ISCHEMIA - A COAGULATION PROBLEM

The causes of perioperative ischemia and myocardial infarction (MI) in coronary artery bypass graft (CABG) patients are almost certainly mul tifactorial, although not well understood. Ultimately, outcome after C ABG is dependent on myocardial preservation and prevention of further myocardial ischemia. The largest number of ST-T-wave events come immed iately after protamine is given, suggesting that re-establishment of c oagulation function after cardiopulmonary bypass (CPB) may be an impor tant event. CPB induces an inflammatory state that involves platelet-e ndothelial-cell interactions and vasospastic responses that result in low flow states in the coronary vasculature. The fibrinolytic system i s activated during CPB, with raised tissue plasminogen activator (tPA) levels and related falls in plasminogen activator inhibitor (PAI-1). PAI-1 levels rise during the postoperative period. There is a huge var iability in human response. However, the patients with the highest tPA surge are not the same patients who have the highest PA1 surge. It co uld be postulated that patients with high PAI-1 levels are at highest risk for early ischemia. New data just being evaluated from the Multic enter Study of Perioperative Ischemia (McSPI) Research Groups' databas e in San Francisco may support the hypothesis that coagulation influen ces perioperative ischemia. The study of approximately 2,400 patients undergoing CABG surgery at 24 major institutions in the United States revealed that intensive care unit (ICU) entry hematocrit was significa ntly related to the risk for postoperative MI. Patients entering the I CU with hematocrits below 24% had the lowest MI rate (3.7%), whereas t hose with hematocrits greater than 34% had the highest rate (8.1%). Pa tients with ICU entry hematocrits below 18% had a zero incidence of pe rioperative MI. One possible explanation for these findings is that pl atelets are involved. As red cells stream down vessels, they marginate the smaller formed elements of the blood. As hematocrit is increased, the number of platelets moved to the outer sides of the vessels incre ases. Therefore, the number of endothelial-platelet interactions would increase over time with higher hematocrits.