Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved. e278 Abstracts Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved M O N D A Y P O S T E R S POSTER SESSION POSTERS’ SESSION PS22: PHARMACOLOGICAL TREATMENT PP.22.01 IMPACT OF FIXED-DOSE COMBINATIONS ON LEFT VENTRICLE MYOCARDIAL STIFFNESS: AMLODIPINE/ LISINOPRIL VS BISOPROLOL/ HYRPOCLOROTHIAZIDE O. Ostroumova, A. Kochetkov. Moscow State University of Medicine and Dentistry named after A. I. Evdokimov, Moscow, Russia Objective: To compare effects of fixed-dose combinations (FDC) of amlodipine/ lisinopril (A/L) versus bisoprolol/hydrochlorothiazide (B/H) on left ventricle (LV) myocardial stiffness (MS) parameters in patients aged 45–65 years with hyperten- sion grade 1–2 without concomitant cardiovascular diseases. Design and method: Prospective, randomized, open-label, controlled study. We examined 60 naive patients with uncomplicated essential hypertension grade 1–2 (mean age 53,6 ± 0,8 years; 31 men). LV end-diastolic stiffness (EDS), LV end-systolic elastance (ESE), LV diastolic elastance (DE) were calculated by the echocardiography (Vivid7, GE) as LV MS parameters. 2-D speckle tracking echocardiography data were acquired for determination of LV myocardial global longitudinal peak strain (LV GLPS). Patients were randomized into 2 groups (30 patients in each group) and received FDC A/L in a start dose of 5/10 mg or FDC B/H in start dose of 2,5/6,25 mg. FDC doses titrated every 14 days to achieve a target blood pressure (BP) < 140/90 mm Hg and the subsequent therapy in se- lected doses combinations for 12 weeks was continued. Results: All patients in both groups have been achieved target level of office BP. No significant differences in BP data were noted between groups at the end of fol- low up. LV GLPS was significantly increased in both groups – from –17,1 ± 0,6% to –18,3 ± 0,6%, p < 0,01 in A/L group; from –17,1 ± 0,5% to -17,9 ± 0,5%, p < 0,05 in B/H group. The increase in LV GLPS was significantly (p < 0,05) higher in A/L group (9,8 ± 3,3%) compared with B/H one (2,7 ± 0,9%). LV EDS was significantly decreased in A/L group (–20,7 ± 2,4%, p < 0,001) as well as in B/H group (-3,5 ± 1,6%, p < 0,01), the decrease in EDS was significantly (p < 0,001) greater in A/L group (–20,7 ± 2,4%) than in B/H group (-3,5 ± 1,6%). LV ESE significantly (p < 0,001) decreased in A/L and B/H groups (–15,4 ± 1,9% and –12,9 ± 1,4%, respectively). The decrease in ESE was significantly (p < 0,05) greater in A/L (–15,4 ± 1,9%) compared with B/H (–12,9 ± 1,4%). LV DE signifi- cantly increased in A/L group (31,6 ± 10,1%; p < 0,05) whereas in contrast in B/H group LV DE significantly decreased (–13,7 ± 4,1%; p < 0,01). Conclusions: FDC A/L shows better positive effect on the LV MS after 12 weeks of treatment compared to B/H in naive middle-age patients with arterial hypertension. PP.22.02 EFFECTS OF NITRATE THERAPY IN MONOCROTALINE-INDUCED PULMONARY HYPERTENSION IN RATS Z. Kmecova, E. Malikova, P. Krenek, J. Klimas. Faculty of Pharmacy, Comenius University in Bratislava, Department of Pharmacology and Toxicology, Bratisla- va, Slovak Republic Objective: Nitric oxide is one of fundamental regulators of vascular tone and is also a crucial factor influencing target organ damage. Multiple organ dysfunction has been described in monocrotaline (MCT)-induced pulmonary hypertension (PH) in rats. Here, we hypothesized that nitrate administration attenuates target organ injury in this experimental PH. Design and method: Male Wistar rats were subcutaneously injected either with 60 mg/kg MCT or with vehicle (CON). Twelve days after MCT injection, 0.3 mM and 1 mM NaNO3 was administered to rats in drinking water for part of the MCT group (MCT+N0.3, MCT+N1), while the rest received correspond- ing dose of natrium in 0.08% solution of NaCl. One month after the MCT in- jection, right ventricular pressure (RVP) was measured invasively. Afterwards, the animals were sacrificed in CO2 and their organs were harvested for fur- ther analysis. Protein expression of endothelial nitric oxide synthase (eNOS), pSer1177eNOS, Hsp90 and caveolin-1 (Cav-1) in right ventricle and lung was evaluated by western blot. Results: MCT injection led to right ventricular hypertrophy, a