Azuma Kohei, Asakura Masanori, Nishimura Koichi, Tahara Saki, Matsumoto Yuki, Manabe Eri, Min Kyung-Duk, Ishihara Masaharu
Department of Cardiovascular and Renal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
J Cardiol Cases. 2022 Feb 20;25(6):385-388. doi: 10.1016/j.jccase.2022.01.005. eCollection 2022 Jun.
Ivabradine is a heart rate (HR)-lowering agent that blocks hyperpolarization-activated cyclic nucleotide-gated channel in the sinus node without a negative inotropic effect on cardiac function. Here we report a case of catecholamine-dependent heart failure, who was intolerant to β blockers, and successfully withdrew catecholamine by administering ivabradine. A 39-year-old male acute decompensated heart failure (ADHF) patient with severe systolic cardiac failure, refractory to diuretic and dobutamine treatment was transferred to our hospital. In addition to titration of dobutamine support, intra-aortic balloon pump, mechanical ventilation, and continuous hemodiafiltration therapy were initiated. These mechanical supports could stabilize ADHF and were removed. Upon stabilization of ADHF, we attempted to initiate a low dose of bisoprolol and taper dobutamine, but the patient could not tolerate even a low dose of bisoprolol nor tapering of dobutamine. Since his HR was consistently above 100 beats per minute and ivabradine was reported to improve stroke volume (SV), we initiated ivabradine, and his SV remarkably increased after initiation. Consequently, the dose of dobutamine was successfully tapered. Also, additional clinical advantage of ivabradine, assessed through hemodynamic parameters, appeared to be a reduction in afterload. < Ivabradine is a heart rate (HR)-lowering agent that blocks the hyperpolarization-activated cyclic nucleotide-gated channel in the sinus node without a negative inotropic effect. In this present catecholamine-dependent advanced heart failure case, the patient could not tolerate even a low dose of bisoprolol nor tapering of dobutamine. Being intolerant to beta-blockers, we initiated the administration of ivabradine. And the initiation of ivabradine resulted in not only the reduction of HR, but also the improvement in stroke volume resulting in the reduction of afterload.>.
伊伐布雷定是一种降低心率（HR）的药物，它可阻断窦房结中的超极化激活环核苷酸门控通道，而对心脏功能无负性肌力作用。在此，我们报告一例儿茶酚胺依赖性心力衰竭患者，该患者对β受体阻滞剂不耐受，通过给予伊伐布雷定成功停用了儿茶酚胺。一名39岁男性急性失代偿性心力衰竭（ADHF）患者，患有严重的收缩性心力衰竭，对利尿剂和多巴酚丁胺治疗无效，被转至我院。除了调整多巴酚丁胺支持剂量外，还启动了主动脉内球囊泵、机械通气和持续血液透析滤过治疗。这些机械支持措施可使ADHF稳定，随后撤除。ADHF病情稳定后，我们试图开始使用低剂量比索洛尔并逐渐减少多巴酚丁胺用量，但该患者甚至不能耐受低剂量比索洛尔，也无法逐渐减少多巴酚丁胺用量。由于其心率持续高于每分钟100次，且据报道伊伐布雷定可改善每搏输出量（SV），我们开始使用伊伐布雷定，用药后其SV显著增加。因此，多巴酚丁胺剂量成功减少。此外，通过血流动力学参数评估，伊伐布雷定的另一个临床优势似乎是可降低后负荷。<伊伐布雷定是一种降低心率（HR）的药物，它可阻断窦房结中的超极化激活环核苷酸门控通道，而对心脏功能无负性肌力作用。在本例儿茶酚胺依赖性晚期心力衰竭病例中，患者甚至不能耐受低剂量比索洛尔，也无法逐渐减少多巴酚丁胺用量。由于对β受体阻滞剂不耐受，我们开始给予伊伐布雷定。伊伐布雷定的使用不仅降低了心率，还改善了每搏输出量，从而降低了后负荷。>
