Association of non-steroidal anti-inflammatory drugs with outcomes in patients with ST-segment elevation myocardial infarction treated with fibrinolytic therapy: an ExTRACT-TIMI 25 analysis

Gibson, C. Michael; Pride, Yuri B.; Aylward, Philip E.; Col, Jacques; Goodman, Shaun G.; Gulba, Dietrich C.; Bergovec, Mijo; Kunadian, Vijayalakshmi; Zorkun, Cafer; Buros, Jacqueline L.; Murphy, Sabina A.; Antman, Elliott M.

doi:10.1007/s11239-008-0264-4

Cited by 19 publications

(4 citation statements)

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“…Despite the proven anti-inflammatory effect of glucocorticoids, it has been reported that their employment could be detrimental due to secondary effects like volume retention, edema, hyperglycemia, and muscular atrophy, preventing its employment in patients with myocardial infarction [17]. The prescription of commonly used NSAIDs has been limited due to the delayed appearance of ischemic necrosis and imminent risk of developing aneurism and rupture [18].…”

Section: Introductionmentioning

confidence: 99%

Clofibrate Treatment Decreases Inflammation and Reverses Myocardial Infarction-Induced Remodelation in a Rodent Experimental Model

et al. 2019

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Myocardial infarction (MI) initiates an inflammatory response that promotes both beneficial and deleterious effects. The early response helps the myocardium to remove damaged tissue; however, a prolonged later response brings cardiac remodeling characterized by functional, metabolic, and structural pathological changes. Current pharmacological treatments have failed to reverse ischemic-induced cardiac damage. Therefore, our aim was to study if clofibrate treatment was capable of decreasing inflammation and apoptosis, and reverse ventricular remodeling and MI-induced functional damage. Male Wistar rats were assigned to (1) Sham coronary artery ligation (Sham) or (2) Coronary artery ligation (MI). Seven days post-MI, animals were further divided to receive vehicle (V) or clofibrate (100 mg/kg, C) for 7 days. The expression of IL-6, TNF-α, and inflammatory related molecules ICAM-1, VCAM-1, MMP-2 and -9, nuclear NF-kB, and iNOS, were elevated in MI-V. These inflammatory biomarkers decreased in MI-C. Also, apoptotic proteins (Bax and pBad) were elevated in MI-V, while clofibrate augmented anti-apoptotic proteins (Bcl-2 and 14-3-3ε). Clofibrate also protected MI-induced changes in ultra-structure. The ex vivo evaluation of myocardial functioning showed that left ventricular pressure and mechanical work decreased in infarcted rats; clofibrate treatment raised those parameters to control values. Echocardiogram showed that clofibrate partially reduced LV dilation. In conclusion, clofibrate decreases cardiac remodeling, decreases inflammatory molecules, and partly preserves myocardial diameters.

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Section: Introductionmentioning

confidence: 99%

Clofibrate Treatment Decreases Inflammation and Reverses Myocardial Infarction-Induced Remodelation in a Rodent Experimental Model

et al. 2019

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“…However, potent anti-inflammatory treatment with glucocorticoids was associated with impaired myocardial healing, development of ventricular aneurysms and high risk of ventricular rupture in clinical studies (53,54). Similar detrimental effects were observed following treatment with non-steroidal anti-inflammatory drugs (55). In consequence, glucocorticoids and non-steroidal anti-inflammatory drugs are contraindicated in patients with AMI by the current clinical guidelines (56).…”

Section: Anti-inflammatory Therapeutic Approaches In Amimentioning

confidence: 96%

Innate Immune Mechanisms in Myocardial Infarction - An Update

Mareş

Marinković

Cotoi

et al. 2018

Revista Romana De Medicina De Laborator

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“…• Нестероидные противовоспалительные средства (за исключением низких доз АСК** в качестве антиагреганта и средних доз ACK** для лечения перикардита) не рекомендуются при ИМпST из-за неблагоприятного влияния на риск сердечно-сосудистых событий [200][201][202].…”

Section: еок Iiab (уур B удд 3)unclassified

2020 Clinical practice guidelines for Acute ST-segment elevation myocardial infarction

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2020

Russ J Cardiol

171

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Association of non-steroidal anti-inflammatory drugs with outcomes in patients with ST-segment elevation myocardial infarction treated with fibrinolytic therapy: an ExTRACT-TIMI 25 analysis

Abstract: Among STEMI patients treated with a fibrinolytic agent and aspirin, use of NSAIDs in the week preceding the incident event was associated with a higher incidence of MI, the composite of death and MI as well as the composite of death, MI, severe heart failure and shock at 30 days.

Cited by 19 publications

References 35 publications

Clofibrate Treatment Decreases Inflammation and Reverses Myocardial Infarction-Induced Remodelation in a Rodent Experimental Model

Clofibrate Treatment Decreases Inflammation and Reverses Myocardial Infarction-Induced Remodelation in a Rodent Experimental Model

Innate Immune Mechanisms in Myocardial Infarction - An Update

2020 Clinical practice guidelines for Acute ST-segment elevation myocardial infarction

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