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The pathophysiology of unstable angina is controversial. Previously, 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. [9] [10] However, sensitive troponin assays reveal rise of cardiac troponin in the ...
In unstable angina, symptoms may appear on rest or on minimal exertion. [6] The symptoms can last longer than those in stable angina, can be resistant to rest or medicine, and can get worse over time. [8] [10] Though ACS is usually associated with coronary thrombosis, it can also be associated with cocaine use. [11]
Generally, diseases outlined within the ICD-10 codes I20-I25 within Chapter IX: Diseases of the circulatory system should be included in this category. Subcategories This category has the following 3 subcategories, out of 3 total.
Angina may present typically with classic symptoms or atypically with symptoms less often associated with heart disease. [19] Atypical presentations are more common in women, diabetics, and elderly individuals. [8] Angina may be stable or unstable. Unstable angina is most often associated with emergent, acute coronary syndromes. [20]
Unstable angina (UA) (also "crescendo angina"; this is a form of acute coronary syndrome) is defined as angina pectoris that changes or worsens or begins suddenly at rest. [12] Unstable angina is a medical emergency and requires urgent medical treatment from a doctor. [5] It has at least one of these three features: [13]
Ischemic cardiomyopathy is a type of cardiomyopathy caused by a narrowing of the coronary arteries which supply blood to the heart. [4] Typically, patients with ischemic cardiomyopathy have a history of acute myocardial infarction, [5] however, it may occur in patients with coronary artery disease, but without a past history of acute myocardial infarction.
The diagnosis of microvascular angina (previously known as cardiac syndrome X – the rare coronary artery disease that is more common in females, as mentioned, is a diagnosis of exclusion. Therefore, usually, the same tests are used as in any person suspected of having coronary artery disease: [ 75 ]
5–10 days (including 'siderophages') 10 days to 2 months: Vessel/endothelial sprouts* 5–10 days: 10 days–4 weeks: 4 weeks: disappearance of capillaries; some large dilated vessels persist: Fibroblast and young collagen* 5–10 days: 2–4 weeks: After 4 weeks; depends on size of infarction; Dense fibrosis: 4 weeks: 2–3 months: No