in trypanosomiasis
• Differences between granulomas in tuberculous and sarcoid myocarditis

Other topics in the section "Pathology of the Cardiovascular System"

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