NSTEMI is a type of heart attack caused by partial or complete occlusion of the coronary artery, leading to cell damage and potential death. It is difficult to distinguish from unstable angina without laboratory findings. Treatment involves anti-ischaemic drugs, thrombolysis, and coronary angiography.
A non-ST-elevation myocardial infarction (NSTEMI) is a type of heart attack caused by partial or nearly complete occlusion of the coronary artery by a thrombus or embolus. With a blocked coronary artery, the heart muscle, or myocardium, becomes ischemic or deficient in blood and oxygen, leading to cell damage and potential cell death. Non-ST-elevation myocardial infarction can only be distinguished from unstable angina (UA) and ST-segment elevation myocardial infarction (STEMI) by laboratory findings only. Compared to STEMI, in which the full thickness of heart muscle supplied by a particular coronary artery is damaged, a non-ST-elevation myocardial infarction involves only the subendocardial region of the heart.
One of the manifestations of heart disease is acute coronary syndrome (ACS), referring to the affected blood vessel, which is the coronary artery. The spectrum of ACS includes angina pectoris, UA, and myocardial infarction. UA and non-ST-elevation myocardial infarction are difficult to distinguish from each other when there are no laboratory findings and are sometimes grouped together and labeled as UA/NSTEMI.
Stable angina is defined as chest or arm discomfort associated and reproducible with stress and physical exertion. It is relieved by resting for 5-10 minutes or by taking sublingual nitroglycerin. Unstable angina is angina that occurs at rest or lasts longer than 10 minutes, is severe or acute, and lasts longer or more frequently than previous episodes. Non-ST-elevation myocardial infarction is diagnosed when a patient has symptoms of UA and develops evidence of myocyte death or necrosis, as detected by elevation of serum cardiac biomarkers, such as troponin and creatinine kinase fraction- MB (CK-MB).
Four factors contribute to the pathophysiology of UA/NSTEMI. The first is the rupture or erosion of an atherosclerotic plaque with the formation of overlapping non-occlusive thrombi. The second factor is dynamic obstruction, such as coronary artery spasm, and the third factor is progressive mechanical obstruction, usually due to thickening of blood vessel walls, as occurs in atherosclerosis. The fourth factor is increased oxygen demand or decreased oxygen supply, as occurs in anemia or increased heart rate. Any of these processes can occur in combination in the development of NSTEMI.
In the electrocardiogram (ECG), the electrical activity of the heart is recorded. Ischemia in NSTEMI is limited to the subendocardium, so the vector or direction of the ST segment is shifted towards it and is typically seen on the ECG as ST segment depression. ECG should be done when a person complains of chest pain and the doctor suspects an underlying cardiovascular problem. ST-segment changes require immediate treatment.
Treatment of UA/NSTEMI involves the use of anti-ischaemic drugs that dilate blood vessels, such as nitrates and beta-blockers. Thrombolysis involves the use of anticoagulant drugs, such as heparin, and antiplatelet drugs, such as aspirin. High-risk patients should undergo coronary angiography and coronary revascularization within 48 to 72 hours. This is to prevent further damage to the myocardium and to restore blood supply to the heart.
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