We read with interest the study by Jacob et al. Its objective was to determine if late use of aspirin before coronary artery bypass grafting (CABG) with valve surgery affects bleeding events and major adverse cardiovascular events. For preoperative aspirin administration, patients were divided in 2 groups: the “early-discontinuation” group had aspirin withdrawal ≥6 days before surgery and the “late-use” group continued aspirin administration within 5 days of surgery. Lack of data concerning an objective quantification of the antiplatelet effect of aspirin constitutes a major drawback of the study. Expected inhibition of platelet function is not always achieved after aspirin administration. A wide variability in platelet response to aspirin therapy has been described with prevalence of aspirin resistance (AR) as defined by platelet function tests ranging from 1% to 45%. In our recent study, we analyzed the proportion of patients with AR before and after the CABG procedure. All patients undergoing CABG were on long-term aspirin therapy, and we observed 31% patients with AR preoperatively. Early discontinuation of aspirin in patients with insufficient platelet inhibition may lead to a further increase in platelet activity and subsequent onset of ischemic events before surgery. There is evidence that certain patients have an accentuated response to usual doses of preoperative aspirin that may result in increased perioperative blood loss. Nevertheless, because AR independently increases the incidence of adverse cardiovascular events as much as pronounced platelet inhibition after aspirin administration increases the incidence of excessive bleeding, it would seem critical to adjust for this variable. When assessing the influence of preoperative aspirin administration management on bleeding and adverse ischemic events, objective quantification of platelet activity inextricably should be considered. Use of suitable point-of-care platelet function analyzers seems to be reasonable for this purpose. By platelet function assessment, it is possible to distinguish patients with AR after aspirin administration and thus a proclivity to ischemic events from patients with an accentuated response to aspirin and thus a proclivity to excessive bleeding. In patients scheduled for procedures involving CABG, individually tailored aspirin administration management based on platelet function testing for sensitivity to an aspirin effect can help decrease bleeding and ischemic events. The role of aspirin should be understood more accurately through an objective quantification of platelet function. Such an approach requires further studies to provide a precise and comprehensive view on the relation between aspirin administration management and bleeding and ischemic events. We congratulate the authors on their elegant and timely research.