eMedicine Specialties > Emergency Medicine > Cardiovascular

Acute Coronary Syndrome: Differential Diagnoses & Workup

Author: Drew Evan Fenton, MD, Hospitalist, Our Health Care Consultants
Contributor Information and Disclosures

Updated: Aug 6, 2009

Differential Diagnoses

Anxiety
Hypertensive Emergencies
Aortic Stenosis
Myocardial Infarction
Asthma
Myocarditis
Cardiomyopathy, Dilated
Pericarditis and Cardiac Tamponade
Esophagitis
Pneumothorax, Iatrogenic, Spontaneous and Pneumomediastinum
Gastroenteritis
Pulmonary Embolism

Workup

Laboratory Studies

  • Troponin I is considered the preferred biomarker for diagnosing myocardial necrosis. Troponins have the greatest sensitivity and specificity in detecting MI, and elevated serum levels are considered diagnostic of MI. They also have prognostic value.
    • For early detection of myocardial necrosis, sensitivity of troponin is superior to that of the creatine kinase–MB (CK-MB). Troponin I is detectable in serum 3-6 hours after an MI, and its level remains elevated for 14 days.
    • Troponin is a contractile protein that normally is not found in serum. It is released only when myocardial necrosis occurs.
    • Troponin should be used as the optimum biomarkers for the evaluation of patients with ACS who have coexistent skeletal muscle injury.
  • Troponin T has similar release kinetics to troponin I, and levels remains elevated for 14 days. False-positive results may occur in patients with renal failure. Minor elevations in troponin T level also identify patients at risk for subsequent cardiac events.
  • Elevated troponin levels may also point to minor myocardial injury due to other causes. Zellweger et al described 4 patients with elevated troponin levels after supraventricular tachycardia without evidence of coronary artery disease and very low risk scores for ACS.1 Similarly, Koller found that endurance athletes may show elevated serum troponin levels in the absence of ACS.2
  • CK-MB levels begin to rise within 4 hours after MI, peak at 18-24 hours, and subside over 3-4 days. A level within the reference range does not exclude myocardial necrosis.
    • The upper limit of normal for CK-MB is 3-6% of total CK. A normal level in the ED does not exclude the possibility of MI. A single assay in the ED has a 34% sensitivity for MI. Serial sampling over periods of 6-9 hours increases sensitivity to approximately 90%. Serial CK-MB over 24 hours detects myocardial necrosis with a sensitivity near 100% and a specificity of 98%.
    • Occasionally, a very small infarct is missed by CK-MB; therefore, troponin levels should be measured for patients suspected to have MI who have negative results from serial CK-MB tests.
    • One study looked at using the 2-hour delta (increase or decrease) of cardiac markers as 1 of 6 criteria in making the diagnosis of ACS and MI. According to one of the Erlanger criteria, an increase in the CK-MB level of 1.5 ng/mL or greater or an increase of the cardiac troponin I level of 0.2 ng/mL or greater over 2 hours in itself would allow one to make the provisional diagnosis of ACS with a high degree of sensitivity and specificity, even if the total levels were within the normal range. Patients with recent MI were also identified by a decreasing curve of CK-MB. Using this 2-hour delta of cardiac markers greatly reduces the number of cases of MI and ACS that are overlooked in patients who are then inappropriately discharged home.
  • Myoglobin, a low-molecular-weight heme protein found in cardiac and skeletal muscle, is released more rapidly from infarcted myocardium than troponin and CK-MB and may be detected as early as 2 hours after MI. Myoglobin levels, although highly sensitive, are not cardiac specific. They may be useful for early detection of MI when performed with other studies.
  • Cardiac markers should be used liberally to evaluate patients with prolonged episodes of ischemic pain, with new changes on ECG, or with nondiagnostic or normal ECGs in whom the diagnosis of ACS or MI is being considered.
  • Complete blood count is indicated to determine if anemia is a precipitant. Transfusion with packed red blood cells may be indicated.
  • A chemistry profile is indicated. Obtain a basic metabolic profile, including a check of blood glucose level, renal function, and electrolytes levels, for patients with new-onset angina. Potassium and magnesium levels should be monitored and corrected. Creatinine levels must be considered before using an angiotensin-converting enzyme (ACE) inhibitor.
  • Other biochemical markers
    • C-reactive protein (CRP) is a marker of acute inflammation. Patients without biochemical evidence of myocardial necrosis but elevated CRP level are at increased risk of an adverse event.
    • Interleukin 6 is the major determinant of acute-phase reactant proteins in the liver, and serum amyloid A is another acute-phase reactant. Elevations of either of these can be predictive in determining increased risk of adverse outcomes in patients with unstable angina.
  • In one study, patients presenting to the ED with suspected myocardial ischemia showing higher levels of inflammatory cytokines were associated with an increased risk of a serious cardiac event during the subsequent 3 months. However, the cytokines have limited ability to predict a serious adverse cardiac event.
  • Erythrocyte sedimentation rate rises above reference range values within 3 days and may remain elevated for weeks.
  • Serum lactase dehydrogenase level rises above the reference range within 24 hours of MI, reaches a peak within 3-6 days, and returns to the baseline within 8-12 days.

