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University of Connecticut Health Center Farmington, CT
Correspondence to: Madalina Macrea, MD, Department of Pulmonary Medicine, University of Connecticut Health Center, MC 1225, 263 Farmington Ave, Farmington, CT 06030; e-mail: minciu-macrea{at}gme.uchc.edu
To the Editor:
We read with great interest the article by Pruszczyk and coworkers (June 2003)1 that reported that patients with pulmonary embolism (PE) and elevated cardiac troponin T (cTnT) levels are at significant risk for a complicated clinical course and fatal outcome. We agree with the authors that risk stratification of hemodynamically stable patients with PE is particularly important because more aggressive therapies such as that with thrombolytic agents may improve outcome. However, we would like to comment on two issues regarding their study.
First, compared with previous studies234 in which authors have excluded coronary artery disease (CAD)-related positive cTnT levels by coronary angiography, cardiac stress-test, or autopsy, Pruszczyk and coworkers1 did not exclude the presence of CAD in any of their patients. Including a detailed history of cardiac risk factors5 in the study is essential, because the severity of CAD may be a confounding factor, especially when almost a third of each category (ie, "survivors" and "nonsurvivors") had known CAD.
Second, 42% of survivors had a positive cTnT finding, which is also emphasized by the authors. This result demonstrates a poor positive predictive value for severe PE. Similar results were found by other studies as well. The cTnT-positive predictive values in studies by Janata et al6 and Konstantinides et al7 were 0.34 and 0.41, respectively. However, very good negative predictive values were found for both cTnT and cardiac troponin I567 in the range of 0.92 to 0.99. In our opinion, the significance of a test assessing cTnT in patients with PE relies on its negative predictive value, and not on its positive predictive value. Therefore, we think that negative cTnT levels obtained during repetitive assays accurately predict which patients with PE will not have a complicated course.
References
Medical University in Warsaw Warsaw, Poland Institute of Lung Diseases Warsaw, Poland
Correspondence to: Piotr Pruszczyk, MD, PhD, Department of Internal Medicine, Hypertension and Angiology, Medical University in Warsaw, Banacha 1a, 02 097 Warsaw, Poland; e-mail: piotr.pruszczyk{at}amwaw.edu.pl
To the Editor:
There is growing evidence that the monitoring of biomarkers, including cardiac troponins and brain natriuretic peptides, is useful in the risk stratification of patients with acute pulmonary embolism (APE).1234 In our opinion, it will be especially useful in the management of patients who are initially hemodynamically stable, because shock or hypotension per se justifies prompt aggressive therapy.
We studied 64 patients with APEs who were normotensive on hospital admission (ie, systolic BP, > 90 mm Hg) and observed biochemical signs of myocardial injury (ie, cardiac troponin T level, > 0.01 ng/mL) in 50% of them.5 Indeed, we did not exclude patients with coronary artery disease (CAD), and it was objectively confirmed or clinically diagnosed in 30% of those patients in the group studied. We agree that CAD might facilitate myocardial injury and cardiac troponin T release in APE patients. The authors of previous articles2 also have pointed out that significant coronary artery stenosis may have been present in some patients included in their studies, thus limiting the specificity of the troponin measurements.
However, myocardial infarctions also have been reported67 in patients with APE and healthy coronary arteries. Moreover, we found no differences in the incidence of CAD among troponin-positive and troponin-negative groups, survivors, or nonsurvivors. It should be underlined that in our study detectable serum troponin levels predicted a fatal outcome and a complicated clinical course (ie, at least one of the following in-hospital events: death; thrombolysis; cardiopulmonary resuscitation; and use of IV catecholamine agents), while the presence of CAD did not. The in-hospital mortality rate in patients who experience submassive APEs has been reported to reach approximately 15%.89 Therefore, it is very important to identify among these patients a high-risk group that should be closely monitored and that may require thrombolysis. Interestingly, all eight in-hospital deaths that were observed in our study occurred in the troponin-positive group (in-hospital mortality rate, 25%).5 Thus, we believe that patients with signs of myocardial injury should be considered as potential candidates for aggressive therapy. However, a multicenter, prospective, randomized trial is needed to address the clinical value biomarkers and to define their optimal levels in a management strategy of patients with submassive APEs.
References
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