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Low cardiac output syndrome (LCOS) and cardiogenic shock (CS) represent life-threatening complications of acute myocardial infarction (AMI), heart failure (HF) or cardiac surgery. Clinically, LCOS presents with hypotension and end-organ hypoperfusion. In CS, the low system oxygen delivery is complicated by a multiorgan dysfunction, which necessitates immediate action. A main treatment strategy, therefore, aims at re-establishing an adequate macrocirculation and microcirculation for the improvement of cellular oxygen supply. Current medical drug therapy for haemodynamic stabilisation is based on vasoactive substances. In early stages, increased systemic vascular resistance often requires vasodilatory drugs, which mediate left ventricular unloading. Nevertheless, application of pure vasodilators might be restricted to certain subgroups of LCOS/CS under the condition of a guided haemodynamic monitoring.1 In the following states of LCOS/CS, therapeutic approaches are mainly based on positive inotropes, which mediate myocardial stimulation and increase heart contractibility. Inotropic drugs effectively enhance myocardial performance. With increasing dosage, however, this potential benefit needs to be judged against the side-effect of raised myocardial oxygen consumption, especially in context of infarct-related LCOS/CS. Vasopressors represent a further option for medical drug therapy of LCOS/CS, but were excluded from this meta-analysis as they are addressed in another Cochrane review.2
Despite the importance of LCOS and CS in clinical praxis, treatment recommendations are limited and controversial. Randomised controlled trials (RCTs) are both difficult to conduct and cost-intensive; so there is an insufficient number of studies investigating treatment strategies for people who become haemodynamically unstable. Most of the existing RCTs just focus on haemodynamic effects. However, …
Contributors This editorial was planned and written by JS based on the systematic review planned, conducted and reported by JS, Eva C. Henrich, Hellen Strobl, Roland Prondzinsky, Sophie Weiche, Holger Thiele, Karl Werdan, Stefan Frantz, and Susanne Unverzagt.
Funding The author has not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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