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Acute Coronary Syndrome Differential Diagnoses

  • Author: David L Coven, MD, PhD; Chief Editor: Eric H Yang, MD  more...
 
Updated: Sep 09, 2015
 
 

Diagnostic Considerations

As many as half of all cases of ACS are clinically silent in that they do not cause the classic symptoms of this syndrome. Consequently, ACS goes unrecognized by the patient. Maintain a high index of suspicion for ACS, especially when evaluating women, patients with diabetes, older patients, patients with dementia, and those with a history of heart failure.

Although ST-segment and T-wave changes are associated with CAD, alternative causes of these findings are left ventricular aneurysm, pericarditis, Prinzmetal angina, early repolarization, Wolff-Parkinson-White syndrome, and drug therapy (eg, with tricyclic antidepressants, phenothiazines).

Increasing public awareness of the typical and atypical presentations of ACS is of the utmost importance for optimal and timely treatment. Many patients do not recognize that their symptoms are cardiac in origin and therefore may delay seeking medical help. Guidelines from the European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA) recommend that patients with established CAD call emergency medical services if they have chest pain that does not resolve after they take a sublingual nitroglycerin tablet.

In patients presenting to the ED with chest pain, a structured diagnostic approach that includes time-focused ED decision points, brief observation, and selective application of early outpatient provocative testing appeared both safe and diagnostically efficient in a study by Scheuermeyer et al. However, some patients with ACS may be discharged for outpatient stress testing on the index ED visit.[17]

Differential Diagnoses

 
 
Contributor Information and Disclosures
Author

David L Coven, MD, PhD Assistant Professor of Clinical Medicine, Columbia University College of Physicians and Surgeons; Director, Cardiology Outpatient Clinic, St Luke’s Site, Attending Physician, Department of Medicine, Division of Cardiology, St Luke’s-Roosevelt Hospital Center

David L Coven, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, Massachusetts Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Jamshid Shirani, MD Director of Cardiology Fellowship Program, Director of Echocardiography Laboratory, Director of Hypertrophic Cardiomyopathy Clinic, St Luke's University Health Network

Jamshid Shirani, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society of Echocardiography, Association of Subspecialty Professors, American College of Cardiology, American College of Physicians, American Heart Association

Disclosure: Nothing to disclose.

Arun Kalyanasundaram, MD, MPH Interventional Cardiology Fellow, Department of Cardiology, Cleveland Clinic

Arun Kalyanasundaram, MD, MPH is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions, Society of General Internal Medicine, Southern Medical Association, Society of Hospital Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic Arizona

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Acknowledgements

Craig T Basson, MD, PhD Gladys and Roland Harriman Professor of Medicine, Director of the Center for Molecular Cardiology, Director of Cardiovascular Research, Division of Cardiology, Department of Medicine, Weill Cornell Medical College; Attending Physician, New York Presbyterian Hospital

Craig T Basson, MD, PhD is a member of the following medical societies: American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA 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.

David FM Brown, MD Associate 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.

Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

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; ProceduresConsult.com Royalty Other

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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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 electrocardiogram (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 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 = 98. Her electrocardiogram (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.
This plot shows changes in cardiac markers over time after the onset of symptoms. Peak A is the early release of myoglobin or creatine kinase isoenzyme MB (CK-MB) after acute myocardial infarction (AMI). Peak B is the cardiac troponin level after infarction. Peak C is the CK-MB level after infarction. Peak D is the cardiac troponin level after unstable angina. Data are plotted on a relative scale, where 1.0 is set at the myocardial-infarction cutoff concentration. Courtesy of Wu et al (1999). ROC = receiver operating characteristic.
Suggested algorithm for triaging patients with chest pain. ACS = ACS; ASA = aspirin; EKG = ECG; MI = myocardial infarction; Rx = treat; STEMI = ST-elevation myocardial infarction. Courtesy of Wu et al (1999).
Use of cardiac markers in the ED. Studies on troponins in ACS.
Use of cardiac markers in the ED. Troponin I levels and cardiac mortality in ACS.
Use of cardiac markers in the ED. Cardiac event rates in the platelet receptor inhibition for ischemic syndrome (PRISM) study based on troponin I results.
Use of cardiac markers in the ED. Effect of time to treatment in patients with acute coronary syndrome (ACS) who are treated with the GIIb/IIIa inhibitor eptifibatide.
Table. TIMI Risk Score for Unstable Angina and NSTEMI [49]
Characteristic Risk Score
History
Age ≥65 years 1
At least 3 risk factors for coronary heart disease 1
Previous coronary stenosis ≥50% 1
Use of aspirin in previous 7 days 1
Presentation
At least 2 anginal episodes in the previous 24 hours 1
ST-segment elevation on admission ECG 1
Elevated levels of serum biomarkers 1
Total Score 0-7
Note: Event rates significantly increased as the TIMI risk score increased in the test cohort in the TIMI IIB study. Rates were 4.7% for a score of 0/1, 8.3% for 2, 13.2% for 3, 19.9% for 4, 26.2% for 5, and 40.9% for 6/7 (P < .001, χ2 test for the trend). The pattern of increasing event rates with increasing TIMI risk score was confirmed in all 3 validation groups (P < .001).
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