Treatment with non-steroidal anti-inflammatory drugs in patients after myocardial infarction – a systematic review

Boulakh, Lena; Gislason, Gunnar

doi:10.1080/14656566.2016.1186648

Cited by 11 publications

(14 citation statements)

References 47 publications

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“…Yet, there is still overwhelming evidence suggesting short-term NSAID treatment increase CVD risks, proposing there is no safe-treatment window. 8,33 Unlike previous studies, we did not observe lower CVD risk with naproxen [5][6][7]34 or celecoxib, 22,28,30 which are the 2 preferred options when NSAID use is unavoidable as recommended by current guidelines. 35 There have been doubts about the superiority of naproxen shown in earlier studies that were heavily biased by the worse outcomes for rofecoxib, which has been withdrawn from the market.…”

Section: Discussioncontrasting

confidence: 90%

Comparative Risks of Nonsteroidal Anti‐inflammatory Drugs on Cardiovascular Diseases: A Population‐Based Cohort Study

Wan

Chan

et al. 2022

The Journal of Clinical Pharma

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Through examining the incidence of cardiovascular diseases (CVDs) among nonsteroidal anti-inflammatory drug (NSAID) users and nonusers, this study aims to compare the risks contributed by different NSAIDs in a Chinese population. The retrospective cohort including 4 298 368 adults without CVD from electronic health records between 2008 and 2017 in Hong Kong was adopted. A total of 4.5% of individuals received NSAIDs including celecoxib, etoricoxib, diclofenac, ibuprofen, indomethacin, mefenamic acid, or naproxen for ≥4 consecutive weeks at baseline. Cox regression, including NSAID use as a time-dependent covariate and adjusted with patient's characteristics, was conducted to examine the association between NSAID exposure and incident CVD. After a median follow-up of 6.9 years (30 million person-years), a total of 258 601 cases of incident CVD was recorded. NSAID use was shown to be associated with a significantly higher risk of CVD (hazard ratio [HR], 1.32 [95%CI, 1.28-1.37]) compared to non-NSAID use. Similar results in coronary heart disease (HR, 1.37 [95%CI,), stroke (HR, 1.27 [95%CI,), and heart failure (HR, 1.25 [95%CI,) were obtained. Overall, similar CVD risk was observed across users of NSAIDs except for etoricoxib, which showed a higher risk (HR, 2.01 [95%CI, 1.63-2.48]). Considering that a higher CVD risk was consistently displayed among NSAID users, NSAIDs should be used cautiously, and the usage of etoricoxib in the Chinese population should be reviewed.

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Section: Discussioncontrasting

confidence: 90%

Comparative Risks of Nonsteroidal Anti‐inflammatory Drugs on Cardiovascular Diseases: A Population‐Based Cohort Study

Wan

Chan

et al. 2022

The Journal of Clinical Pharma

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“…Inhibition of COX‐1‐induced prostaglandins in the gastric mucosa by traditional NSAIDs is often associated with gastrointestinal toxicity, including peptic ulcer disease. Thus, selective COX‐2 inhibitors were introduced in the late 1990s in an attempt to develop anti‐inflammatory strategies without the risk of gastrointestinal side effects (Boulakh and Gislason, ).…”

Section: Broad Anti‐inflammatory Interventionsmentioning

confidence: 99%

Anti‐inflammatory therapies in myocardial infarction: failures, hopes and challenges

