Long-term myocardial effects of noninvasive ventilation in patients with obesity hypoventilation syndrome.

INTRODUCTION: Chronic effects of noninvasive ventilation on myocardial function in patients with obesity hypoventilation syndrome (OHS) are scarcely understood. The aim of the present study was to evaluate the long-term effects of volume-targeted bilevel positive airway pressure ventilation (BiPAP) on cardiac parameters and myocardial biomarkers in patients with OHS. METHODS: Clinically stable patients with OHS referred to the tertiary center for the initiation of long-term BiPAP therapy were consecutively enrolled. At baseline, all participants underwent overnight cardiorespiratory polygraphy. BiPAP therapy using volume-targeted spontaneous/timed mode delivered via an oro-nasal mask was initiated. Beat-to-beat noninvasive monitoring by impedance cardiography was used to assess heart function at baseline and after 3 and 12 months of BiPAP use. Serum troponin 1, N-Terminal Pro-B-Type Natriuretic Peptide (NT-ProBNP), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) were monitored. RESULTS: Thirteen patients (10 men; mean age, 55.8 ± 9.8 years; mean body mass index of 47.8 ± 5.9 kg/m2) were recruited. From baseline to 3, and to 12 months of BiPAP use, left ventricular stroke volume (SV), ejection time (LVET), and ejection time index significantly increased (P = 0.030; P < 0.001; P = 0.003, respectively), while heart rate and systolic time ratio significantly decreased (P = 0.004; P = 0.034, respectively). Reductions in serum NT-proBNP, IL-6 and TNF-α were observed (P = 0.045; P = 0.018; P = 0.003, respectively). No significant changes in serum troponin were detected throughout the study. CONCLUSIONS: The present findings of increased SV, in association with lengthening of LVET, reductions of NT-proBNP and reductions in circulatory inflammatory markers in patients with stable OHS and chronic moderate-to-severe daytime hypercapnia treated with BiPAP over 1 year support the role of this therapeutic mode in such patients.

Acute hemodynamic effects of non-invasive ventilation in patients with obesity hypoventilation syndrome.

OBJECTIVE: To evaluate the acute effects of volume-targeted non-invasive ventilation (NIV) on hemodynamic parameters assessed by impedance cardiography in patients with obesity hypoventilation syndrome (OHS). BACKGROUND: Despite the well-described beneficial effects of NIV using volume-targeted pressure support ventilation modes on respiration in OHS patients, questions were raised about the impact of this treatment on the cardiovascular system. METHODS: In 15 patients (10 men; mean age, 55.8±9.3 years) impedance cardiography recordings were taken at baseline, after 120 minutes while on NIV and 20 minutes after NIV termination. A repeated-measures analysis of variance was used for comparisons. RESULTS: Compared to baseline, a reduction in heart rate (from 80±11 to 73±10 beats per min, p<0.05) was observed on NIV whereas the stroke volume and cardiac index remained stable throughout all three assessed intervals (p=0.347, p=0.344; respectively). The pre-ejection period increased on NIV (from 113±16 to 127±20 ms, p<0.05), and the left ventricular ejection time increased after NIV termination compared to baseline (from 259±25 to 269±25 ms, p<0.05). CONCLUSION: Volume-targeted NIV may acutely improve systolic time intervals without any negative impact on the left ventricular function in OHS patients (Tab. 2, Ref. 17).

[Malignant fibrous histiocytoma as a rare cause of acute limb ischemia]. / Malígny fibrózny histiocytóm ako raritná prícina akútnej koncatinovej ischémie.

Malignant fibrous histiocytoma (MFH) represents a rare malignant affection of heart and aorta. Its clinical presentation depends on the localisation, size, degree of invasion and metastasis. Previously, relatively few cases of acute tumour mass embolisation into the visceral and limb arterial system were described in the literature. In the present case study we describe a case of acute ischemia of both lower extremities caused by thromboembolic mass of MFH cells. According to literary sources this tumour type is characterized by poor prognosis as it was in the case of our patient.

Increased resting energy expenditure and insulin resistance in male patients with moderate-to severe obstructive sleep apnoea.

Obstructive sleep apnoea (OSA) has been associated with disturbances in energy metabolism and insulin resistance, nevertheless, the links between OSA severity, resting energy expenditure (REE) and insulin resistance (homeostasis model assessment, HOMA-IR) remained unexplored. Therefore, we investigated the effects of OSA severity on REE, and relationships between REE and HOMA-IR in patients with OSA. Forty men [mean (SD) age 49.4 (11.4) years] underwent overnight polysomnography; REE was assessed using indirect calorimetry. REE adjusted for fat-free mass (FFM) was higher in patients with moderate-to severe OSA [n=24; body mass index (BMI) 31.1 (2.7) kg.m(-2); apnoea-hypopnoea index (AHI)>/=15 episodes.h(-1)] compared to participants with no clinically significant OSA (n=16; BMI 30.3 (2.2) kg.m(-2); AHI<15 episodes.h(-1)) [median (interquartile range) 30.4 (26.1-31.3) versus 25.8 (24.6-27.3) kcal.kg(-1).24 h(-1), p=0.005)]. AHI and oxygen desaturation index (ODI) were directly related to REE/FFM (p=0.001; p<0.001, respectively) and to HOMA-IR (p<0.001 for both). In stepwise multiple linear models, REE/FFM was independently predicted by ODI (p<0.001) and age (p=0.028) (R(2)=0.346); HOMA-IR was independently predicted by ODI only (p<0.001, R(2)=0.457). In conclusion, male patients with moderate-to severe OSA have increased REE paralleled by impaired insulin sensitivity. Severity of nocturnal intermittent hypoxia reflected by ODI is an independent predictor of REE/FFM and HOMA-IR.

