Is it an MI, angina, or something else?

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When a patient presents with chest pain, follow this doctor’s guidelines to quickly reach an accurate diagnosis and initiate life-saving treatment.

For some time, cardiologists have called MIs and unstable angina “acute coronary syndrome,” or ACS. The new nomenclature makes sense because ST-elevation MI (STEMI), non-ST-elevation MI (NSTEMI), and unstable angina have overlapping clinical presentations and call for similar evaluation and management strategies. Knowing the precise condition you’re dealing with will guide the course of treatment and the urgency with which you pursue that course.

The diagnosis of ACS begins with a thorough history that includes:
• the nature of any anginal symptoms
• whether there is a prior history of CAD
• the patient’s age and gender
• the presence of any CAD risk factors.1,2

Substernal chest pain that is provoked by exertion and relieved by rest or nitroglycerin is considered typical angina and carries a high risk for unstable CAD.3

Also associated with a high risk of ACS is chest pain that radiates to one or both arms or is accompanied by nausea, vomiting, or diaphoresis.4 Symptoms not typically associated with CAD, such as discomfort radiating to the jaw, neck, or ear, may be considered “anginal equivalents” if they are predictably associated with exertion. New-onset or worsening exertional dyspnea is the most common “anginal equivalent” in the elderly.2

Patients with previously diagnosed CAD who develop new or worsening symptoms are at particularly high risk for multivessel CAD.2 Men older than 60 are also at greater risk. The risk for severe obstructive or multivessel CAD increases with age, and older patients with ACS are more likely to have atypical symptoms.2 Even patients who lack major CAD risk factors, such as hypertension, diabetes, hyperlipidemia, and tobacco use, are considered to be at high risk if they have typical anginal symptoms.

The Rouan clinical decision rule can help predict which patients with chest pain and a normal or nonspecific ECG are at higher risk of MI5 (Table 1).

Physical examination

A brief, targeted physical examination is important to aid appropriate initial triage of any patient with possible ACS. The first priority is rapid assessment of the airway, breathing, and circulation, plus the patient’s general condition and vital signs. Jugular venous distension or rales may suggest pulmonary edema or acute heart failure. The heart should be evaluated for murmurs or gallops.

Assessment of the patient’s peripheral pulses can help determine the presence of systemic vascular disease. It is also important to evaluate for signs of stroke or the presence or absence of hypoperfusion (is the patient cool, clammy, pale, or ashen?).2 Once the initial assessment is completed, a more detailed physical examination can help you formulate a differential diagnosis and evaluate for other causes of chest pain or anginalike symptoms.

Testing

Important initial testing for a possible ACS includes a 12-lead ECG and a chest x-ray, plus a complete blood count, blood chemistries, and serum markers for myocardial damage.

The ECG findings most strongly predictive of MI are ST-segment elevation, Q waves, or a conduction defect, such as a left bundle branch block (LBBB), especially if they are new compared with a previous ECG. New T-wave inversion also increases the likelihood of MI.

ST-segment elevation >0.2 mV in the anteroseptal leads identifies patients who may benefit from reperfusion therapy for an acute STEMI. Mortality risk appears to rise with increasing numbers of leads showing ST changes. ST depression in leads V1 through V4 accompanied by tall R waves in right precordial leads and upright T waves may suggest a posterior infarction.2

Other ECG criteria that may help confirm ischemia in the presence of LBBB and a typical anginal history include:
• ST elevation ≥0.1 mV in leads with a positive QRS and
• ST depression ≥0.1 mV in V1-V3, and ST elevation ≥0.5 mV in leads with a negative QRS.2

An ECG showing ST-segment depression in a patient who has anginal symptoms suggests either unstable angina or NSTEMI. Transient ST-segment changes that are present with symptoms and resolve when symptoms dissipate are particularly suggestive of underlying CAD. Differential diagnoses that should also warrant consideration in patients with ST-segment or T-wave changes include left ventricular aneurysm, pericarditis, Prinzmetal’s angina, early repolarization, Wolff-Parkinson-White syndrome, and use of such medications as phenothiazines and tricyclic antidepressants.1

Serial ECGs should be monitored for acute evolution of ischemia during initial evaluation. Note, however, that up to 6% of patients with chest pain and a normal ECG will ultimately be found to have had an acute MI or unstable angina.1

