American College of Cardiology

BRAUNWALD ET AL., MANAGEMENT OF PATIENTS WITH UNSTABLE ANGINA AND NON-ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION UPDATE
http://www.acc.org/clinical/guidelines/unstable/incorporated/index.htm

ACC/AHA 2002 Guideline Update for the Management of Patients With Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction

A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina)

Appendix 1

Acute coronary syndrome—any constellation of clinical signs or symptoms suggestive of AMI or UA. This syndrome includes patients with AMI, STEMI, NSTEMI, enzyme-diagnosed MI, biomarker-diagnosed MI, late ECG-diagnosed MI, and UA. This term is useful to generically refer to patients who ultimately prove to have 1 of these diagnoses to describe management alternatives at a time before the diagnosis is ultimately confirmed. This term is also used prospectively to identify those patients at a time of initial presentation who should be considered for treatment of AMI or UA. Probable acute coronary syndrome is a term that is commonly used, and this represents the primary consideration of patients on initial presentation. Possible acute coronary syndrome is useful as a secondary diagnosis when an alternate diagnosis seems more likely but an acute ischemic process has not been excluded as a possible cause of the presenting symptoms.

Acute myocardial infarction—an acute process of myocardial ischemia with sufficient severity and duration to result in permanent myocardial damage. Clinically, the diagnosis of permanent myocardial damage is typically made when there is a characteristic rise and fall in cardiac biomarkers indicative of myocardial necrosis that may or may not be accompanied by the development of Q waves on the ECG. Permanent myocardial damage may also be diagnosed when histological evidence of myocardial necrosis is observed on pathological examination.

Angina pectoris—a clinical syndrome typically characterized by a deep, poorly localized chest or arm discomfort that is reproducibly associated with physical exertion or emotional stress and relieved promptly (i.e., less than 5 min) with rest or sublingual NTG. The discomfort of angina is often hard for patients to describe, and many patients do not consider it to be "pain." Patients with UA may have discomfort with all the qualities of typical angina except that episodes are more severe and prolonged and may occur at rest with an unknown relationship to exertion or stress. In most, but not all, patients, these symptoms reflect myocardial ischemia that results from significant underlying CAD.

Angiographically significant coronary artery disease—CAD is typically judged "significant" at coronary angiography if there is greater than 70% diameter stenosis, assessed visually, of greater than 1 major epicardial coronary segments or greater than 50% diameter stenosis of the left main coronary artery. The term "significant CAD" used in these guidelines does not imply clinical significance but refers only to an angiographically significant stenosis.

Coronary artery disease—although a number of disease processes other than atherosclerosis can involve coronary arteries, in these guidelines, the term "CAD" refers to the atherosclerotic narrowing of the major epicardial coronary arteries.

Enzyme- or biomarker-diagnosed acute myocardial infarction—diagnostic elevation of cardiac enzymes or biomarkers (e.g., troponin) that indicates definite myocardial injury in the absence of diagnostic ECG changes (Q waves or ST-segment deviation).

Ischemic heart disease—a form of heart disease with primary manifestations that result from myocardial ischemia due to atherosclerotic CAD. This term encompasses a spectrum of conditions, ranging from the asymptomatic preclinical phase to AMI and sudden cardiac death.

Likelihood—used in these guidelines to refer to the probability of an underlying diagnosis, particularly significant CAD.

Myocardial ischemia—a condition in which oxygen delivery to and metabolite removal from the myocardium fall below normal levels, with oxygen demand exceeding supply. As a consequence, the metabolic machinery of myocardial cells is impaired, leading to various degrees of systolic (contractile) and diastolic (relaxation) dysfunction. Ischemia is usually diagnosed indirectly through techniques that demonstrate reduced myocardial blood flow or its consequences on contracting myocardium.

Non-Q-wave myocardial infarction—an AMI that is not associated with the evolution of new Q waves on the ECG. The diagnosis of non-Q-wave MI is often difficult to make soon after the event and is commonly made only retrospectively on the basis of elevated cardiac enzyme levels.

Non-ST-segment elevation myocardial infarction—NSTEMI is an acute process of myocardial ischemia with sufficient severity and duration to result in myocardial necrosis (see Acute Myocardial Infarction). The initial ECG in patients with NSTEMI does not show ST-segment elevation; the majority of patients who present with NSTEMI do not develop new Q waves on the ECG and are ultimately diagnosed as having had a non-Q-wave MI. NSTEMI is distinguished from UA by the detection of cardiac markers indicative of myocardial necrosis in NSTEMI and the absence of abnormal elevation of such biomarkers in patients with UA.

Post-myocardial infarction angina—UA occurring from 1 to 60 days after an AMI.

Reperfusion-eligible acute myocardial infarction—a condition characterized by a clinical presentation compatible with AMI accompanied by ST-segment elevation or new LBBB or anterior ST-segment depression with upright T waves on ECG.

Unstable angina—an acute process of myocardial ischemia that is not of sufficient severity and duration to result in myocardial necrosis. Patients with UA typically do not present with ST-segment elevation on the ECG and do not release biomarkers indicative of myocardial necrosis into the blood.

Variant angina—a clinical syndrome of rest pain and reversible ST-segment elevation without subsequent enzyme evidence of AMI. In some patients, the cause of this syndrome appears to be coronary vasospasm alone, often at the site of an insignificant coronary plaque, but a majority of patients with variant angina have angiographically significant CAD.