[What do we know about the cardiovascular toxicity of the NSAIDs?].
Following the arterial thrombotic risk of rofecoxib (myocardial infarct and cerebral ischemic accidents) that led to its withdrawal from the market, the other coxibs then the NSAIDs have also been blacklisted. The factors responsible for the cardiovascular risk associated with the ingestion of the NSAIDs, selective or not, are not clearly identified. The objective of this review was to collect the available data from the literature, in order to better evaluate of the risk and its causes, principally on the basis of the results of randomised studies, but also of case reports and meta-analyses. There is an increase in the risk of arterial thrombotic events under coxibs and traditional NSAIDs, however the risk is variable for both classes. The cardiovascular risk linked to celecoxib seems variable and modest, and at a standard dose and for usual treatment durations, the risk is probably inexistant. While the real risk of classical NSAIDs is difficult to appreciate from the available results, it can be concluded that the cardiovascular risk of naproxen is low. While part of the cardiovascular consequences of rofecoxib could be associated with increased arterial pressure, these effects are not exclusive to the coxibs since they have been observed with the conventional NSAIDs. However the increase in arterial pressure cannot probably explain everything. Similarly the cardiac insufficiency associated more particularly with rofecoxib, especially in some groups of patients (very old subjects) is not a new type of complication and does not seem to be more frequent with coxibs than with classical NSAIDs. No short-term arterial thrombotic risk of the coxibs and NSAIDs has been clearly demonstrated.
Sibilia
Jean
J
Service de Rhumatologie,CHU de Strasbourg, Hôpital de Hautepierre, Strasbourg 67000. jean.sibilia@chru-strasbourg.fr
Deray
Gilbert
G
Montalescot
Gilles
G
D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000009:adverse effects*; D002318:Cardiovascular Diseases / Q000139:chemically induced*; D016022:Case-Control Studies; D000068579:Celecoxib; D052246:Cyclooxygenase 2 Inhibitors / Q000008:administration & dosage / Q000009:adverse effects; D016861:Cyclooxygenase Inhibitors / Q000009:adverse effects*; D004008:Diclofenac / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives; D005500:Follow-Up Studies; D006801:Humans; D007555:Isoxazoles / Q000008:administration & dosage / Q000009:adverse effects; D007783:Lactones / Q000008:administration & dosage / Q000009:adverse effects; D015201:Meta-Analysis as Topic; D008875:Middle Aged; D009288:Naproxen / Q000008:administration & dosage / Q000009:adverse effects; D011720:Pyrazoles / Q000008:administration & dosage / Q000009:adverse effects; D016032:Randomized Controlled Trials as Topic; D012307:Risk Factors; D013449:Sulfonamides / Q000008:administration & dosage / Q000009:adverse effects; D013450:Sulfones / Q000008:administration & dosage / Q000009:adverse effects; D013927:Thrombosis / Q000139:chemically induced; D013997:Time Factors; D000096926:Benzenesulfonamides
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000068579:Celecoxib; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D004008:Diclofenac; D007555:Isoxazoles; D007783:Lactones; D009288:Naproxen; D011720:Pyrazoles; D013449:Sulfonamides; D013450:Sulfones; C116926:rofecoxib; C406224:valdecoxib; D000096926:Benzenesulfonamides; C409945:parecoxib; C473384:lumiracoxib