[Comparison of the results of surgical and endovascular treatment in patients with peripheral arterial disease of the lower extremities in the femoropopliteal region]. / Porovnanie výsledkov pouzitia chirurgickej a endovaskulárnej liecby u pacientov s periférnym artériovým ochorením dolných koncatín vo femoropopliteálnej oblasti.

INTRODUCTION: Results of previous studies comparing bypass surgery and percutaneous transluminal angioplasty in peripheral artery disease are ambiguous. Therefore, the aim of our study was to analyse and compare the long-term results of surgical and endovascular revascularisation in patients with peripheral artery disease in the femoropopliteal region. MATERIAL AND METHODS: 255 patients with peripheral artery disease who underwent bypass surgery or percutaneous transluminal angioplasty for newly diagnosed infrainguinal lesions in the femoropopliteal region were retrospectively identified and analyzed. Clinical and technical success, primary and secondary patency, improvement of critical limb ischaemia symptoms and improvement of the claudication interval were assessed within 1 year following treatment. Secondary evaluated outcomes were complications including haematoma after intervention, the need for revascularization and need for amputation of the thigh within 1 year after the intervention. Clinical outcomes were statistically evaluated as odds ratio and confidence interval. RESULTS: Patients were divided into two groups: the first one was formed by 93 (36.47%) patients who underwent bypass surgery, the second one consisted of 162 (63.53%) patients who underwent endovascular therapy - percutaneous transluminal angioplasty. We could not find differences in clinical and technical success, primary and secondary patency and claudication interval improvement between the treatment groups within 1 year of follow-up after the intervention. In comparison to the endovascular group, we observed a 1.85 times higher rate of clinical improvement of critical limb ischaemia symptoms after 1 year following the intervention in the bypass surgery group patients OR 1.85 (1.10-3.10), p=0.020. Multiple logistic regression analysis showed that type of intervention was the only predictor of improvement in critical limb ischemia symptoms, independently of claudication interval before intervention, age, gender, active smoking, diabetes mellitus, hypertension and ischaemic heart disease (p=0,004). The bypass surgery group had a higher incidence of haematoma due to intervention than the endovascular group OR 4.23 (1.27-14.15), p=0.019. No differences were detected between the treatment groups in the need for revascularisation or amputation of the thigh within 1 year following intervention. CONCLUSION: The use of bypass surgery has been associated with a higher rate of clinical improvement in critical limb ischaemia symptoms after 1 year of intervention and presence of haematoma after the intervention. No differences were detected between patients with peripheral artery disease in the femoropopliteal region treated by bypass surgery or percutaneous transluminal angioplasty in clinical and technical success, primary and secondary patency, nor in the improvement of the claudication interval during 1 year of follow-up. We also could not observe differences in the need for revascularisation or amputation of the thigh within 1 year following the intervention.

Effects of hypoxia on adipose tissue expression of NFκB, IκBα, IKKγ and IKAP in patients with chronic obstructive pulmonary disease.

Recently we observed increased adipose tissue (AT) expression of CD40-related signaling proteins but no activation of tumor necrosis factor-α or CD68 in patients with chronic sustained hypoxia resulting from chronic obstructive pulmonary disease (COPD). Transcription factor nuclear factor-κB (NFκB) is involved in cellular responses to hypoxia and activates the proinflammatory gene expression with concomitant upregulation of its own repressors--inhibitors of κB (IκB) in an auto feedback loop. Inhibitor of kappaB kinase (IKK)-γ and inhibitor of kappaB kinase complex-associated protein (IKAP) are further regulatory proteins involved in NFκB signaling. In this study, we hypothesized that chronic sustained hypoxia significantly relates to IκBα, IKKγ and IKAP within the AT in COPD patients. In 20 patients with stable disease, samples of subcutaneous AT were analyzed using real-time PCR. Although no significant differences were observed between two groups categorized by median PaO2 in NFκB (p = 0.065), gene expressions of IκBα, IKKγ and IKAP were all higher in hypoxemic patients (p = 0.033; p = 0.050; p = 0.010, respectively). In multivariate analyses, PaO2 independently predicted AT IκBα, IKKγ and IKAP (R (2) = 0.490, p = 0.012; R (2) = 0.586, p = 0.002; R (2) = 0.504, p = 0.009, respectively). In conclusion, our data suggest significant AT upregulation of IκBα, IKKγ and IKAP by chronic sustained hypoxia in COPD patients.

