Utilidad clínica de la troponina I en la tromboembolia pulmonar / Clinical usefulness of troponin I in acute pulmonary embolism

Fundamento: La troponina cardíaca I (cTnI) se considera un marcador sensible de daño miocárdico en la tromboembolia pulmonar (TEP) aguda con implicaciones pronósticas, aunque los valores considerados patológicos son variables. Pacientes y método: En pacientes consecutivos con TEP objetivamente demostrada por angiografía pulmonar con tomografía computarizada (TC) helicoidal se midieron los valores de la cTnI. Los pacientes se clasificaron radiológicamente como TEP central o periférica y se clasificaron hemodinámicamente como TEP masiva, submasiva o no masiva (según las cifras de presión arterial sistólica y pro-B de péptido natriurético). Se constató el retraso diagnóstico (RD) desde el inicio de la clínica y la mortalidad a los 30 días. Resultados: Se evaluaron 164 pacientes (edad media de 70 años [desviación estándar {DE} de 15] con 76 varones [46%]). El RD fue de 5 días (diferencia intercuartílica [DIQ] de 12) (mediana de la cTnI con RD superior a 5 días de 0,003¼g/l [DIQ de 0,103] y con RD inferior a 5 días de 0,05¼g/l [DIQ de 0,096]; p< 0,05). Un valor de la cTnI superior o igual a 0,5 ocurrió en 11 pacientes (7%).Resultados: Los valores de la cTnI superiores o iguales a 0,03¼g/l se asociaron a TEP central (AUC [area under the curve área bajo la curva ] ROC [receiver operating characterisric curva de eficacia diagnóstica ] de 0,7059; intervalo de confianza [IC] del 95%: 0,6643 a 0,7475; sensibilidad de 0,75; especificidad de 0,69; valor predictivo positivo [VPP] de 0,75, y valor predictivo negativo [VPP] de 0,69) y se asociaron a TEP masiva y submasiva (AUC ROC de 0,7685; sensibilidad de 0,86; especificidad de 0,66; VPP de 0,72, y VPN de 0,82), pero no a mortalidad (AUC ROC de 0,5394). Resultados: En el análisis de regresión logística, los valores de la cTnI no fueron predictores independientes de TEP central, de TEP masiva o submasiva ni de muerte a los 30 días

Background: Troponin-I (cTp-I) is considered a sensitive biomarker of myocardial injury in acute pulmonary thromboembolism (PE) with prognosis implications, though abnormal levels vary among reports. Patients and Methods: cTp-I was measured in consecutive patients objectively diagnosed of PE by means of pulmonary angiography made with helicoidal CT. Patients were classified radiologically as central or peripheral PE and hemodynamically as massive, submassive or non-massive according to the pulmonary vessel occluded and systolic blood pressure and ProBNP levels respectively. We checked also the delay in diagnosis (DD) and 30-days all-causes mortality rate. Results: We evaluated 164 patients; the mean age was 70 (15) years, males: 76 (46%). Median DD was 5 [interquartile range (IQ) 12) days. Median cTp-I in patients with DD>5 was 0.003¼g/L (IQ 0.072)¼g/L while in patients with DD<5 was 0.05¼g/L (IQ 0.096) (p<0.05). cTp-I higher than 0.5¼g/L occurred in 11 (7%) patients. Results: Levels of cTp-I higher than 0.03¼g/L were associated with central PE, (AUROC 0.7059 CI95% 0.6643 0.7475, sensitivity 0.75, specificity 0.69, PPV 0.75 and NPV 0.69) and massive and submassive PE (AUROC 0.7685, CI95% 0.7288 0.8082 sensitivity 0.86, specificity 0.66, PPV 0.72 and NPV 0.82), but they were not associated with mortality (AUROC 0.5394).Results: In a multivariate analysis cTp-I did not show to be an independent predictor of central, massive and submassive PE or all causes death. Conclusions: In this study cTp-I was not a proper biomarker of the size of pulmonary vessel occluded, the degree of hemodynamic derangement or short-term mortality. The delay in diagnosis could influence the usefulness of cTp-I

[Clinical usefulness of troponin I in acute pulmonary embolism]. / Utilidad clínica de la troponina I en la tromboembolia pulmonar.

BACKGROUND: Troponin-I (cTp-I) is considered a sensitive biomarker of myocardial injury in acute pulmonary thromboembolism (PE) with prognosis implications, though abnormal levels vary among reports. PATIENTS AND METHODS: cTp-I was measured in consecutive patients objectively diagnosed of PE by means of pulmonary angiography made with helicoidal CT. Patients were classified radiologically as central or peripheral PE and hemodynamically as massive, submassive or non-massive according to the pulmonary vessel occluded and systolic blood pressure and ProBNP levels respectively. We checked also the delay in diagnosis (DD) and 30-days all-causes mortality rate. RESULTS: We evaluated 164 patients; the mean age was 70 (15) years, males: 76 (46%). Median DD was 5 [interquartile range (IQ) 12) days. Median cTp-I in patients with DD>5 was 0.003microg/L (IQ 0.072)microg/L while in patients with DD<5 was 0.05microg/L (IQ 0.096) (p<0.05). cTp-I higher than 0.5microg/L occurred in 11 (7%) patients. Levels of cTp-I higher than 0.03microg/L were associated with central PE, (AUROC 0.7059 CI95% 0.6643-0.7475, sensitivity 0.75, specificity 0.69, PPV 0.75 and NPV 0.69) and massive and submassive PE (AUROC 0.7685, CI95% 0.7288-0.8082 sensitivity 0.86, specificity 0.66, PPV 0.72 and NPV 0.82), but they were not associated with mortality (AUROC 0.5394). In a multivariate analysis cTp-I did not show to be an independent predictor of central, massive and submassive PE or all causes death. CONCLUSIONS: In this study cTp-I was not a proper biomarker of the size of pulmonary vessel occluded, the degree of hemodynamic derangement or short-term mortality. The delay in diagnosis could influence the usefulness of cTp-I.