A non-ST-elevation myocardial infarction (NSTEMI) is a type of heart attack that is caused by the partial or almost full occlusion of the coronary artery by a thrombus or an embolus. With an occluded coronary artery, the heart muscle, or myocardium, becomes ischemic, or deficient in blood and oxygen supply, leading to cell injury and potential cell death. A non-ST-elevation myocardial infarction can only be distinguished from unstable angina (UA) and ST-elevation myocardial infarction (STEMI) with laboratory results. In comparison to STEMI, wherein the full thickness of the heart muscle supplied by a particular coronary artery becomes injured, 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), in reference 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 results, and they are sometimes lumped together and labeled as UA/NSTEMI.
Stable angina is defined as chest or arm discomfort that is associated and reproducible with stress and physical exertion. It is relieved by resting for 5 to 10 minutes or through intake of sublingual nitroglycerin. Unstable angina is angina which occurs at rest or for longer than 10 minutes, is severe or acute, and lasts longer or more frequent than previously experienced episodes. A non-ST-elevation myocardial infarction is given as a diagnosis when a patient has the symptoms of UA and develops evidence of myocyte death or necrosis, as detected through the elevation of serum cardiac biomarkers, such as troponin and creatinine kinase-MB fraction (CK-MB).
Four factors contribute to the pathophysiology of UA/NSTEMI. First is the rupture or erosion of an atherosclerotic plaque with superimposed non-occlusive thrombus formation. Second is dynamic obstruction, such as coronary artery spasm, and the third factor is progressive mechanical obstruction, usually due to thickened blood vessel walls, as what happens in atherosclerosis. The fourth factor is increased oxygen demand or decreased oxygen supply, as what happens in anemia or increased heart rates. Any of these processes may occur in combination in the development of NSTEMI.
In electrocardiogram (ECG), the electrical activity of the heart is recorded. The ischemia in NSTEMI is limited to the subendocardium, thus the vector or direction of the ST segment is shifted toward it and is typically seen on ECG as ST-segment depression. ECG should be done when a person complains of chest pain and the doctor suspects an underlying cardiovascular problem. Changes in the ST segment require immediate treatment.
Treatment of UA/NSTEMI involves the use of anti-ischemic drugs that dilate the blood vessels, such as nitrates and beta-blockers. Lysis of the thrombus involves using anti-coagulation drugs, such as heparin, and antiplatelet drugs, such as aspirin. High-risk patients should undergo coronary angiography and coronary artery revascularization within 48 to 72 hours. This is to prevent further myocardial injury and to restore the blood supply of the heart.