There are no very effective measures for the prevention and treatment of viral myocarditis. The research progress in the treatment of viral myocarditis in recent years is reviewed below. Anti-inflammatory drugs: Non-steroidal anti-inflammatory drugs have been used empirically in the treatment of acute viral myocarditis. The use of indomethacin, sodium salicylate, and ibuprofen in the early stage of the disease can aggravate the disease; the late application did not aggravate the lesion, but also did not see beneficial effects. Therefore, the use of NSAIDs should be avoided in the acute phase of the disease, and this treatment should be limited in the chronic phase. Antiviral agents In animal studies of myocarditis, the use of antiviral agents such as ribavirin at the early stage of the disease (especially during the infection period and within 4 days of infection) was effective in inhibiting viral replication, reducing myocardial damage, and improving survival, but no significant effect was seen with later use. The same agents have no significant clinical efficacy when used in humans. In addition, the efficacy of recombinant alpha interferon and polyclonal immunoglobulin is similar to that of antiviral agents. Immunosuppressive therapy Animal studies have shown that immunosuppressive agents used in the treatment of acute myocarditis can aggravate myocardial necrosis and increase mortality. The combination of prednisone and thiothiopurine has been used in the treatment of myocarditis in humans, and the results were the same in both groups compared to the conventional treatment group [1]. In another study of patients with myocarditis (left ventricular ejection fraction ≤45%) in combination with heart failure, immunological tests showed that patients with a strong early inflammatory response were less ill, but those with high T-cell counts were more ill and had higher mortality. The results of the trial showed that immunosuppressive therapy did not further improve left ventricular ejection fraction or reduce mortality, suggesting that immunosuppressive therapy should not be routinely applied in myocarditis. However, suppression of the T-cell damage response at the right time may also be beneficial in some patients. The application of adrenocorticotropic hormones may improve heart failure and reduce or eliminate severe arrhythmias (e.g., high atrioventricular block) in severe myocarditis, probably by suppressing inflammation and edema in myocarditis, eliminating metabolic reactions, and reducing the effects of toxins [3]. In experiments, hormones inhibit the synthesis and release of interferon, accelerate viral proliferation, and cause aggravation of infection, so it is currently considered unnecessary to use them in general patients, especially within the first 10 days of onset. However, clinical practice has proved that hormones should be applied to patients with severe disease to tide over the critical period. For those who are not effectively treated by other methods or have a strong immune response, hormones can also be considered within 10 days to 1 month after the onset of the disease. For patients with myocarditis in general, the use of hormones and cyclosporine as immunosuppressive therapy has not been shown to be beneficial. Alpha and beta blockers Adrenergic blockers have a mixed effect on acute myocarditis. Metoprolol has no beneficial effect on myocardial fibrosis and increases mortality. The α1 blocker bunazosin, started early in the infection, has a protective effect on the myocardium, probably related to its vasodilatory properties. Calcium antagonists In a mouse model, the myocardial inflammatory response and myocardial fibrosis were significantly reduced in the treatment group with calcium antagonists (verapamil) compared with the control group, and the efficacy may be related to the authorship of verapamil on the coronary microvascular system. Verapamil significantly promoted the replication of coxsackie B virus-ribonucleic acid in cardiac myocytes. It is suggested that the use of verapamil may be detrimental in the clinical treatment of acute viral myocarditis or transient arrhythmias caused by viral infections. High doses of vitamin C are commonly used clinically. Animal experiments have confirmed that the use of vitamin C at the same time of infection can reduce myocardial damage, and the efficacy of the drug after 1 week of infection is not significant, suggesting that vitamin C should be used at an early stage. The use of certain measures to interfere with the effect of perforin Perforin is a protein present in the eosinophilic granules in the cytoplasm of killer effector cells such as cytotoxic T cells and natural killer cells. Cell-mediated cytotoxicity is now shown to be the main pathogenesis of viral myocarditis. In contrast, perforin is one of the major effector molecules released by cytotoxic effector cells such as cytotoxic T cells and natural killer cells to kill target cells. It is expressed and released by natural killer cells and cytotoxic T cells infiltrating the myocardium of viral myocarditis and acts on the myocardial cell membrane. It forms transmembrane tunnel-like pores and causes cell death under the synergistic action of granzyme. It can be seen that the use of certain measures to interfere with the effect of perforin may have some effect on the prevention and treatment of the disease. Angiotensin-converting enzyme inhibitors Studies in a mouse model of coxsackievirus B3 myocarditis have shown that captopril has a good protective effect on the myocardium, whether administered concurrently with coxsackievirus B3 infection or short-term after 1 week. In particular, it reduced myocardial weight, myocardial inflammation, myocardial fibrosis and myocardial calcification, and improved congestive heart failure when applied early. In a study comparing the efficacy of enalapril and captopril, it was found that although enalapril also reduced myocardial weight, only captopril improved survival and myocardial injury. It is thought that the shared efficacy of converting enzyme inhibitors may be based on the reduction of cardiac afterload or the inhibition of protein synthesis. The mechanism of the unique efficacy of captopril has been suggested to be related to the sulfhydryl group and oxygen radical scavenging properties of captopril, as well as its modulatory effects on the bradykinin system (dilating coronary vessels and preventing vasospasm).