Category: Professional Posters
Purpose: In acute heart failure, elevated heart rate is a common phenomenon but a strong predicting factor for poor prognosis. However, the role of beta-blockers is limited in this setting due to its negative inotropic effect. Ivabradine has comparable chronotropic effect with that of beta-blockers but without affecting contractility. However, its clinical evidence on hemodynamic stability and heart rate variability in acute heart failure patients is limited. The aim of this study was to evaluate the impact of ivabradine on hemodynamic stability and heart rate variability in patients with acute heart failure.
Methods: Between April 2016 and February 2017, eleven consecutive patients with acute heart failure, sinus rhythm with heart rate of 70 bpm or more and left ventricular ejection fraction (LVEF) less than 40%, were began with ivabradine at the dose of 2.5-5 mg twice daily during hospitalization. In order to evaluate hemodynamic impact of ivabradine objectively, the study utilized a non-invasive hemodynamic system using bio-impedence measurements to detect cardiac contractility, stroke volume, blood pressure and vascular resistance. Heart rate variability parameters were collected using holter monitor. Data was obtained before initiation of ivabradine, one week and one month after initiation of ivabradine.
Results: The mean age of study subjects was 57. The leading cause of heart failure was ischemic heart disease (46%), followed by uremic cardiomyopathy (18%). Ivabradine was initiated in 63% of the patients within the first 72 hours after admission. No patients were requiring inotropic therapy at the time of initiation of ivabradine. The mean heart rate was significantly decreased after initiation of ivabradine: 92.2±12.59 bpm at baseline; 78.7±11.21 bpm at one week (p=0.004); 76.64±12.94 bpm at one month (p=0.031). Cardiac contractility index was similar in one week but significantly increased at one month compared to that at baseline: 28.11±12.89 at baseline; 32.78±12.92 at one week (p=0.334); 36.8±10.92 at one month (p=0.019). Stroke volume index, cardiac index, mean arterial pressure, systemic vascular resistance, and heart rate variability were similar before and after initiation of ivabradine. LVEF was significantly improved from 26.4% to 45.6% within three months after discharge (p=0.003). New York Heart Association functional class was significantly improved at one week and one month (p=0.004). NT-proBNP was reduced within two weeks after ivabradine initiation though the difference was not statistically significant (p=0.145). One patient (9%) experienced bradycardia while on ivabradine. In-hospital mortality rate and three-month readmission rate were 0%.
Conclusion: Ivabradine was effective in reducing heart rate without significantly affecting cardiac index, blood pressure, and heart rate variability in patients with acute heart failure in sinus rhythm. Since Ivabradine was well-tolerated, it might be considered as a treatment option in patients with acute heart failure in sinus rhythm with elevated heart rate. Further study with larger sample size is warranted to confirm the findings of this study.