Chapter 3 Unstable Angina and Non-ST Elevation Myocardial Infarction
Definitions
Epidemiology
Coronary artery disease (CAD) is the leading cause of death in the United States. UA and NSTEMI account for over 5 million emergency department visits and over 1 million admissions per year. Most deaths from UA or NSTEMI are due to sudden death or acute myocardial infarction (AMI).
Pathogenesis
Clinical Features
Initial Evaluation and Probability of ACS
The evaluation of UA and NSTEMI involves two major steps. The first step is to determine whether the patient is experiencing ACS. The second step is to determine the patient’s risk of an adverse outcome. Aside from a thorough history and physical examination, an EKG and cardiac injury markers (CK with MB fraction, troponin I, or troponin T) should be obtained in persons with possible ACS.
According to the ACC/AHA Guidelines, the possibility that a constellation of signs and symptoms are due to ACS may be stratified as follows:
History of chest or left arm pain or discomfort, or occurrence of prior angina equivalent. History of myocardial infarction or CAD
History
Aside from the sex and age of the patient, the history should focus on the patient’s symptoms and presence of risk factors, including history of CAD. Typical angina is pain, pressure, or discomfort located in the chest or arm that reliably occurs with physical activity or emotional stress, and is relieved with rest or sublingual nitroglycerin. Some patients may have other symptoms, such as jaw, neck, epigastric, or upper extremity discomfort or pain that has a clear association with activity or stress; such events may be considered anginal equivalents. Elderly patients and patients with diabetes mellitus may present with atypical symptoms of angina, including new onset dyspnea on exertion, fatigue, or diaphoresis. History findings of older age, male sex, chest or left upper extremity discomfort, or pain are most consistent with acute cardiac ischemia.
Pleuritic chest pain, lower abdominal pain, well-localized chest pain, or fleeting pain lasting a few seconds is not consistent with angina. However, presence of these symptoms does not necessarily exclude ACS. Up to 22% of patients with stabbing chest pain may be diagnosed with acute ischemia.
A history of myocardial infarction and older age results in a higher risk of severe or multi-vessel CAD. Diabetes mellitus and hypertension increase the risk of adverse outcomes.
Physical Examination
The physical examination should focus on determining:
Vital signs, including blood pressure in each arm, heart rate, respiratory rate, and oxygen saturation, should be determined.
Findings that suggest severe disease or increased risk of adverse outcomes include new-onset mitral regurgitation or evidence of left ventricular dysfunction (pulmonary crackles, S3 gallop). The presence of cardiogenic shock portends high mortality rates of up to 60% and should be treated as a medical emergency.
Electrocardiogram
A 12-lead EKG should be obtained while the patient is symptomatic. ST segment deviation > 0.05 mV or T-wave inversions greater than 0.2 mV during an episode of angina that resolve when the patient is asymptomatic is highly suggestive of ACS. Continuous 12-lead EKG monitoring may also be performed. Patients with suspected or documented ACS should be observed with telemetry monitoring.
Box 3-1 lists the non-ACS causes of ST segment and T wave changes.
Cardiac Injury Markers
Cardiac injury markers should be obtained on presentation and every 8 hours for the first 24 hours. Often, an EKG is performed at the same time.
Troponins
Troponin I and Troponin T are markers of cardiac injury. Troponins are more specific and sensitive than CK for the diagnosis of myocardial infarction and may also allow for risk-stratification. Troponins are useful for diagnosis of recent myocardial infarction within 2 weeks of onset that may otherwise be missed by creatine kinase assays. Due to their increased sensitivity, troponins may also be elevated when CK–MB levels are normal, allowing for detection of “micro-infarctions.”
Troponin levels correlate with the risk of death in patients with ACS. Patients with normal EKG findings and CK–MB levels but with elevated troponin levels have a higher risk of death than do patients with normal troponin levels. Patients with increased troponin levels may also benefit from more aggressive anti-platelet and anti-coagulation therapy.
Creatine Kinase
Measurement of CK–MB has traditionally been used in the diagnosis of myocardial injury. CK-MB is superior to troponins for early diagnosis of myocardial infarction, but it has lower sensitivity for the diagnosis of myocardial infarction > 36 hours after the event. CK-MB has a shorter half-life than troponins, which may be useful for the diagnosis of recurrent myocardial infarction.
Early Risk Stratification
Early risk-stratification (for short-term risk of death or non-fatal MI) allows identification of patients who may benefit from more aggressive anti-platelet and anti-coagulation therapy and early angiography. Two systems will be described here. The ACC/AHA Guidelines from 2002 allow risk-stratification based on history, physical examination and EKG findings, and cardiac marker levels. The Thrombolysis in MI (TIMI) risk score was developed and validated based on data from large clinical trials. It uses seven clinical variables to stratify patients into high-, medium-, and low-risk categories (Box 3-2).
Box 3-2 Early Risk Stratification in UA/NSTEMI
From Braunwald E, Antman EM, Beasley JW, et al. ACC/AHA 2002 guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients with Unstable Angina). 2002. Available at: http://www.acc.org/clinical/guidelines/unstable/unstable.pdf.