significant increase in the mass of lung and interestingly, a significant decrease in the mass of kidney compared to CON. However, these changes were absent in the MCT+N1 when compared to CON, while administration of 0.3 mM NaNO3 was inefficient to pre- vent organ remodelling. RVP was significantly elevated in all groups that received MCT injection and nitrate therapies were unable to prevent this increase. Protein expression of Hsp90 in right ventricle was increased by 53% in MCT and by 54% in MCT+N0.3 group when compared to controls (P < 0.05), but not in MCT+N1. Protein expression of Cav-1 was significantly decreased in MCT+N0.3 group by 63% in right ventricle and by 68% in lung compared to controls (P < 0.01). Ex- pressions of other studied proteins remained stable. Conclusions: After 1 mM NaNO3 administration, we noted the attenuation of MCT-induced increase of right ventricular mass and lung, and the preservation of kidney weight, compared to control group suggesting positive effect of nitrates on tissue remodelling. Interestingly, this was in accordance with the attenuation of increased Hsp90 expression in right ventricles of MCT+N1 rats. PP.22.03 IMPROVEMENT OF HYPERTENSION INDUCED HFPEF BY INHIBITION OF LATE SODIUM-INFLUX AND MAGNESIUM K. Kisters, B. Gremmler. Med. Clinic I St. Anna Hospital, Herne, Germany Objective: Heart insufficiency with preserved ejection fraction -HFpEF- (or dia- stolic Relaxation disorder) is a consequence of left ventricular dysfunction induced by a long-term hypertension. It is observed as well despite effective treatment with antihypertensive drugs. The analysis and quantification of the diastolic relaxation disorder is feasible using tissue-doppler-echocardiography by registration of the E’A’- ratio. Typical clinical symptoms are dyspnea and angina pectoris equivalents. An influence on heart failure with preserved ejection fraction may be induced by the drug ranolazine. Ranolazine inhibits the ischemic generated late sodium influx (I Na-late) and reduces consequently the ischemic induced intracellular sodium - and calcium overload. Upon this mechanism the calcium dependent diastolic left ventricular wall tension will be decreased. We hypothesized that ranolazine will improve hypertensive induced diastolic dys- function through this mechanism. Design and method: We report about 15 patients with essential hypertension (7 male and 8 female, aged 72.7 +/– 9.8 years) with normal renal function (serum creatinine 0.9 +/– 0.2 mg/dl) with exclusion of a macrocoronary induced isch- emia, which complained of dyspnoea and/or angina pectoris equivalents under moderate exercise. A coincidental exercise induced hypertension was excluded. Despite efficient continuation of the antihypertensive treatment all these patients showed a diastolic relaxation disorder with normal LV systolic function. After educational advertising ranolazine (375 mg, 2  d.) was administerd ad- ditionally. As a sodium magnesium antiport was described in hypertensive cells earlier, we measured ionized and plasma magnesium before and after treatment, too. Results: During observation time of this study,blood-pressure and heart rate showed no significant changes to values pre-treatment. The patients by themselves reported a subjective amelioration using a standard questionaire. After 10.3 +/– 3.1 days a significant (p < 0.01) decrease of the diastolic relax- ation disorder was measured in the control of tissue-doppler-measurement (ini- tial E’A’ratio = 0.598 +/– 0.131 versus E’A’ratio under ranolazine treatment with 0.766 +/– 0.179). This normalization of E’A’- index (as a parameter of diastolic relaxation disorder) was observed in all 15 patients. Plasma and ionized magnesium values showed no significant change under rano- lazine treatment. Conclusions: The addition of ranolazine in hypertensive heart disease is safe and effective. PP.22.04 SYSTOLIC BLOOD PRESSURE AND POTASSIUM REGULATION K. Kisters 1 , L. Reither 2 , H. Gell 2 , M. Moser 2 , K. Pichlkastner 2 , I. Viebahn 3 , H. Stossier 3 , M. Harb 3 , S. Porta 2,3 . 1 Med. Clinic I St. Anna Hospital, Herne, Germany, 2 Theresian Military Academy, Wiener Neustadt, Austria, 3 Institute of Applpied Stress Research, Dillach, Austria