Aspirin Resistance Incidence and Associations Between Aspirin Effect and Outcomes in Cardiac Surgery.

BACKGROUND: When, and on whom, aspirin should be ceased before elective cardiac surgery is controversial. This study assessed the incidence of preoperative aspirin resistance and whether the quantitative antiplatelet effect of aspirin was associated with perioperative outcomes. METHODS: Aspirin-induced antiplatelet effect was measured by multiple electrode aggregometry in 250 adult cardiac surgical patients within 24 hours before surgery. Aspirin resistance was defined by a normal platelet function testing result for those who had continued taking aspirin until the day before the platelet function testing. RESULTS: Aspirin resistance was observed in 16 (11.9%) patients (95% confidence interval [CI], 7.4-18.4). Of the 250 patients included, 75 (30%) required allogeneic blood product transfusion subsequently. Aspirin induced antiplatelet effect (odds ratio [OR], 0.991 per unit increment in the area under the curve on the platelet function testing, with a smaller area indicating more platelet inhibition; 95% CI, 0.982-0.999; P = .035), a higher EuroSCORE [European System for Cardiac Operative Risk Evaluation] II risk (OR, 1.184 per EuroSCORE II risk percentage increment; 95% CI, 1.017-1.379; P = .001), and a lower body mass index (OR, 0.926 per unit increment; 95% CI, 0.867-0.990; P = .024) were the only factors independently associated with requiring perioperative allogeneic blood product transfusion. CONCLUSIONS: The degree of aspirin effect immediately before cardiac surgery was weakly associated with the risks of postoperative bleeding and allogeneic blood product transfusion, suggesting that measuring aspirin-induced antiplatelet effect before cardiac surgery may be useful as an adjunct in optimizing patient blood management for patients who are at high risk of bleeding and requiring allogeneic blood transfusion.

The role of contact system in septic shock: the next target? An overview of the current evidence.

BACKGROUND: Septic shock remains challenging to intensive care units worldwide, despite recent documented improvement in mortality over the years. Multiple new therapies have been attempted without success in large clinical trials. Evidence concerning the role of the contact system and bradykinin on septic shock physiological manifestations is shown by this article. OBJECTIVES: The objective of the study is to review the current evidence linking contact system activation and septic shock, as well as efficacy of available therapies targeting this pathophysiological pathway and to evaluate the potential of further researching the matter. RESULTS: Multiple animal studies are already available and suggestive of a meaningful role of contact system activation on septic shock. However, human trials are still scarce, and the ones available are not enough to establish such a strong connection. Furthermore, attempted therapies have been successful across multiple species, but not as much in humans. Therefore, contact system and septic shock relationship remains plentiful in questions to be answered in the coming years or decades. CONCLUSIONS: Whether the contact system is not as relevant in humans as it is in animals or there is only lack of evidence remains to be explained. The subject is an attractive open field for further research aiming to aid in tackling such a burdensome condition.