scholarly journals The effect of levosimendan on right ventricular function in patients with heart dysfunction: a systematic review and meta-analysis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yaoshi Hu ◽  
Zhe Wei ◽  
Chaoyong Zhang ◽  
Chuanghong Lu ◽  
Zhiyu Zeng

AbstractLevosimendan exerts positive inotropic and vasodilatory effects. Currently, its effects on right heart function remain uncertain. This systematic review and meta-analysis is intended to illustrate the impacts of levosimendan on systolic function of the right heart in patients with heart dysfunction. We systematically searched electronic databases (PubMed, the Cochrane Library, Embase and Web of Science) up to November 30, 2020, and filtered eligible studies that reported the impacts of levosimendan on right heart function. Of these, only studies whose patients suffered from heart dysfunction or pulmonary hypertension were included. Additionally, patients were divided into two groups (given levosimendan or not) in the initial research. Then, RevMan5.3 was used to conduct further analysis. A total of 8 studies comprising 390 patients were included. The results showed that after 24 h of levosimendan, patients’ right ventricular fractional area change [3.17, 95% CI (2.03, 4.32), P < 0.00001], tricuspid annular plane systolic excursion [1.26, 95% CI (0.35, 2.16), P = 0.007] and tricuspid annular peak systolic velocity [0.86, 95% CI (0.41, 1.32), P = 0.0002] were significantly increased compared to the control group. And there is an increasing trend of cardiac output in levosimendan group [1.06, 95% CI (− 0.16, 2.29), P = 0.09 ] .Furthermore, patients’ systolic pulmonary arterial pressure [− 5.57, 95% CI (− 7.60, − 3.54), P < 0.00001] and mean pulmonary arterial pressure [− 1.01, 95% CI (− 1.64, − 0.37), P = 0.002] were both significantly decreased, whereas changes in pulmonary vascular resistance [− 55.88, 95% CI (− 206.57, 94.82), P = 0.47] were not significant. Our study shows that in patients with heart dysfunction, levosimendan improves systolic function of the right heart and decreases the pressure of the pulmonary artery.

2013 ◽  
Vol 106 (2) ◽  
pp. 141-146 ◽  
Author(s):  
Michelle L. Freeman ◽  
Carolyn Landolfo ◽  
Robert E. Safford ◽  
Cesar A. Keller ◽  
Michael G. Heckman ◽  
...  

2014 ◽  
Vol 23 (134) ◽  
pp. 476-487 ◽  
Author(s):  
Robert Naeije ◽  
Alessandra Manes

Pulmonary arterial hypertension (PAH) is a right heart failure syndrome. In early-stage PAH, the right ventricle tends to remain adapted to afterload with increased contractility and little or no increase in right heart chamber dimensions. However, less than optimal right ventricular (RV)–arterial coupling may already cause a decreased aerobic exercise capacity by limiting maximum cardiac output. In more advanced stages, RV systolic function cannot remain matched to afterload and dilatation of the right heart chamber progressively develops. In addition, diastolic dysfunction occurs due to myocardial fibrosis and sarcomeric stiffening. All these changes lead to limitation of RV flow output, increased right-sided filling pressures and under-filling of the left ventricle, with eventual decrease in systemic blood pressure and altered systolic ventricular interaction. These pathophysiological changes account for exertional dyspnoea and systemic venous congestion typical of PAH. Complete evaluation of RV failure requires echocardiographic or magnetic resonance imaging, and right heart catheterisation measurements. Treatment of RV failure in PAH relies on: decreasing afterload with drugs targeting pulmonary circulation; fluid management to optimise ventricular diastolic interactions; and inotropic interventions to reverse cardiogenic shock. To date, there has been no report of the efficacy of drug treatments that specifically target the right ventricle.


2021 ◽  
Vol 8 ◽  
Author(s):  
Longxiang Su ◽  
Pan Pan ◽  
Huaiwu He ◽  
Dawei Liu ◽  
Yun Long

Pulse pressure variation (PPV) is a mandatory index for hemodynamic monitoring during mechanical ventilation. The changes in pleural pressure (Ppl) and transpulmonary pressure (PL) caused by mechanical ventilation are the basis for PPV and lead to the effect of blood flow. If the state of hypovolemia exists, the effect of the increased Ppl during mechanical ventilation on the right ventricular preload will mainly affect the cardiac output, resulting in a positive PPV. However, PL is more influenced by the change in alveolar pressure, which produces an increase in right heart overload, resulting in high PPV. In particular, if spontaneous breathing is strong, the transvascular pressure will be extremely high, which may lead to the promotion of alveolar flooding and increased RV flow. Asynchronous breathing and mediastinal swing may damage the pulmonary circulation and right heart function. Therefore, according to the principle of PPV, a high PPV can be incorporated into the whole respiratory treatment process to monitor the mechanical ventilation cycle damage/protection regardless of the controlled ventilation or spontaneous breathing. Through the monitoring of PPV, the circulation-protective ventilation can be guided at bedside in real time by PPV.


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