ABSTRACT
Two decades ago, perioperative myocardial infarction was thought to be primarily a result of myocardial oxygen supply-demand imbalance. All anesthetists could do to protect the heart of the patient was to avoid cardiovascular instability and hope for the best. That view has changed almost beyond recognition. As described in chapter 2, from the 1980s onwards there has been an explosion of knowledge about the pathophysiology of coronary artery disease. It has become clear that in the nonsurgical setting, myocardial infarction results from atherosclerotic plaque rupture, thrombosis, and embolization and that this is a dynamic and complex process. We have come to understand that the environment produced by surgery can facilitate this pernicious process; both the release of inflammatory mediators and the activation of the coagulation system can help to fuel the fire of inflammation and thrombus formation on an active coronary plaque. This is discussed in depth in chapter 4. Our changing understanding of the pathophysiology of myocardial infarction has been matched by a changing view of the natural history of myocardial infarction and angina. Previously, myocardial infarction was seen as a dichotomous event; patients had either suffered an infarction or not. A patient who presented with chest pain but no ECG changes would have his cardiac enzymes checked and if these were normal he would be sent on his way with a reassurance that he had not had a heart attack. The development of the cardiac troponin assays over the past 10 years has changed this. It is now understood that there is a spectrum of myocardial injury characterized by increasing levels of cardiac troponin release. The acute coronary syndromes embrace a range of conditions from unstable angina, through non-ST segment myocardial infarction to full blown “Q-wave” infarction. It has become clear that even a small amount of cardiac troponin release portends future problems and means that the patient is likely to suffer further cardiac events in the future. This is discussed in more depth in chapter 3 by Smith and Pepper.
