Thanks.

It seems Famotidine has not historically been associated with Qt interval elongation (prolongation).

 

There are a few reports on that - usually individual case reports of seriously ill patients with comorbidities:

https://www.amjmed.com/article/S0002-9343(99)00328-9/fulltext Famotidine and acquired long QT syndrome August 16, 2004

 

But there are more convincing ones as well:

https://pubmed.ncbi.nlm.nih.gov/25253561/ Analysis of an ECG record database reveals QT interval prolongation potential of famotidine in a large Korean population April 2015

 

And there is a counter study saying Famotidine is not associated with Qt interval elongation:

https://www.researchgate.net/publication/10819177_Famotidine_does_not_induce_long_QT_syndrome_Experimental_evidence_from_in_vitro_and_in_vivo_test_systems Famotidine does not induce long QT syndrome: Experimental evidence from in vitro and in vivo test systems April 2003

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 Ca(2+) concentration.

https://eurjther.com/content/files/sayilar/14/buyuk/9.pdf

Acquired long QT syndrome associated with famotidine has rarely been reported (3,4). To the best of our knowledge the reported patient is the seventh case in the English-language literature.

The mechanism of famotidine-induced long QT is not clearly understood. However, ranitidine - the other H2receptor antagonist - has been shown to inhibit cholinesterase, which may lead to an increase in the acetylcholine level at the nerve endings.

Ranitidine associated bradycardia has been reported in the English-language literature (6), however to the best of our knowledge, ranitidine associated long QT syndrome had not been reported in the literature.

 

While searching for - Fluvoxamine qt prolongation:

https://pubmed.ncbi.nlm.nih.gov/25560394/ Fluvoxamine by itself has potential to directly induce long QT syndrome at supra-therapeutic concentrations Feb 2015

Fluvoxamine was intravenously administered in three escalating doses of 0.1, 1 and 10 mg/kg over 10 min with a pause of 20 min between the doses. The low dose provided therapeutic plasma drug concentration, whereas the middle and high doses attained approximately 10 and 100 times of the therapeutic ones, respectively. Supra-therapeutic concentration of fluvoxamine exerted the negative chronotropic, inotropic and hypotensive effects; and suppressed the atrioventricular nodal and intraventricular conductions, indicating inhibitory actions on Ca2+ and Na+ channels, whereas it delayed the repolarization in a reverse use-dependent manner, reflecting characteristics of rapidly activating delayed rectifier K+ current channel-blocking property. Fluvoxamine prolonged the terminal repolarization phase at 100 times higher concentration than the therapeutic, indicating its proarrhythmic potential. Thus, fluvoxamine by itself has potential to directly induce long QT syndrome at supra-therapeutic concentrations.

 

https://pubmed.ncbi.nlm.nih.gov/24259697/ A comparison of the risk of QT prolongation among SSRIs Oct 2013

Studies demonstrate possible dose-related clinically significant QT prolongation with escitalopram. Fluoxetine, fluvoxamine, and sertraline at traditional doses demonstrate a lack of clinically significant increases in QTc in the majority of studies. Further, paroxetine monotherapy shows a lack of clinically significant QTc prolongation in all studies. However, case reports or reporting tools still link these SSRIs with QTc prolongation. Fluoxetine, escitalopram, and sertraline used in post-acute coronary syndrome patients did not demonstrate risk of QTc prolongation.

 

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