Key result
Levosimendan increases LVEF by ~4% and reduces all-cause mortality in patients with LVSD.
Why the study?
Levosimendan is used in heart failure, but its impact on ventricular remodelling in patients with left ventricular systolic dysfunction remained unclear.
Does levosimendan improve ventricular remodelling in patients with left ventricular systolic dysfunction?
Meta-Analysis (n=7,968)
Does levosimendan improve ventricular remodelling in patients with left ventricular systolic dysfunction?
Effect estimate: MD 3.62 (95% CI 2.88, 4.35)
p-value: p=< 0.00001
Levosimendan improves ventricular remodelling and reduces all-cause mortality in patients with left ventricular systolic dysfunction, though it is associated with increased risks of hypotension and arrhythmias.
Supports levosimendan in LV systolic dysfunction despite side-effect risks; confirms remodelling and mortality benefits across 66 RCTs.
Heart failure is the final stage of several cardiovascular diseases, and the key to effectively treating heart failure is to reverse or delay ventricular remodelling. Levosimendan is a novel inotropic and vasodilator agent used in heart failure, whereas the impact of levosimendan on ventricular remodelling is still unclear. This study aims to investigate the impact of levosimendan on ventricular remodelling in patients with left ventricular systolic dysfunction. Electronic databases were searched to identify eligible studies. A total of 66 randomized controlled trials involving 7968 patients were included. Meta-analysis results showed that levosimendan increased left ventricular ejection fraction [mean difference (MD) = 3.62, 95% confidence interval (CI) (2.88, 4.35), P < 0.00001] and stroke volume [MD = 6.59, 95% CI (3.22, 9.96), P = 0.0001] and significantly reduced left ventricular end-systolic volume [standard mean difference (SMD) = -0.52, 95% CI (-0.67, -0.37), P < 0.00001], left ventricular end-diastolic volume index [SMD = -1.24, 95% CI (-1.61, -0.86), P < 0.00001], and left ventricular end-systolic volume index [SMD = -1.06, 95% CI (-1.43, -0.70), P < 0.00001]. In terms of biomarkers, levosimendan significantly reduced the level of brain natriuretic peptide [SMD = -1.08, 95% CI (-1.60, -0.56), P < 0.0001], N-terminal pro-brain natriuretic peptide [SMD = -0.99, 95% CI (-1.41, -0.56), P < 0.00001], and interleukin-6 [SMD = -0.61, 95% CI (-0.86, -0.35), P < 0.00001]. Meanwhile, levosimendan may increase the incidence of hypotension [risk ratio (RR) = 1.24, 95% CI (1.12, 1.39), P < 0.0001], hypokalaemia [RR = 1.57, 95% CI (1.08, 2.28), P = 0.02], headache [RR = 1.89, 95% CI (1.50, 2.39), P < 0.00001], atrial fibrillation [RR = 1.31, 95% CI (1.12, 1.52), P = 0.0005], and premature ventricular complexes [RR = 1.86, 95% CI (1.27, 2.72), P = 0.001]. In addition, levosimendan reduced all-cause mortality [RR = 0.83, 95% CI (0.74, 0.94), P = 0.002]. In conclusion, our study found that levosimendan might reverse ventricular remodelling when applied in patients with left ventricular systolic dysfunction, especially in patients undergoing cardiac surgery, decompensated heart failure, and septic shock.
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Wang et al. (2024) conducted a meta-analysis in Left ventricular systolic dysfunction (n=7,968). Levosimendan was evaluated on Left ventricular ejection fraction (MD 3.62, 95% CI 2.88, 4.35, p=< 0.00001). Levosimendan increased left ventricular ejection fraction (MD 3.62; 95% CI 2.88-4.35; P<0.00001) and reduced all-cause mortality in patients with left ventricular systolic dysfunction.
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