Serum markers commonly used to evaluate a patient with a suspected ACS include creatine kinase (CK), its MB subform (CK-MB), and troponin T (TnT) and troponin I (TnI). Serial measurements to assess for repeated elevations of CK-MB can be used to detect recurrent infarction following an initial event.2 CK-MB has low sensitivity for detecting infarction during the first six hours after the onset of symptoms, but a CK-MB >6.0 ng/mL within nine hours of presentation for emergency care modestly increases the likelihood of MI or death in the next 30 days.6

Both TnT and TnI are relatively insensitive during the first six hours after myocardial injury, but elevated levels of either troponin (TnT >2 ng/mL or TnI >1 ng/mL) support the diagnosis of MI or ACS and increase the likelihood of death or recurrent MI within 30 days. A normal level of either troponin 6-72 hours after the onset of chest pain provides strong evidence against ACS if the ECG is normal or near-normal.7,8

One study found that among emergency department (ED) patients with chest pain and an essentially normal ECG, only 0.3% with a normal TnI and 1.1% with a normal TnT at six hours suffered death or acute MI in the next 30 days.9 Thus, individuals with chest pain and a low-risk history, a normal or near-normal ECG, and normal troponins can safely be evaluated as outpatients.

Elevations in serum myoglobin occur as early as two hours after symptom onset due to ischemic injury, but myoglobins are relatively nonspecific to cardiac muscle and their use has not been widely adopted. Overall, CK-MB and perhaps myoglobin are the most efficient markers for diagnosis of MI within six hours of symptom onset, while TnT and TnI are much more cardiac-specific and more efficient for late diagnosis of MI.1

Initial stabilization and assessment Initial management should focus on rapid stabilization and assessment. While obtaining a focused history of cardiac symptoms and risks and performing an exam to specifically assess the patient’s stability, emergency personnel should place the patient on a cardiac monitor, administer oxygen, and obtain a 12-lead ECG.

Oral aspirin and oral or IV beta blockers should be given to all patients who do not have contraindications. Nitroglycerin, given sublingually, transcutaneously, or by IV, is useful for initial relief of chest discomfort, and morphine sulfate can both relieve pain that is unresponsive to nitroglycerin and help relieve pulmonary vascular congestion. ECG findings can then lead to classification of the patient into one of three risk categories: STEMI, NSTEMI, or inconclusive and in need of further testing (Table 2).2,10

Patients with STEMI. Patients with anginal chest pain and ST-segment elevation >1 mm in two or more contiguous precordial leads or two or more adjacent limb leads, or those with new LBBB, are diagnosed with STEMI based on history and ECG alone. These patients typically have complete occlusion of a coronary vessel, and the primary intervention should be revascularization with either fibrinolytics or mechanical percutaneous coronary intervention (PCI) (angioplasty with or without stenting).

The choice between fibrinolysis or PCI depends on the ability of the local facility to provide prompt intervention. Absolute contraindications to fibrinolytic therapy are any prior intracranial hemorrhage, known presence of a structural cerebrovascular lesion, known malignant intracranial neoplasm (primary or metastatic), ischemic stroke within three months (except acute ischemic stroke within three hours), suspected aortic dissection, active bleeding or bleeding diathesis (excluding menses), significant closed head trauma or facial trauma within three months.2,10

Relative contraindications to fibrinolysis include history of chronic, severe, poorly controlled hypertension; severe uncontrolled hypertension (systolic BP>180 mm Hg or diastolic BP >110 mm Hg on presentation); history of ischemic stroke more than three months before; dementia, or known intracranial pathology not covered in previously noted contraindications; traumatic or prolonged (>10 minutes) cardiopulmonary resuscitation or major surgery within the past three weeks; recent (within the past two to four weeks) internal bleeding; noncompressible vascular punctures; prior exposure (more than five days ago) or allergic reaction to streptokinase/ anistreplase (if these are the agents to be used); pregnancy; active peptic ulcer; and current use of anticoagulants.2,10

In their guidelines, the American College of Cardiology and the American Heart Association found no evidence to support bypassing hospitals without PCI capability in favor of transport to facilities that can provide primary PCI. The guidelines do recommend prompt intervention based on ECG diagnosis without delaying management to obtain cardiac enzymes or consult with the patient’s primary physician.

In short, when the diagnosis is STEMI, the more severe form of MI, time (to revascularization) is of the essence.10

Patients with NSTEMI or unstable angina.

