Use of medical therapies before pulmonary endarterectomy in chronic thromboembolic pulmonary hypertension patients with severe hemodynamic impairment.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare complication of acute pulmonary embolism, characterized by non-resolving fibro-thrombotic obstructions of large pulmonary arteries. Pulmonary endarterectomy (PEA) is the treatment of choice for the disease, significantly improving survival. Patients with worse hemodynamic profile have worse prognosis after surgery, raising the question of whether the use of medical therapy prior to surgery to optimize hemodynamics could improve outcomes. The aim of this study was to evaluate the role of medical therapy pre-PEA, according to the hemodynamic profile at the diagnosis. We retrospectively analyzed all patients submitted to PEA, from January 2013 to December 2017. Functional, clinical and hemodynamic data were collected to evaluate the main prognostic determinants. Patients were stratified according to the hemodynamic severity and use of targeted therapies prior to surgery. A total of 108 patients were included. Thirty-five patients (32,4%) used targeted therapy pre-PEA. The use of medical therapy delayed the surgical procedure by about 7 months. There was no difference in overall survival between patients that received targeted therapy and those treated only with supportive therapy (87.8% vs 80.3%, respectively, p = 0.426). Nevertheless, when analyzing the group of patients with severe hemodynamic impairment, defined by low cardiac output(<3.7L/min) at baseline, patients treated with targeted therapies presented a significantly better one-year survival. In higher-risk CTEPH patients, characterized by the presence of low cardiac output, the use of targeted therapies prior to PEA was associated with better outcome, suggesting a potential role for pre-operative use of medical treatment in this particular subgroup.

Pleurodesis induced by talc or silver nitrate: evaluation of collagen and elastic fibers in pleural remodeling.

This study evaluated the extracellular matrix (collagen and elastic fibers) in pleurodesis induced by intrapleural talc (TL) or silver nitrate (SN). Study subjects were 420 rabbits divided into two groups and sacrificed from 15 min to 12 months after the injection of the sclerosing agents at intervals previously defined. Pleural adhesions and fibrosis were graded (0-4), and the collagen and elastin were quantified. The maximum score of the pleural adhesions was observed two months after TL (2.80 +/- 0.99) and 15 days after SN (3.75 +/- 0.25). More intense pleural adhesions were observed in the SN group from day 5 (p < 0.05). Pleural thickness and pleural fibrosis were, in general, significantly higher after SN (p < 0.05). Increased deposition of collagen and elastin was observed in both groups but was more evident in the SN group. In the TL group, a linear correlation was observed between pleural adhesions and fibrosis (r = 0.775), between pleural adhesions and collagen (r = 0.779), and between fibrosis and collagen (r = 0.709). In the SN group, these correlations were acceptable (r = 0.605, 0.665, and 0.663). The elastin presented a correlation of 0.707 (p < 0.001) in the TL group and of 0.564 (p < 0.001) in the SN group. In conclusion, intrapleural 0.5% silver nitrate and talc (400 mg/kg) are effective in the induction of pleurodesis. However, the intensity of adhesions and the richness of collagen after SN, in combination with the early onset of tissue remodeling, demonstrate the local superiority of this agent. Considering the easy availability and instillation, the low cost, and the absence of important side effects, silver nitrate might be considered as a sclerosing agent to induce pleurodesis in humans.

Effects of air pollution on blood pressure and heart rate variability: a panel study of vehicular traffic controllers in the city of São Paulo, Brazil.

AIMS: Evaluating the effects of air pollution on Sao Paulo city's vehicular traffic controllers by means of risk indicators for cardiovascular diseases. METHODS AND RESULTS: Twenty-four hour blood pressure recordings and an electrocardiogram were obtained in 48 healthy, non-smoking vehicular traffic controllers, aged 31-55 years, during three periods: winter 2000, summer 2001, and winter 2001. Effects of air pollutants on the outcomes were estimated using linear regression based on generalized estimated equations, controlling for age, body mass index, humidity, and temperature. An interquartile range (IQR) increase in CO (1.1 p.p.m.) was associated with increases of 2.6 mmHg (95% CI 1.0, 4.2), 1.8 mmHg (95% CI 0.8, 2.8), and 2.4 mmHg (95% CI 1.1, 3.6) in systolic, diastolic, and mean 24 h ambulatory blood pressures. SO(2) also had relevant effects on blood pressure. On heart rate variability, an IQR increase of SO2 (9.6 microg/m3) was negatively associated with the standard deviation (SD) of normal RR intervals (SDNN) -7.93 ms (95% CI -15.3, -0.6). CONCLUSION: This study supplies biological plausibility for observational studies on air pollution-related cardiovascular morbidity and mortality.

Heterogeneous remodeling of lung vessels in idiopathic pulmonary fibrosis.

Recently, several reports suggest differences in the vascularization of the various histopathologic patterns of parenchymal remodeling seen in usual interstitial pneumonia (UIP). In this study, we sought to validate the importance of vascular remodeling in patients with idiopathic pulmonary fibrosis (IPF) and to examine the relationship between vascular remodeling and parenchymal remodeling or pulmonary function. Open lung biopsies were performed in 57 patients with IPF, and vascular changes in alternating areas of parenchymal remodeling (UIP histologic patterns) were studied. Quantitative analysis of the internal area, internal perimeter, wall thickness, and surrounding cellularity of medium or large pulmonary arteries, as well as their distribution according to air/parenchymal ratios, was performed. Semiquantitative analysis also was used to determine the grade of vascular occlusion. An inverse association was found between vascularization and UIP parenchymal remodeling (p < 0.05); that is, the decreased internal luminal area and perimeter as well as the increased wall thickness run in parallel with progression from alveolar collapse toward severe mural-organizing fibrosis with honeycombing. Vascular regression (diminished internal area and perimeter of vessels) was also associated with higher FEV(1), FVC, and RV values (r = 0.48, p< 0.05), reflecting a tight relationship between vascular remodeling and pulmonary function. A progressive regression of vascularization, reflected by different degrees of luminal occlusion after vascular remodeling, coincided with parenchymal remodeling (alveolar collapse, mural-organizing fibrosis, and honeycombing). This vascular regression may be responsible for the impaired wound healing and progressive fibroproliferation found in patients with IPF. Further studies are needed to determine whether this relationship is causal or consequential.