Management of Unstable Angina and Non-ST Elevation Myocardial Infarction

Yuri B. Pride

Eli V. Gelfand

I. GENERAL PRINCIPLES AND DEFINITIONS

A. More than 6 million patients present to the emergency department with chest pain annually in the United States.

B. More than 1.1 million patients are admitted to the hospital each year in the United States with an acute coronary syndrome (ACS).

C. Eighty percent of ACS patients do not have ST-segment elevations on an initial ECG and have unstable angina or non-ST-segment elevation myocardial infarction (UA/NSTEMI).

II. PATHOPHYSIOLOGY

A. UA/NSTEMI is caused by either rupture of a vulnerable atherosclerotic plaque or erosion of endothelium revealing underlying atherosclerotic debris followed by the formation of thrombus.

B. In contrast to ST-segment elevation MI (STEMI), in UA/NSTEMI, the intracoronary thrombus is typically only partially occlusive, although intermittent periods of occlusion and subsequent reperfusion are common.

C. There is embolization of the thrombus fragments downstream, causing additional myocardial ischemia and necrosis.

D. The sequence of events in UA/NSTEMI is

1. Rupture or erosion of a vulnerable atherosclerotic plaque.

2. Platelet activation, aggregation, and adhesion.

3. Secondary activation of plasma coagulation cascade.

4. Coronary vasoconstriction.

5. Imbalance in myocardial oxygen and demand.

6. Downstream embolization of platelet microaggregates, thrombus, and atherosclerotic debris.

III. GENERAL ASPECTS OF DIAGNOSIS

A. Based on new or accelerating symptoms of coronary ischemia, with or without ECG changes.

B. Elevation of cardiac troponin beyond 99th percentile of normal distinguishes NSTEMI from UA.

C. ECG changes in UA/NSTEMI may include:

1. ST-segment depressions.

2. Transient ST-segment elevations.

3. New T-wave inversions.

IV. INITIAL EVALUATION AND RISK STRATIFICATION OF SUSPECTED UA/NSTEMI

A. Focused history should concentrate on the nature of anginal symptoms, prior history of coronary artery disease (CAD), and traditional cardiovascular risk factors.

B. Physical examination is directed toward assessment of

1. Possible precipitants of UA/NSTEMI, such as hypertension, thyroid disease, anemia, or arrhythmias.

2. Hemodynamic effects of UA/NSTEMI, such as congestive heart failure and arrhythmia.

3. Important alternate diagnoses; for example, acute pericarditis, pulmonary embolism, or aortic dissection.

C. 12-lead ECG should be interpreted within 10 minutes of the patient’s arrival to the emergency department.

1. If initial ECG is not diagnostic of ACS, follow-up ECG should be performed every 15 to 30 minutes to evaluate for evolving ST-segment elevations or depressions.

2. Posterior leads V₇-V₉ should be utilized to enhance detection of posterior MI if there are ST-segment depressions in the anterior precordial leads (V₁-V₃).

D. Cardiac biomarkers, preferably cardiac-specific troponin, should be measured.

1. For patients presenting within 6 hours of symptom onset, considerations are to

a. Measure myoglobin (a very early marker of myocardial necrosis) along with troponin.

b. Repeat troponin levels in 6 to 8 hours or as guided by timing of symptom onset.

2. Additional biomarkers, such as total CK-MB mass, B-type natriuretic peptide (BNP), or N-terminus proBNP (NT-pro-BNP), may have additional prognostic information in UA/NSTEMI.

E. Among patients with new left bundle branch block or a concerning history without diagnostic ECG changes, consideration should be given to performing bedside echocardiography to assess for regional wall motion abnormalities.

F. Focused evaluation for other causes of chest discomfort should be undertaken (Table 32-1).

G. Based on the clinical history, ECG and initial laboratory, and imaging tests, patients are assigned the probability of having ACS. Further triage and management decisions are made accordingly.

