Charles A. Henrikson, MD, MPH; Eric E. Howell, MD; David E. Bush, MD; J. Shawn Miles, MD; Glenn R. Meininger, MD; Tracy Friedlander; Andrew C. Bushnell, MD; Nisha Chandra-Strobos, MD
Acknowledgments: The authors thank Edward Bessman, MD, for administrative support; Johann Brandes, MD, for assistance with patient follow-up; and Angel Sampedro for assistance with data analysis.
Grant Support: By a National Heart, Lung and Blood Institute Training grant #T32-HLO7227-26 (Dr. Henrikson).
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Nisha Chandra-Strobos, MD, Division of Cardiology, Johns Hopkins Bayview Medical Center, 4940 Eastern Avenue, Baltimore, MD 21224; e-mail, email@example.com.
Current Author Addresses: Drs. Henrikson, Miles, and Meininger: Division of Cardiology, Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, MD 21205.
Dr. Howell: Divison of General Internal Medicine, Johns Hopkins Bayview Medical Center, 4940 Eastern Avenue, Baltimore, MD 21224.
Drs. Bush, Chandra-Strobos, and Ms. Friedlander: Division of Cardiology, Johns Hopkins Bayview Medical Center, 4940 Eastern Avenue, Baltimore, MD 21224.
Dr. Bushnell: Division of Emergency Medicine, University of Vermont, 111 Colchester Ave., Burlington, VT 05401.
Author Contributions: Conception and design: C.A. Henrikson, E.E. Howell, D.E. Bush, N. Chandra-Strobos.
Analysis and interpretation of the data: C.A. Henrikson, E.E. Howell, D.E. Bush, N. Chandra-Strobos.
Drafting of the article: C.A. Henrikson.
Critical revision of the article for important intellectual content: C.A. Henrikson, E.E. Howell, D.E. Bush, J.S. Miles, G.R. Meininger, T. Friedlander, A.C. Bushnell, N. Chandra-Strobos.
Final approval of the article: C.A. Henrikson, E.E. Howell, D.E. Bush, J.S. Miles, G.R. Meininger, T. Friedlander, A.C. Bushnell, N. Chandra-Strobos.
Provision of study materials or patients: E.E. Howell, A.C. Bushnell, N. Chandra-Strobos.
Statistical expertise: C.A. Henrikson, D.E. Bush.
Administrative, technical, or logistic support: N. Chandra-Strobos.
Collection and assembly of data: C.A. Henrikson, E.E. Howell, J.S. Miles, G.R. Meininger, T. Friedlander, A.C. Bushnell.
The belief that chest pain relief with nitroglycerin indicates the presence of active coronary artery disease is common. However, this hypothesis has not been tested.
To define the diagnostic and prognostic value of chest pain relief with nitroglycerin.
Prospective observational cohort study.
Urban community teaching hospital.
459 consecutive patients with chest pain admitted through the emergency department who received nitroglycerin from emergency services personnel or an emergency department nurse. Follow-up was obtained by telephone contact at 4 months.
Chest pain relief was defined as a decrease of at least 50% in patients' self-reported pain within 5 minutes of the initial dose of sublingual or spray nitroglycerin. Active coronary artery disease was defined as any elevated serum enzyme levels, coronary angiography demonstrating a 70% or greater stenosis, or a positive exercise test result.
Nitroglycerin relieved chest pain in 39% of patients (181 of 459). In patients with active coronary artery disease as the likely cause of their chest pain, 35% (49 of 141) had chest pain relief with nitroglycerin. In contrast, in patients without active coronary artery disease, 41% (113 of 275) had chest pain relief (P > 0.2). Four-month clinical outcomes were similar in patients with or without chest pain relief with nitroglycerin (P > 0.2).
These data suggest that, in a general population admitted for chest pain, relief of pain after nitroglycerin treatment does not predict active coronary artery disease and should not be used to guide diagnosis.
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Henrikson CA, Howell EE, Bush DE, Miles JS, Meininger GR, Friedlander T, et al. Chest Pain Relief by Nitroglycerin Does Not Predict Active Coronary Artery Disease. Ann Intern Med. 2003;139:979-986. doi: 10.7326/0003-4819-139-12-200312160-00007
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Published: Ann Intern Med. 2003;139(12):979-986.
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