Yelizaveta Medina, Asif Khan, Jonathon Spagnola, James Lafferty
{"title":"Resolution of Sinus Tachycardia Secondary to Hyperthyroidism With Ivabradine.","authors":"Yelizaveta Medina, Asif Khan, Jonathon Spagnola, James Lafferty","doi":"10.14740/jocmr4940","DOIUrl":null,"url":null,"abstract":"<p><p>Currently, ivabradine is not approved for the treatment of sinus tachycardia secondary to hyperthyroidism. We aimed to increase the recognition of ivabradine as an effective alternative to, or combination with, beta-blockers in controlling sinus tachycardia secondary to hyperthyroidism. Elevated thyroid hormone levels enhance cardiac performance through a positive chronotropic effect, resulting in an increased heart rate (HR), an effect brought on by increasing the <i>I<sub>f</sub></i> funny current at sinoatrial node (SAN). Ivabradine is a novel, dose-dependent selective inhibitor of <i>I<sub>f</sub></i> channels. By decreasing SAN pacemaker activity, ivabradine allows for selective reduction of HR with a resultant increase in ventricular filling time. This mechanism sets ivabradine apart from the typical rate-reducing medications, namely beta-blockers and calcium channel blockers, which simultaneously decrease HR and myocardial contractility. We describe a case of hyperthyroidism-induced sinus tachycardia, resistant to maximal doses of beta-blocker, which was successfully managed by ivabradine. After excluding other causes of tachycardia, such as anemia, hypovolemic states, structural heart disease, drug abuse, and infection, ivabradine was given off-label for symptomatic relief of hyperthyroidism-induced sinus tachycardia. Within 24 h, HR steadily decreased to the low 80s. Our patient had a unique presentation in which he presented with hyperthyroidism-induced sinus tachycardia with no relief after administration of maximal dose of beta-blocker. Ivabradine was then given, with resolution of sinus tachycardia within 24 h.</p>","PeriodicalId":15431,"journal":{"name":"Journal of Clinical Medicine Research","volume":"15 6","pages":"336-339"},"PeriodicalIF":0.0000,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d4/f0/jocmr-15-336.PMC10332879.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Clinical Medicine Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14740/jocmr4940","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/6/29 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Currently, ivabradine is not approved for the treatment of sinus tachycardia secondary to hyperthyroidism. We aimed to increase the recognition of ivabradine as an effective alternative to, or combination with, beta-blockers in controlling sinus tachycardia secondary to hyperthyroidism. Elevated thyroid hormone levels enhance cardiac performance through a positive chronotropic effect, resulting in an increased heart rate (HR), an effect brought on by increasing the If funny current at sinoatrial node (SAN). Ivabradine is a novel, dose-dependent selective inhibitor of If channels. By decreasing SAN pacemaker activity, ivabradine allows for selective reduction of HR with a resultant increase in ventricular filling time. This mechanism sets ivabradine apart from the typical rate-reducing medications, namely beta-blockers and calcium channel blockers, which simultaneously decrease HR and myocardial contractility. We describe a case of hyperthyroidism-induced sinus tachycardia, resistant to maximal doses of beta-blocker, which was successfully managed by ivabradine. After excluding other causes of tachycardia, such as anemia, hypovolemic states, structural heart disease, drug abuse, and infection, ivabradine was given off-label for symptomatic relief of hyperthyroidism-induced sinus tachycardia. Within 24 h, HR steadily decreased to the low 80s. Our patient had a unique presentation in which he presented with hyperthyroidism-induced sinus tachycardia with no relief after administration of maximal dose of beta-blocker. Ivabradine was then given, with resolution of sinus tachycardia within 24 h.
目前,伊伐布雷定尚未被批准用于治疗甲亢继发的窦性心动过速。我们的目标是让更多人认识到伊伐布雷定可有效替代或联合β-受体阻滞剂控制甲亢继发的窦性心动过速。甲状腺激素水平升高可通过正性时序效应提高心脏性能,从而导致心率(HR)增加,这种效应是通过增加窦房结(SAN)的滑稽电流产生的。伊伐布雷定是一种新型、剂量依赖性的 If 通道选择性抑制剂。通过降低 SAN 起搏器的活性,伊伐布雷定可选择性地降低心率,从而延长心室充盈时间。这种机制使伊伐布雷定有别于典型的降心率药物,即同时降低心率和心肌收缩力的β受体阻滞剂和钙通道阻滞剂。我们描述了一例甲状腺功能亢进引起的窦性心动过速病例,患者对最大剂量的β-受体阻滞剂产生耐药性,伊伐布雷定成功地控制了患者的病情。在排除其他心动过速原因(如贫血、低血容量状态、结构性心脏病、药物滥用和感染)后,患者在标签外使用伊伐布雷定对甲亢诱发的窦性心动过速进行对症缓解。24 小时内,心率稳步下降至 80 多分。我们的患者有一个独特的病例,他出现甲状腺功能亢进诱发的窦性心动过速,服用最大剂量的β-受体阻滞剂后症状仍无缓解。随后他服用了伊伐布雷定,窦性心动过速在 24 小时内得到缓解。