Introduction

Traditionally, ischemic heart disease has been divided into several separate syndromes: stable coronary artery disease, unstable angina (UA)(1,2), non-Q wave myocardial infarction (MI), and Q wave MI. However, the understanding of the conversion of a stable atherosclerotic lesion to a ruptured plaque with thrombosis has provided a unifying hypothesis for the etiology of acute coronary syndromes (ACS)(3-7). The concept of myocardial ischemia as a spectrum provides a framework for understanding the patho-genesis, clinical features, treatment and outcome of patients across the nexus of myocardial ischemia (Fig. 1).

However, a new paradigm for ACS emerged with the results of the Thrombolysis in Myocardial Ischemia (TIMI) IIIB trial: while fibrinolytic therapy is clearly beneficial in patients with ST segment elevation (STE) (8), no benefit was observed in patients without STE (9). Thus, it was observed that pharmacologic reperfusion therapy applies only to patients with STEMI, and is not indicated for patients without STEMI (8-10) Angio-

From: Contemporary Cardiology: Management of Acute Coronary Syndromes, Second Edition Edited by: C. P. Cannon © Humana Press Inc., Totowa, NJ

Wave Stemi

Fig. 1. The spectrum of myocardial ischemia. The various clinical syndromes of coronary artery disease can be viewed as a spectrum, ranging from patients with stable angina to those with acute Q wave MI. Across the spectrum of the ACS, atherosclerotic plaque rupture leads to coronary artery thrombosis: in acute Q wave MI, which usually presents with STE on the electrocardiogram, complete coronary occlusion is present. In those with UA or non-Q wave MI, a flow-limiting thrombus is usually present. In patients with stable angina, thrombus is rarely seen. The overall treatment objective is to move the patients back to a stable lesion. In acute STEMI, the objective over the first minutes to hours is to open the artery and achieve reperfusion. In patients with UA and non-STEMI, the goal is to stabilize or passivate the active thrombotic lesion over a period of hours to days. Then, over a period of months to years, the goal is to try to heal the lesion with risk-factor reduction with treatment of hyper-cholesterolemia, hypertension, diabetes, and smoking cessation, in an attempt to reduce the likelihood of subsequent rupture of the coronary plaques. Adapted with permission from ref. 135.

Fig. 1. The spectrum of myocardial ischemia. The various clinical syndromes of coronary artery disease can be viewed as a spectrum, ranging from patients with stable angina to those with acute Q wave MI. Across the spectrum of the ACS, atherosclerotic plaque rupture leads to coronary artery thrombosis: in acute Q wave MI, which usually presents with STE on the electrocardiogram, complete coronary occlusion is present. In those with UA or non-Q wave MI, a flow-limiting thrombus is usually present. In patients with stable angina, thrombus is rarely seen. The overall treatment objective is to move the patients back to a stable lesion. In acute STEMI, the objective over the first minutes to hours is to open the artery and achieve reperfusion. In patients with UA and non-STEMI, the goal is to stabilize or passivate the active thrombotic lesion over a period of hours to days. Then, over a period of months to years, the goal is to try to heal the lesion with risk-factor reduction with treatment of hyper-cholesterolemia, hypertension, diabetes, and smoking cessation, in an attempt to reduce the likelihood of subsequent rupture of the coronary plaques. Adapted with permission from ref. 135.

graphic studies have shown that this difference in outcome is due to the initial status of the infarct-related artery, which usually exhibits 100% occlusion in STEMI (11,12), in contrast to a patent, but severly stenotic coronary lesion in non-STE ACS (13,14)

Thus, because of the advent of acute reperfusion therapy, the old distinction of Q wave vs non-Q wave MI (usually made days following MI) is no longer as useful for acute management. Instead, a classification of STEMI vs non-STE ACS provides the critical information regarding the pathophysiology and acute management of the patient. Patients with UA and non-STEMI share a similar pathophysiology, although the non-STEMI patients are at higher risk of subsequent events and appear to benefit more from more aggressive antithrombotic and interventional therapies.

Accordingly, in this book, separate sections are devoted to the management of these two broad types of patients with ACS, those with STEMI and those with non-STE ACS. It should be noted that STE is not a perfectly sensitive marker of acute occlusion (15), and thus new technologies for proper identification and triage of patients with ACS are being evaluated extensively, as reviewed in Chapters 7 and 8. There are more than 1.8 million patients admitted every year to hospitals in the United States, with approx 1.42 million patients with UA/non-STEMI as compared with approx 400,000 patients with acute STEMI (16).

Stable Unstable Non-Q Angina Angina Wave Ml

Q wave Ml

Q wave Ml

Sudden Death

Asymptomatic

Micro-infarction

Sudden Death

Siient Ischemia

ST Elevation Ml

Fig. 2. The complete clinical spectrum of myocardial ischemic syndromes.

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