The effects of nonselective non-aspirin non-steroidal anti-inflammatory medications on the risk of nonfatal myocardial infarction and their interaction with aspirin

Kimmel, Stephen E.; Berlin, Jesse A.; Reilly, Muredach P.; Jaskowiak, Jane; Kishel, Lori; Chittams, Jesse; Strom, Brian L.

doi:10.1016/j.jacc.2003.08.064

Cited by 109 publications

(100 citation statements)

References 24 publications

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“…Of them, two articles based on the General Practice Research Database (GPRD) (García Rodríguez et al 2000;Watson et al 2002) and another one based on a case-control study in Philadelphia (Kimmel et al 2004) were excluded because their study population overlapped with that of more recent versions. However, we did consider additional sub-analyses if they were provided only in the earliest versions (e.g.…”

Section: Methodsmentioning

confidence: 99%

“…However, we did consider additional sub-analyses if they were provided only in the earliest versions (e.g. RR estimates for individual tNSAID) (Kimmel et al 2004). In addition, one study originally excluded for not presenting results with non-users as a reference was used in a comparison of Naproxen users with users of other tNSAIDs (Rahme et al 2002).…”

Section: Methodsmentioning

confidence: 99%

“…Pooled estimates for cohort and nested casecontrol studies were relatively similar. However, there was significant heterogeneity within case-control studies, which reported both the highest (Johnsen et al 2005) and the lowest (Kimmel et al 2004(Kimmel et al & 2005 RR estimates (table 2). Demographic characteristics.…”

Section: Minireviewmentioning

confidence: 99%

“…For studies that allowed aspirin use, in which 15-30% of the persons used aspirin, the pooled RR was 1.03 (95% CI: 0.96-1.10) for naproxen and 1.10 (95% CI: 1.04-1.16) for ibuprofen, compared with no NSAID use (Ray et al 2002a & b;Schlienger et al 2002;Mamdani et al 2003 Watson et al 2002;Kimmel et al 2004;Lévesque et al 2005). Fewer studies evaluated the interaction between aspirin and coxibs.…”

Section: Minireviewmentioning

confidence: 99%

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Non‐Steroidal Antiinflammatory Drugs and the Risk of Acute Myocardial Infarction

Hernández–Dı́az

Varas‐Lorenzo

Rodrı́guez

2006

Basic Clin Pharma Tox

178

126

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Whether non-aspirin non-steroidal antiinflammatory drugs (NSAIDs) affect the risk of myocardial infarction is unclear. Also, it is unknown whether the effect varies by individual NSAIDs. To summarize the evidence from published observational studies on the risk of myocardial infarction associated with both traditional NSAIDs (tNSAIDs) and selective inhibitors of cyclooxygenase-2 (Coxibs), the authors conducted a systematic review of cohort and case-control studies on NSAIDs and myocardial infarction published between 2000 and 2005. Sixteen original studies were selected according to predefined criteria. Two researchers independently extracted the data on individual study characteristics and results. The authors calculated pooled relative risk (RR) estimates of myocardial infarction for specific NSAIDs compared with no NSAID use, tested the heterogeneity of effects, and evaluated potential reasons for heterogeneity. The pooled RR of myocardial infarction was 0.98 (95% confidence interval (CI): 0.92-1.05) for naproxen, 1.07 (95% CI: 1.02-1.12) for ibuprofen, 1.44 (95% CI: 1.32-1.56) for diclofenac, 0.96 (95% CI: 0.90-1.02) for celecoxib, and 1.26 (95% CI: 1.17-1.36) for rofecoxib (all doses). The pooled RR for rofecoxib at doses Ͼ25 mg/day was 1.78 (95% CI: 1.36-2.34), and 1.18 (95% CI: 1.07-1.31) for doses AE25 mg/day. The RR associated with naproxen was 0.83 (95% CI: 0.72-0.90) among non-users of low-dose aspirin. The RR associated with rofecoxib (all doses) was 1.39 (95% CI: 1.25-1.54) among subjects without a history of myocardial infarction. The risk of myocardial infarction varies with individual NSAIDs. An increased risk was observed for diclofenac and rofecoxib, the latter one with a clear dose-response trend. There was a suggestion of a small increased risk with ibuprofen. Also, data suggest a small reduced risk for naproxen present only in non-users of aspirin, mainly people free of clinically apparent vascular disease.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Minireviewmentioning

confidence: 99%

Section: Minireviewmentioning

confidence: 99%

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Non‐Steroidal Antiinflammatory Drugs and the Risk of Acute Myocardial Infarction

Hernández–Dı́az

Varas‐Lorenzo

Rodrı́guez

2006

Basic Clin Pharma Tox

178

126

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“…Aspirin given 2 hours before a daily dose of ibuprofen successfully inhibits platelet aggregation 1 ; however, ibuprofen administered 3 times per day competitively prevents aspirin from accessing its target serine and inhibiting platelet aggregation ( Figure 1C). Some post hoc analyses [5][6][7] suggested that patients taking both aspirin and ibuprofen had more cardiovascular events than patients taking either drug alone, although others found no clinical risk. 8,9 J.D.…”

Section: The Aspirin-ibuprofen Drug-drug Interactionmentioning

confidence: 99%

Controversies in Antiplatelet Therapy for Patients With Cardiovascular Disease

Lau

2005

Circulation

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Antiplatelet Therapy in Non–ST-Segment Elevation Acute Coronary Syndromes

Schulman

2004

JAMA

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A 63-year-old man presented to the emergency department with 8 hours of waxing-and-waning substernal chest pressure. The patient had previously undergone coronary artery bypass graft surgery in 1992, with the left internal mammary anastomosed to the left anterior descending artery and a reverse saphenous vein graft anastomosed to a large circumflex marginal vein. The right coronary artery was nondominant and without disease. Following coronary artery bypass graft surgery, the patient returned to an active lifestyle without symptoms. Relevant medical history also included hypertension and hypercholesterolemia. Medications included aspirin, 325 mg/d, a 3-hydroxy-3methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (statin), and an angiotensin-converting enzyme inhibitor combined with a low-dose diuretic.Physical examination results were notable for a blood pressure of 126/70 mm Hg and a heart rate of 70/min. Lung fields were clear. The S 1 and S 2 were normal, but there was an S 4 gallop. Distal pulses were intact. His admission electrocardiogram (FIGURE 1) demonstrated diffuse ischemic changes, including ST-segment elevation in lead aVR. Laboratory evaluation demonstrated the following values: peak troponin I, 5.65 ng/mL (reference range, 0-0.50 ng/mL); creatine kinase, 603 U/L (reference range, 24-170 U/L); and creatine kinase-MB fraction, 14% (reference range, 0%-3%).

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The effects of nonselective non-aspirin non-steroidal anti-inflammatory medications on the risk of nonfatal myocardial infarction and their interaction with aspirin

Abstract: In the absence of aspirin use, NANSAIDs are associated with reduced odds of MI. In those using aspirin, NANSAIDs do not provide additional protection. Additional study is needed to determine the clinical impact of using NANSAIDs along with aspirin for cardioprotection.

Cited by 109 publications

References 24 publications

Non‐Steroidal Antiinflammatory Drugs and the Risk of Acute Myocardial Infarction

Non‐Steroidal Antiinflammatory Drugs and the Risk of Acute Myocardial Infarction

Controversies in Antiplatelet Therapy for Patients With Cardiovascular Disease

Antiplatelet Therapy in Non–ST-Segment Elevation Acute Coronary Syndromes

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