| Only in recent years have we come to appreciate the diagnostic and therapeutic continuum represented by acute coronary syndromes. When patients present to the emergency room with chest discomfort and an abnormal electrocardiogram, it is frequently easy to diagnose an acute coronary syndrome. But, if there is not classic ST-segment elevation (and reciprocal ST depression), it may be difficult to determine whether unstable angina or a non-Q (currently known as a non-ST elevation) MI is the correct diagnosis. Only through subsequent observation, serial clinical, ECG, and enzyme assessment can the appropriate diagnosis be made. Beyond the diagnostic dilemma, there is a pathophysiological and therapeutic continuum. These patients typically have coronary atherosclerotic plaque fissure, erosion, or frank rupture; there has been some loss of integrity of the diseased vessel wall with resultant platelet-thrombus formation. In response to this acute presentation, we administer aspirin, heparin, and anti-ischemic medications. Only in patients with ST-segment elevation (unless there is a posterior MI or bundle branch block) is there consideration for fibrinolytic therapy. Indeed, recent large-scale clinical trials have, for the first time, particularly focused on acute coronary syndromes. For example, the large-scale 2nd Global Utilization of Strategies to Open Occluded Arteries (GUSTO-II) enrolled over 12,000 patients ranging from ST elevation to unstable angina. |
| Over this span of time, several new therapeutics have been tested, and there is now important evidence to support their clinical application. These include new fibrinolytics, such as reteplase, as assessed in GUSTO-III, low-molecular-weight heparins, direct thrombin inhibitors, and the platelet glycoprotein IIb/IIIa inhibitors. The primary intent of this monograph is to capture the essence of the |
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