Elsevier

American Heart Journal

Volume 140, Issue 3, September 2000, Pages 379-384
American Heart Journal

Acute Ischemic Heart Disease
D -Dimer is an early diagnostic marker of coronary ischemia in patients with chest pain,☆☆

Presented in part at the XIXth Congress of the European Society of Cardiology, 24-28 August 1997, Stockholm; and the XIII World Congress of Cardiology, 26-30 April 1998, Rio de Janeiro.
https://doi.org/10.1067/mhj.2000.108823Get rights and content

Abstract

Background Chest pain is a frequent symptom in the emergency department and often presents a diagnostic challenge. Because coronary thrombosis is a hallmark of acute ischemic syndromes, the substrates of the coagulation and fibrinolysis cascades may be markers of coronary ischemia. The objective of this study was to determine the diagnostic value of several hemostatic markers in patients presenting to the emergency department (ED) with chest pain syndromes. Methods Two hundred fifty-seven consecutive patients with acute chest pain were studied in this prospective study conducted in an urban ED. D- Dimer levels were measured at admission to the ED in all patients. We also measured thrombin-antithrombin complexes, prothrombin fragment 1+2, activated factor VII, and fibrinogen. We used regression analysis to estimate the likelihood of myocardial infarction and the diagnostic value of D -dimer. Results D -Dimer and fibrinogen levels were significantly higher in patients with acute ischemic events (myocardial infarction and unstable angina) than in nonischemic patients (P <.01 and P =.02, respectively). The other hemostatic markers were not significantly elevated in patients with ischemic events. D -Dimer level >500 μg/L had an independent diagnostic value for myocardial infarction and increased the diagnostic sensitivity of the electrocardiogram and history from 73% to 92%. Conclusion D -Dimer, an expression of ongoing thrombus formation and lysis, is a marker of substantial incremental value for the early diagnosis of acute coronary syndromes presenting with chest pain. It adds independent information to the traditional assessment for myocardial infarction. D -Dimer can be incorporated into clinical decision models in the ED. (Am Heart J 2000;140:379-84.)

Section snippets

Methods

This prospective study enrolled 300 consecutive patients admitted to a teaching hospital ED for acute chest pain from September 15, 1996, to January 18, 1997. All patients were 25 years or older and came to the ED with a chief symptom of central or left-sided chest pain. Only patients with onset of symptoms <6 hours were eligible for study. Informed consent was obtained from all patients, and the study protocol was approved by the local ethics committee.

The physician on duty took the medical

Results

One hundred sixty-two patients (63%) were diagnosed with nonischemic chest pain from the following causes: musculoskeletal pain (n = 79), anxiety (n = 50), pain of gastrointestinal origin (n = 15), tachyarrhythmias (atrial flutter and fibrillation) (n = 10), pericarditis (n = 2), pneumothorax (n = 2), pulmonary embolism (n = l), bronchial asthma (n = l), pneumonia (n = l), and urticaria (n = l).

Fifty-eight patients (23%) had UA, and 37 patients (14%) had MI develop. Twenty-one patients (57%)

Discussion

These results suggest that D -dimer measurement can improve clinical decision models to facilitate risk stratification. We found substantially increased D -dimer levels in patients with MI and UA. Our findings also provide a clinically useful D -dimer threshold in MI (>500 μg/L), which added to the conventional diagnosis in the ED and increased the diagnostic sensitivity for MI from 73% to 92%. TAT, F1+2, and activated factor VII provided no additional diagnostic information for patients with

Acknowledgements

We thank the emergency team for their support. We also thank Ms Rosa Felices for technical assistance and Dr J. Soler for his critical review.

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    Partly supported by a grant from the Comisión Interministerial de Ciencia y Tecnología (CICYT); SAF 96/0058 Spain.

    ☆☆

    Reprint requests: Robert S. Schwartz, MD, Division of Cardiovascular Diseases, Mayo Clinic, 200 First St SW, Rochester, MN 55905.E-mail: [email protected]

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