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Karin Janata Universitätsklinik für Notfallmedizin,
Allgemeines Krankenhaus Wien, Währinger Gürtel 18-20/6D, A-1090
Vienna, Austria Correspondence to: M
Mullner
marcus.muellner{at}univie.ac.at
Right ventricular function is an important prognostic
factor for pulmonary embolism.1 Massive pulmonary embolism
may lead to right ventricular failure, reduced left ventricular output, and even death.2 Cardiac troponins are routinely applied
markers of minor and major myocardial damage in patients with acute
coronary syndromes. In small case series, troponin concentrations were raised in patients with massive pulmonary embolism.
3 4
The role of troponin as a prognostic factor is, however, unclear. We
assessed the association between serum concentrations of cardiac troponin T and severity of pulmonary embolism as well as the role of
troponin T as a predictor of mortality.
We assessed 136 consecutive patients who were admitted to the
emergency department of a tertiary care university hospital between
December 1999 and November 2001 with pulmonary embolism, confirmed by
computed tomography or scintigraphy. Two patients with terminal illness
and seven patients admitted after cardiac arrest out of hospital were
excluded. In 106 patients troponin concentrations were determined in
the first 12 hours after admission (Elecsys 2010; Roche, Mannheim,
Germany). The severity of the event was classified according to the
grading system by Grosser (see table A on bmj.com).5 Right
ventricular strain in the electrocardiogram was defined as right bundle
branch block, T wave inversion in precordial leads, or
S1Q3T3 pattern. We used Spearman's
correlation and the Wilcoxon rank sum test and constructed a receiver
operating characteristic curve based on sensitivities and
specificities, using various troponin values as cut offs to determine
mortality in hospital. We used routine data; studies using such data
are not routinely reviewed by the local ethical review board.
The median age of patients was 60 (interquartile range 43-72)
years; 74 (58%) were female. Six had fulminant pulmonary embolism, in
37 it was massive, in 62 it was submassive, and in one it was minor.
With increasing severity of pulmonary embolism troponin concentrations
also increased (r=0.56, P<0.001). The median troponin concentration in patients with signs of right ventricular strain in the
electrocardiogram was 0.03 ng/ml (interquartile range <0.01 to 0.06)
and in patients without these signs <0.01 ng/ml (<0.01 to <0.01,
P<0.001). Ninety three patients underwent echocardiography, of whom 63 (68%) had signs of right ventricular strain1; the median
troponin concentration in patients with signs of right ventricular
strain was 0.03 ng/ml compared with <0.01 ng/ml (P<0.001) in patients
without right ventricular strain.
Five of 106 patients with troponin measurements died in hospital (5%);
troponin concentrations were higher in patients who died than in
survivors (0.18 ng/ml (0.09 to 0.18) v <0.01 ng/ml (<0.01
to 0.03), P<0.001). A cut-off value for troponin of 0.09 ng/ml was a
suitable predictor for death in hospital (figure). The area under the
curve was 0.92 (95% confidence interval 0.82 to 1.0), and the cut-off
value had a sensitivity of 0.80 (0.49 to 1.0) and a specificity of 0.92 (0.87 to 0.97). The negative predictive value was 0.99 (0.93 to 1.00)
and the positive predictive value 0.34 (0.10 to
0.59).
Raised concentrations of troponin T are associated with a higher
in-hospital mortality in patients with pulmonary embolism. The major
limitation of this study is that we do not know in how many patients
pulmonary embolism remained undetected. We assume that missed cases had
only minor symptoms and probably a good prognosis. Another limitation
is that in 21 of the 127 eligible patients (17%) troponin was not
measured. Patients with missing troponin values were younger (median 47 years v 60 years, P=0.014). The proportion of
missing troponin values was similar in survivors and non-survivors
(17%). Overall, we believe that this selection bias does not
invalidate our conclusion. Whether troponin measurement can be used as
a tool for clinical decision making
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Participants, methods, and results
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Receiver operating characteristic curve of cardiac troponin T and
mortality. The values at the curve indicate the respective
concentrations of cardiac troponin T
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Participants, methods, and...
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for example, deciding whether to
give thrombolytic treatment
needs confirmation in larger prospective studies.
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Acknowledgments |
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Contributors: KJ collected the data for the pulmonary embolism registry, interpreted the data, and wrote the article. MH interpreted the data and wrote the article. ANL interpreted the data and critically revised the article. MM analysed and interpreted the data, wrote the article, and is, together with KJ, the guarantor for this paper.
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Footnotes |
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Funding: None.
Competing interests: MM works part time as an editor with the BMJ but had nothing to do with the peer review of this paper.
An extra table appears on
bmj.com
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References |
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| 1. |
Kasper W, Konstantinides S, Geibel A, Tiede N, Krause T, Just H.
Prognostic significance of right ventricular afterload stress detected by echocardiography in patients with clinically suspected pulmonary embolism.
Heart
1997;
77:
346-349 |
| 2. | Lualdi JC, Goldhaber SZ. Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. Am Heart J 1995; 130: 1276-1282[CrossRef][Web of Science][Medline]. |
| 3. |
Meyer T, Binder L, Hruska N, Luthe H, Buchwald AB.
Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction.
J Am Coll Cardiol
2000;
36:
1632-1636 |
| 4. |
Giannitsis E, Muller-Bardorff M, Kurowski V, Weidtmann B, Wiegand U, Kampmann M, et al.
Independent prognostic value of cardiac troponin T in patients with confirmed pulmonary embolism.
Circulation
2000;
102:
211-217 |
| 5. |
Grosser KD.
Lungenembolie. Erkennung und differentialtherapeutische Probleme [Pulmonary embolism problems in identifying and treating the condition].
Internist
1980;
21:
273-282[Medline].
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(Accepted 15 August 2002)
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