Key result
Levosimendan significantly improved left ventricular fractional shortening (0.32 vs. 0.23, P=0.005) and reduced cardiomyocyte apoptosis compared with vehicle in mice with viral myocarditis.
Why the study?
Does levosimendan improve ventricular function and reduce apoptosis in a mouse model of acute coxsackievirus myocarditis?
RCT (n=39)
randomized
Does levosimendan improve ventricular function and reduce apoptosis in a mouse model of acute coxsackievirus myocarditis?
Levosimendan improves ventricular function and inhibits cardiomyocyte apoptosis in a murine model of acute viral myocarditis, suggesting potential utility in acute heart failure caused by myocarditis.
No immediate clinical implications in viral myocarditis; leaves open potential benefits pending human trials.
BACKGROUND: Acute heart failure is a potentially fatal manifestation of viral myocarditis. Development of myocardial damage in myocarditis involves cardiomyocyte apoptosis. Levosimendan is a novel calcium sensitizing inotropic agent with anti-apoptotic properties. We studied the feasibility of inotropic treatment with levosimendan and its effects on apoptosis in experimental acute heart failure caused by coxsackievirus myocarditis. MATERIALS AND METHODS: Adolescent BALB/c mice were infected with myocarditic Woodruff variant of coxsackievirus B3 (2 x 10(4) plaque-forming units). Mice were randomized into those receiving levosimendan 0.33 mg kg(-1) (total dose 1 mg kg(-1) day(-1)) (n = 20) or vehicle (n = 19) given orally by gauge three times a day for 7 days after infection. Left ventricular function was evaluated by transthoracic echocardiography and the mice were euthanized on day 7. Histopathology, amount of virus in the heart (virus titration assay) and cardiomyocyte apoptosis (TUNEL assay) were studied. Uninfected untreated control mice were also studied. RESULTS: Infection resulted in histopathologically severe myocarditis and significant impairment of left ventricular function. Levosimendan treatment significantly improved ventricular function (fractional shortening 0.32 +/- 0.04 vs. 0.23 +/- 0.05, P = 0.005; contractility 0.60 +/- 0.12 vs. 0.39 +/- 0.14, P = 0.007 and myocardial performance index 0.36 +/- 0.06 vs. 0.62 +/- 0.15, P < 0.0001) compared with vehicle. Levosimendan also reduced cardiomyocyte apoptosis (0.26 +/- 0.08% vs. 0.44 +/- 0.15% in vehicle, P = 0.008), but did not have an effect on areas of myocardial necrosis or inflammation, or the amount of virus in the heart. Levosimendan treatment did not affect mortality (total mortality 63%). CONCLUSIONS; Levosimendan improves ventricular function and inhibits cardiomyocyte apoptosis; therefore, it is suggested as a potentially feasible therapy in acute heart failure caused by viral myocarditis.
No takes yet. Share an insight, caveat, or question.
Latva‐Hirvelä et al. (2009) conducted an RCT in acute heart failure caused by coxsackievirus myocarditis (n=39). Levosimendan vs. vehicle was evaluated on Left ventricular function (fractional shortening) (p=0.005). Levosimendan significantly improved left ventricular fractional shortening (0.32 vs. 0.23, P=0.005) and reduced cardiomyocyte apoptosis compared with vehicle in mice with viral myocarditis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: