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WOS: 000414152700007, PubMed ID: 28248408, Background: The association between mortality and localization of central thrombus in hemodynamically stable patients with pulmonary embolism (PE) is unclear. Sufficient data are not available to help clinicians to select between low molecular weight heparin (LMWH), unfractionated heparin (UFH) and thrombolytics for the management of central thrombus. The present study aims to investigate whether central thrombus in the pulmonary artery affects 30-day mortality rate, and to compare the outcomes of different treatment approaches in patients with central thrombus. Methods: This multi-central, prospective, observational study included 874 hemodynamically stable patients with PE confirmed by multidetector computed tomography scan. The localization of the emboli was evaluated and categorized as central (saddle or at least one main pulmonary artery), lobar or distal. The primary study outcome was 30-day all-cause mortality. Results: Localization of the emboli was central in 319 (36.5%) patients, lobar in 264 (30.2%) and distal in 291 (33.2%) patients. Seventy-four (8.5%) patients died during the 30-day follow-up period. All-cause mortality rate was 11.9%, 6.8% and 6.2% in patients with central, lobar, and distal emboli, respectively (p < 0.001). Multivariate analysis did not show that hemodynamically stable central thrombus was an independent predictor of mortality. Additionally, mortality rate was not significantly different between UFH, LMWH and thrombolytic therapy groups. Conclusions: The present study showed that central thrombus was not an independent predictor of mortality in hemodynamically stable PE patients. LMWH and UFH were similarly effective in the treatment of this patient group.

Previous studies have indicated that high levels of urinary albumin excretion (UAE) are associated with an increased incidence of cardiovascular morbidity and mortality. This study examined the association between UAE and obstructive sleep apnea syndrome (OSAS). The study included 35 newly diagnosed OSAS patients and 11 nonapneic controls. Subjects with diabetes mellitus, hypertension, a history of renal failure, cardiac failure, coronary heart disease, collagen tissue disease, high serum creatinine, and urinary infection, and who use angiotensin-converting enzyme inhibitors and were women were excluded from the study. A single void morning urine sample at the baseline examination was used to measure UAE. There were no significant differences in the age, body mass index (BMI), and smoking habits of the OSAS patients and controls. UAE of the OSAS group was significantly higher than that of the control group (23.3 +/- 6.1 microg/min vs. 6.5 +/- 2.1 microg/min, respectively; P = 0.002). UAE was positively correlated to length of time spent at an oxygen saturation of90% (r = 0.503, P = 0.002) and BMI (r = 0.361, P = 0.033). Regression analyses (r (2) = 0.504, P0.0001) showed that the length of time spent at an oxygen saturation of90% (P0.0001) was risk factor for UAE, independent of age and BMI. Our study supports the notion that low-grade UAE is associated with non-hypertensive/non-diabetic OSAS, independent of age and BMI. Low-grade UAE may be a marker for subclinical vascular damage that predisposes OSAS patients to future cardiovascular disease.

Objective: Obesity and obstructive sleep apnea (OSA) and systemic inflammation may interact through biochemical pathways. Neopterin (NP) is a monocyte/macrophage activation marker produced by macrophages in response to interferon-gamma secreted by activated T lymphocytes. This study examines the association between NP, obesity and OSA. Patients and methods: The study included 22 newly diagnosed OSA (+) patients and 18 OSA patients. Subjects with history of coronary artery disease, transplant patients, history of alcohol and drug abuse, history of HIV and any other significant medical. illnesses such as active infections, autoimmune disease, malignancy, liver disease, pulmonary disease (COPD, asthma, ...), neuromuscular disease, patients on immunomodulating therapy or HMG-CoA reductase inhibitors were excluded. Results: There were no significant differences in age, body mass index (BMI), and smoking habits of the OSA (+) patients and OSA (-) patients. Serum NP levels did not show any significant difference between the OSA (+) patients and OSA (-) patients, however, NP levels were positively correlated with BMI (r = 0.320, p = 0.044). There was no significant correlation between NP and any of the polysomnographic parameters. The result of stepwise regression analyses (r 2 = 0.320, p < 0.001) showed that high serum NP levels (p = 0.004) and apnea-hypopnea index (AHI) were a risk factor for elevated Epworth sleepiness score, independent of BMI. Conclusion: We suggest that serum NP levels correlate with BMI. There was a significant relationship between serum NP levels and excessive daytime sleepiness in OSA patients.