Imaging Studies

  • Chest radiograph may demonstrate complications of ischemia, such as pulmonary edema, or it may provide clues to alternative causes of symptoms, such as thoracic aneurysm or pneumonia.
  • Echocardiogram often demonstrates wall motion abnormalities due to ischemia. It is of limited value in patients whose symptoms have resolved or in those with preexisting wall motion abnormalities. However, echocardiogram may be useful in identifying precipitants for ischemia, such as ventricular hypertrophy and valvular disease.
  • Radionuclide myocardial perfusion imaging has been shown to have favorable diagnostic and prognostic value in this setting, with an excellent early sensitivity to detect acute myocardial infarction (MI) not achieved by other testing modalities.
    • A normal resting perfusion imaging study has been shown to have a negative predictive value of more than 99% in excluding MI. Observational and randomized trials of both rest and stress imaging in the ED evaluation of patients with chest pain have demonstrated reductions in unnecessary hospitalizations and cost savings compared with routine care.
    • Perfusion imaging has also been used in risk stratification after MI and for measurement of infarct size to evaluate reperfusion therapies. Novel "hot spot" imaging radiopharmaceuticals that visualize infarction or ischemia are currently undergoing evaluation and hold promise for future imaging of ACS. (See Myocardial Ischemia - Nuclear Medicine and Risk Stratification.)
  • Recent advances include dual-source 64-slice CT scanners that can do a full scan in 10 seconds and produce high-resolution images that allow fine details of the patient's coronary arteries to be seen. This technology allows for noninvasive and early diagnosis of coronary artery disease and thus earlier treatment before the coronary arteries become more or completely occluded. It allows direct visualization of not only the lumen of the coronary arteries but also plaque within the artery. Dual-source 64-slice CT scanning is being used with intravenous contrast to determine if a stent or graft is open or closed.
  • Technetium-99m (99mTc) tetrofosmin single-photon emission computed tomography (SPECT) is a useful method to exclude high-risk patients among patients with chest pain in the emergency department.
  • Resting cardiac magnetic resonance imaging (MRI) has exhibited diagnostic operating characteristics suitable for triage of patients with chest pain in the ED. Performed urgently to evaluate chest pain, MRI accurately detected a high fraction of patients with ACS, including patients with enzyme-negative unstable angina. MRI can identify wall thinning, scar, delayed enhancement (infarction), and wall motion abnormalities (ischemia). Coronary artery assessment may be coupled with magnetic resonance (MR) angiography in the future.

Other Tests

  • ECG is the most important ED diagnostic test for angina. It may show changes during symptoms and in response to treatment, which would confirm a cardiac basis for symptoms. It also may demonstrate preexisting structural or ischemic heart disease (left ventricular hypertrophy, Q waves). A normal ECG or one that remains unchanged from the baseline does not exclude the possibility that chest pain is ischemic in origin. Changes that may be seen during anginal episodes include the following:
    • Transient ST-segment elevations (fixed changes suggest acute MI) may be observed. In patients with elevated ST segments, consider LV aneurysm, pericarditis, Prinzmetal angina, early repolarization, and Wolff-Parkinson-White syndrome as possible diagnoses.
    • Dynamic T-wave changes (inversions, normalizations, or hyperacute changes) may be observed. In patients with deep T-wave inversions, consider CNS events or drug therapy with tricyclic antidepressants or phenothiazines.
    • ST depressions may be junctional, downsloping, or horizontal.
    • Diagnostic sensitivity may be increased by performing right-sided leads (V4 R), posterior leads (V8, V9), and serial recordings.
A 50-year-old man with type 1 diabetes mellitus a...

