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Cardiopulmonary Exercise Testing (CPET) is a standardized, non-invasive procedure assessing pulmonary, cardiovascular, hematopoietic, and skeletal muscle functions during a symptom-limited test. Few studies have examined whether CPET is of prognostic value in Systemic Sclerosis (SSc), a disease characterized by highly increased cardiorespiratory morbidity and mortality. To examine the prognostic value of CPET in SSc patients without baseline pulmonary hypertension (PH). Sixty-two consecutive SSc patients underwent CPET, Pulmonary Function Tests (PFTs) and echocardiography at baseline. Four patients with Right Ventricular Systolic Pressure ≥ 40 mmHg, were excluded. Participants repeated PFTs approximately every 3 years. At the end of the follow-up period [median (IQR): 9.79 (2.78) years] patient vital status was recorded. Cox Regression analysis was used to identify predictors of deterioration of PFTs and 10-year survival. Median (IQR) age of 58 patients (90% women) at baseline was 54.0 (15.0) years, whereas 10-year survival was 88%. Baseline respiratory Oxygen uptake (VO2max) predicted PFT deterioration, defined either as a decline in FVC ≥ 10% or a combined decline in FVC 5%-9% plus DLCO ≥ 15%, during follow-up, after correction for age, gender and smoking status (HR: 0.874, 95%CI: 0.779–0.979, p = 0.021). In addition, lower baseline VO2max (HR = 0.861, 95%CI:0.739–1.003, p = 0.054) and DLCO (HR = 0.957, 95%CI: 0.910–1.006 p = 0.088), as well as male gender (HR = 5.68, 95%CI: 1.090–29.610 p = 0.039) and older age (HR = 1.069, 95%CI: 0.990–1.154, p = 0.086) were associated, after adjustment, with an increased risk for death. In the absence of baseline PH, CPET indices may predict pulmonary function deterioration and death in SSc patients during a nearly 10-year follow-up period.

Obstructive sleep apnea syndrome (OSAS) is common in adult population and it is associated with increased morbidity and mortality, especially due to cardiovascular disease (CVD). Both diagnosis, based on polysomnography, and treatment with continuous positive airway pressure (CPAP), carry a potentially high cost. The present study aims to analyze the cost-effectiveness of CPAP treatment versus no treatment, in the long-term, as it examines the effect of this treatment on the incidence of CVD.A Markov model was constructed to observe the disease evolution in patients with OSAS based on published evidence. Data on treatment costs were collected from public hospitals in Greece. Within each cycle of the model, each patient may remain free of CVD, may develop CVD, may die due to a cause related to CVD, or may die from other causes. The model begins at the age of 55 years in a severe OSAS patient (apnea-hypopnea index ≥30/h) and lasts for 45 years.Within the limitation of the model, CPAP was found to be a cost-effective strategy versus no treatment, due to the reduction of the cost for the CVD treatment, when the analysis was restricted to the male population. Moreover, CPAP was found to be clinically more effective than no treatment, as it increases life expectancy in both males and females.CPAP was found to be clinically more effective therapy than no treatment in relation to CVD and a cost-effective strategy in males with severe OSAS.

Cyclophosphamide is considered the treatment of choice for interstitial lung disease (ILD) secondary to systemic sclerosis (SSc), albeit having a minimal effect. Although controlled evidence does not exist, mycophenolate is used increasingly in clinical practice as an alternative. We aimed to compare the long-term efficacy of these drugs. Patients from our SSc cohort who received mycophenolate for over 1 year for progressive ILD were 1:1 matched for age, gender, and baseline forced vital capacity (FVC ±3 %) with cyclophosphamide-treated patients. Changes in FVC, total lung capacity (TLC), diffusion capacity for carbon monoxide (DLCO), and high-resolution computed tomography (HRCT) scans were compared between groups. Changes in pulmonary function tests (PFTs) over at least 1 year in six unmatched control patients, who had denied mycophenolate or cyclophosphamide, also were examined. FVC, TLC, and DLCO did not change significantly in either mycophenolate (from 79.0 ± 12.5 to 80.2 ± 8.1 to 81.2 ± 11.4, from 71.5 ± 16.1 to 74.3 ± 10.8 to 71.8 ± 13.0, from 56.8 ± 12.0 to 55.2 ± 9.9 to 50.6 ± 8.5, respectively) or cyclophosphamide group (from 77.3 ± 12.5 to 79.7 ± 10.3 to 82.5 ± 12.9, from 64.7 ± 14.9 to 68.6 ± 16.0 to 66.1 ± 15.5, from 53.1 ± 14.3 to 56.4 ± 13.5 to 56.3 ± 6.7, respectively), after 1 or 2 years of treatment. PFTs also remained stable in the control group. In either the mycophenolate or cyclophosphamide groups, six patients remained stable, three improved, and one deteriorated according to the definitions of the American Thoracic Society. However, and despite the fact that patients in the cyclophosphamide group had more extended ILD at baseline, a deterioration of lung HRCT findings at 2 years was noticed after mycophenolate (from 10.0 ± 8.9 to 12.7 ± 8.2, p = 0.039) but not after cyclophosphamide. Although these results derive from patients selected for receiving at least 1 year of treatment and therefore they do not represent an intention-to-treat cohort, an eagerness to replace cyclophosphamide by mycophenolate in SSc-associated ILD treatment is not supported.

