A classification of unstable angina revisited

CW Hamm, E Braunwald - Circulation, 2000 - Am Heart Assoc
CW Hamm, E Braunwald
Circulation, 2000Am Heart Assoc
Unstable angina is a critical phase of coronary heart disease with widely variable symptoms
and prognosis. A decade ago, a classification of unstable angina based on clinical
symptoms was introduced. This system was then validated by prospective clinical studies to
correlate with the prognosis and was linked to angiographic and histological findings. It has
been used to categorize patients in many large clinical trials. In recent years, the
pathophysiological roles of platelet activation and inflammation in unstable angina have …
Abstract
—Unstable angina is a critical phase of coronary heart disease with widely variable symptoms and prognosis. A decade ago, a classification of unstable angina based on clinical symptoms was introduced. This system was then validated by prospective clinical studies to correlate with the prognosis and was linked to angiographic and histological findings. It has been used to categorize patients in many large clinical trials. In recent years, the pathophysiological roles of platelet activation and inflammation in unstable angina have been elucidated. Subsequently, improved markers of myocardial injury, acute-phase proteins, and hemostatic markers that may be associated with clinical outcomes have been identified. Particularly, cardiac-specific troponin T and troponin I have been shown to represent the best predictors of early risk in patients with angina at rest. Accordingly, it is suggested that the original classification be extended by subclassifying one large group of unstable angina patients, ie, those with angina at rest within the past 48 hours (class IIIB), into troponin-positive (Tpos) and troponin-negative (Tneg) patients. The 30-days risk for death and myocardial infarction is considered to be up to 20% in class IIIB-Tpos but <2% in class IIIB-Tneg patients. Initial results suggest that troponins may function as surrogate markers for thrombus formation and can effectively guide therapy with glycoprotein IIb/IIIa antagonists or low-molecular-weight heparins. These observations provide additional impetus for adding the measurement of these markers to the clinical classification and represent a novel concept of treating these high-risk patients.
Am Heart Assoc