Resolution of Sinus Tachycardia Secondary to Hyperthyroidism With Ivabradine

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(f) funny current at sinoatrial node (SAN). Ivabradine is a novel, dose-dependent selective inhibitor of I(f) 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.