Viral infection occasionally triggers myocarditis (inflammation and necrosis of the heart muscle) which can result in serious, acute heart failure. The first signs of this condition may be flu-like symptoms which evolve into non-specific chest discomfort, shortness of breath or palpitations. The majority of patients recover spontaneously but others have continuing heart problems which require medication and can be severe enough to cause death.
The effect of hormone treatment on viral myocarditis remains controversial. The review authors conducted a thorough search of the medical literature. Eight randomised trials with 719 patients which met the inclusion criteria compared hormone treatment plus conventional therapy with no hormone. Hormone treatment did not reduce mortality from viral myocarditis. Improvements in heart function were found but the trials were of low quality and small size so this finding must be regarded as uncertain. Further trials comparing hormone treatment in people suffering viral myocarditis with placebo are warranted. There are no conflicts of interest in the review.
For people diagnosed with viral myocarditis and low LVEF, corticosteroids do not reduce mortality. They may improve cardiac function but the trials were of low quality and small size so this finding must be regarded as uncertain. High-quality, large-scale RCTs should be careful designed to determine the role of corticosteroid treatment for viral myocarditis. Adverse events should also be carefully evaluated.
Myocarditis is defined as inflammation of the myocardium accompanied by myocellular necrosis. Experimental evidence suggests that autoimmune mechanisms follow viral infection, resulting in inflammation and necrosis in the myocardium. However, the use of corticosteroids as immunosuppressives for this condition remains controversial.
The existing review was updated. The primary objective of this review is to assess the beneficial and harmful effects of treating acute or chronic viral myocarditis with corticosteroids. The secondary objective is to determine the best dose regimen.
We searched the Cochrane Central Register of Controlled Trials (CENTRAL, Issue 7 of 12, 2012) on The Cochrane Library, MEDLINE OVID (1946 to July Week 2, 2012), EMBASE OVID (1980 to Week 29, 2012), BIOSIS Previews (1969 to 20 July 2012), ISI Web of Science (1970 to 20th July, 2012), and LILACS (from its inception to 25 July, 2012) , Chinese Biomed Database, CNKI and WANFANG Databases (from their inception to 31 December 2012). We applied no language restrictions.
Randomised controlled trials (RCTs) of corticosteroids for viral myocarditis compared with no intervention, placebo, supportive therapy, antiviral agents therapy or conventional therapy, including trials of corticosteroids plus other treatment versus other treatment alone, irrespective of blinding, publication status, or language.
Two review authors extracted data independently. Results were presented as risk ratios (RRs) and mean differences (MDs), both with 95% confidence intervals (CIs).
Eight RCTs (with 719 participants) were included in this update. The trials were small in size and methodological quality was poor. Viral detection was performed in 38% of participants, among whom 56% had positive results. Mortality between corticosteroids and control groups was non-significant (RR, 0.93, 95% CI 0.70 to 1.24). At 1 to 3 months follow-up, left ventricular ejection fraction (LVEF) was higher in the corticosteroids group compared to the control group (MD 7.36%, 95% CI 4.94 to 9.79), but there was substantial heterogeneity. Benefits were observed in LVEF in two trials with 200 children given corticosteroids (MD 9.00%, 95% CI 7.48 to 10.52). New York Heart Association (NYHA) class and left ventricular end-stage systole diameter (LVESD) were not affected. Creatine phosphokinase (CPK) (MD -104.00 U/L, 95% CI -115.18 to -92.82), Isoenzyme of creatine phosphate MB (CKMB) (MD 10.35 U/L, 95% CI 8.92 to 11.78), were reduced in the corticosteroids group compared to the control group, although the evidence is limited to small participant numbers. There were insufficient data on adverse events.