It is useful to note that there are several other groups of patients who fall on this spectrum of myocardial ischemia (Fig. 2) Among patients with stable coronary artery disease, many apparently stable patients have active lesions, which are prone to rupture over the subsequent months and years (17). Although most patients remain clinically stable (18), it is estimated that nearly all of these patients with "stable" coronary artery disease have subclinical plaque rupture events (19,20).
Between patients with stable angina and those with UA are a high-risk group with clinically stable symptoms, yet significant ambulatory ischemia that can be detected by ambulatory Holter monitoring (21,22). Similarly, between patients with UA and non-STEMI, a patient may have what has been called a microinfarction (23) or infarctlet with a very small elevation of cardiac markers such as troponin T or I (24-26).
At the extreme right of the spectrum of ischemic heart disease (Fig. 2) are patients with sudden cardiac death. Many patients have an acute coronary occlusion as the etiology of the cardiac arrest. However, with aggressive emergency medical services which respond rapidly and treat with advanced cardiac life support (ACLS) procedures, more patients are presenting with resuscitated "sudden cardiac death" (27). Indeed, the National Heart Attack Alert Program (NHAAP) has as one of its major goals the improvement of emergency medical systems and early identification and treatment of acute MI patients as a means to reduce the overall mortality from MI (28-31). If more patients with cardiac arrest can be successfully resuscitated in the pre-hospital setting, they may become candidates for reperfusion and other therapies for ACS.
Atherothrombosis is a silent process that usually commences 20-30 yr prior a patient's presentation with a clinical syndrome (3,4). Hypercholesterolemia, hypertension, diabetes, smoking and other coronary risk factors damage the endothelium which initiates the atherosclerotic process (3,4,32), When the endothelium is dysfunctional, macrophages bind to endothelial adhesion molecules and can infiltrate the endothelial cell. Low density lipoprotein (LDL) molecules are able to penetrate into the vessel wall, the macrophages digest the LDL, becoming foam cells, which thereby create a lipid-filled atherosclerotic plaque (4,33). Oxidized LDL may also have a direct toxic affect on the endothelium and smooth muscle cells, which contribute to the instability of the atherosclerotic plaque.
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