The pathophysiology of unstable angina is the reduction of coronary flow due to transient platelet aggregation on apparently normal endothelium, coronary artery spasms, or coronary thrombosis.
A type of angina pectoris that is irregular.
Classified as a type of acute coronary syndrome (ACS).
It may be difficult to distinguish unstable angina from non-ST elevation myocardial infarction (NSTEMI).
Unstable angina starts with atherosclerosis, progresses through inflammation to yield an active unstable plaque, which undergoes thrombosis and results in acute myocardial ischemia, which, if not reversed, results in cell necrosis.
Unstable angina was assumed to be angina pectoris caused by disruption of an atherosclerotic plaque with partial thrombosis and possibly embolization or vasospasm leading to myocardial ischemia.
Unstable angina differs from NSTEMI in whether the ischemia is severe enough to cause sufficient damage to the heart muscle to release detectable markers of injury, typically troponin T or troponin.
Fifty percent of people with unstable angina will have evidence of necrosis of the heart’s muscular cells manifested by 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.
It is considered in patients with ischemic symptoms suggestive of an ACS and no elevation in troponin, with or without ECG changes indicative of ischemia.
Because an elevation in troponin may not be detectable for up to 12 hours after presentation, unstable and NSTEMI are frequently indistinguishable at initial evaluation.
More than 1 million hospitalizations annually.
Unstable angina refers to sudden-onset angina at rest, and angina lasting more than 15 minutes.
Such symptoms of unstable angina are usually grouped with similar conditions as the acute coronary syndrome.
As these may precede a heart attack, they require urgent medical attention and are, in general, treated in similar fashion to myocardial infarction.
Unstable angina is grouped with similar conditions as the acute coronary syndrome.
Unstable angina is defined as angina pectoris that changes or worsens.
It has at least one of these three features:
It occurs at rest or with minimal exertion.
64% of all unstable angina events occur between 22:00 and 08:00 when patients are at rest.
In stable angina, the developing atheroma is protected with a fibrous cap.
This cap may rupture in unstable angina, allowing blood clots to precipitate and further decrease the area of the coronary vessel’s lumen.
This above explains why, in many cases, unstable angina develops independently of activity.
Unstable angina is severe and of new onset, within the prior 4–6 weeks.
Unstable angina occurs with a crescendo pattern, meaning it is distinctly more severe, prolonged, or frequent than before.
Unstable angina may occur at rest, which may be a serious indicator of an impending heart attack.
Presentations include rest angina usually lasting more than 20 minutes, new onset of severe angina of less than two months duration, and a crescendo pattern of occurrence with increased intensity, duration, frequency or any combination of these factors.
Unstable angina is characterized:
Severe chest pain and of onset within 1 month.
Occurs with a crescendo pattern brought on by less activity, more severe, more prolonged or increased frequency than previously.
6-8% of patients have a nonfatal myocardial infarction or die within the first year after diagnosis.
Evidence of leukocyte activation and degranulation is found in patients with unstable angina.
For patients with unstable angina and non-ST-elevation myocardial infarction should be treated with a combination of aspirin and clopidrogrel at presentation and continued for 9-12 months when aspirin should be continued alone indefinitely.
For unstable angina nitroglycerin can be used immediately to dilate the venous system and reduce the circulating blood volume, reducing the work and oxygen demand of the heart.
Nitroglycerin causes peripheral venous and artery dilation reducing cardiac preload and afterload, decreasing stress on the heart and therefore lower the oxygen demand of the heart’s muscle cells.
Antiplatelet drugs can help reduce the progression of atherosclerotic plaque formation.
Anticoagulants are also indicated.