Influence of aspirin on inflammatory markers in patients after acute myocardial infarction

Solheim, Svein; Arnesen, Harald; Eikvar, Lars; Hurlen, Mette; Seljeflot, Ingebjørg

doi:10.1016/s0002-9149(03)00897-x

Cited by 53 publications

(34 citation statements)

References 149 publications

(168 reference statements)

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“…Several previous studies demonstrated anti--inflammatory effect of low doses of ASA and clopidogrel, mainly in patients with CAD [18][19][20][21][22][23][24][25]. The results of subanalysis of Physician's Health Study suggested that cardioprotective effect of ASA correlated with its anti-inflammatory effect [26].…”

Section: Discussionmentioning

confidence: 96%

Effect of ASA dose doubling versus switching to clopidogrel on plasma inflammatory markers concentration in patients with type 2 diabetes and high platelet reactivity: The AVOCADO study

Rosiak

Postuła²,

Kapłon‐Cieślicka³

et al. 2013

Cardiol J

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Section: Discussionmentioning

confidence: 96%

Effect of ASA dose doubling versus switching to clopidogrel on plasma inflammatory markers concentration in patients with type 2 diabetes and high platelet reactivity: The AVOCADO study

Rosiak

Postuła²,

Kapłon‐Cieślicka³

et al. 2013

Cardiol J

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“…Primary prevention with ASA is widely applied, however, not only because of its cardioprotective impact but also because there is increasing evidence of chemoprotection by ASA against cancer (96). Regarding its effect on the inflammatory response, the reduction of CRP levels by ASA has also been confirmed in other patient cohorts including subgroups with stable CAD (97) and ACS (98,99). Furthermore, ASA treatment reduces levels of IL-6, MCP-1, transforming growth factor-β (TGF-β), and TNF-α (97-100) but does not affect platelet-leukocyte interactions (101) (▶ Table 3).…”

Section: Platelets Inflammation and Antiinflammatory Drugs In Acs Anmentioning

confidence: 99%

Platelets, inflammation and anti-inflammatory effects of antiplatelet drugs in ACS and CAD

Müller¹,

Chatterjee²,

Rath³

et al. 2015

Thromb Haemost

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SummaryPlatelets play a pivotal role in chronic inflammation leading to progression of atherosclerosis and acute coronary events. Recent discoveries on novel mechanisms and platelet-dependent inflammatory targets underpin the role of platelets to maintain a chronic inflammatory condition in cardiovascular disease. There is strong and clinically relevant crosslink between chronic inflammation and platelet activation. Antiplatelet therapy is a cornerstone in the prevention and treatment of acute cardiovascular events. The benefit of antiplatelet agents has mainly been attributed to their direct anti-aggregatory impact. Some anti-inflammatory off-target effects have also been described. However, it is unclear whether these effects are secondary due to inhibition of platelet activation or are caused by direct distinct mechanisms interfering with inflammatory pathways. This article will highlight novel platelet associated targets that contribute to inflammation in cardiovascular disease and elucidate mechanisms by which currently available antiplatelet agents evolve anti-inflammatory capacities, in particular by carving out the differential mechanisms directly or indirectly affecting platelet mediated inflammation. It will further illustrate the prognostic impact of antiplatelet therapies by reducing inflammatory marker release in recent cardiovascular trials.

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“…associated with lower levels of inflammatory markers. [28] REFERENCES Strengths and limitations of study and is azurophilic granules of human neutrophils.…”

Section: Resultsmentioning

confidence: 99%

Study of leukocytic hydrolytic enzymes in patients with acute stage of coronary heart disease

Patil¹,

Karnik²,

Chavan³

2007

Indian J Med Sci

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ABSTRACTwomen] with the diagnosis of AMI or unstable BACKGROUND: Coronary heart disease (CHD) is a major killer worldwide. Atherosclerosis, which is the basis of CHD, is believed to be an inflammatory disorder. Though various aspects of atherosclerosis are extensively studied, leukocytic hydrolytic enzymes are not studied very well with respect to CHD. AIM: This study was planned to assess changes associated with leukocytic hydrolases in CHD patients. SETTING AND DESIGN: A tertiary care hospital; case-control study. MATERIALS AND METHODS: 106 patients with acute myocardial infarction, 60 patients with unstable angina and 45 healthy controls were included in the study. Acid phosphatase, lysozyme, adenosine deaminase (ADA) and cathepsin-G levels were estimated from leukocytes. Reduced glutathione (GSH) and malondialdehyde (MDA) levels were measured. STATISTICAL ANALYSIS: Statistical comparison of data was done using student's ttest (unpaired). Correlation difference was calculated by using Pearson correlation coefficient. RESULTS: Significantly higher levels of acid phosphatase, lysozyme, ADA with lower levels of cathepsin G in leukocytes were observed in CHD group. We also found significantly higher levels of serum MDA with lower concentrations of blood GSH in CHD group. In diabetic CHD group, significantly higher levels of leukocytic acid phosphatase, lysozyme, ADA and serum MDA with lower levels of cathepsin G and blood GSH were observed. CONCLUSIONS: Our study indicates that leukocyte hydrolytic enzymes, mainly acid phosphatase, lysozyme and ADA were more active in CHD patients and may contribute to inflammation related with CHD. Its also indicates that leukocyte cathepsin-G may have antiinflammatory role.

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Influence of aspirin on inflammatory markers in patients after acute myocardial infarction

Cited by 53 publications

References 149 publications

Effect of ASA dose doubling versus switching to clopidogrel on plasma inflammatory markers concentration in patients with type 2 diabetes and high platelet reactivity: The AVOCADO study

Effect of ASA dose doubling versus switching to clopidogrel on plasma inflammatory markers concentration in patients with type 2 diabetes and high platelet reactivity: The AVOCADO study

Platelets, inflammation and anti-inflammatory effects of antiplatelet drugs in ACS and CAD

Study of leukocytic hydrolytic enzymes in patients with acute stage of coronary heart disease

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