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Background: Decline in oxygen uptake efficiency (OUE), especially during exercise, is found in patients with chronic heart failure. In this study we aimed to test the validity and usefulness of OUE in evaluating gas exchange abnormality of patients with idiopathic pulmonary arterial hypertension (IPAH). Methods: We retrospectively investigated the cardiopulmonary exercise test (CPET) with gas exchange measurements in 32 patients with confirmed IPAH. All patients also had resting hemodynamic measurements and pulmonary function test (PFT). Sixteen healthy subjects, matched by age, sex, and body size were used as controls, also had CPET and PFT measurements. Results: In IPAH patients, the magnitude of absolute and percentage of predicted (%pred) oxygen uptake efficiency slope (OUES) and oxygen uptake efficiency plateau (OUEP), as well as several other CPET parameters, were strikingly worse than healthy subjects (P<0.0001). Pattern of changes in OUE in patients is similar to that in controls, In IPAH patients, OUE values at rest, warming up, anaerobic threshold and peak exercise were all significantly lower than in normal (P<0.0001). OUEP%pred, better than OUES%pred, correlated significantly with New York Heart Association (NYHA) functional Class (r = −0.724, P<0.005), Total Pulmonary Vascular Resistance (TPVR) (r = −0.694, P<0.005), diffusing capacity for carbon monoxide (DLCO) (r = 0.577, P<0.05), and the lowest ventilation versus CO2 output ratio during exercise (LowestV˙E/V˙CO2) (r = −0.902, P<0.0001). In addition, the coefficient of variation (COV) of OUEP was lower (20.9%) markedly than OUES (34.3%) (P<0.0001). Conclusions: In patients with IPAH, OUES and OUEP are both significantly lower than the healthy subjects. OUEP is a better physiological parameter than OUES in evaluating the gas exchange abnormality of patients with IPAH. [ABSTRACT FROM AUTHOR]

Background: Chronic kidney disease and occurrence of atrial fibrillation (AF) are closely related. No studies have examined whether renal impairment (RI) without severe renal dysfunction is associated with the occurrence of AF. Methods: Unilateral RI with mild renal insufficiency was induced in beagles by embolization of small branches of the renal artery in the left kidney for 2 weeks using gelatin sponge granules in the model group (n = 5). The sham group (n = 5) underwent the same procedure, except for embolization. Parameters associated with RI and renal function were tested, cardiac electrophysiological parameters, blood pressure, left ventricular pressure, and AF vulnerability were investigated. The activity of the sympathetic nervous system, renin-angiotensin-aldosterone system, inflammation, and oxidative stress were measured. Histological studies associated with atrial interstitial fibrosis were performed. Results: Embolization of small branches of the renal artery in the left kidney led to ischemic RI with mild renal insufficiency. The following changes occurred after embolization. Heart rate and P wave duration were increased. Blood pressure and left ventricular systolic pressure were elevated. The atrial effective refractory period and antegrade Wenckebach point were shortened. Episodes and duration of AF, as well as atrial and ventricular rate during AF were increased in the model group. Plasma levels of norepinephrine, renin, and aldosterone were increased, angiotensin II and aldosterone levels in atrial tissue were elevated, and atrial interstitial fibrosis was enhanced after 2 weeks of embolization in the model group. Conclusions: We successfully established a model of RI with mild renal insufficiency in a large animal. We found that RI with mild renal insufficiency was associated with AF in this model. [ABSTRACT FROM AUTHOR]

Aims: To investigate the association of ABCG1, GALNT2 and HMGCR genes promoter DNA methylation with coronary heart disease (CHD) and explore the interaction between their methylation status and the CHD patients' clinical characteristics in Han Chinese population. Methods and results: Methylation-specific polymerase chain reaction (MSP) technology was used to examine the role of the aberrant gene promoter methylation in CHD in Han Chinese population. A total of 85 CHD patients and 54 participants without CHD confirmed by angiography were recruited. 82.8% of the participants with ABCG1 gene promoter hypermethylation have CHD, while only 17.4% of the participants without hypermethylation have it. The average age of the participants with GALNT2 gene promoter hypermethylation is 62.10±8.21, while that of the participants without hypermethylation is 57.28±9.87; in the former group, 75.4% of the participants have CHD, compared to only 50% in the latter group. As for the HMGCR gene, the average age of the participants with promoter hypermethylation is 63.24±8.10 and that of the participants without hypermethylation is 57.79±9.55; its promoter hypermethylation is likely to be related to smoking. Our results indicated a significant statistical association of promoter methylation of the ABCG1 gene with increased risk of CHD (OR = 19.966; 95% CI, 7.319–54.468; P*<0.001; P*: adjusted for age, gender, smoking, lipid level, hypertension, and diabetes). Similar results were obtained for that of the GALNT2 gene (OR = 2.978; 95% CI, 1.335–6.646; P* = 0.008), but not of HMGCR gene (OR = 1.388; 95% CI, 0.572–3.371; P* = 0.469). Conclusions: The present work provides evidence to support the association of promoter DNA methylation status with the risk profile of CHD. Our data indicates that promoter DNA hypermethylation of the ABCG1 and GALNT2 genes, but not the HMGCR gene, is associated with an increased risk of CHD. CHD, smoking and aging are likely to be the important factors influencing DNA hypermethylation. [ABSTRACT FROM AUTHOR]