Key result
Cytokines generated by activated immune cells are increasingly recognized as important factors in the pathogenesis of myocarditis and cardiomyopathy, potentially causing myocardial damage via nitric oxide.
This review highlights the pathophysiological role of cytokines and nitric oxide in mediating myocardial damage and negative inotropism in myocarditis and dilated cardiomyopathy.
Cytokine pathways may identify therapeutic targets in myocarditis; leaves open confirmation in prospective trials.
Myocarditis is thought to be caused by various viruses, and accumulating evidence links viral myocarditis with the eventual development of dilated cardiomyopathy. Recently the importance of hepatitis C virus infection was noted in patients with dilated cardiomyopathy. Cytokines are increasingly recognized as an important factor in the pathogenesis and pathophysiology of myocarditis and cardiomyopathy. Elevated circulating cytokines have been reported in patients with heart failure, and various cytokines have been shown to depress myocardial contractility in vitro and in vivo. A number of recent studies showed that cytokines generated by activated immune cells cause an increase in NO (nitric oxide) via induction of NO synthase. Increased generation of NO may induce negative inotropism and myocardial damage. This review discusses the etiology and pathogenesis of myocarditis and cardiomyopathy from this point of view.
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Akira Matsumori (1996) conducted a review in Myocarditis and cardiomyopathies. Cytokines was evaluated. Cytokines generated by activated immune cells are increasingly recognized as important factors in the pathogenesis of myocarditis and cardiomyopathy, potentially causing myocardial damage via nitric oxide.
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