Clinical investigations
Clinical usefulness and prognostic value of elevated cardiac troponin I levels in acute pulmonary embolism

https://doi.org/10.1016/S0002-8703(02)94704-6Get rights and content

Abstract

Background

Right ventricular myocardial ischemia and injury contribute to right ventricular dysfunction and failure during acute pulmonary embolism. The objective of this study was to evaluate the clinical usefulness of cardiac troponin I (cTnI) in the assessment of right ventricular involvement and short-term prognosis in acute pulmonary embolism

Methods

Thirty-eight patients with acute pulmonary embolism were included in the study. Clinical characteristics, right ventricular involvement, and clinical outcome were compared in patients with elevated levels of serum cTnI versus patients with normal levels of serum cTnI.

Results

Among the study population (n = 38 patients), 18 patients (47%) had elevated cTnI levels (mean ± SD 1.6 ± 0.7 ng/mL, range 0.7–3.7 ng/mL, median, 1.4 ng/mL), and comprised the cTnI-positive group. In the other 20 patients, the serum cTnI levels were normal (≤0.4 ng/mL), and they comprised the cTnI-negative group. In the cTnI-positive group (n = 18 patients), 12 patients (67%) had right ventricular dilatation/hypokinesia, compared with 3 patients (15%) in the cTnI-negative group (n = 20 patients, P = .004). Right ventricular systolic pressure was significantly higher in the cTnI-positive group (51 ± 8 mm Hg vs 40 ± 9 mm Hg, P = .002). Cardiogenic shock developed in a significantly higher number of patients with elevated serum cTnI levels (33% vs 5%, P = .01). In patients with elevated cTnI levels, the odds ratio for development of cardiogenic shock was 8.8 (95% CI 2.5–21).

Conclusions

Patients with acute pulmonary embolism with elevated serum cTnI levels are at a higher risk for the development of right ventricular dysfunction and cardiogenic shock. Serum cTnI has a role in risk stratification and short-term prognostication in patients with acute pulmonary embolism.

Section snippets

Study population

The medical records of 130 consecutive patients with acute pulmonary embolism who were treated in Long Island College Hospital between January 1998 and December 2000 were reviewed retrospectively. The investigations used to diagnose pulmonary embolism were helical computed tomography and ventilation perfusion scans. Of 130 patients, 62 patients had serum cTnI levels measured on admission. Patients were excluded from the study when they had a history of myocardial infarction or coronary

Results

Of 38 study patients in whom acute pulmonary embolism was diagnosed, 18 (47%) had elevated serum cTnI levels (mean ± SD 1.6 ± 0.7 ng/mL, range 0.7–3.7 ng/mL, median 1.4 ng/mL) and comprised the cTnI-positive group. In the other 20 patients, the serum cTnI levels were normal (≤0.4 ng/mL), and these patients comprised the cTnI-negative group. The clinical and electrocardiographic characteristics of both groups are summarized in Table I. Shortness of breath was the most common presenting complaint

Discussion

As early as 1939, it was recognized that acute pulmonary embolism might cause myocardial ischemia and injury.13 In animal models, a significant deterioration in coronary blood flow and concomitant decrease in the contractile performance of the right ventricle during episodes of acute pulmonary embolism have been demonstrated.14, 15 Pulmonary artery occlusion has been shown to cause a selective decrease in myocardial blood flow to the right ventricular subendocardium, resulting in subendocardial

Conclusions

Patients with acute pulmonary embolism and elevated serum cTnI levels are at a higher risk for developing right ventricular dysfunction and cardiogenic shock. Therefore, cTnI has a role, as an adjunct to the clinical assessment and echocardiography, for risk stratification and short-term prognostication in patients with acute pulmonary embolism.

References (22)

  • E.M Antman et al.

    Cardiac-specific troponin I levels to predict the risk of mortality in patients with acute coronary syndromes

    N Eng J Med

    (1996)

    • Cited by (0)

    View full text
    Copyright © 2003 Mosby, Inc. All rights reserved.