Central Versus Peripheral Pulmonary Embolism: Analysis of the Impact on the Physiological Parameters and Long-term Survival.

BACKGROUND: Studies aimed at assessing whether the emboli lodged in the central pulmonary arteries carry a worse prognosis than more peripheral emboli have yielded controversial results. AIMS: To explore the impact on survival and long-term prognosis of central pulmonary embolism. PATIENTS AND METHODS: Consecutive patients diagnosed with acute symptomatic pulmonary embolism by means of computed tomography (CT) angiography were evaluated at episode index and traced through the computed system of clinical recording and following-up. Central pulmonary embolism was diagnosed when thrombi were seen in the trunk or in the main pulmonary arteries and peripheral pulmonary embolism when segmental or subsegmental arteries were affected. RESULTS: A total of 530 consecutive patients diagnosed with pulmonary embolism were evaluated; 255 patients had central pulmonary embolism and 275 patients had segmental or subsegmental pulmonary embolism. Patients with central pulmonary embolism were older, had higher plasma levels of N-terminal of the prohormone brain natriuretic peptide (NT-ProBNP), troponin I, D-dimer, alveolar-arterial gradient, and shock index (P < .001 for each one). Patients with central pulmonary embolism had an all-cause mortality of 40% while patients with segmental or subsegmental pulmonary embolism (PE) had an overall mortality of 27% and odds ratio of 1.81 [confidence interval (CI) 95% 1.16-1.9]. Survival was lower in patients with central PE than in patients with segmental or subsegmental pulmonary embolism, even after avoiding confounders (P = .018). CONCLUSIONS: Apart from a greater impact on hemodynamics, gas exchange, and right ventricular dysfunction, central pulmonary embolism associates a shorter survival and an increased long-term mortality.

N-terminal Pro-B type natriuretic peptide as long-term predictor of death after an acute pulmonary embolism.

BACKGROUND AND OBJECTIVE: After an acute pulmonary embolism few long-term prognostic factors have shown to be of practical use. We hypothesized that, as in heart failure, natriuretic peptides could serve as biomarkers of a late deleterious prognosis. PATIENTS AND METHODS: Consecutive patients admitted to an Internal Medicine ward diagnosed with acute pulmonary embolism were traced through the computerized system of clinical episodes of Navarra Health System and by telephone calls. On hospitalization, standard evaluation was made, previous history of cancer and cardiac disease was recorded, and N-terminal ProB-type natriuretic peptide (NT-ProBNP), D-dimer and Troponin I were measured. In the analysis all-causes death was considered. RESULTS: Two hundred and thirty-four patients were traced, median age 75 [interquartile range (IQR) 16] years old, women 51%. At a median time of 9.5 (IQR 29) months 52 (22%) patients had died, 38 (73%) dead patients had NT-ProBNP higher than 850 ng/L. NT-ProBNP in dead patients was 2.741 (IQR 7.420)ng/L and 662 (IQR 2.517)ng/L in survivors (p<0.001). Age (OR 4.37 CI 95% 1.04-1.16) and NT-ProBNP (OR 1.49 CI 95% 1-1.002) showed to be independent factors of mortality. Between the 3rd and 20th month after the diagnosis, a level of NT-ProBNP higher than 850 ng/L (sensitivity 0.86, specificity 0.45 and negative predictive value 0.92) was associated with a lower survival (p=0.019), hazard ratio 1.89, OR 7.67 (CI 95% 1.52-39.44) for this period. CONCLUSION: Besides the unchangeable age, plasma level of NT-ProBNP measured on acute pulmonary embolism could predict longer-term all-cause death.

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.

[Prognostic significance of the hepatopulmonary syndrome in liver cirrhosis]. / Significado pronóstico del síndrome hepatopulmonar en la cirrosis hepática.

BACKGROUND AND OBJECTIVE: The prognosis of hepatopulmonary syndrome (HPS) has been only rarely investigated. PATIENTS AND METHOD: We investigated the survival of 32 cirrhotic patients, 14 (44%) with HPS and 18 with a normal gaseous exchange (NGE), and the associated factors. RESULTS: During a mean (standard deviation) of 56 (27) months, 9 patients in the HPS group (relative risk: 0.64) and 4 patients in the NGE group (relative risk: 0.22) died. The odds ratio was 6.42 (p < 0.01; 95% confidence interval, 0.04-0.80). Patients in the HPS group died after 44 (31) months, while patients in the NGE group died 65 (21) months after inclusion (p < 0.05). Overall, 46% of deaths were liver related. Factors associated with death were the right to left shunting and the increased plasmatic renin levels. Of note, the plasmatic volume and diffusing capacity were protective. CONCLUSIONS: The coexistence of HPS worsens the prognosis in liver cirrhosis.