Inotropic and vasodilator strategies in patients with a heart attack (acute myocardial infarction) and cardiogenic shock or low cardiac output

Cardiogenic shock occurring in 5% to 10% of patients with acute myocardial infarction still remains a life-threatening complication. As regards treatment options with inotropic and vasoactive drugs for infarct related cardiogenic shock, there is only very little evidence generated by randomised controlled trials.

We included four small randomised controlled trials with a total of 66 participants. Mortality rates ranged from 18% to 47% in the four studies. Only one inotropic drug and one vasodilative were studied in four different comparisons with other active drugs or placebo.

Levosimendan showed a trend towards beneficial haemodynamic effects and improved survival rates, but this evidence was based on very limited data which were insufficient to draw robust conclusions. This means that there is no trial evidence for inotropic or vasodilator drugs which shows convincing benefits and confirmed superiority regarding haemodynamic management or survival rates.

Authors' conclusions: 

At present there are no robust and convincing data to support a distinct inotropic or vasodilator drug based therapy as a superior solution to reduce mortality in haemodynamically unstable patients with CS or low cardiac output complicating AMI.

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Background: 

The recently published German-Austrian S3 Guideline for the treatment of infarct related cardiogenic shock (CS) revealed a lack of evidence for all recommended therapeutic measures.

Objectives: 

To determine the effects in terms of efficacy, efficiency and safety of cardiac care with inotropic agents and vasodilator strategies versus placebo or against each other for haemodynamic stabilisation following surgical treatment, interventional therapy (angioplasty, stent implantation) and conservative treatment (that is no revascularization) on mortality and morbidity in patients with acute myocardial infarction (AMI) complicated by CS or low cardiac output syndrome (LCOS).

Search strategy: 

We searched CENTRAL, MEDLINE (Ovid), EMBASE (Ovid) and ISI Web of Science, registers of ongoing trials and proceedings of conferences in January 2013. Reference lists were scanned and experts in the field were contacted to obtain further information. No language restrictions were applied.

Selection criteria: 

Randomised controlled trials in patients with AMI complicated by CS or LCOS.

Data collection and analysis: 

Data collection and analysis were performed according to the published protocol. All trials were analysed individually. Hazard ratios (HRs) and odds ratios with 95% confidence intervals (CI) were extracted but not pooled because of high heterogeneity between the control group interventions.

Main results: 

Four eligible, very small studies were identified from a total of 4065 references. Three trials with high overall risk of bias compared levosimendan to standard treatment (enoximone or dobutamine) or placebo. Data from a total of 63 participants were included in our comparisons, 31 were treated with levosimendan and 32 served as controls. Levosimendan showed an imprecise survival benefit in comparison with enoximone based on a very small trial with 32 participants (HR 0.33; 95% CI 0.11 to 0.97). Results from the other similarly small trials were too imprecise to provide any meaningful information about the effect of levosimendan in comparison with dobutamine or placebo. Only small differences in haemodynamics, length of hospital stay and the frequency of major adverse cardiac events or adverse events overall were found between study groups.

Only one small randomised controlled trial with three participants was found for vasodilator strategies (nitric oxide gas versus placebo) in AMI complicated by CS or LCOS. This study was too small to draw any conclusions on the effects on our key outcomes.

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