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Acute
Myocardial
Infarction
Description/Etiology
Acute myocardial infarction (AMI; also called heart attack) is the rapid development of myocardial necrosis (i.e.,
death of an area of heart muscle) due to an inadequate supply of oxygen. AMI is most commonly caused by a
thrombus that blocks a coronary artery previously narrowed from the buildup of fatty plaque. Additional causes
include coronary artery spasm, embolic infarction, arteritis, and cocaine-induced vasospasm.
Diagnosis of AMI is based on patient history, clinical presentation, and indirect evidence of myocardial necrosis,
using biochemical, electrocardiographic, and imaging modalities. AMI should be differentiated from acute coronary
syndrome with or without stable or unstable angina pectoris; anxiety; aortic stenosis or dissection; gastroesophageal
reflux disease (GERD); esophageal spasm or biliary colic; musculoskeletal or neurologic chest wall pain; chronic
obstructive pulmonary disease (COPD); pulmonary embolism; spontaneous pneumothorax; and pericarditis.
Treatment involves emergency department evaluation, admission to and stabilization in the coronary care unit (CCU)
or intensive care unit (ICU), oxygen supplementation, medications, restriction of physical activities, and possibly
surgical or percutaneous coronary reperfusion procedures. Percutaneous or surgical reperfusion procedures include
coronary angiography with percutaneous coronary intervention (PCI) with or without stenting to open blocked
coronary arteries. Other coronary reperfusion procedures include intraaortic balloon counter pulsation and coronary
artery bypass grafting (CABG) surgeries performed via conventional, off-pump, or minimally invasive direct, robotic,
or endoscopic techniques. Constant electrocardiographic and hemodynamic monitoring is essential. Prognosis
varies and depends largely on the size, type, severity, and location of infarct and the amount of remaining functional
cardiac muscle. In general, prognosis worsens with advanced age or the presence of arrhythmias, post-AMI angina,
pericarditis, or concomitant illnesses (e.g., diabetes mellitus), and improves with appropriate use of beta-blockers or
lipid-lowering medications. Potential complications include recurrent or persistent chest pain, heart failure, stroke,
deep vein thrombosis, pulmonary embolism, pulmonary edema, ventricular and/or papillary muscle rupture, mitral
insufficiency, cardiogenic shock, cardiac arrest, and death.
Risk Factors
ICD-9
410.9
Authors
Leonard L. Buckley, MD
Tanja Schub, BS
Reviewers
Darlene A. Strayer, RN, MBA
Cinahl Information Systems
Glendale, California
Nursing Practice Council
Glendale Adventist Medical Center
Glendale, California
Editor
Diane Pravikoff, RN, PhD, FAAN
Cinahl Information Systems
Risk factors for AMI include tobacco smoking, obesity, age > 40 years, sedentary lifestyle, being male, being a
postmenopausal female, high-fat diet, family history of premature onset (age < 55 for women or age < 45 for men)
of AMI, diabetes mellitus, and hypertension. Other risk factors include elevated levels of homocysteine, C-reactive
protein (CRP), low-density lipoprotein, or fibrinogen; use of birth control pills, cocaine, or amphetamines; and
psychological factors (e.g., depression, anger, hostility, chronic stress).
Assessment
44 Patient History
Assessment for personal or family history of angina or other heart problems is critical because physical
examination can be unremarkable in MI
Serum cardiac enzymes and specific cardiac biomarkers, including cardiac specific troponin T (cTnT) and
March 9, 2012
cardiac specific troponin I (cTnI), creatinine kinase (CK) and CK-MB isoenzymes, lactate dehydrogenase
(LDH) and LDH1 isoenzyme, homocysteine, and CRP, may be elevated, indicating cardiac muscle necrosis
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general informational overview of the subject for the healthcare professional. Cinahl Information Systems, 1509 Wilson Terrace, Glendale, CA 91206
CBC may reveal anemia, elevated WBCs, or elevated erythrocyte sedimentation rate (ESR), indicating inflammatory processes. Triglycerides and lowdensity lipoprotein (LDL) and/or very low-density lipoprotein (VLDL) cholesterol may be elevated; levels of high-density lipoprotein (HDL) cholesterol
may be lowered
Repeat or serial 12-lead EKG may show ST-segment elevation or depression and the presence of new Q waves or peaked T waves
Echocardiography will evaluate for wall motion abnormalities; chest X-ray will evaluate for the presence of aortic dissection or heart failure
Myocardial perfusion scanning, the most commonly used cardiac nuclear medicine procedure in patients with AMI, visualizes blood-flow patterns to
the heart walls. Nuclear ventriculography studies (e.g., radionucleotide ventriculography [RNV] or multiple gate acquisition [MUGA] scan) using the
radioactive isotopes technetium-99m or thallium-201 and 64-slice CT scans may be ordered to evaluate for damage to cardiac muscle
Treatment Goals
Assess patients anxiety level and coping ability; provide emotional support and educate about AMI etiology, potential complications, treatment risks and
benefits, and individualized prognosis; request referral to a mental health clinician, as appropriate, for counseling on strategies for coping with having a
life-threatening condition
Red Flags
44 Clopidogrel therapy should be discontinued for at least 57 days before elective CABG
44 Nitrates should not be administered in patients who have recently used PDE-5 inhibitors (e.g., sildenafil)
44 Closely monitor high-risk patients (e.g., those with pre-existing kidney disease, heart failure, volume depletion) for contrast-induced acute kidney injury by
measuring serum creatinine levels once daily for 5 days after coronary angiography
Note
44 Recent review of the literature has found no updated research evidence on this topic since previous publication on July 15, 2011
References
Cabello, J. B., Burls, A., Emparanza, J. I., Bayliss, S., & Quinn, T. (2010). Oxygen therapy for acute myocardial infarction. Cochrane Database of Systematic Reviews, 6, Art. No.: CD007160. doi: 10.1002/14651858.CD007160.pub2.
Christ, M., Popp, S., Pohlmann, H., Poravas, M., Umarov, D., Bach, R., & Bertsch, T. (2010). Implementation of high sensitivity cardiac troponin T measurement in the emergency department. American Journal of Medicine, 123(12), 1134-1142.
De Luca, L., Tomai, F., Verdoia, M., & De Luca, G. (2010). Evaluation and management of special subgroups after primary percutaneous coronary intervention. American Heart Journal, 160(6 Suppl 1), S22-S27.
Wooding, F. G., Lee, J., & Arenas, I. A. (2012). Myocardial infarction, ST-segment elevation (STEMI). In F. J. Domino (Ed.), The 5-minute clinical consult 2012 (20th ed., pp. 868-869). Philadelphia: Wolters Kluwer Health/Lippincott
Williams & Wilkins.
Zafari, A. M., Afonso, L. C., Aggarwal, K., Bessman, E., Coven, D. L., Desser, K. B., Setnik, G. (2012, February 13). Myocardial infarction. Medscape Reference. Retrieved March 1, 2012, from
http://emedicine.medscape.com/article/155919-overview