Classification and Idiopathic Fiedler Myocarditis
There is still no universally accepted classification of inflammatory heart muscle diseases. In pathology, it is customary to distinguish non-specific, granulomatous, giant-cell, secondary, and idiopathic forms.
Of particular interest is idiopathic Fiedler myocarditis. This is a diagnosis of exclusion, as its exact etiology remains unknown. Viral infections, medications, and allergic mechanisms are suspected to play a role. In 25% of patients, the pathology is combined with myositis, myasthenia gravis, or thymomas.
The disease occurs in an acute form (with rapid fatal outcome) or latently. 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 are likely of myogenic origin. Over time, foci of necrosis develop in the center of these infiltrates. Subsequently, they undergo scarring, leading to marked cardiosclerosis.
Bacterial and Parasitic Myocarditis
Bacterial infections occur less frequently than viral ones. Their pathogenesis is primarily driven by bacterial toxins or an allergic reaction to the infection. Typically, the process starts 2–3 weeks after the onset of the primary 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 features multiple pinhead-sized abscesses containing staphylococci, streptococci, and occasionally pathogenic fungi. Complications depend on localization: subendocardial foci threaten abscess formation on the internal 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 protozoan and helminthic 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 composed of lymphocytes, neutrophils, and eosinophils form around the foci of myofibrillar necrosis. The process can transition into a latent form with sclerosis (while the parasites remain viable), lead to arrhythmias, or result in cardiac aneurysm formation.
Infectious-Allergic and Toxic Forms
The main pathogenetic link 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 occur in the stroma (often perivascular), accompanied by the accumulation of serous exudate and foci of myofibrillar necrosis. Infiltrates are diffuse or focal, 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. Macroscopic examination reveals cardiomegaly, chamber dilation (especially of the left ventricle), and endocardial fibrosis. Microscopically, cardiomyocytes alternate (hypertrophied and atrophied), with perinuclear vacuoles visible. The stroma shows reticular cardiosclerosis and large scars. The hallmark feature is granulomas composed of lymphocytes, histiocytes, and Langhans giant cells located within 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.