Decongestive effects of levosimendan in cardiogenic shock induced by postpartum cardiomyopathy.

BACKGROUND: Catecholamines and/or levosimendan have been proposed for haemodynamic restoration during cardiogenic shock (CS). In CS induced by post-partum cardiomyopathy (PPCM), levosimendan might be particularly favourable. The aim of this study was to evaluate the haemodynamic and echocardiographic effects of levosimendan in patients with CS, in particular in patients with PPCM-induced CS. METHODS: Twenty-eight patients with refractory CS were retrospectively included in the study. Among them, a cohort of 8 women with PPCM-induced CS was included. All patients were treated with levosimendan (loading dose followed by a continuous infusion for 24 h) and were invasively monitored, including a pulmonary artery catheter, for 48hours. Echocardiographic measurements were performed at baseline and during follow-up. RESULTS: Significant improvements in haemodynamic parameters were observed 48 h after starting levosimendan. The cardiac index increased (+1.2±0.6L/min, P<0.001) and filling pressures decreased (pulmonary artery occlusion pressure, PAOP: -11.2±4.3mmHg, P<0.001; right-atrial pressure, RAP: -6.1±4.9mmHg, P<0.001). The left ventricular ejection fraction was significantly higher at 48 h compared to baseline (38% [34-46%] versus 27% [22-30%], P<0.001). Despite similar characteristics at baseline, in the subgroup of patients with PPCM, more profound decongestive effects at 48hours were observed: PAOP (13±2 versus 17±4mmHg, P=0.007) and RAP (12±4 versus 17±4mmHg, P=0.006) were significantly lower in the PPCM subgroup compared to the non-PPCM subgroup. CONCLUSIONS: Haemodynamics and left-ventricular ejection fraction rapidly improved after treatment with levosimendan. In patients with PPCM-induced CS, a more profound reduction of congestion was observed.

Acute heart failure and cardiogenic shock: a multidisciplinary practical guidance.

PURPOSE: Acute heart failure (AHF) causes high burden of mortality, morbidity, and repeated hospitalizations worldwide. This guidance paper describes the tailored treatment approaches of different clinical scenarios of AHF and CS, focusing on the needs of professionals working in intensive care settings. RESULTS: Tissue congestion and hypoperfusion are the two leading mechanisms of end-organ injury and dysfunction, which are associated with worse outcome in AHF. Diagnosis of AHF is based on clinical assessment, measurement of natriuretic peptides, and imaging modalities. Simultaneously, emphasis should be given in rapidly identifying the underlying trigger of AHF and assessing severity of AHF, as well as in recognizing end-organ injuries. Early initiation of effective treatment is associated with superior outcomes. Oxygen, diuretics, and vasodilators are the key therapies for the initial treatment of AHF. In case of respiratory distress, non-invasive ventilation with pressure support should be promptly started. In patients with severe forms of AHF with cardiogenic shock (CS), inotropes are recommended to achieve hemodynamic stability and restore tissue perfusion. In refractory CS, when hemodynamic stabilization is not achieved, the use of mechanical support with assist devices should be considered early, before the development of irreversible end-organ injuries. CONCLUSION: A multidisciplinary approach along the entire patient journey from pre-hospital care to hospital discharge is needed to ensure early recognition, risk stratification, and the benefit of available therapies. Medical management should be planned according to the underlying mechanisms of various clinical scenarios of AHF.