Prior aspirin use in unstable angina patients with modified plasma inflammatory markers and endothelial nitric oxide synthase in neutrophils.
BACKGROUND
Prior use of aspirin in patients with acute coronary syndrome has been associated with a lower incidence of acute myocardial infarction. The aim of this study was to explore if prior aspirin therapy in unstable angina (UA) patients could modify systemic inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) and the expression of endothelial nitric oxide synthase (eNOS) in neutrophils.


METHODS
Unstable angina was defined as transient S-T segment changes without significant increases in CK and CK-MB. We studied 50 consecutive patients admitted to hospital within 24 h after the onset of chest pain. The number of patients with prior aspirin was significantly higher (n = 32) than those not taking aspirin (n = 18) on admission.


RESULTS
Plasma levels of IL-6 and ICAM-1 were significantly increased in the UA patients when compared with the healthy control volunteers (n = 20) used as a reference for normal values. Plasma levels of both IL-6 and ICAM-1 were reduced in patients taking aspirin. There were no differences in the plasma levels of TNF-alpha between the UA patients and the control volunteers. The eNOS protein expression was also higher in neutrophils from the UA patients taking aspirin than in those not taking aspirin.


CONCLUSIONS
Patients taking aspirin before UA showed a lower systemic inflammatory response and higher eNOS protein expression in their neutrophils
Mateos-Cáreres
P J
PJ
Cardiovascular Research and Hypertension Laboratory, Fundación Jiménez Díaz, Madrid, Spain.
García-Méndez
A
A
Farré
J
J
Sánchez de Miguel
L
L
Gómez
J
J
de Andres
R
R
Rico
L
L
Romero
J
J
López-Farré
A
A
D000368:Aged; D000789:Angina, Unstable / Q000188:drug therapy* / Q000276:immunology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D001241:Aspirin / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D003327:Coronary Disease / Q000150:complications / Q000276:immunology; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000276:immunology; D004730:Endothelium, Vascular / Q000276:immunology; D005260:Female; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications / Q000276:immunology; D018836:Inflammation Mediators / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D009504:Neutrophils / Q000201:enzymology*; D019001:Nitric Oxide Synthase / Q000032:analysis*; D052250:Nitric Oxide Synthase Type III; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D000894:Anti-Inflammatory Agents, Non-Steroidal; D015415:Biomarkers; D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D001241:Aspirin