Circulatory and adipose tissue leptin and adiponectin in relationship to resting energy expenditure in patients with chronic obstructive pulmonary disease.

Increases in resting energy expenditure (REE) likely contribute to weight loss in various chronic diseases. In chronic obstructive pulmonary disease (COPD), relationships between the ventilatory impairment and increased REE, and between disturbances in adipokines and weight loss were previously described. Therefore, we investigated serum levels and adipose tissue expression of leptin and adiponectin, and their relationships to REE in patients with COPD. In 44 patients with stable COPD (38 male; age 62.3+/-7.2 years), REE was assessed using indirect calorimetry. Subcutaneous adipose tissue samples were analyzed using real-time PCR. From underweight [n=9; body mass index (BMI) <20.0 kg.m(-2)], to normal weight-overweight (n=24, BMI=20.0-29.9 kg.m(-2)) and obese patients (n=11; BMI>/=30 kg.m(-2)), REE adjusted for body weight decreased (32.9+/-6.1 vs. 26.2+/-5.8 vs. 23.9+/-6.6 kcal.kg(-1).24 h(-1), p=0.006), serum levels and adipose tissue expression of leptin increased (p<0.001 for both), and serum and adipose tissue adiponectin decreased (p<0.001; p=0.004, respectively). REE was inversely related to serum and adipose tissue leptin (R=-0.547, p<0.001; R=-0.458, p=0.002), and directly to serum adiponectin (R=0.316, p=0.039). Underweight patients had increased REE compared to normal weight-overweight patients, in association with reductions in serum and adipose tissue leptin, and increased serum adiponectin, suggesting a role of adipokines in energy imbalance in COPD-related cachexia.

Carotid intima-media thickness in patients with chronic obstructive pulmonary disease.

OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is associated with increased cardiovascular morbidity and mortality. Several large population-based cohort studies identified an association between reduced lung function and increased intima-media thickness (IMT). Nevertheless, a vast majority of subjects in these studies did not suffer from COPD and thus it remains unclear whether IMT differs among various stages of COPD severity. The aim of the present pilot study was to evaluate IMT in central European patients with moderate, severe and very severe COPD. METHODS: In forty-nine patients (34 men, 15 women; mean age 66.1 +/- 10.9 years) with COPD, the combined thickness of intima and media layers of the common carotid arteries was measured using B-mode ultrasound imaging. RESULTS: Increased cardiovascular disease risk as evidenced by carotid IMT values greater or equal to 75th percentile were present in 14 (28.6%), whereas IMT hypertrophy (IMT values greater or equal 0.80 mm) was present in 24 (49.0%) of patients. Average IMT in the entire cohort was 0.85 +/- 0.21 mm, with no significant differences from stage II to stages III and IV of COPD. CONCLUSION: Present results indicate a high prevalence of IMT hypertrophy and increased cardiovascular disease risk as assessed by carotid ultrasonography in COPD patients with a broad spectrum of airway obstruction severity. The lack of differences in carotid IMT between various stages of lung impairment severity suggests that atherosclerosis starts early in the course of COPD. Therefore, the need to screen patients for the presence of concomitant atherosclerosis in early stages of COPD severity may be warranted (Tab. 2, Ref. 33).

[Osteoporosis in chronic obstructive pulmonary disease]. / Osteoporóza pri chronickej obstrukcnej chorobe pl'úc.

Patients with chronic obstructive pulmonary disease (COPD) are at increased risk of osteoporosis because of their age, limited physical activity, low body mass index, smoking, hypogonadism, malnutrition, and use of corticosteroids. Systemic inflammation represents an additional pathomechanism contributing to the development of osteoporosis in COPD patients. Males in their mid to late 60s with a smoking history of greater than 60 pack-years have a prevalence rate of vertebral fractures similar to, and possibly greater than, postmenopausal women greater than or equal to 65 years old: in patients with severe COPD, up to 50-70% have osteoporosis or osteopenia, and up to 24-30% have compression vertebral fractures. Correlates of osteoporosis in COPD are mainly measures of body composition, disease severity and the use of corticosteroids, although causality has not been proven. Systemic corticosteroids remain the most common cause of drug-related osteoporosis, and a meta-analysis concluded that the use of more than 6.25 mg prednisone daily led to decreased bone mineral density (BMD) and increased fracture risk. In contrast, the effects of the long-term use of inhaled corticosteroids on BMD remain debatable. Effects of treatment of osteoporosis have not been investigated in samples consisting of COPD patients only but the recommendations follow the general recommendations for the diagnosis and treatment of osteoporosis. Early recognition of BMD loss is essential, and assumes close interdisciplinary cooperation between respirologists and reumatologists. Longitudinal follow-up to assess determinants of osteoporosis in COPD and randomised placebo-controlled trials on the effects of treatment of osteoporosis in patients with COPD only are warranted. In the future, novel therapeutical strategies such as monoclonal antibodies against osteoclasts activators may prove their beneficial effects in the treatment of COPD-related osteoporosis.