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J Am Coll Cardiol, 1999; 33:107-118 © 1999 by the American College of Cardiology Foundation |
a Rush Heart Institute and Rush Medical College, Rush-Presbyterian-St. Luke’s Medical Center, Chicago, Illinois, USA
Manuscript received May 6, 1998; revised manuscript received August 11, 1998, accepted September 10, 1998.
Address for correspondence: Dr. Lloyd W. Klein, Cardiology Section, Jelke Pavilion, Suite 1035, Rush-Presbyterian-St. Luke’s Medical Center, 1653 W. Congress Pkwy, Chicago, Illinois 60612
lklein{at}rpslmc.edu
Objectives. The goal of this review is to reevaluate the unstable coronary syndromes in the setting of new therapies and biochemical markers.
Background. Patients with acute coronary syndromes comprise a large subset of many cardiology practices. Patients with unstable angina (UA) and non-Q wave myocardial infarction (NQMI) may sustain a small amount of myocardial loss but have significant amounts of viable, yet ischemic, myocardium, placing them at high risk for future cardiac events. In the past, enzyme differentiation of NQMI from UA was considered important to assess prognosis and direct therapy.
Methods. Manuscripts published in peer-reviewed journals over the past three decades were reviewed and selected for this review. Recent abstracts were also considered and cited where appropriate.
Results. In the late 1990’s, although UA and NQMI remain parts of a spectrum, it is apparent that the distinction between these two entities is no longer sufficient to identify high risk patients; rather, specific electrocardiographic changes, aspects of the clinical history, newer biochemical markers, and angiographic findings help to better distinguish higher risk individuals from a large patient population with unstable coronary syndromes and these factors usually determine therapy.
Conclusions. Based on these results, it is likely that newer therapies such as glycoprotein IIb/IIIa receptor antagonists, low molecular weight heparins, and coronary stents will be directed toward these high risk patients.
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