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Communications to the Editor |

Cardiac Troponins in Acute Pulmonary EmbolismCardiac Troponins in Acute Pulmonary Embolism FREE TO VIEW

Piotr Pruszczyk, MD, PhD; Marcin Szulc, MD, PhD; Adam Torbicki, MD, PhD
Author and Funding Information

Affiliations: Medical University of Warsaw Institute for Lung Diseases Warsaw, Poland,  University of Wisconsin-Madison Medical School Madison, WI

Correspondence to: Piotr Pruszczyk, MD, PhD, Department of Internal Medicine and Hypertension, Medical University of Warsaw, Banacha 1a, 02-097 Warsaw, Poland; e-mail: piotr.pruszczyk@amwaw.edu.pl



Chest. 2002;122(6):2264-2265. doi:10.1378/chest.122.6.2264
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To the Editor:

It was with great interest that we read the review article on major pulmonary embolism (PE) that was published in CHEST by Wood (March 2002).1However, although the author emphasized the fact that transmural right ventricular (RV) infarctions were found at autopsy in some patients who died due to massive PEs despite unchanged coronary arteries,2he did not mention that plasma cardiac troponin levels may be elevated in approximately 30% of patients with PEs, which suggests the occurrences of ongoing myocardial damage.3 Moreover, Giannitsis et al3reported that although elevated cardiac troponin T (cTnT) levels often have been found in patients in the setting of shock or hypotension, this biochemical marker of myocardial injury is in fact an independent risk factor for fatal outcomes in patients with PEs. Increased plasma troponin levels were also commonly found in patients with preserved systemic systolic pressure but echocardiographic signs of RV strain.45

While the presence of shock or hypotension justifies aggressive therapy, patients with submassive PEs (ie, preserved systemic systolic pressure, but the presence of echocardiographic signs of RV overload) constitute a group in which, despite increased mortality, the use of thrombolytic treatment is controversial.67 Clearly, more precise criteria for the identification of patients with PEs in whom heparin therapy alone is not sufficient are needed.8 In the discussed review, it was suggested that the identification of residual deep venous thrombosis can be a discriminator of patients who may benefit from more aggressive treatment. However, recurrent PE is only one of the potential causes of a fatal outcome. Progressive irreversible RV heart failure may precipitate death. Our unpublished data indicate that repetitive cTnT measurements using a sensitive method (electrochemiluminescence method ECLIA; Roche Diagnostics GmbH; Mannheim, Germany) [detection limit, > 0.01 ng/mL] revealed myocardial injury in 50% of 64 hemodynamically stable patients with PEs and a systemic systolic pressure of at least 90 mm Hg. During the in-hospital period, eight patients died (in-hospital mortality rate, 12.5%). Interestingly, in all these patients elevated cTnT levels were found. Thus, the in-hospital mortality rate reached 25% in this group, contrasting with no mortality in patients without detectable cTnT levels despite having acute PEs (p = 0.048 [Fisher exact test]). Therefore, we believe that elevated plasma levels of cardiac troponins help to identify a subgroup of normotensive patients who are at high risk and who may benefit from more aggressive treatment.

Although no formal recommendations can be made, in our institutions patients with submassive PEs, defined according to European Society of Cardiology criteria,7 and concomitant elevated plasma cTnT levels, indicating myocardial injury, form a high-risk group and are considered for thrombolysis after determining the individual’s risk of bleeding. We suggest that the determination of plasma cardiac troponin levels may be helpful in therapeutic triage in patients with submassive PEs and that a long-due multicenter prospective trial assessing the value of thrombolysis in patients with submassive PEs also should addressly the clinical value of such a management strategy.

Grifoni, S, Olivotto, I, Cecchini, P, et al (2000) Short-term clinical outcome of patients with acute pulmonary embolism, normal blood pressure, and echocardiographic right ventricular dysfunction.Circulation101,2817-2822. [PubMed] [CrossRef]
 
Goldhaber, SZ, Haire, WD, Feldstein, ML, et al Alteplase versus heparin in acute pulmonary embolism: randomized trial assessing right-ventricular function and pulmonary perfusion.Lancet1993;341,507-511. [PubMed]
 
Hamel, E, Pacouret, G, Vincentelli, D, et al Thrombolysis or heparin therapy in massive pulmonary embolism with right ventricular dilation: results from a 128-patient monocenter registry.Chest2001;120,120-125. [PubMed]
 
Miller, GAH, Sutton, GC Acute massive pulmonary embolism: clinical and haemodynamic findings in 23 patients studied by cardiac catheterization and pulmonary arteriography.Br Heart J1970;32,518-523. [PubMed]
 
Carson, JL, Kelley, MA, Duff, A, et al The clinical course of pulmonary embolism.N Engl J Med1992;326,1240-1245. [PubMed]
 
Giannitisis, E, Muller-Bardoff, M, Kurowski, V, et al Independent prognostic value of cardiac troponin T in patients with confirmed pulmonary embolism.Circulation2000;102,211-217. [PubMed]
 
Meyer, T, Binder, L, Hruska, N, et al Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction.J Am Coll Cardiol2000;36,1632-1636. [PubMed]
 

Cardiac Troponins in Acute Pulmonary Embolism

To the Editor:

Contemporary risk stratification issues in patients with pulmonary embolism (PE) are ostensibly confined to patients who are hemodynamically stable with right ventricular dysfunction (HSRVD). This is because there is reasonable consensus that thrombolytic therapy is appropriate for hemodynamically unstable PE patients and that the mortality rate for hemodynamically stable PE patients without right ventricular dysfunction who have been treated with heparin is extremely low (0 to 1%).12 In combined studies13 requiring objective PE confirmation and echocardiography, the overwhelming majority (> 96%) of HSRVD patients will survive when treated with heparin alone. Hence, the specificity and positive predictive value of right ventricular dysfunction as a mortality predictor in HSRVD patients is extraordinarily poor. This has prompted the search to identify the determinants for the small subset of HSRVD patients whose conditions have the potential to deteriorate and to provide a discriminator for the use of thrombolytic therapy in such patients.

