Left ventricular hypertrophy inhibition in expermiental hypertension

GOMEZ LLAMBI H; D SUAREZ; G OTTAVIANO; A MÜLLER; N PAGLIA; M OTERO LOSADA; J MILEI

Milán

Congreso; 21st Annual Scientific meeting of European Society of Hypertension; 2011

LEFf VENTRICULAR HYPERTROPHY INHIBITION IN EXPERIMENTALHYPERTENSIONAutor/es:GOMEZ-LLAMBI H.; SUAREZ D.; OTTAVIANO G; MULLER A; PAGLIA N.;OTERO-LOSADA M.; MILEI J.Lugar:MilanReunión:Congreso; 21st. European Meeting on Hypertension (ESH); 2011Institución organizadora:European Meeting on Hypertension (ESH)Resumen:The left véntricular hypertrophy (LVH) has be en traditionally described as a protectivemechanism to prevent cardiac failure. Paradoxically in epidemiological studies LVI hasbeen associated with an increment in cardiac morbidity and mortality. In genetichypertension (SHR) the LVH is associated with the development of Hypertension .. In thesame sense pharmacological treatment with different drugs norrnalize the Blood Pressureand regress the LVH in this gene tic model of hypertension Several reports suggest thatLVH is not necessary to prevent cardiac failure, opening the possibility to inhibit hisdevelopment . Objectives. Evaluate the chronic therapeutic effects with different drugs onhypertension and LVH during sixteen months of treatment. Methods. Male SHR rats(n=84) and WKY (n=18)8 weeks old were selected .SHR rats were divided according thedifferent drugs administrate in l)L :(Losartan 30 mg kg/day) (n= 18) 2)H: (hydralazina11mg kg/day (n=18) 3) R: (Rosuvastatina 10 mg kg/day )(n=18) 4) C : (Carvedilol20mgkg/day) (n=12) 5) G :( no drugs )(n:::18) and 6) WKY : wistar kyoto (n=18) as controlnormotensive group. AlI the measures were done in awake conditions. Systolic bloodpressure (SBP) was periodically measured by tail-cuff plethysmography. 2).Echocardiograms (Aloka 550, 7.5 Mhz transducer) were obtained before and at 6, 12 and16 months of treatment. The echocardiography transducer was positioned to obtain thelong and the short axis , the apical view of four chambers and five chambers(includingaorta).From the long axis we have obtain a M mode view of left ventricular chamber.Diastolic (DD) and Systolic Diameters (SD), shortening fraction (SF)(DD-SD/DD*100)Septal Diastolic Thickness (SDT), Posterior Diastolic Thickness(PDT), Heart Rate (HR),Left Ventricular Mass (LVM) : 1,04* [(DD+ PDT + SDT)3 - DD3]. corrected for BodyWeight (LVM/BW), Left Ventricular End Diastolic Volume (LVDV) :(0,85 x DD3) , LeftVentricular End Systolic Volumes (LVSV) :(0,85 *SD3), Systolic Volume (SV) :( LVDVLVSV),Cardiac Output (CO): (SV *HR) and Ejection Fraction (EF): (LVSVLVSV/LVDV*100 were recorded. Euthanasia was practiced at the end ofmonth 16. Leftventricular weights (LVW) were measured and they were corrected for BW (LVW/BW).Results. Groups were indistinguishable according with BW. SBP values were (rnrnHg):154 ±3 (L), 137 ±1 (H), 190 ±3 (R)*, 206 ±3 (SHR)*, 183 ±1 (C)*, 141 ±1 (WKY). P<0.05vs. WKY, L, and H .Ventricular Pump function and ventricular contractile parameters(SF), were depressed in SHR , R, and C compared to L, H and WKY groups. Surprisinglyhigh SBP values in C group were not followed with LVH . Conclusions. 1) Thedevelopment of hypertension trough the life in this model of gene tic hypertension induceVentricular Hypertrophy and a deterioration of cardiac function 2) The normalization ofblood pressure either Losartan or Hydralazine was followed by inhibition of ventricularhypertrophy and a preservation of cardiac function.- 3) The light antihypertensive effectof Rosuvastatin did not prevent either the ventricular depression in cardiac function or thehypertrophy 4) The light antihypertensive effect of Carvedilol , did not prevent theventricular depression in cardiac function but paradoxically inhibits the ventricularhypertrophy. This protective effect of carvedilol could be associated either a beta blockereffect expressed trough reduction in the Heart rate and Cardiac Output or anantiproliferative effect.