Right ventricular wall thickness and activity of sodium/hydrogen exchanger in young population with essential hypertension

ESCUDERO EM; ENNIS IL; MASSARUTTI C; PINILLA OA; VILLA-ABRILLE MCM; BRODA D; CINGOLANI HE

Congreso; Joint Meeting ESH-ISH-Hypertension; 2014

ESH-ISH

Objective The present study was projected to analyze the wall thickness of right ventricle ( RV) and its relationship with the sodium/hydrogen exchanger (NHE) activity in thrombocytes as no hemodynamics signal, over a young population with essential arterial hypertension (HT). Design and method 750 medical students (20.48± 0.07 years old) for La Plata School of Medicine were included in the study. 47 were HT indicating a prevalence of 6% . These 47 HT and 45 normotensive (NT) randomized of the general population configured our reference group. LV mass index (LVMI) and RV wall thickness (RVWT) was obtained, to characterized ventricular structure, by echocardiographic study. In 24/47 students (13 HT, 11 NT) it was determined in thrombocytes, by a sample of blood of peripheral vein, the velocity of intracellular pH (pHi) recuperation as expression of NHE activity. Results LVMI was higher in HT group (HT: 77.07 ± 2.21g/m2; NT: 69.36 ± 2.02 g/m2 p<0.01) as an answer to pressure overloading. The RVWT also was higher in HT (HT: 4 ± 0.05 mm; NT: 3 ± 0.06 mm- p< 0.01), showing a modification of RV structure in HT. On the other hand the HT had a higher velocity of pHi recuperation after an acidify pulse, pointing the increase NHE activity in the thrombocytes, respect to NT (HT: 0.32 ± 0.03 Ph/s, NT: 0.24 ± 0.01Ph/s p<0.03). Conclusions Analyzing the results we conclude that in this young population the increases of blood pressure produced structural changes in LV represented for the increase in LV mass and in RV as showed by the increment in wall ventricular thickness. As the higher expression and activity of NHE was associated with the intracellular pathway to produce hypertrophy, the finding that the NHE had more activity in trombocyte in our observation, allow as to inferring that this activity could be increment in the RV muscle fibers and would be responsible of the non hemodynamic answer of the RV in systemic hypertension.