Residual pulmonary thromboemboli after acute pulmonary embolism.

BACKGROUND: After an acute pulmonary embolism (PE), the complete resolution of thromboemboli may not be routinely achieved. The rate of persistence may depend on the time and the diagnostic technique used for evaluation. PATIENTS AND METHODS: Patients were diagnosed with acute PE by means of computed tomography angiography (CTA). While they were receiving anticoagulant therapy, a second CTA was used to explore the rate of persistence of residual thromboemboli. During the initial episode, the plasma levels of Troponin I and natriuretic peptide, patient demographics, and hemodynamic and gas exchange data were evaluated as risk factors for persistence of pulmonary thromboemboli. RESULTS: In this study 166 patients were diagnosed. A second CTA was not made in 46 (28%) patients for different reasons. In 120 (72%) patients a second CTA was made 4.5 [SD2.34] months after the initial episode (range 2-12 months). Complete clearance of thrombi occurred in 89 (74%, 95% CI 65-81) patients. Residual thrombi remained in 31 (26%, 95% CI 18-34) patients. In 6%, 13% and 81% of the patients the size of the residual thrombi was greater, similar to and smaller than initially diagnosed, respectively. The risk factors for residual thrombi included the thrombotic burden (OR 1.95), the alveolar to arterial difference of oxygen (OR 1.64), and the clinical antecedents of venous thromboembolic disease (OR 0.65). CONCLUSIONS: After 4.5 months of anticoagulant therapy, residual pulmonary thromboemboli persisted in 26% of the patients. The risk factors for residual thromboemboli include a greater initial thrombotic burden, a deeper gas exchange disturbation and a history of previous venous thromboembolism.

[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.

N-terminal pro-B-type natriuretic peptide predicts the burden of pulmonary embolism.

BACKGROUND: In acute pulmonary embolism (PE), brain natriuretic peptides are markers of right ventricular dysfunction and they could point out the size of the occluded pulmonary vessel. METHODS: N-terminal pro-B-type natriuretic peptide (BNP) was measured in 93 consecutive outpatients diagnosed with acute PE by means of helical computed tomography. Central PE was diagnosed when thrombotic material was seen in the main trunk or right or left main branches of the pulmonary artery, and peripheral PE was diagnosed when thrombi were seen exclusively in segmental or subsegmental arteries. RESULTS: Central PE occurred in 51 (55%) patients and peripheral PE in 42 (45%). Plasma level of pro-BNP greater than 500 ng/L was independently associated with central PE. The area under the receiver operating characteristic curve was 0.753 (CI 95% 0.700-0.806), sensitivity 0.82 (CI 95% 0.69-0.91), specificity 0.67 (CI 95% 0.50-0.79), positive predictive value 0.75 (CI 95% 0.61-0.85), and negative predictive value 0.76 (CI 95% 0.58-0.87). Six (6%) patients died, 3 from PE, 2 from brain hemorrhage, and 1 from advanced gallbladder cancer. N-terminal pro-BNP level was greater than 500 ng/L in all patients who died. The area under receiver operating characteristic curve for death was 0.712 (CI 95% 0.635-0.789), sensitivity 0.10 (CI 95% 0.04-0.22), specificity 1 (CI 95% 0.88-1), positive predictive value 1 (CI 95% 0.51-1), and negative predictive value 0.42 (CI 95% 0.32-0.53). CONCLUSIONS: Preliminary data suggest that N-terminal pro-BNP levels higher than 500 ng/L could serve as indicator of the burden of PE and perhaps as a predictor of death.

[Hepatopulmonary syndrome: relationship with liver dysfunction and systemic hemodynamic disorder]. / Síndrome hepatopulmonar: relación con el grado de disfunción hepática y el trastorno hemodinámico de la cirrosis hepática.

BACKGROUND AND OBJECTIVE: The hepatopulmonary syndrome (HPS) causes an increased alveolar to arterial gradient of oxygen and in advanced phases hypoxemia, as the result of pulmonary vasodilation. In liver cirrhosis, it has been demonstrated the existence of splachnic vasodilation and also in other vascular beds. Our main objectives were to know the hemodynamic status, the renal function and the condition of some humoral systems in patient diagnosed of HPS. PATIENTS AND METHOD: We studied consecutively 32 cirrhotic patients Divided in two groups, a group of 18 cirrhotic patients with normal gaseous exchange (NGE), and another group of 14 cirrhotic patients diagnosed of HPS by contrast-enhanced transthoracic echocardiography and/or lung and brain scintigraphy with 99Tc albumin macroaggregates. They were all in rest in bed, upon alcohol and tobacco abstinence and on a diet of 50 mEq of sodium. Cardiovascular drugs were all withheld during 4 days in order to reach steady state. RESULTS: Patients of the HPS group were characterized by a more advanced index of Child-Pugh and presence of clubbing and vascular spiders. They presented a greater degree of hypoxemia in a sitting position, greater hypocapnia and smaller transference factor values (TLCO). They also showed a hyperkinetic circulatory condition characterized by smaller arterial blood pressure, greater cardiac index, smaller vascular resistances and greater femoral flows, with smaller clearance of creatinine, elimination of urinary sodium, urinary volume/24 h and an increased plasmatic volume, accompanied with a greater activation of the renin-angiotensin-aldosterone axis and a greater urinary elimination of nitrites and nitrates. CONCLUSIONS: The pulmonary vasodilation that explains the HPS is a constitutive part of the systemic vasodilation occurring in liver cirrhosis, and it is related to the degree of liver dysfunction as measured by the classification of Child-Pugh. The greater activation of the renin-aldosterone system and the rise of the plasmatic volume express a highest grade of arterial underfilling caused by an increment in the nitric oxide production.