The role of levosimendan in acute heart failure complicating acute coronary syndrome: A review and expert consensus opinion.

Acute heart failure and/or cardiogenic shock are frequently triggered by ischemic coronary events. Yet, there is a paucity of randomized data on the management of patients with heart failure complicating acute coronary syndrome, as acute coronary syndrome and cardiogenic shock have frequently been defined as exclusion criteria in trials and registries. As a consequence, guideline recommendations are mostly driven by observational studies, even though these patients have a particularly poor prognosis compared to heart failure patients without signs of coronary artery disease. In acute heart failure, and especially in cardiogenic shock related to ischemic conditions, vasopressors and inotropes are used. However, both pathophysiological considerations and available clinical data suggest that these treatments may have disadvantageous effects. The inodilator levosimendan offers potential benefits due to a range of distinct effects including positive inotropy, restoration of ventriculo-arterial coupling, increases in tissue perfusion, and anti-stunning and anti-inflammatory effects. In clinical trials levosimendan improves symptoms, cardiac function, hemodynamics, and end-organ function. Adverse effects are generally less common than with other inotropic and vasoactive therapies, with the notable exception of hypotension. The decision to use levosimendan, in terms of timing and dosing, is influenced by the presence of pulmonary congestion, and blood pressure measurements. Levosimendan should be preferred over adrenergic inotropes as a first line therapy for all ACS-AHF patients who are under beta-blockade and/or when urinary output is insufficient after diuretics. Levosimendan can be used alone or in combination with other inotropic or vasopressor agents, but requires monitoring due to the risk of hypotension.

Ivabradine versus metoprolol for heart rate reduction before coronary computed tomography angiography.

Several studies have demonstrated the correlation of heart rate (HR) and image quality in coronary computed tomography angiography. Beta-blocker administration is critical because of its negative inotropic effect. Ivabradine is a selective HR-lowering agent that exclusively inhibits the I(f) current in sinoatrial node cells without having any effect on cardiac contractility or atrioventricular conduction. A total of 120 patients were randomized to oral premedication with ivabradine 15 mg or metoprolol 50 mg. HR and blood pressure (BP) were measured before the administration of premedication and immediately before coronary computed tomographic angiography. The mean time between premedication administration and follow-up was 108 ± 21.5 minutes for ivabradine and 110 ± 22.2 minutes for metoprolol (p = NS). When comparing groups, there were no significant differences in reduction of HR (-11.83 ± 8.6 vs -13.20 ± 7.8 beats/min, p = NS) and diastolic BP (-5.05 ± 14.2 mm Hg vs -4.08 ± 10.8 mm Hg, p = NS), whereas the decrease of systolic BP was significantly lower in patients who received ivabradine compared to those in the metoprolol group (-3.95 ± 13.6 vs -13.65 ± 17.3 mm Hg, p <0.001). In the subgroup of patients who were receiving long-term ß-blocker therapy, significantly stronger HR reduction was achieved with ivabradine (-13.19 ± 5.4 vs -10.04 ± 6.0 beats/min, p <0.05), while the decrease in systolic BP was less (-2.00 ± 13.6 vs -15.04 ± 20.8 mm Hg, p <0.05) compared to metoprolol. In conclusion, ivabradine decreases HR before coronary computed tomographic angiography sufficiently, with significantly less depression of systolic BP compared to metoprolol.