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Aspirin is the key treatment in the secondary prevention of atherothrombosis. Interindividual variability of response has been linked to a higher risk for ischemic events. The aim of this study was to identify clinical and biologic factors predicting high on-aspirin platelet reactivity (HPR) in a high-risk, "real-world" population of vascular patients. All platelet testing performed from 2011 to 2013 in consecutive patients receiving long-term treatment with aspirin for coronary or cerebrovascular disease was retrospectively analyzed. Indications for platelet testing were recurrent ischemic events or high-risk angioplasty. HPR was defined as aggregation intensity =20% using light-transmission aggregometry with arachidonic acid 0.5 mg/ml. Collagen-epinephrine platelet function analysis was also performed (threshold <165 seconds). Cardiovascular risk factors, usual biologic parameters, and antiplatelet treatment were recorded. A total of 1,508 patients were included (mean age 63 years, 71% men, 23% with diabetes). Antiplatelet treatment was aspirin alone in 333 patients and dual-antiplatelet therapy in 1,175 patients. HPR was found in 11.1% of patients. In multivariate analysis, independent predictive factors of HPR on light-transmission aggregometry with arachidonic acid were diabetes mellitus (odds ratio [OR] 2.10, 95% confidence interval [CI] 1.39 to 3.16), age (OR 1.25, 95% CI 1.06 to 1.47), fibrinogen level (OR 1.20, 95% CI 1.02 to 1.42), and von Willebrand factor level (OR 1.06, 95% CI 1.03 to 1.09). On light-transmission aggregometry with arachidonic acid and collagen-epinephrine platelet function analysis, fibrinogen remained the main factor associated with HPR (OR 1.33, 95% CI 1.19 to 1.61). Similar results were found in patients treated with aspirin alone or dual-antiplatelet therapy. A fibrinogen level >4.0 g/L was associated with a 3.9-fold increased risk for HPR in patients aged <75 years. In conclusion, fibrinogen level was the major predictor of HPR on aspirin in this large population of high-risk vascular patients. [ABSTRACT FROM AUTHOR]

Background: The great majority of successfully resuscitated out-of-hospital cardiac arrest (OHCA) patients will subsequently die during their ICU and hospital stay. Several studies have previously described the main causes of OHCA but the impact of aetiology on the outcome and the timing and value of diagnostic procedures such as coronary angiogram remains controversial. Methods: We analysed the causes of cardiac arrest in a prospective database from a tertiary reference. We compared the mortality observed in the subgroups of patients with a cardiac or a non-cardiac cause of arrest. Results: 983 patients were admitted from January 2000 to August 2008.In patients without an obvious non-cardiac cause of arrest, a coronary angiogram followed if necessary by a coronary angioplasty was performed at admission. The median age was 58 years (range 84.39) and 74% were male. Past or current cigarette smoking was noted in 54%, hypertension in 35% and hypercholesterolemia in 23%. The causes of OHCA were an acute coronary syndrome (ACS=Gr1) in 389 pts (40%), primary ventricular arrhythmia (VT-FV=Gr2) in 154 pts (16%), cardiac failure (=Gr3) in 35 pts (3%), acute respiratory failure (=Gr4) in 186 pts (19%), neurological failure (=Gr5) in 41 pts (4%), unknown (=Gr6) in 71 pts (7%) and others causes(=Gr7) in 104 pts (11%). Overall, the mortality rate of the entire cohort was 68%; mortality rates observed in each subgroup are displayed in the figure. Display Omitted [Copyright &y& Elsevier]

Background: Diabetes is associated with a high rate of events after acute coronary syndrome and percutaneous coronary intervention despite aspirin treatment. Once daily aspirin might not provide 24-hour stable biological efficacy in patients with diabetes. We compared the biological efficacy of the same daily dose of aspirin given either once (OPD) or divided twice per day in a population of diabetic patients with previous coronary artery disease. Methods: Ninety-two consecutive diabetic patients with at least 1 criteria of time-dependent aspirin efficacy, elevated high-sensibility C-reactive protein (hs-CRP), fibrinogen, platelet count, or active smoking were prospectively included. Consecutive patients were randomly treated with 150-mg aspirin daily given either OPD (150 mg in the morning) or twice per day (75 mg in the morning and 75 mg in the evening) in a crossover study. The main outcome was platelet reactivity to arachidonic acid (0.5 mg/mL) measured by light transmission aggregometry at trough level before morning aspirin intake. Results: Mean maximum aggregation intensity triggered by arachidonic acid was 19.7% ± 15.4% on OPD and 11.9% ± 10.4% on twice per day (P < .0001). Biological resistance (maximum aggregation intensity ≥20%) was observed in 42% of patients on OPD and 17% on twice per day (P < .001). Of the 39 patients with biological resistance on OPD, 24 (62%) overcame resistance on twice per day. Of the 16 resistant on twice per day, only 1 patient (6%) overcame resistance on OPD. Results were concordant with global evaluation of platelet reactivity by Platelet Function Analyzer-100. A better twice per day efficacy was independent of clopidogrel cotreatment. Conclusion: In a population of diabetic patients with coronary artery disease and a high risk of time-dependent aspirin resistance, aspirin divided twice per day can significantly decrease the rate of biological loss of efficacy at trough level. [ABSTRACT FROM AUTHOR]