COVID-19: Fluvoxamine is not effective in preventing disease severity and increase the risk of heart failure

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In one meta-analysis of comparing three drugs – Fluvoxamine, Paxlovid and Molnupiravir, only Fluvoxamine reflected the most cases of deaths (and in all cases heart failures!) https://www.tandfonline.com/doi/pdf/10.1080/07853890.2022.2034936

A study in December 2021 already highlighted that Fluvoxamine is not effective in preventing disease severity. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8745642/

BA.2 and its emerging variants are adapt at replicating very fast in the other parts of the human host including the lower respiratory tract and also building up huge reservoirs in the heart, liver, kidneys, CNS system, gastrointestinal and male reproductive organs.

These indirectly affects the heart in a multitude of ways and those who are taking Fluvoxamine, already known to cause arrhythmia, they are actually increasing the risk of heart failure.

https://www.goodrx.com/classes/ssris/ssris-what-you-should-know-side-effects
 
https://www.jstage.jst.go.jp/article/jts/40/1/40_33/_article

— Fluvoxamine is one of the typical selective serotonin-reuptake inhibitors. While its combined use with QT-prolonging drugs has been contraindicated because of the increase in plasma concentrations of such drugs, information is still limited whether fluvoxamine by itself may directly prolong the QT interval.

We examined electropharmacological effects of fluvoxamine together with its pharmacokinetic profile by using the halothane-anesthetized dogs (n = 4). 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

 Worse for those with SCN5A mutations and suffer from Brugada syndrome, they will have a high risk of death if they have COVID and are also given Fluvoxamine. https://academic.oup.com/europace/article/12/2/282/430346
 

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