When there is profound and sustained ischemic to a portion of the myocardium the cells deprived of oxygen cannot survive, and local death of tissue (necrosis) develops in the involved Area. This destructive process is termed acute myocardial infarction. The event that produces this irreversible tissue damage (infarction) is often called a coronary thrombosis, a coronary occlusion, a coronary, or a heart attack. These latter terms are used synonymously in clinical practice to describe what properly should be designated acute myocardial infarction.
With few exceptions acute myocardial infarction results from advanced atherosclerosis of the coronary arteries. The final insult of progressive coronary atherosclerosis usually occurs when one of the main coronary arteries or its branches becomes occluded. Although the narrowing process is gradual, the obstruction takes place suddenly in most instances. The exact reason that a coronary artery blocks off at a certain moment is not fully understood, but three main causes have been incriminated: 1) a clot may develop on the roughened surface of an atherosclerotic plaque and occlude the lumen of the artery; 2) the atherosclerotic lesions may irritate the underlying arterial wall, causing bleeding beneath the plaque (subintimal hemorrhage), which dislodges the plaque and obstructs the artery, 3) a piece of a large plaque may break off and block a small distal artery. Although all of these mechanisms offer a logical explanation for the suddenness of the event, it is now clear that none oftlicni can account foral/ myocardial infarctions. Autopsy studies have shown, for instance, that acute myocardial infarction can occur even though the coronary arteries have no clots and are not completely obstructed. In these latter instances, it is presumed that at a particular moment the heart is faced with an enormous oxygen demand (e.g., during intense physical activity, such as shoveling snow) which cannot be met by the available blood supply through partially narrowed arteries. In effect, even though the coronary arteries are not completely obstructed, the persistent myocardial demand for oxygen simply overwhelms the limited supply and tissue necrosis develops because of’ this relative oxygen deprivation. Another possibility is that coronary artery spasm may be superimposed on existing coronary artery disease, causing a partially narrowed vessel to close completely during the transient spasm. (Although this is an attractive concept, the role of coronary artery spasm in acute myocardial infarction has not been determined as yet.)
The site of an infarction depends fundamentally on which coronary artery (or arteries) is blocked. When the left coronary artery or its branches are occluded, the infarction involves primarily the anterior wall of the left ventricle and is called an anterior infarction. Occlusion of the right coronary artery results in infarction of the inferior (diaphragmatic) wall of the left ventricle—an inferior infarction. Very often more than one area of the left ventricle is damaged by the ischemic process; in these cases more specific terms are used to describe the location of the infarct. For example, if the infarction involves both the anterior and lateral walls of the left ventricle, it is termed an anterolateral infarction. Similarly, damage to the anterior wall of the left ventricle and to the interventricular septum is called an anteroseptal infarction.
Myocardial infarction involving the right ventricle alone is very rare because this chamber receives a relatively greater proportion of blood for its (smaller) muscle mass than the left ventricle, and also has less oxygen requirements. However, right ventricular infarction is not uncommon in conjunction with inferior myocardial infarction. This relationship is understandable since the right ventricle and the inferior wall of the left ventricle share a common blood supply through the right coronary artery. Nevertheless, the frequency of these combined infarctions was not appreciated until the recent introduction of radionuclide methods for the diagnosis of acute myocardial infarction (as described in the next chapter). With these (and other) means it has been shown that at least 25% of patients with acute inferior myocardial infarction also have some evidence of right ventricular damage.
The extent of an infarction is determined first by the size of the vessel obstructed and second by the capacity of the collateral circulation to bring addi-. tional blood to the oxygen-deprived areas. If there is widespread myocardial necrosis extending through and through the entire ventricular wall (from the endocardium to the pericardium), the infarction is termed transinural (Figure 1.7A). Lesser degrees of damage which do not involve the full thickness of the ventricular wall are categorized as nontransmural infarctions (Figure 1.713). Other descriptive terms for nontransmural infarctions are intramural and subendocardial infarctions.
In the early stages of acute myocardial infarction there are, at least in concept, three zones of tissue damage (Figure 1.8). The first zone consists of necrotic myocardial tissue that has been irreversibly destroyed by prolonged deprivation of oxygen. Surrounding this dead tissue is a second zone (zone of injury) in which the myocardial cells, although injured and jeopardized, may still survive if adequate circulation to the area is restored. Zone 3, called the zone of ischemic, represents cells that have not received adequate oxygen but can be expected to recover unless the ischemic process worsens. In effect, the ultimate size of an infarction may depend on the fate of the zones of injury and ischemic. (These latter zones are not actually distinct or separate areas as the foregoing description suggests. Instead, they appear histologically as a combined outer zone surrounding the central zone of necrosis. This outer zone is diffuse and consists of patchy areas of necrotic, injured and ischemic tissues, merging with normal myocardium. Because of its in-between location and status, this peripheral zone is usually described as the border zone or twilight zone.)
Once the coronary circulation is interrupted and a myocardial infarction occurs, a series of events follows which places life and death in balance. This book is concerned with these events and describes a concept of specialized care, known as intensive coronary care, designed to lower the death rate from acute myocardial infarction.