Factors associated with parasympathetic activation following exercise in patients with rheumatoid arthritis: a cross-sectional study

Background Patients with rheumatoid arthritis (RA) have an increased risk for cardiovascular disease (CVD) with poor parasympathetic function being implicated as an underlying factor. Factors related to parasympathetic function, commonly assessed by heart rate recovery (HRR) following maximal exercise, are currently not known in RA. We aimed to explore the association between HRR with CVD risk factors, inflammatory markers, and wellbeing in patients with RA. Methods Ninety-six RA patients (54.4 ± 12.6 years, 68 % women) completed a treadmill exercise test, during which heart rate (HR) was monitored. HRR1 and HRR2 were defined as the absolute change from HR peak to HRR 1 min post HR peak and 2 min post HR peak, respectively. Cardiorespiratory fitness, CVD risk factors, and serological markers of inflammation were measured in all patients. The Framingham Risk Score (FRS) was used as an assessment of global risk for CVD events, and wellbeing was assessed by questionnaires. Results Mean HRR1 and HRR2 were 29.1 ± 13.2 bpm and 46.4 ± 15.3 bpm, respectively. CVD risk factors as well as most inflammatory markers and measures of wellbeing were inversely correlated with HRR1 and HRR2. Multivariate regression analyses revealed that 27.9 % of the variance in HRR1 and 37.9 % of the variance in HRR2 was explained collectively by CVD risk factors, measures of inflammation, and wellbeing (p = 0.009, p = 0.001 respectively), however no individual measure was independently associated with HRR1 or HRR2. Conclusion Parasympathetic activation was associated with overall CVD risk, arthritis-related burden and wellbeing in patients with RA

Role of ATP decrease in secretion induced by mitochondrial dysfunction in guinea-pig adrenal chromaffin cells

The mechanism related to mitochondrial dysfunction-induced catecholamine (CA) secretion in dispersed guinea-pig adrenal chromaffin cells was investigated using amperometry and confocal laser microscopy. Application of CCCP, which does not stimulate generation of reactive oxygen species (ROS), reversibly induced CA secretion, whereas application of either cyanide or oligomycin (OL), a stimulator for ROS, enhanced CA secretion to a smaller extent. The CCCP-induced secretion was abolished by removal of external Ca2+ ions and was markedly diminished by D600. The mitochondrial membrane potential, measured using rhodamine 123, was rapidly lost in response to CCCP, but did not change noticeably during a 3 min exposure to OL. Prior exposure to OL markedly facilitated depolarization of the mitochondrial membrane potential in response to cyanide. The mitochondrial inhibitors rapidly produced an increase in Magnesium Green (MgG) fluorescence in the absence of external Ca2+ and Mg2+ ions, an increase that was larger in the cytoplasm than in the nucleus. The rank order of potency in increasing MgG fluorescence among the inhibitors was similar to that in increasing secretion. Thus, mitochondrial inhibition rapidly decreases [ATP] and the mitochondrial dysfunction-induced secretion is not due to ROS generation or to mitochondrial depolarization, but is possibly mediated by a decrease in ATP

CHRONIC POST-THROMBOEMBOLIC PULMONARY HYPERTENSION DEVELOPMENT IN A PATIENT WITH HEREDITARY THROMBOPHILIA: A CASE REPORT

Objective: to describe a clinical case of chronic post-thromboembolic pulmonary hypertension (CTEPH) development and progression in a patient with recurrent pulmonary thromboembolism (PTE) and hereditary thrombophilia.Materials and methods. Patient K., female, 50 years old, was hospitalized in the 1st therapeutic department of N.I. Pirogov First City Clinical Hospital with complaints of shortness of breath, occurring at rest and exacerbating after minimal physical activity, dry cough, chest heaviness, swelling of the lower extremities (mainly right one). The patient had a history of deep venous thrombosis (DVT) of the lower extremities, PTE, splenectomy, and long glucocorticosteroid drugs intake for thrombocytopenic purpura. The patient underwent different examinations in the hospital, including evaluation of laboratory tests in dynamics, echocardiography, contrast-enhanced multislice computed tomography of the pulmonary artery and its branches, perfusion lung scintigraphy, right heart catheterization.Results. After examination the patient was diagnosed with multiple segmental and subsegmental perfusion defects of both lungs; we also observed signs of pulmonary hypertension (PH) at echocardiography, proved by right heart catheterization. Also the patient was diagnosed with inherited thrombophilia. The patient was included in the register of PH-patients, thromboendarterectomy together with administration of special medications, approved for use in patients with pulmonary arterial hypertension (PAH-specific therapy) were recommended.Conclusion. This article describes the main features of CTEPH, its diagnostics and treatment in patients with CTEPH after PTE