Patients with anginal chest pain and ischemic ECG changes that do not meet criteria for STEMI may have an NSTEMI or unstable angina, possibly due to a partially or intermittently occluding coronary thrombus. Fibrinolysis is not indicated for these patients (and is potentially harmful), but important elements of evaluation include serial ECGs, serial measurements of serum cardiac markers, and evaluation for other nonischemic pathology.

Patients in this category benefit from admission to a hospital or dedicated chest-pain unit for close monitoring, further evaluation, and risk stratification. Those with certain clinic indicators are at particularly high risk of cardiac disease and warrant further invasive testing with angiography (Table 3). Any elevation of TnT or TnI during the first 24 hours in this group of patients also predicts increased cardiac risk and probably warrants angiographic investigation.1,10

Patients with normal or nondiagnostic ECG changes. Patients with anginal chest pain and a normal or nondiagnostic ECG are at relatively low risk of ACS, although underlying CAD cannot be entirely excluded based only on the immediate evaluation in the ED. Evaluation of these patients should focus on stratification based on CAD risk factors, monitoring for serial ECG changes or cardiac enzyme elevations in patients at moderate CAD risk, and consideration of further testing to clarify the presence or absence of CAD.10

Exercise stress ECG testing can aid in assessment of patients at low-to-moderate risk of CAD based on history, symptoms, and risk factors; exercise or chemical stress testing with nuclear or echocardiographic imaging can aid in the evaluation of patients who are at higher cardiac risk or are unable to run on a treadmill. If exercise stress testing is used, the Duke Treadmill Score can provide helpful diagnostic information (Table 4 and 5).

The American College of Cardiology has a Web site that offers versions of its unstable angina, NSTEMI, and other guidelines that are downloadable to a PDA. Go to www.acc.org/qualityandscience/clinical/palm_download.ht.

Follow-up

All patients who present with a possible ACS should be assessed for long-term cardiac risk after initial stabilization and management. For patients not found to have cardiac disease, primary cardiac prevention is still important.

Dr. Cayley is assistant professor in the Department of Family Medicine, University of Wisconsin School of Medicine and Public Health, in Eau Claire, and practices at the UW Health Augusta Family Medicine Clinic in Augusta, Wis.

References

1. 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: www.acc.org/qualityandscience. Accessed February 7, 2007.

2. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction—executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol. 2004;44:671-719. Available at: www.acc.org. Accessed February 7, 2007.

3. Gibbons RJ, Balady GJ, Bricker JT, et al. ACC/AHA 2002 guideline update for exercise testing: summary article. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines). Circulation. 2002;106:1883-1892. Available at: http://circ.ahajournals.org. Accessed February 7, 2007.

4. Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA. 2005;294:2623-2629.

5. Rouan GW, Lee TH, Cook EF, et al. Clinical characteristics and outcome of acute myocardial infarction in patients with initially normal or nonspecific electrocardiograms (a report from the Multicenter Chest Pain Study). Am J Cardiol. 1989;64:1087-1092.

6. McCord J, Nowak RM, Hudson MP, et al. The prognostic significance of serial myoglobin, troponin I, and creatine kinase-MB measurements in patients evaluated in the emergency department for acute coronary syndrome. Ann Emerg Med. 2003;42:343-350.

7. Ebell MH, Flewelling D, Flynn CA. A systematic review of troponin T and I for diagnosing acute myocardial infarction. J Fam Pract. 2000;49:550-556.

8. Ebell MH, White LL, Weismantel D. A systematic review of troponin T and I values as a prognostic tool for patients with chest pain. J Fam Pract. 2000;49:746-753.

9. Hamm CW, Goldmann BU, Heeschen C, et al. Emergency room triage of patients with acute chest pain by means of rapid testing for cardiac troponin T or troponin I. N Engl J Med. 1997;337:1648-1653.

10. ECC Committee, Subcommittees, and Task Forces of the American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: Stabilization of the Patient with Acute Coronary Syndromes. Circulation. 2005;112(24 Suppl):IV-89-IV-110. Available at: http://circ.ahajournals.org. Accessed February 7, 2007.

11. Kwok JM, Miller TD, Christian TF, et al. Prognostic value of a treadmill exercise score in symptomatic patients with nonspecific ST-T abnormalities on resting ECG. JAMA. 1999;282:1047-1053.

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