Residual deep venous thrombosis was proposed as a possible discriminator because recurrent PE is the primary cause of death (PE-related deaths) in patients surviving the first hour of an acute episode. “Progressive irreversible right ventricular failure precipitating death” in HSRVD patients has not been reported independently of recurrent PE and is unlikely. As early as 1970, Miller and Sutton4recognized that significant hemodynamic improvement occurs in ≤ 24 h after occurrence of the acute event, which is probably related to mechanical fracturing of the clot and the fibrinolytic system. In the Prospective Investigation of Pulmonary Embolism Diagnosis study,5 none of the almost 400 patients who were hemodynamically stable upon presentation died of progressive RV failure.

It is appealing to speculate that troponins could function as a discriminator for thrombolytic therapy in HSRVD patients. However, in the only reported study6to comment on outcome, only 53% of hemodynamically unstable patients and 35% of HSRVD patients were troponin-positive. Specific outcome data on the latter group were not provided. Troponin elevations also have been reported in 20% of hemodynamically stable PE patients with normal right ventricular function.7 Until further data are available, the use of troponins as a thrombolytic discriminator should remain speculative and should await the results of clinical trials that have been designed to examine the issue.

References
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.Circulation2000;101,2817-2822. [PubMed] [CrossRef]
 
Goldhaber, SZ, Haire, WD, Feldstein, ML, et al Alteplase versus heparin in acute pulmonary embolism: randomized trial assessing right-ventricular function and pulmonary perfusion.Lancet1993;341,507-511. [PubMed]
 
Hamel, E, Pacouret, G, Vincentelli, D, et al Thrombolysis or heparin therapy in massive pulmonary embolism with right ventricular dilation: results from a 128-patient monocenter registry.Chest2001;120,120-125. [PubMed]
 
Miller, GAH, Sutton, GC Acute massive pulmonary embolism: clinical and haemodynamic findings in 23 patients studied by cardiac catheterization and pulmonary arteriography.Br Heart J1970;32,518-523. [PubMed]
 
Carson, JL, Kelley, MA, Duff, A, et al The clinical course of pulmonary embolism.N Engl J Med1992;326,1240-1245. [PubMed]
 
Giannitisis, E, Muller-Bardoff, M, Kurowski, V, et al Independent prognostic value of cardiac troponin T in patients with confirmed pulmonary embolism.Circulation2000;102,211-217. [PubMed]
 
Meyer, T, Binder, L, Hruska, N, et al Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction.J Am Coll Cardiol2000;36,1632-1636. [PubMed]
 

Figures

Tables

References

Grifoni, S, Olivotto, I, Cecchini, P, et al (2000) Short-term clinical outcome of patients with acute pulmonary embolism, normal blood pressure, and echocardiographic right ventricular dysfunction.Circulation101,2817-2822. [PubMed] [CrossRef]
 
Goldhaber, SZ, Haire, WD, Feldstein, ML, et al Alteplase versus heparin in acute pulmonary embolism: randomized trial assessing right-ventricular function and pulmonary perfusion.Lancet1993;341,507-511. [PubMed]
 
Hamel, E, Pacouret, G, Vincentelli, D, et al Thrombolysis or heparin therapy in massive pulmonary embolism with right ventricular dilation: results from a 128-patient monocenter registry.Chest2001;120,120-125. [PubMed]
 
Miller, GAH, Sutton, GC Acute massive pulmonary embolism: clinical and haemodynamic findings in 23 patients studied by cardiac catheterization and pulmonary arteriography.Br Heart J1970;32,518-523. [PubMed]
 
Carson, JL, Kelley, MA, Duff, A, et al The clinical course of pulmonary embolism.N Engl J Med1992;326,1240-1245. [PubMed]
 
Giannitisis, E, Muller-Bardoff, M, Kurowski, V, et al Independent prognostic value of cardiac troponin T in patients with confirmed pulmonary embolism.Circulation2000;102,211-217. [PubMed]
 
Meyer, T, Binder, L, Hruska, N, et al Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction.J Am Coll Cardiol2000;36,1632-1636. [PubMed]
 
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.Circulation2000;101,2817-2822. [PubMed] [CrossRef]
 
Goldhaber, SZ, Haire, WD, Feldstein, ML, et al Alteplase versus heparin in acute pulmonary embolism: randomized trial assessing right-ventricular function and pulmonary perfusion.Lancet1993;341,507-511. [PubMed]
 
Hamel, E, Pacouret, G, Vincentelli, D, et al Thrombolysis or heparin therapy in massive pulmonary embolism with right ventricular dilation: results from a 128-patient monocenter registry.Chest2001;120,120-125. [PubMed]
 
Miller, GAH, Sutton, GC Acute massive pulmonary embolism: clinical and haemodynamic findings in 23 patients studied by cardiac catheterization and pulmonary arteriography.Br Heart J1970;32,518-523. [PubMed]
 
Carson, JL, Kelley, MA, Duff, A, et al The clinical course of pulmonary embolism.N Engl J Med1992;326,1240-1245. [PubMed]
 
Giannitisis, E, Muller-Bardoff, M, Kurowski, V, et al Independent prognostic value of cardiac troponin T in patients with confirmed pulmonary embolism.Circulation2000;102,211-217. [PubMed]
 
Meyer, T, Binder, L, Hruska, N, et al Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction.J Am Coll Cardiol2000;36,1632-1636. [PubMed]
 
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