Huang

Frangogiannis

2018

British J Pharmacology

217

159

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In the infarcted heart, the damage-associated molecular pattern proteins released by necrotic cells trigger both myocardial and systemic inflammatory responses. Induction of chemokines and cytokines and up-regulation of endothelial adhesion molecules mediate leukocyte recruitment in the infarcted myocardium. Inflammatory cells clear the infarct of dead cells and matrix debris and activate repair by myofibroblasts and vascular cells, but may also contribute to adverse fibrotic remodelling of viable segments, accentuate cardiomyocyte apoptosis and exert arrhythmogenic actions. Excessive, prolonged and dysregulated inflammation has been implicated in the pathogenesis of complications and may be involved in the development of heart failure following infarction. Studies in animal models of myocardial infarction (MI) have suggested the effectiveness of pharmacological interventions targeting the inflammatory response. This article provides a brief overview of the cell biology of the post-infarction inflammatory response and discusses the use of pharmacological interventions targeting inflammation following infarction. Therapy with broad anti-inflammatory and immunomodulatory agents may also inhibit important repair pathways, thus exerting detrimental actions in patients with MI. Extensive experimental evidence suggests that targeting specific inflammatory signals, such as the complement cascade, chemokines, cytokines, proteases, selectins and leukocyte integrins, may hold promise. However, clinical translation has proved challenging. Targeting IL-1 may benefit patients with exaggerated post-MI inflammatory responses following infarction, not only by attenuating adverse remodelling but also by stabilizing the atherosclerotic plaque and by inhibiting arrhythmia generation. Identification of the therapeutic window for specific interventions and pathophysiological stratification of MI patients using inflammatory biomarkers and imaging strategies are critical for optimal therapeutic design. Abbreviations11β-HSD, 11-β hydroxysteroid dehydrogenase;

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“…Sriuttha et al 11 18 RCT (45,705 participants) Nderitu et al 12 7 studies: 5 CO, 1 CC, 1 CS Zhang et al 13 15 studies: 10 studies with general population (n = 1,609,136): 5 nCC, 5 CC 5 studies with chronic renal failure patients (n = 106,681), CC Asghar et al 14 19 studies: 12 CC, 4 CO, 3 RCT Yaxley et al 15 , 9 studies: 5 CO, 4 CC (12,418 participants and 23,877 controls) Villa et al 16 19 studies Ungprasert et al 17 7 studies: 4 CC, 3 CO (7,543,805 participants) Liu et al 18 5 studies: 3 CC, 2 CO Seshasai et al 19 9 RCT (over 100,000 participants) Whitlock et al 20 7 studies: 6 CO, 1 RCT Boulakh et al 21 14 studies: 2 dbRT, 10 CO, 2 CC Ungprasert et al 22 6 studies: 3 CC, 3 CO García Rodríguez et al 23 4 CO, 2 nCC Salvo et al 24 29 MA Scott et al 25 21 studies: 5 CC, 2 CO, 12 RCT Varas-Lorenzo et al 26 25 studies: 8 CO, 14 nCC, 3 CC McGettigan et al 27 51 studies: 30 CC (184,946 cardiovascular events) 21 CO (2.7×10 6 exposed individuals). Mackenzie et al 28 17 RCT Major et al 29 3 clinical trials (4,468 participants and 16,740 person-years of follow-up) Luni et al 30 6 studies: 1 CO, 5 CC Lee et al 31 4 RCT Bem et al 32 28 controlled studies RCT: randomized clinical trial; CO: cohort; CC: case-control; CS: cross-sectional; nCC: nested case-control in a cohort; dbRT: randomized double-blind trial; MA: meta-analysis.…”

Section: Authors Studies Included In the Reviewmentioning

confidence: 99%

Safety considerations during prescription of non-steroidal anti-inflammatory drugs (NSAIDs), through a review of systematic reviews

2021

An Sist Sanit Navar

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Treatment with non-steroidal anti-inflammatory drugs in patients after myocardial infarction – a systematic review

Cited by 11 publications

References 47 publications

Comparative Risks of Nonsteroidal Anti‐inflammatory Drugs on Cardiovascular Diseases: A Population‐Based Cohort Study

Comparative Risks of Nonsteroidal Anti‐inflammatory Drugs on Cardiovascular Diseases: A Population‐Based Cohort Study

Anti‐inflammatory therapies in myocardial infarction: failures, hopes and challenges

Safety considerations during prescription of non-steroidal anti-inflammatory drugs (NSAIDs), through a review of systematic reviews

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