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Cardiovascular risk with cyclooxygenase inhibitors: general problem with substance specific differences?

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Abstract

Randomised clinical trials and observational studies have shown an increased risk of myocardial infarction, stroke, hypertension and heart failure during treatment with cyclooxygenase inhibitors. Adverse cardiovascular effects occurred mainly, but not exclusively, in patients with concomitant risk factors. Cyclooxygenase inhibitors cause complex changes in renal, vascular and cardiac prostanoid profiles thereby increasing vascular resistance and fluid retention. The incidence of cardiovascular adverse events tends to increase with the daily dose and total exposure time. A comparison of individual selective and unselective cyclooxygenase inhibitors suggests substance-specific differences, which may depend on differences in pharmacokinetic parameters or inhibitory potency and may be contributed by prostaglandin-independent effects. Diagnostic markers such as N-terminal pro brain natriuretic peptide (NT-proBNP) or high-sensitive C-reactive protein might help in the early identification of patients at risk, thus avoiding the occurrence of serious cardiovascular toxicity.

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Notes

  1. Serious cardiovascular event were defined by the APTC (Anti-platelet Trialists’ Collaboration) composite endpoint: cardiac death, non-fatal myocardial infarction and stroke including hemorrhagic stroke and excluding peripheral events.

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Conflict of interest

G. Geisslinger has received grant support and honoraria for occasional lectures from Aventis, MSD, Mundipharma and Pfizer during the past 5 years.

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Tegeder, I., Geisslinger, G. Cardiovascular risk with cyclooxygenase inhibitors: general problem with substance specific differences?. Naunyn Schmied Arch Pharmacol 373, 1–17 (2006). https://doi.org/10.1007/s00210-006-0044-7

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