Background: Tranexamic acid reduces blood loss and transfusion requirements in cardiac surgery but may increase the risk of coronary graft thrombosis. We previously reported the 30-day results of a trial evaluating tranexamic acid for coronary artery surgery. Here we report the 1-year clinical outcomes.Methods: Using a factorial design, we randomly assigned patients undergoing coronary artery surgery to receive aspirin or placebo and tranexamic acid or placebo. The results of the tranexamic acid comparison are reported here. The primary 1-year outcome was death or severe disability, the latter defined as living with a modified Katz activities of daily living score of less than 8. Secondary outcomes included a composite of myocardial infarction, stroke, and death from any cause through to 1 year after surgery.
Results:The rate of death or disability at 1 year was 3.8% in the tranexamic acid group and 4.4% in the placebo group (relative risk, 0.85; 95% confidence interval, 0.64-1.13; P ¼ .27), and this did not significantly differ according to aspirin exposure at the time of surgery (interaction P ¼ .073). The composite rate of myocardial infarction, stroke, and death up to 1 year after surgery was 14.3% in the tranexamic acid group and 16.4% in the placebo group (relative risk, 0.87; 95% CI, 0.76-1.00; P ¼ .053).
Conclusions:In this trial of patients having coronary artery surgery, tranexamic acid did not affect death or severe disability through to 1 year after surgery. Further work should be done to explore possible beneficial effects on late cardiovascular events.
Neurocognitive dysfunction after cardiac surgery can present with diverse clinical phenotypes, which include postoperative delirium, postoperative cognitive dysfunction, and stroke, and it presents a significant healthcare burden for both patients and providers. Neurologic monitoring during cardiac surgery includes several modalities assessing cerebral perfusion and oxygenation (near-infrared spectroscopy, transcranial Doppler and jugular venous bulb saturation monitoring) and those that measure cerebral function (processed and unprocessed electroencephalogram), reflecting an absence of a single, definitive neuromonitor. This narrative review briefly describes the technologic basis of these neuromonitoring modalities, before exploring their use in clinical practice, both as tools to predict neurocognitive dysfunction, and with a bundle of interventions designed to optimize cerebral oxygen supply, with the aim of reducing postoperative delirium and cognitive dysfunction following cardiac surgery.
Acute kidney injury (AKI) is common after cardiac surgery. To date, there are no specific pharmacological therapies. In this review, we summarise the existing evidence for prevention and management of cardiac surgery-associated AKI and outline areas for future research. Preoperatively, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers should be withheld and nephrotoxins should be avoided to reduce the risk. Intraoperative strategies include goal-directed therapy with individualised blood pressure management and administration of balanced fluids, the use of circuits with biocompatible coatings, application of minimally invasive extracorporeal circulation, and lung protective ventilation. Postoperative management should be in accordance with current KDIGO AKI recommendations.
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