Abstract
Introduction: Whether in patients with acute central sub-massive or non-massive pulmonary embolism, mild troponin I increase (> 0.03 μg/L) predicts in-hospital occurrence of hemodynamic instability and death independent to prognostically relevant clinical, laboratory and echocardiographic information is not fully established. Methods and results: We evaluated consecutively patients admitted to the Emergency Room for pulmonary embolism; those in stable hemodynamics in whom central pulmonary embolism was confirmed by spiral-computed tomography were recruited. All participants underwent standardized study protocol, including clinical and diagnostic evaluation for assessment of severity of pulmonary embolism; therapy was established accordingly; troponin I was measured, but treatment protocol was not affected by knowledge of troponin I levels. Of 90 patients enrolled in the study, 33 (37%) developed hemodynamic instability during hospitalization (on average, 90 h ± 20 from admission). Troponin I was > 0.03 μg/L in 56% of the study population at admission, and predicted occurrence of hemodynamic instability during hospitalization (adjusted hazard ratio 9.8, 95% confidence interval 1.2-79.2), independent to age, gender, co-morbidity, systolic blood pressure, CK-MB, echocardiographic right ventricular dysfunction and other covariates. Twelve patients died during hospitalization (mean time to event 107 h ± 24 from admission); troponin I > 0.03 μg/L predicted mortality in univariate analysis, but not after accounting for age, sex and clinical variables. Nevertheless, higher troponin as continuous variable correlated with higher likelihood of in-hospital death (adjusted likelihood ratio 2.2/μg/L, 95% confidence interval 1.1-4.3) in multivariate analysis. In a further multivariate model, CK-MB predicted mortality independent of covariates and troponin I. Conclusions: In patients with acute central sub-massive or non-massive pulmonary embolism, even mild increase in troponin I > 0.03 μg/L may provide relevant short-term prognostic information independent to clinical, laboratory and echocardiographic data.
| Original language | English |
|---|---|
| Pages (from-to) | 351-357 |
| Number of pages | 7 |
| Journal | International Journal of Cardiology |
| Volume | 124 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Mar 14 2008 |
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Keywords
- Outcome
- Pulmonary embolism
- Troponin
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Increased troponin I predicts in-hospital occurrence of hemodynamic instability in patients with sub-massive or non-massive pulmonary embolism independent to clinical, echocardiographic and laboratory information. / Gallotta, Giovanni; Palmieri, Vittorio; Piedimonte, Vincenzo; Rendina, Domenico; De Bonis, Silvana; Russo, Vittorio; Celentano, Aldo; Di Minno, Matteo N D; Postiglione, Alfredo; Di Minno, Giovanni.
In: International Journal of Cardiology, Vol. 124, No. 3, 14.03.2008, p. 351-357.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Increased troponin I predicts in-hospital occurrence of hemodynamic instability in patients with sub-massive or non-massive pulmonary embolism independent to clinical, echocardiographic and laboratory information
AU - Gallotta, Giovanni
AU - Palmieri, Vittorio
AU - Piedimonte, Vincenzo
AU - Rendina, Domenico
AU - De Bonis, Silvana
AU - Russo, Vittorio
AU - Celentano, Aldo
AU - Di Minno, Matteo N D
AU - Postiglione, Alfredo
AU - Di Minno, Giovanni
PY - 2008/3/14
Y1 - 2008/3/14
N2 - Introduction: Whether in patients with acute central sub-massive or non-massive pulmonary embolism, mild troponin I increase (> 0.03 μg/L) predicts in-hospital occurrence of hemodynamic instability and death independent to prognostically relevant clinical, laboratory and echocardiographic information is not fully established. Methods and results: We evaluated consecutively patients admitted to the Emergency Room for pulmonary embolism; those in stable hemodynamics in whom central pulmonary embolism was confirmed by spiral-computed tomography were recruited. All participants underwent standardized study protocol, including clinical and diagnostic evaluation for assessment of severity of pulmonary embolism; therapy was established accordingly; troponin I was measured, but treatment protocol was not affected by knowledge of troponin I levels. Of 90 patients enrolled in the study, 33 (37%) developed hemodynamic instability during hospitalization (on average, 90 h ± 20 from admission). Troponin I was > 0.03 μg/L in 56% of the study population at admission, and predicted occurrence of hemodynamic instability during hospitalization (adjusted hazard ratio 9.8, 95% confidence interval 1.2-79.2), independent to age, gender, co-morbidity, systolic blood pressure, CK-MB, echocardiographic right ventricular dysfunction and other covariates. Twelve patients died during hospitalization (mean time to event 107 h ± 24 from admission); troponin I > 0.03 μg/L predicted mortality in univariate analysis, but not after accounting for age, sex and clinical variables. Nevertheless, higher troponin as continuous variable correlated with higher likelihood of in-hospital death (adjusted likelihood ratio 2.2/μg/L, 95% confidence interval 1.1-4.3) in multivariate analysis. In a further multivariate model, CK-MB predicted mortality independent of covariates and troponin I. Conclusions: In patients with acute central sub-massive or non-massive pulmonary embolism, even mild increase in troponin I > 0.03 μg/L may provide relevant short-term prognostic information independent to clinical, laboratory and echocardiographic data.
AB - Introduction: Whether in patients with acute central sub-massive or non-massive pulmonary embolism, mild troponin I increase (> 0.03 μg/L) predicts in-hospital occurrence of hemodynamic instability and death independent to prognostically relevant clinical, laboratory and echocardiographic information is not fully established. Methods and results: We evaluated consecutively patients admitted to the Emergency Room for pulmonary embolism; those in stable hemodynamics in whom central pulmonary embolism was confirmed by spiral-computed tomography were recruited. All participants underwent standardized study protocol, including clinical and diagnostic evaluation for assessment of severity of pulmonary embolism; therapy was established accordingly; troponin I was measured, but treatment protocol was not affected by knowledge of troponin I levels. Of 90 patients enrolled in the study, 33 (37%) developed hemodynamic instability during hospitalization (on average, 90 h ± 20 from admission). Troponin I was > 0.03 μg/L in 56% of the study population at admission, and predicted occurrence of hemodynamic instability during hospitalization (adjusted hazard ratio 9.8, 95% confidence interval 1.2-79.2), independent to age, gender, co-morbidity, systolic blood pressure, CK-MB, echocardiographic right ventricular dysfunction and other covariates. Twelve patients died during hospitalization (mean time to event 107 h ± 24 from admission); troponin I > 0.03 μg/L predicted mortality in univariate analysis, but not after accounting for age, sex and clinical variables. Nevertheless, higher troponin as continuous variable correlated with higher likelihood of in-hospital death (adjusted likelihood ratio 2.2/μg/L, 95% confidence interval 1.1-4.3) in multivariate analysis. In a further multivariate model, CK-MB predicted mortality independent of covariates and troponin I. Conclusions: In patients with acute central sub-massive or non-massive pulmonary embolism, even mild increase in troponin I > 0.03 μg/L may provide relevant short-term prognostic information independent to clinical, laboratory and echocardiographic data.
KW - Outcome
KW - Pulmonary embolism
KW - Troponin
UR - http://www.scopus.com/inward/record.url?scp=39749100597&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=39749100597&partnerID=8YFLogxK
U2 - 10.1016/j.ijcard.2006.03.096
DO - 10.1016/j.ijcard.2006.03.096
M3 - Article
VL - 124
SP - 351
EP - 357
JO - International Journal of Cardiology
JF - International Journal of Cardiology
SN - 0167-5273
IS - 3
ER -