Specialty cardiology ICD-9-CM 411.1 MedlinePlus 000201 | ICD-10 I20.0 DiseasesDB 13530 MeSH D000789 | |
Unstable angina (UA) is a type of angina pectoris that is irregular. It is also classified as a type of acute coronary syndrome (ACS).
Contents
It can be difficult to distinguish unstable angina from non-ST elevation (non-Q wave) myocardial infarction (NSTEMI). They differ primarily in whether the ischemia is severe enough to cause sufficient damage to the heart's muscular cells to release detectable quantities of a marker of injury (typically troponin T or troponin I). Unstable angina is considered to be present in patients with ischemic symptoms suggestive of an ACS and no elevation in troponin, with or without ECG changes indicative of ischemia (e.g., ST segment depression or transient elevation or new T wave inversion). Since an elevation in troponin may not be detectable for up to 12 hours after presentation, UA and NSTEMI are frequently indistinguishable at initial evaluation.
Pathophysiology
Unstable angina is angina pectoris caused by disruption of an atherosclerotic plaque with partial thrombosis and possibly embolization or vasospasm.
Diagnosis
Unstable angina is characterized by at least one of the following:
- Occurs at rest or minimal exertion and usually lasts more than 20 minutes (if nitroglycerin is not administered)
- Being severe (at least Canadian Cardiovascular Society Classification 3) and of new onset (i.e. within 1 month)
- Occurs with a crescendo pattern (brought on by less activity, more severe, more prolonged or increased frequency than previously).
Fifty percent of people with unstable angina will have evidence of necrosis of the heart's muscular cells based on elevated cardiac serum markers such as creatine kinase isoenzyme (CK)-MB and troponin T or I, and thus have a diagnosis of non-ST elevation myocardial infarction.
Management
Nitroglycerin can be used immediately to widen the coronary arteries and help increase blood flow to the heart. In addition, nitroglycerin causes peripheral venous and artery dilation reducing cardiac preload and afterload. These reductions allow for decreased stress on the heart and therefore lower the oxygen demand of the heart's muscle cells.
Antiplatelet drugs such as aspirin and clopidogrel can help reduce the progression of atherosclerotic plaque formation, as well as combining these with an anticoagulant such as a low molecular weight heparin.