Ischemia-modified albumin levels in patients with acute decompensated heart failure treated with dobutamine or levosimendan: IMA-HF study.

OBJECTIVE: Ischemia-modified albumin (IMA) is a sensitive biomarker of myocardial ischemia. However, data on IMA levels in acute heart failure (HF) are still lacking. In this study, we aimed to evaluate serum IMA levels in acute decompensated HF and the effects of dobutamine and levosimendan treatments on IMA levels. METHODS: This was a prospective, multicenter study that included 70 patients hospitalized with acute decompensated HF and left ventricular ejection fraction < 35%. Blood samples for IMA measurements were obtained on admission and 24-48 h after the initiation of HF therapy. Twenty-nine patients were treated with standard HF therapy, 18 received levosimendan, and 23 received dobutamine in addition to standard of care. A single serum specimen was also collected from 32 healthy individuals each. IMA concentrations were measured by the albumin cobalt binding colorimetric assay, and the results were given in absorbance units (AU). Independent and paired sample t-tests, Mann-Whitney U test, and Wilcoxon signed-rank test were used for the analysis. RESULTS: In patients with acute decompensated HF, the serum concentration of IMA was significantly higher than those of healthy subjects (0.894 ± 0.23 AU vs. 0.379 ± 0.08 AU, p < 0.001). Overall, the IMA levels significantly decreased after 24-48 h of HF therapy (0.894 ± 0.23 AU and 0.832 ± 0.18 AU, p = 0.013). Furthermore, the IMA levels were also found to significantly decrease with standard HF therapy (1.041 ± 0.28 vs. 0.884 ± 0.15 AU, p = 0.041), with levosimendan (0.771 ± 0.18 vs. 0.728 ± 0.18 AU, p = 0.046) and also with dobutamine (0.892 ± 0.18 vs. 0.820 ± 0.13 AU, p = 0.035). CONCLUSION: Patients with acute decompensated HF had elevated IMA levels, and appropriate HF therapy significantly reduced the serum IMA levels. Dobutamine or levosimendan did not increase the IMA levels, suggesting a lower potential in inducing myocardial ischemia when used in recommended doses.

Ivabradine treatment prevents dobutamine-induced increase in heart rate in patients with acute decompensated heart failure.

BACKGROUND: Ivabradine is a heart rate (HR)-lowering agent acting by inhibiting the If-channel. Dobutamine does increase the HR and has some deleterious effects on myocardium. So, we aimed to evaluate whether ivabradine treatment blunts a dobutamine-induced increase in HR. METHODS: The main study population consisted of 58 acute decompensated heart failure patients requiring inotropic support with left-ventricular ejection fraction below 35%, who were randomized to ivabradine (n = 29) or control (n = 29). All patients underwent Holter recording for 6 h and then dobutamine was administered at incremental doses of 5, 10 and 15 µg/kg/min, with 6-h steps. Holter recording was continued during dobutamine infusion. Ivabradine 7.5 mg was given at the initiation of dobutamine and readministered at 12 h of infusion. Also, a nonrandomized beta-blocker group with 15 patients receiving beta-blocker was included in the analysis. Control and beta-blocker groups did not receive ivabradine. RESULTS: In the control group, mean HR gradually and significantly increased at each step of dobutamine infusion (81 ±â€Š11, 90 ±â€Š16, 97 ±â€Š14 and 101 ±â€Š16 b.p.m., respectively; P = 0.001), whereas no significant increase in HR was observed in the ivabradine group (82 ±â€Š17, 82 ±â€Š15, 85 ±â€Š14 and 83 ±â€Š12 b.p.m., respectively; P = 0.439). Mean HR was also found to significantly increase during dobutamine infusion in the beta-blocker group (75 ±â€Š13, 82 ±â€Š13, 86 ±â€Š14 and 88 ±â€Š13 b.p.m., respectively; P = 0.001). The median increase in HR from baseline was significantly higher in the control group compared to those in the ivabradine group (5 vs. 2 b.p.m.; P = 0.007 at first step, 13 vs. 5 b.p.m.; P = 0.001 at second step and 18 vs. 6 b.p.m.; P = 0.0001 at third step of dobutamine, respectively). CONCLUSIONS: Ivabradine treatment prevents dobutamine-induced increase in HR and may be useful in reducing HR-related adverse effects of dobutamine.