Heart failure therapy in myocarditis and ICMP should, according to references, follow the recommendations of cardiological societies. However, some studies proved the positive or negative impact of some medicaments on prognosis and inflammatory changes and the myocardial remodelation [130, 131, 132, 134, 135, 136, 137].

The basis of the therapy is ACE-inhibitors, eventually sartans, beta-blockers (in acute phase administered after the stabilization of a patient´s state of health), diuretics and antagonist of mineralocorticoid receptors [24, 26, 98, 99, 100]. To sustain the adequate cardiac output, dopamine or dobutamine is indicated in some cases [102].

ACE-inhibitors disturb the effect of angiotensin-converting enzyme which transforms biologically inactive angiotensin I into biologically active angiotensin II which increases, by binding on its receptors, among others the system blood pressure. Sartans are blockers of the receptor for angiotensin II and are indicated in patients with the intolerance of ACE-inhibitors [130].

In treatment with ACE-inhibitors and sartans, besides their cardiological effect, there is described even a positive influence on the inflammatory reaction, cardiac remodelation and progression of myocarditis in DCMP, respectively ICMP [131, 132]. In mouse models, administration of captopril and losartan led to a significant reduction of inflammatory damage to the myocardium [131]. However, more distinct reduction of inflammation, necrosis, severity and incidence of myocarditis was observed in mice receiving captopril. The reduction of inflammatory reaction could be according to the study´s conclusions caused by the reduction of local inflammatory reaction and thus by the decreased amount of T lymphocytes involving in the inflammation. The direct mechanism is however still not quite clear.

Therapy with beta-blockers should be according to the recommendations initiated after the stabilization of a patient´s state of health [99]. By contrast, in later phases, it is described positive effect of specific beta-blockers on prognosis and inflammatory reaction. In a study comparing the effect of carvedilol, metoprolol and propranolol, carvedilol had positive effects on almost all researched parameters. It decreased not just the severity of myocarditis, but also mRNA expression of inflammatory cytokines [132]. Two other beta-blockers did not have any or just minor influence. By contrast, in another study with mice infected with Coxsackie B3 virus, a negative influence of administration of metoprolol on the myocarditis prognosis in the acute phase was observed [133]. In mice treated with metoprolol, the research proved increased viral replication, necrosis and inflammation. The mortality rate of mice in this group was 60 % higher than in a control group.

The most commonly indicated diuretics are loop diuretics which inhibit the transport of sodium and chloride ions in the loop oh Henle [134]. A Japanese study with mice models proved positive effect of Torasemide on myocardial fibrosis and remodelation [135]. Favourable influence on the myocardial fibrosis was put in connection with the decrease of levels of TNF beta1, collagen III and aldosterone synthetases and possible influence on the activity of angiotensin II and aldosterone.

Favourable effect on the myocardial remodelation was proved even at antagonist of aldosterone eplerenone [136] and at some calcium channel blockers, which are not however recommended in the therapy of acute heart failure [43, 93]. A similar effect was described even at ivabradine which reduced mortality in mice models by more than 30 % and reduced also the extent of fibrosis, expression of pro-inflammatory cytokines TNF alpha, IL-1beta and IL-6 and led to the improvement of the left ventricular function and to the normalization of its dimensions [137].

The indication of digoxin is full of contradiction in the case of acute heart failure in myocarditis. According to the references, its indication is documented just in some specific cases, however, on the other hand, a Japanese study from 1999 proved a negative influence of digoxin on viral myocarditis in mice models when it increased the extent of the myocardial necrosis and fibrosis [138].

Author of the opening picture: Benjah-bmm27.

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References:

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26) COOPER L. T., JR., KNOWLTON K. U. Chapter 67: Myocarditis. In.: D.P., ZIPES, MANN D.L., LIBBY P., BONOW R.O. a BRAUNWALD E. (eds.). Braunwald´s Heart Disease: A Textbook of Cardiovascular medic Tenth edition. Philadelphia: Elsevier Saunders, 2015. pp. 1589–1602. ISBN 978-1-4557-5133-4.

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