The purpose of this study was to investigate the role of a fatty meal before bedtime, on sleep characteristics and blood pressure in patients with obstructive sleep apnea (OSA). Recently diagnosed, by full polysomnography (PSG), patients with OSA (n = 19) were included. These underwent PSG for additional two consecutive nights. Two hours before the PSG examination, a ham and cheese sandwich of 360 kcal was served to all patients, at first night, while a fatty meal of 1,800 kcal was served before the second PSG examination. Comparisons were performed between the last two examinations in terms of PSG data and morning and night blood pressure measurements. After the fatty meal, a significant increase was observed in total sleep time (p = 0.026) in the Apnea–Hypopnea Index (AHI) (p = 0.015), as well as in the absolute number of obstructive and central apneas (p = 0.032 and p = 0.042, respectively) compared to the previous night. Conversely, distribution of sleep stages and indices of nocturnal hypoxia (average and minimum SpO2 and sleep time with SpO2

Obstructive sleep apnea syndrome (OSAS) is associated with obesity and insulin resistance. Visfatin is an insulin-mimicking adipokine, which is considered a link between obesity and insulin resistance. Aim of this study was to evaluate levels of plasma visfatin in patients with severe OSAS and examine their potential correlation with sleep characteristics and several biochemical parameters.Nondiabetic patients with severe OSAS (Apnea Hypopnea Index30/h, n = 32) and healthy controls (Apnea Hypopnea Index5/h, n = 12), examined with polysomnography, underwent a biochemical analysis to estimate fasting levels of visfatin, glucose, insulin, C-peptide, and lipid profile.The two groups were matched for age and body mass index (BMI). OSAS patients had significantly higher fasting insulin levels (p = 0.045), but no difference was shown in visfatin between patients and controls (p = 0.585). In OSAS patients, visfatin levels correlated positively with sleep latency (r = 0.539, p = 0.01) and triglyceride levels (r = 0.584, p = 0.036) and negatively with total sleep time, percentage of stage 2 and REM sleep, and LDL-cholesterol levels (r = -0.659 and p = 0.001; r = -0.496 and p = 0.019; r = -0.577 and p = 0.005; r = -0.804 and p = 0.003, respectively). No association was found, however, between visfatin levels and HOMA index or indices of nocturnal hypoxia.In patients with severe OSAS, visfatin levels are associated with characteristics of sleep architecture. However, there is no correlation between visfatin and insulin resistance or nocturnal hypoxia.

Marathon racing is a strenuous exercise that has a profound effect on many laboratory parameters. Participants in marathon races may require abstinence of exercise and the performance of laboratory assays several days after the event. The aim of this study was to evaluate the possible changes in blood cell count and biochemical parameters observed in participants in a marathon 3 days before and 3 days after and before and immediately after a cardiopulmonary exercise test. Incremental cycle ergometry up to maximal capacity was performed in 7 marathon runners, 3 days before and 3 days after the race. The % peak oxygen consumption (peak %VO(2)) achieved was statistically significantly lower after than before the race ( p = 0.02). No statistically significant differences were observed in cardiac frequency ( p = 0.148) or blood cell count ( p = 0.501). Also, the concentration of sodium, potassium, calcium, magnesium, lactate dehydrogenase (LDH), phosphocreatine kinase (CPK) and glucose, measured before and immediately after the pulmonary exercise test, did not differ significantly ( p < 0.5). A significant percentage of the laboratory results were outside the standard reference rates. According to our data, exercise performance, as expressed by peak %VO(2), continued to be decreased in marathon runners 3 days after the race. The blood cell count and biochemical parameters did not differ significantly but many marathon runners were outside the standard reference rates. Unfortunately, only 7 subjects were available for this study. Further studies with larger samples and with samples obtained at multiple times during and after exercise are needed to clarify the effects of long-distance running.