No available QT/arrhythmia reports.

Analysis of an ECG record database reveals QT interval prolongation potential of famotidine in a large Korean population.

Yun, J., Hwangbo, E., Lee, J. et al. Analysis of an ECG Record Database Reveals QT Interval Prolongation Potential of Famotidine in a Large Korean Population. Cardiovasc Toxicol 15, 197–202 (2015). https://doi.org/10.1007/s12012-014-9285-8

Based on an analysis of QT/QTc intervals from a database of ECG recordings from a large Korean population (ECG-ViEW, 710,369 ECG recordings from 371,401 individuals), we observed that famotidine administration induced a prolonged QTc interval (above 480 ms, p < 0.05 compared to before-treatment, based on a McNemar test). Furthermore, famotidine induced QT prolongations in 10 out of 14 patients with hypocalcemia and 11 out of 13 patients with hypomagnesemia [difference of mean between before and after famotidine administration; 38.00 ms (95% confidence interval 2.72-73.28) and 67.08 ms (95% confidence interval 24.94-109.21), p < 0.05 and p < 0.01 by paired t test, respectively]. In vitro, the IC50 of famotidine for human-ether-a-go-go gene (hERG) channel inhibition was higher than 100 μM as determined by automated patch clamp hERG current assay, implying that hERG channel inhibition is not the underlying mechanism for QT prolongation. These results suggest that famotidine administration increases a proarrhythmic potential, especially in subjects with electrolytes imbalance.

Famotidine and long QT syndrome.

Ken W Lee, Steven R Kayser, Richard H Hongo, Zian H Tseng, Melvin M Scheinman, Famotidine and long QT syndrome, The American Journal of Cardiology, Volume 93, Issue 10, 2004, Pages 1325-1327, ISSN 0002-9149, https://doi.org/10.1016/j.amjcard.2004.02.025.

It is possible that acquired long QT syndrome associated with certain nonantiarrhythmic drugs manifests itself only under unusually stressful conditions that leave patients susceptible to repolarization abnormalities. Although the occurrence of TdP associated with famotidine appears rare, it may be under-recognized because of its occurrence in critically ill patients with other concurrent potential explanations for long QT and TdP.

Famotidine does not induce long QT syndrome: experimental evidence from in vitro and in vivo test systems

Atsushi Sugiyama, Yoshioki Satoh, Akira Takahara, Yuji Nakamura, Masao Shimizu-Sasamata, Shuichi Sato, Keiji Miyata, Keitaro Hashimoto, Famotidine does not induce long QT syndrome: experimental evidence from in vitro and in vivo test systems, European Journal of Pharmacology, Volume 466, Issues 1–2, 2003, Pages 137-146, ISSN 0014-2999, https://doi.org/10.1016/S0014-2999(03)01559-0.

The effects of famotidine on the cardiac repolarization process were assessed using four different levels of test systems described in the draft stage guideline ICH S7B. A supratherapeutic concentration of famotidine (10−5 M), which is >8 times higher than Cmax obtained after its therapeutic dose, neither inhibited human ether-a-go-go-related gene (HERG) K+ current expressed in human embryonic kidney 293 (HEK293) cells nor affected any of the action potential parameters of guinea pig papillary muscles. Therapeutic (0.3 mg/kg, i.v.) to supratherapeutic doses (3–10 mg/kg, i.v.) of famotidine did not affect the repolarization process of the halothane-anesthetized canine model, while only supratherapeutic doses exerted the positive chronotropic, inotropic and dromotropic effects without affecting the mean blood pressure. Moreover, supratherapeutic doses of famotidine (1–10 mg/kg, i.v.) neither induced torsades de pointes nor prolonged QT interval in the canine chronic atrioventricular conduction block model. These results suggest that famotidine possesses no cardiovascular effects at a therapeutic dose, while it may exert cardiostimulatory actions after drug overdoses that might potentiate the proarrhythmic potential of co-administered cardiotonic agents by increasing the intracellular Ca2+ concentration.