No abstract

Myocardial ischemia reperfusion injury contributes to adverse cardiovascular outcomes after myocardial ischemia, cardiac surgery or circulatory arrest. Primarily, no blood flow to the heart causes an imbalance between oxygen demand and supply, named ischemia (from the greek isch-, restriction and -haema, blood), resulting in damage or dysfunction of the cardiac tissue. Instinctively, early and fast restoration of blood flow has been established to be the treatment of choice to prevent further tissue injury. Indeed, the use of thrombolytic therapy or primary percutaneous coronary intervention is the most effective strategy for reducing the size of a myocardial infarct and improving the clinical outcome. Unfortunately, restoring blood flow to the ischemic myocardium, named reperfusion, can also induce injury. This phenomenon was therefore termed myocardial ischemia reperfusion injury. Subsequent studies in animal models of acute myocardial infarction suggest that myocardial ischemia reperfusion injury accounts for up to 50% of the final size of a myocardial infarct. Consequently many researchers aim to understand the underlying molecular mechanism of myocardial ischemia reperfusion injury to find therapeutic strategies ultimately reducing the final infarct size. Despite of the identification of numerous therapeutic strategies at the bench, many of them are just in the process of being translated to bedside. In the current review, we will discuss the most striking basic science findings made during the last decades that are currently under clinical evaluation, with the ultimate goal to treat patients who are suffering from myocardial ischemia and reperfusion associated tissue injury.

Summary The platelet‐mapping assay of the thromboelastograph was used to measure platelet aggregation and to examine the effect of cardiopulmonary bypass on multiple platelet receptors and the role of altered receptor activity in postoperative bleeding. The percentage platelet aggregation for collagen, adenosine diphosphate and arachidonic acid was measured in 40 patients divided post‐hoc into high‐ or low‐bleeding groups depending on postoperative 24‐h chest tube output. Platelet aggregation was lower after cardiopulmonary bypass compared to before it using collagen (mean (SD) 45 (25) vs 19 (12) %, p < 0.001), adenosine diphosphate (76 (23) vs 35 (24) %, p < 0.001), and arachidonic acid (61 (33) vs 31 (35) %, p < 0.001). Only platelet aggregation as measured using collagen pre‐ and post‐cardiopulmonary bypass was significantly less in the high‐ compared to the low‐bleeding group. This finding was significantly correlated with the 24‐h chest tube drainage, and it predicted postoperative bleeding with a sensitivity of 83% and a specificity of 68%. Therefore, platelet aggregation is reduced following cardiopulmonary bypass, and this may play a role in predicting postoperative blood loss.

This pilot study showed that pharmacologically dosed oral GLN therapy prior to cardiac surgery was safe, well tolerated, and feasible. GLN therapy reduced myocardial injury and clinical complications in this small randomized, blinded feasibility trial. These data indicate that a larger trial of preoperative GLN therapy in patients undergoing cardiac surgery is needed to confirm clinical benefit.

Physicians who leave practice are a heterogeneous group. Most participants' performance warranted some formal education; few demonstrated global educational needs. The data from this study justify mandates that physicians demonstrate competence through an objective testing process prior to returning to practice. Emerging patterns regarding the performance of the reentering physician may help guide future policy.