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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 ...
Information card published by the National Heart, Lung, and Blood Institute urging people with symptoms of angina to call the emergency medical services.. Because of the relationship between the duration of myocardial ischemia and the extent of damage to heart muscle, public health services encourage people experiencing possible acute coronary syndrome symptoms or those around them to ...
Wellens' syndrome is an electrocardiographic manifestation of critical proximal left anterior descending (LAD) coronary artery stenosis in people with unstable angina. Originally thought of as two separate types, A and B, it is now considered an evolving wave form, initially of biphasic T wave inversions and later becoming symmetrical, often ...
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]
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]
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]
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
Differential diagnosis hibernating myocardium , silent ischemia, myocardial infarction , acute pericarditis , myocarditis , pulmonary embolism Myocardial stunning or transient post-ischemic myocardial dysfunction is a state of mechanical cardiac dysfunction that can occur in a portion of myocardium without necrosis after a brief interruption in ...