[Tumor necrosis factor alpha and interferon alpha in patients with myocarditis.].

Aim: To elucidate the role of tumor necrosis factor alpha (TNF alpha) and interferon alpha (INF alpha) in pathogenesis of infectious-immune myocarditis (M) and myocarditic cardiosclerosis (MCS).

Material And Methods: Patients with infectious-immune myocarditis (n=27) and myocarditic cardiosclerosis with symptoms of heart failure (n=19). Blood levels of TNF alpha and INF alpha were measured by immune enzyme analysis.

Results: Mean levels of INF alpha and TNF alpha in patients with M (75+/-47 and 304+/-102 rg/ml respectively) were significantly higher than in patients with MCS and healthy donors (31+/-14 and 83+/-39; 38+/-18 95+/-58 rg/ml, respectively, p<0.05). Levels of INF alpha and TNF alpha significantly differed between patients with benign and malignant course of M (99+/-46 and 354+/-100; 39+/-10 227+/-42 rg/ml, p<0.05). Phytohemagglutinine induced TNF alpha production by leucocytes in patients with malignant M (1432+/-515 rg/ml) was higher (p<0.05) while in patients with benign M (131+/-54 rg/ml) lower (p<0.01) than in healthy donors (255+/-98 rg/ml). Patients with malignant compared with those with benign course of myocarditis had lower ejection fraction (25.9+/-12.1 and 42.5+/-11,2%, respectively, p<0.003) and higher inhospital mortality (16.6 and 0%, respectively).

Conclusion: It is most probable that factors of regulation of INF alpha and TNF alpha production occupy an import place among mechanisms of malignant transformation of myocarditis.