Part of the acute coronary syndrome spectrum. Usually caused by a partial or near-complete occlusion of a coronary artery resulting in compromised blood flow to myocardium with subsequent myocardial injury or infarction as demonstrated by elevation in troponin.
There are differences in typical presentation between the sexes. Male patients typically present with chest pressure/discomfort lasting at least several minutes, at times accompanied by sweating, dyspnea, nausea, and/or anxiety. Women present more commonly with middle/upper back pain or dyspnea and similar associated symptoms.
Symptoms are indistinguishable from those of unstable angina. However, non-ST-elevation myocardial infarction (MI) is differentiated from unstable angina by a rise of troponin.
ECG is the first-line investigation in all patients and should not be delayed for history, examination, or other tests.
Early risk stratification and treatment with anti-ischemic (beta-blockers, nitrates), anticoagulant (heparin), and dual antiplatelet agents (aspirin plus a P2Y12 receptor inhibitor) is needed. Higher-risk patients should be considered for an early invasive strategy (coronary angiography and revascularization in 12-24 hours).
Complications are progression or worsening of MI, heart failure, cardiogenic shock, arrhythmias, and death.
Non-ST-elevation myocardial infarction (NSTEMI) is an acute ischemic event causing myocyte necrosis. The initial ECG may show ischemic changes such as ST depressions, T-wave inversions, or transient ST elevations; however, it may also be normal or show nonspecific changes. If persistent ST elevation, evidence of posterior MI, or a new left bundle-branch block is present, then the patient should be evaluated as an ST-elevation myocardial infarction. NSTEMI, therefore, encompasses a broad spectrum of ischemic injury to the myocardium, which is detected by elevation of troponin. It can be distinguished from unstable angina pectoris by normal serial troponin.
History and exam
- atherosclerosis (history of angina, myocardial infarction, stroke, transient ischemic attack, peripheral vascular disease)
- family history of premature coronary artery disease (CAD)
- age >65 years
- obesity and metabolic syndrome phenotype
- physical inactivity
- cocaine use
- stent thrombosis or restenosis
- chronic kidney disease
- surgical procedures (including intraoperative and postoperative periods)
- sleep apnea
Assistant Professor of Medicine
Director of Cardiology
University of North Carolina
CSD was previously the Director of Cardiac Rehab for Chatham Hospital, which was financially set up as a consultancy relationship, until 2017. CSD has spoken (unpaid) at the Update in Cardiology and Update in Internal Medicine Conferences at UNC for the last 5 years. CSD has served as the PI for the Dal-GeneE (site now closed) and the ACCELERATE Trials at the University of North Carolina (trial now completed). Each trial required paid travel to an investigator meeting.
Dr Cody S. Deen would like to gratefully acknowledge Dr Sripal Bangalore, Dr Mina Owlia, Dr Thomas Vanhecke, and Dr Dena Krishnan, the previous contributors to this topic.
SB, MO, TEV, and DK declare that they have no competing interests.
University of Texas MD Anderson Cancer Center
NP declares that he has no competing interests.
Department of Emergency Medicine
Beth Israel Medical Deaconess Center
EU declares that he has no competing interests.
Associate Professor of Medicine
Department of Cardiovascular Medicine
DLB declares that he has no competing interests.
East Surrey Hospital
Surrey and Sussex NHS Trust
SB declares that she has no competing interests.
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