may be one of them [1,4]. We suggest that more patients in the elevated cTnI group could have received thrombolysis, decided by the clinicians in charge who were worried about potential RV dysfunction. And last, there was a higher prevalence (sometimes significant) of risk factor for coronary artery diseases (older patient, male sex, smoking, diabetes, hyperten- sion, history of coronary artery disease) in the elevated cTnI group. Thus, even if they excluded one obvious episode of acute coronary syndrome, we cannot exclude other underlying ongoing myocardial ischemia in this group. It could even be argued that any cause of hemodynamic instability (pulmonary embolism, severe sepsis, hypovolemia, hypoxia, etc) could have resulted in more patients with elevated cTnI in a group with more coronary risk factors and that elevated cTnI is a risk factor for complicated clinical course whatever the initial pathologic condition may be [5]. We especially strongly disagree with their conclusions. First, based on the methodological biases mentioned above, we believe that they cannot state that high cTnI should be guiding the decision on patient admission. Secondly to our knowledge, there are no current guidelines recommending that patients with PE without shock but RV failure should received thrombolysis; this is still a matter of debate [6-8]. In fact, we agree that cTnI is probably associated with echocardiographic RV dysfunction, which is generally associated with higher mortality [9]. However, we believe that the study by Aksay et al is not strong enough (because of lack of good methodology) to demonstrate it. Further research should focus on PE and biomarker (cTnI and natriuretic peptides) testing in patients with PE with RV failure but without shock and should be evaluated into formal guidelines and management [10,11]. Samuel Delerme MD Patrick Ray MD Department of Emergency Medicine and Surgery Centre Hospitalo-Universitaire (CHU) Pitie-Salpetriere Assistance-Publique Hopitaux de Paris (AP-HP) Universite Pierre et Marie Curie-Paris 6 75013 Paris, France E-mail address: patrick.ray@psl.aphp.fr doi:10.1016/j.ajem.2007.04.009 References [1] Aksay E, Yanturali S, Kiyan S. Can elevated troponin I levels predict complicated clinical course and inhospital mortality in patients with acute pulmonary embolism? Am J Emerg Med 2007;25:138-43. [2] Fischer JE, Bachmann LM, Jaeschke R. A readers' guide to the interpretation of diagnostic test properties: clinical example of sepsis. Intensive Care Med 2003;29:1043-51. [3] Maziere F, Medimagh S, Birolleau S, et al. Comparison of troponin I and NT-proBNP for risk stratification in patients with pulmonary embolism. European Journal of Emergency Medicine 2007 [in press]. [4] Jerjes-Sanchez C, Ramirez-Rivera A, de Lourdes M, et al. Streptoki- nase and heparin versus heparin alone in massive pulmonary embolism: a randomized controlled trial. J Thromb Thrombolysis 1995;2:227-9. [5] Lim W, Qushmaq I, Devereaux PJ, et al. Elevated cardiac troponin measurements in critically ill patients. Arch Intern Med 2006;166: 2446-54. [6] Goldhaber SZ. Thrombolytic therapy for patients with pulmonary embolism who are hemodynamically stable but have right ventri- cular dysfunction: pro. Arch Intern Med 2005;165:2197-9 [discussion 2204-2195]. [7] Konstantinides S, Geibel A, Heusel G, et al. Heparin plus alteplase compared with heparin alone in patients with submassive pulmonary embolism. N Engl J Med 2002;347:1143-50. [8] Thabut G, Logeart D. Thrombolysis for pulmonary embolism in patients with right ventricular dysfunction: con. Arch Intern Med 2005;165:2200-3 [discussion 2204-2205]. [9] Kostrubiec M, Pruszczyk P, Bochowicz A, et al. Biomarker-based risk assessment model in acute pulmonary embolism. Eur Heart J 2005;26: 2166-72. [10] Grifoni S, Olivotto I, Cecchini P, et al. Short-term clinical outcome of patients with acute pulmonary embolism, normal blood pressure, and echocardiographic right ventricular dysfunction. Circulation 2000;101:2817-22. [11] Logeart D, Lecuyer L, Thabut G, et al. Biomarker-based strategy for screening right ventricular dysfunction in patients with non-massive pulmonary embolism. Intensive Care Med 2007;33:286-92. Reply to cardiac troponin and risk stratification in pulmonary embolism Reviewer 1: I disagree with the author's concern about clinical features of patients presenting with pulmonary embolism (PE) to the emergency department (ED). I think emergency physicians commonly meet complicated patients with PE because those patients have more serious complaints and they tend to present to EDs rather than hospital polyclinics or the offices of private physicians. Therefore, it is not surprising that these patients revealed serious deviations in vital parameters and elevated cardiac troponin I (cTnI) levels more frequently. Moreover, the prevalence of elevated cTnI level in patients with PE is reported to be up to 52% in literature [1]. In addition, the study revealed frequent right ventricular dysfunction in patients with elevated cTnI; so they were mostly hemodynamically unstable. Mehta et al [2] reported a higher rate (33%) of cardiogenic shock in patients with elevated cTnI levels. Although there is no universally accepted clinical practice using thrombolytic drugs in hemodynamically stable patients with PE and right ventricular dysfunction on echocardiography, according to the clinical policy of the American College of Emergency Physicians on the critical issues in the evaluation and management of patients presenting with pulmonary embolism, emergency physicians should consider fibrinolytic therapy for those patients as a level C recommendation [3]. I agree with some of Dr Ray's comments. First of all, this study has methodological limitations inherent to all retro- spective studies. Myocardial ischemia cannot be excluded in the study patients. However, even if the study design was prospective, this is not an ethical approach because excluding acute coronary ischemia in patients with PE needs extra invasive investigation such as a coronary angiography during the critical period for these patients (this limitation, however, 236 Correspondence