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To propose a test to evaluate endothelial function, based on VO(2) on-transition kinetics in sub-anaerobic threshold (AT) constant load exercise, we tested healthy subjects and patients with ischemic-hypertensive cardiopathy by two cardiopulmonary tests on a cycle ergometer endowed with an electric motor to overcome initial inertia: a pre-test and, after at least 24 h, one 6 min constant load exercise at 90 % AT. We measured net phase 3 VO(2)-on kinetics and, by phase 2 time constant (tau), valued endothelial dysfunction. We found shorter tau in repeated tests, shorter time between first and second test, by persisting endothelium-dependent arteriolar vasodilatation and/or several other mechanisms. Reducing load to 80 % and 90 % AT did not produce significant changes in tau of healthy volunteers, while in heart patients an AT load of 70 %, compared to 80 % AT, shortened tau (delta=4.38+/-1.65 s, p=0.013). In heart patients, no correlation was found between NYHA class, ejection fraction (EF), and the two variables derived from incremental cycle cardio-pulmonary exercise, as well as between EF and tau; while NYHA class groups were well correlated with tau duration (r=0.92, p=0.0001). Doxazosin and tadalafil also significantly reduced tau. In conclusion, the O(2) consumption kinetics during the on-transition of constant load exercise below the anaerobic threshold are highly sensitive to endothelial function in muscular microcirculation, and constitute a marker for the evaluation of endothelial dysfunction.

Background Left ventricular hypertrophy (LVH) is an independent and powerful risk factor for cardiovascular events and death. Serum uric acid (SUA) may induce LVH, on one hand, through an inflammatory effect which promotes cardiac hypertrophy and, on the other, through an activation of the renin-angiotensin-aldosterone system which generates hypertrophy and hyperplasia of myocytes and fibrosis of the heart Objectives Aim of the study was to investigate the correlation between SUA levels and left ventricular mass in a group of hypertensive patients Methods We evaluated 51 patients (mean age 74±10 years; range 49-87, F 37.7%; M 62.3%) with essential hypertension. Each patient underwent a standardized medical history and clinical examination, laboratory tests and echocardiographic assessment with the determination of left ventricular mass index (LVMI) Results Mean value of SUA was 6.68±2 mg/dl. Mean blood pressure (MAP) was 95±12 mmHg. A positive significant correlation between SUA and LVMI (P=0.029) was observed. After adjusting for MAP and age in standard multiple linear regression analysis, SUA level remains independently associated with LVMI suggesting that increased urate levels are associated with a higher myocardial mass. Conclusions Our results demonstrate that SUA is independently associated with LVMI and suggest that the combination of hyperuricemia with LVH could be a powerful predictor of cardiovascular events References Yoshio Iwashima, Takeshi Horio, Kei Kamide, Hiromi Rakugi, Toshio Ogihara and Yuhei Uric Acid, Left Ventricular Mass Index, and Risk of Cardiovascular Disease in Essential Hypertension. Hypertension 2006;47:195-202; Ayako Yoshimura, Hisashi Adachi, Yuji Hirai, Mika Enomoto, Ako Fukami, Eita Kumagai, Kyoko Ohbu, Sachiko Nakamura, Aya Obuchi, Yume Nohara, Tsutomu Imaizumi. Serum Uric Acid Is Associated With the Left Ventricular Mass Index in Males of a General Population. Int Heart J, January 2014 Cristiana Catena, GianLuca Colussi, Frine Capobianco, Gabriele Brosolo and Leonardo A. Sechi. Uricaemia and left ventricular mass in hypertensive patients. Eur J Clin Invest 2014;44(10):972-981 Disclosure of Interest None declared

Background Rheumatoid arthritis(RA) is a chronic autoimmune inflammatory disease. The inflammatory process causes joint destruction and disability. Patients have a shorter life expectancy and a relative risk of cardiovascular (CV) disease ranging from 1.5 to 4.0 with an increase in CV morbidity and mortality of 1.5 fold compared with the general population. The chronic inflammation seen in RA have its main effectors in factor alfa tumor necrosis (TNF) and interleukin 6 (IL-6) that, in addition to playing a key role in the initiation of joint damage and progression of atherosclerotic disease, are also potent inducers of the renin angiotensin system (RAS). The latter could contribute in these patients to the development of an early and accelerated CV damage. Objectives To evaluate the possible presence of hyperactivation of RAS and its association with the activity parameters of RA, with traditional risk factors and premature CV organ damage Methods there were evaluated 17 (F) patients (pts) with RA receiving stable therapy (3 months) with DMARDs or anti-TNF alpha, in the absence of previous CVevents and/or traditional risk factors. All pts underwent a visit with rheumatologic evaluation of patient history, activity of RA (DAS28), pain (VAS), quality of life (HAQ), patient GH. Blood samples were collected for the evaluation of: lipid profile, indices of insulin resistance (HOMA-IR), indices of activity of rheumatoid arthritis (autoantibodies, inflammatory markers) and CV risk according to risk charts based on the Framinghamstudy. The CV organ damage was assessed by imaging techniques such as Pulse Wave Velocity (PWV) and Augmentation Index (AIx), Intima-media thickness (IMT) and ankle-brachial index (ABI). From a sample of the patient’s blood leukocytes were separated and subsequently extracted RNA to perform Real time qPCR to verify the expression of Angiotensin II and AT1 and AT2 receptors. The mean disease duration was 9 ±7 years; the mean age (pts all female) was 55 ± 12 years. FR was positive in 49%, antiCC and ANA respectively in 64% and 59% Results data, though preliminary, showed a statistically significant correlation between the density of receptors for angiotensin II (AT1R and AT2R) and, respectively, the values of ABI(p Conclusions The results obtained so far make attractive and plausible the initial assumption and could, if confirmed in further continuation of the study, help to explain the paradoxical development of vascular disease in patients with RA and apparent low CV risk with important therapeutic implications Disclosure of Interest None Declared