ASPIRIN: the best NSAID
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Aspirin reduces C-recative Protein (MI reduction)

Aspirin lowers the inflammation within artery walls that is essential part of the development of atherosclerosis.  Thus not only does it reduce the formation of thrombi, it also slows or blocks atherosclerosis process.  The reduction in MI from the taking of aspirin is due both to the anti-platelet and anti-inflammatory properties of aspirin.  C-reactive protein (CRP) is a marker for inflammation which initiates the plaque formation process leading to atherosclerosis and MI.  For those who had an MI those not taking aspirin the CRP was 50% lower. 

 

 

(Circulation. 1999;100:793-798.)
© 1999 American Heart Association, Inc.

 

Increased Proinflammatory Cytokines in Patients With Chronic Stable Angina and Their Reduction By Aspirin

Ignatios Ikonomidis, MD; Felicita Andreotti, MD, PhD; Emanouel Economou, MD; Christodoulos Stefanadis, MD, FESC; Pavlos Toutouzas, MD, FESC; Petros Nihoyannopoulos, MD, FESC

From The Imperial College School of Medicine, National Heart & Lung Institute, Cardiology Department, Hammersmith Hospital, London, UK, and the Department of Cardiology (E.E., C.S., P.T.), Ippokration Hospital, Athens, Greece.

Correspondence to Petros Nihoyannopoulos, MD, FACC, FESC, Imperial College School of Medicine, National Heart & Lung Institute, Cardiology Department, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK. E-mail petros@rpms.ac.uk.

Ignatios Ikonomidis, MD; Felicita Andreotti, MD, PhD; Emanouel Economou, MD; Christodoulos Stefanadis, MD, FESC; Pavlos Toutouzas, MD, FESC; Petros Nihoyannopoulos, MD, FESC

From The Imperial College School of Medicine, National Heart & Lung Institute, Cardiology Department, Hammersmith Hospital, London, UK, and the Department of Cardiology (E.E., C.S., P.T.), Ippokration Hospital, Athens, Greece.

Correspondence to Petros Nihoyannopoulos, MD, FACC, FESC, Imperial College School of Medicine, National Heart & Lung Institute, Cardiology Department, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK. E-mail petros@rpms.ac.uk.

Background—Proinflammatory cytokines released by injured endothelium facilitate interaction of endothelial cells with circulating leukocytes and thus may contribute to development and progression of atherosclerosis. We investigated whether cytokines and C-reactive protein (CRP) are indicative of myocardial ischemia or of diseased vessels and whether they are influenced by aspirin treatment in patients with chronic stable angina.

Methods and Results—Plasma macrophage colony stimulating factor (MCSF), IL-1b, IL-6, and CRP were measured in 60 stable patients after 48-hour Holter monitoring and in 24 matched controls. All patients had angiographic documentation of disease and positive exercise ECGs. Patients with ischemia on Holter monitoring (n=40) received aspirin or placebo in a 6-week, randomized, double blind, crossover trial. Blood sampling was repeated at the end of each treatment phase (3 weeks). Compared to controls, patients had more than twice median MCSF (800 versus 372 pg/mL), IL-6 (3.9 versus 1.7 pg/mL), and CRP (1.25 versus 0.23 mg/L) levels (P<0.01 for all comparisons). MCSF was related to ischemia on Holter monitoring (P<0.01), to low ischemic threshold during exercise (P<0.01), and together with IL-1b to number of diseased vessels (P<0.05). MCSF, IL-6, and CRP were all reduced after 6 weeks of aspirin treatment (P<0.05).

Conclusions—These findings suggest that cytokines are associated with both ischemia and anatomic extent of disease in patients with stable angina. Reduced cytokine and CRP levels by aspirin may explain part of aspirin's therapeutic action.

 

 

 

 

 

 

Effect of Short-Term Aspirin Use on C-Reactive Protein

Journal of Thrombosis and Thrombolysis, Vol. 9, No. 1, January 2000, pages 37-41.

 

The effect of aspirin on C-reactive protein as a marker of risk in unstable angina .  Journal of the American College of Cardiology , Volume 37 , Issue 5 , Pages 1266 - 1270 S . Kennon

Abstract

OBJECTIVES

This study was designed to assess the interaction between aspirin and C-reactive protein (CRP) release in unstable angina.

BACKGROUND

C-reactive protein release in acute coronary syndromes may be a response to myocardial necrosis or may reflect the inflammatory process that drives atherogenesis. Aspirin has the potential to influence CRP release, either by its anti-inflammatory activity or by reducing myocardial necrosis. The clinical significance of this potential interaction has not previously been tested.

METHODS

We conducted a prospective cohort study of 304 consecutive patients admitted with non-ST-elevation acute coronary syndromes. Serial blood samples were obtained for CRP and troponin I assay. End points were cardiac death and nonfatal myocardial infarction during follow-up for 12 months.

RESULTS

A total of 174 patients (57%) were taking aspirin before admission. Patients taking aspirin had lower troponin I concentrations throughout the sampling period, only 45 (26.0%) having concentrations >0.1 mg/l compared with 48 (37.8%) patients not taking aspirin (p = 0.03). Maximum CRP concentrations were also lower in patients taking aspirin (8.16 mg/l [3.24 to 24.5]) than in patients not taking aspirin (11.3 mg/l [4.15 to 26.1]), although the difference was not significant. However, there was significant interaction (p = 0.04) between prior aspirin therapy and the predictive value of CRP concentrations for death and myocardial infarction at 12 months. Thus, odds ratios (95% confidence intervals) for events associated with an increase of 1 standard deviation in maximum CRP concentration were 2.64 (1.22–5.72) in patients not pretreated with aspirin compared with 0.98 (0.60–1.62) in patients pretreated with aspirin.

CONCLUSIONS

The association between CRP and cardiac events in patients with unstable angina is influenced by pretreatment with aspirin. Modification of the acute-phase inflammatory responses to myocardial injury is the major mechanism of this interaction.

 

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Disclaimer:  The information, facts, and opinions provided here is not a substitute for professional advice.  It only indicates what JK believes, does, or would do.  Always consult your primary care physician for any medical advice, diagnosis, and treatment.