A 50-year-old man with type 1 diabetes mellitus and hypertension presents after experiencing 1 hour of midsternal chest pain that began after eating a large meal. Pain is now present but is minimal. Aspirin is the single drug that will have the greatest potential impact on subsequent morbidity. In the setting of ongoing symptoms and ECG changes, nitrates titrated to 10% reduction in blood pressure and symptoms, beta-blockers, and heparin are all indicated. If the patient continues to have persistent signs and/or symptoms of ischemia, addition of a glycoprotein IIb/IIIa inhibitor should be considered.

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A 50-year-old man with type 1 diabetes mellitus a...

A 50-year-old man with type 1 diabetes mellitus and hypertension presents after experiencing 1 hour of midsternal chest pain that began after eating a large meal. Pain is now present but is minimal. Aspirin is the single drug that will have the greatest potential impact on subsequent morbidity. In the setting of ongoing symptoms and ECG changes, nitrates titrated to 10% reduction in blood pressure and symptoms, beta-blockers, and heparin are all indicated. If the patient continues to have persistent signs and/or symptoms of ischemia, addition of a glycoprotein IIb/IIIa inhibitor should be considered.


A 62-year-old woman with a history of chronic sta...

A 62-year-old woman with a history of chronic stable angina and a "valve problem" presents with new chest pain. She is symptomatic on arrival, complaining of shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure 140/90 mm Hg and heart rate is 98. Her ECG is as shown. She is given nitroglycerin sublingually, and her pressure decreases to 80/palpation. Right ventricular ischemia should be considered in this patient.

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A 62-year-old woman with a history of chronic sta...

A 62-year-old woman with a history of chronic stable angina and a "valve problem" presents with new chest pain. She is symptomatic on arrival, complaining of shortness of breath and precordial chest tightness. Her initial vital signs are blood pressure 140/90 mm Hg and heart rate is 98. Her ECG is as shown. She is given nitroglycerin sublingually, and her pressure decreases to 80/palpation. Right ventricular ischemia should be considered in this patient.


More on Acute Coronary Syndrome

Overview: Acute Coronary Syndrome
Differential Diagnoses & Workup: Acute Coronary Syndrome
Treatment & Medication: Acute Coronary Syndrome
Follow-up: Acute Coronary Syndrome
Multimedia: Acute Coronary Syndrome
References
Further Reading
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References

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Further Reading

Clinical guidelines

Clinical policy: critical issues in the evaluation and management of adult patients with non-ST-segment elevation acute coronary syndromes.Fesmire FM, Decker WW, Diercks DB, Ghaemmaghami CA, Nazarian D, Brady WJ, Hahn S, Jagoda AS, American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of adult patients with non-ST-segment elevation acute coronary syndromes. Ann Emerg Med 2006 Sep;48(3):270-301 Antithrombotic therapy for non-ST-segment elevation acute coronary syndromes. American College of Chest Physicians evidence-based clinical practice guidelines (8th edition).Harrington RA, Becker RC, Cannon CP, Gutterman D, Lincoff AM, Popma JJ, Steg G, Guyatt GH, Goodman SG. Antithrombotic therapy for non-ST-segment elevation acute coronary syndromes: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008 Jun;133(6 Suppl):670S-707S.

Use of cardiac biomarkers for acute coronary syndromes. Laboratory medicine practice guidelines: evidence-based practice for point-of-care testing. Storrow AB, Apple FS, Wu AH, Jesse R, Francis G, Christenson RH. Use of cardiac biomarkers for acute coronary syndromes. In: Laboratory medicine practice guidelines: evidence-based practice for point-of-care testing. Washington (DC): National Academy of Clinical Biochemistry (NACB); 2006. p. 13-20.

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Keywords

acute coronary syndrome, ACS, ACS treatment, ACS causes, ACS symptoms, ST-elevation myocardial infarction, STEMI, non-ST-elevation myocardial infarction, NSTEMI, ACS, angina, myocardial ischemia, acute myocardial ischemia, myocardial infarction, MI, coronary artery disease, coronary heart disease, heart disease, chest pain

atherosclerotic plaques, variant angina, Prinzmetal angina, coronaryvasospasm, stable angina, unstable angina, hypertension, diabetes mellitus, smoking, hypercholesterolemia, hyperlipidemia

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Contributor Information and Disclosures

Author

Drew Evan Fenton, MD, Hospitalist, Our Health Care Consultants
Drew Evan Fenton, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Edward Bessman, MD, Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University
Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School
Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD, Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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