Diclofenac and acute myocardial infarction in patients with no major risk factors

Jick, Susan S.; Kaye, James A.; Jick, Hershel

doi:10.1111/j.1365-2125.2007.02942.x

Cited by 17 publications

(18 citation statements)

References 12 publications

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“…Despite the use of the same database, the results cannot directly be compared because of varying definitions of the exposure timewindows, different time-periods included and matching variables. Taking this into account, the overall results of the present cohort study were broadly similar to most of the previously published GPRD studies [30][31][32][33][34][35][36]. A recent GPRD case-control study concluded that long-term use of diclofenac was associated with substantially increased risks of MI, whilst this conclusion did not apply to ibuprofen or naproxen [35].…”

Section: Discussionsupporting

confidence: 87%

“…General Practice Research Database has been used in several other studies to study the risk of MI in patients using traditional NSAIDs [30][31][32][33][34][35][36] or selective Cox-2 inhibitors [37]. Despite the use of the same database, the results cannot directly be compared because of varying definitions of the exposure timewindows, different time-periods included and matching variables.…”

Section: Discussionmentioning

confidence: 99%

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Does the varied use of NSAIDs explain the differences in the risk of myocardial infarction?

Staa

Rietbrock²,

Setakis³

et al. 2008

Journal of Internal Medicine

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Abstract. van Staa T-P, Rietbrock S, Setakis E, Leufkens HGM (Medicines and Healthcare Products Regulatory Agency, London, UK; Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Utrecht, The Netherlands). Does the varied use of NSAIDs explain the differences in the risk of myocardial infarction? J Intern Med 2008; 264: 481-492.Objective. To investigate the risk of myocardial infarction (MI) with diclofenac, ibuprofen and naproxen, taking into account the exposure patterns.Design. Retrospective cohort study using the General Practice Research Database.Setting. UK primary care. Subjects. Patients aged 40+ years prescribed a traditional nonsteroidal anti-inflammatory drug (NSAID).The control cohort was frequency matched by disease risk score.Intervention. Observational comparisons of MI rates.Results. The study included 729294 NSAID users and 443047 controls. The relative rate (RR) for MI increased with cumulative and daily dose (RR = 1.05 with 0-4 prior prescriptions and RR = 1.49 with 30+; RR = 1.05 with daily dose of <1200 mg ibuprofen and RR = 1.96 with dose of ‡2400 mg per day; for diclofenac, the RR was 1.13 with <150 mg per day and 2.03 with ‡300 mg per day). Diclofenac users had higher risks of MI (RR = 1.21) than ibuprofen (RR = 1.04) or naproxen (RR = 1.03) users, but exposure varied between these drugs. Taking into account these exposure differences, it was found that the risk of MI was comparable in current and past long-term users. The patterns of hazard rates (i.e. absolute risks) of MI were similar in patients using ibuprofen, diclofenac or naproxen with similar history of NSAID use. There was no statistical difference between ibuprofen, diclofenac and ibuprofen in the linear trends for cumulative dose or daily dose.Conclusions. Long-term users of traditional NSAIDs have an increased risk of MI that is probably explained by the underlying disease severity. Most of the differences in MI risk between diclofenac, ibuprofen or naproxen may be explained by their varied use.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Does the varied use of NSAIDs explain the differences in the risk of myocardial infarction?

Staa

Rietbrock²,

Setakis³

et al. 2008

Journal of Internal Medicine

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“…They also discovered a cumulating risk for MI with diclofenac up to 2.03 at >300mg compared to 1.13 at <150 mg. Jick et al further specified the dependence of an escalation of relative risk with the number of prescriptions of tNSAID (diclofenac, ibuprofen and naproxen) and found only for diclofenac an increase up to a RR of 2. [40]. The study by GarciaRodriguez confirms these results as it found that the risk increased with current NSAID intake, treatment duration and daily dose [42].…”

Section: Clinical Data For An Association Of Diclofenac With Atherothsupporting

confidence: 83%

“…Jick et al analyzed in a nested case control study cases of AMI associated with diclofenac, ibuprofen or naproxen intake in patients with no major risk factors and found an adjusted risk ratio for diclofenac of 1.30 vs. 1.10 in naproxen or ibuprofen users. Diclofenac showed an increasing risk ratio up to 2 with increasing numbers of prescriptions [40]. Similar results were obtained by van Staa et al, who scanned the General Practice Research Database like Jick et al In this analysis, the relative risk for AMI increased with numbers of prescriptions and raising dosages, resulting in a cumulative risk of 1.21 for diclofenac and 1.04 and 1.03 for ibuprofen and naproxen respectively [41].…”

Section: Clinical Data For An Association Of Diclofenac With Atherothsupporting

confidence: 75%

A Review on the Risk of Myocardial Infarction Associated with the NSAID Diclofenac

Krötz

Struthmann²

2010

CHDDT

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The popular over-the counter analgesic drug diclofenac has recently been associated with increased rates of myocardial infarction among patients with cardiovascular risk as well as among healthy populations. Although other traditional non-steroidal anti-inflammatory drugs (tNSAID) have also been accused to exert this risk, literature data at present gives reason to believe that the hazard of myocardial infarction is mainly associated with diclofenac. Large retrospective analyses of clinical data have repeatedly shown that diclofenac, similar as some selective COX-2 inhibitors, increases the propensity to experience adverse cardiovascular and atherothrombotic events. These associations cannot be explained with the deteriorating effect of NSAID on arterial hypertension, as the statistical associations only have been found conclusively for diclofenac and not for other tNSAID. The reasons for this novel side-effect of diclofenac may be based on the specific pharmacology of diclofenac, which, similar to selective COX-2 inhibitors, alters vascular levels of platelet active prostaglandins in a way that favours arterial thrombosis. In this review, we summarize the clinical evidence about adverse atherothrombotic events associated with diclofenac and dissect the pharmacological reasons beyond this phenomenon in comparison to other tNSAID.

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“…A positive dose-response relationship has been demonstrated for both diclofenac and ibuprofen and risk of coronary artery disease. [37][38][39][40] Whether or not an increased risk of ischemic stroke exists at higher doses for these or other NSAIDs requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

Use of non‐steroidal anti‐inflammatory drugs and risk of ischemic and hemorrhagic stroke in the Australian veteran community

Mangoni

Woodman

Gilbert

et al. 2010

Pharmacoepidemiology and Drug

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Diclofenac and acute myocardial infarction in patients with no major risk factors

Cited by 17 publications

References 12 publications

Does the varied use of NSAIDs explain the differences in the risk of myocardial infarction?

Does the varied use of NSAIDs explain the differences in the risk of myocardial infarction?

A Review on the Risk of Myocardial Infarction Associated with the NSAID Diclofenac

Use of non‐steroidal anti‐inflammatory drugs and risk of ischemic and hemorrhagic stroke in the Australian veteran community

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