1. In patients with noncardiac chest pain, a search is undertaken in the ED for the underlying cause.

TABLE 32-1 Differential Diagnosis of Chest Discomfort

Conditions with immediate life-threatening potential

ACS
Acute aortic dissection
Pulmonary embolism/infarction
Esophageal rupture
Tension pneumothorax

Other common conditions

Acute pericarditis
Gastroesophageal reflux disease
Costochondritis and related musculoskeletal conditions
Acute myocarditis
Transient apical ballooning syndrome (“takotsubo-type” cardiomyopathy)
Esophageal spasm
Pleurisy
Referred pain from abdominal organs, particularly the spleen and gallbladder

2. Patients with stable angina benefit from uptitration of antianginal therapy with or without observation in a dedicated chest pain unit.

3. Patients with possible UA/NSTEMI who have a nondiagnostic ECG and normal initial cardiac biomarkers are observed for at least 6 to 12 hours from symptom onset.

a. If recurrent ischemic pain or follow-up studies are positive, treatment for definite ACS is initiated.

b. If there is no further pain and ECG/biomarkers remain within the range of normal, a stress test should be considered.

i. If stress test demonstrates inducible ischemia or new regional left ventricular (LV) systolic dysfunction, therapy for ACS is started.

ii. If stress test is negative, a diagnosis of noncardiac chest pain is likely and arrangements should be made for outpatient follow-up.

4. Among patients with a nondiagnostic ECG and negative cardiac biomarkers, coronary computed tomography (CT) can also be considered. It has a high negative predictive value, and it may help determine patients who are safe for discharge from the emergency department.

5. Patients with probable/definite UA/NSTEMI are admitted to a coronary care or telemetry unit for continuous cardiac monitoring, risk stratification, antithrombotic and antianginal therapy, and consideration of revascularization.

H. Patients with UA/NSTEMI must be risk stratified, as certain therapies have been shown to benefit only high-risk patients.

I. TIMI risk score (Table 32-2) provides a rapid way of assessing the patient’s risk.

1. Has been prospectively validated in UA/NSTEMI.

TABLE 32-2 TIMI Risk Score for UA/NSTEMI

Age ≥65 y	1 pt
Prior coronary stenoses >50%	1 pt
≥3 Risk factors for CAD	1 pt
Use of aspirin in the preceding 24 h	1 pt
≥2 Anginal events in the preceding 24 h	1 pt
ST-segment changes	1 pt
Elevated cardiac biomarkers	1 pt
Total possible score	0-7 pts
Adapted from Antman EM, Cohen M, Bernink PJ, et al. The TIMI risk score for unstable angina/non-ST elevation MI: a method for prognostication and therapeutic decision making. JAMA 2000;284(7):835-842.

2. Useful in predicting short-term (14 to 30 days) major adverse cardiovascular events (death, MI, or recurrent ischemia) and long-term (1-year) mortality.

3. Higher-risk score identifies patients who progressively benefit from aggressive therapy with low molecular weight heparin (LMWH), glycoprotein (GP) IIb/IIIa inhibitors, and early invasive strategy.

V. MANAGEMENT OF UA/NSTEMI

A. General aspects of care.

1. Dual goals in management of UA/NSTEMI must be taken into account at all times.

a. Immediate relief of myocardial ischemia.

b. Prevention of adverse outcomes, specifically [re]infarction, death, and future heart failure.

2. The overall management plan is described in Figure 32-1.

3. The general plan of management of patients with UA/NSTEMI should develop as follows.

a. Establish basic care and monitoring: oxygen, continuous ECG monitoring, and resuscitation equipment.

b. Administer analgesic and anti-ischemic therapy: beta-blockers, nitrates, and morphine.

c. Define risk using a standardized scoring system (see above).

d. Determine the appropriate overall treatment strategy.

i. Early invasive strategy: planned cardiac catheterization within 4 to 48 hours with revascularization where feasible.