LEFT VENTRICULAR HYPERTROPHY INHIBITION IN EXPERIMENTAL HYPERTENSION

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

Milan

Congreso; 21st. European Meeting on Hypertension (ESH); 2011

European Meeting on Hypertension (ESH)

The left ventricular hypertrophy (LVH) has been traditionally described as a protective mechanism to prevent cardiac failure. Paradoxically in epidemiological studies LVI has been associated with an increment in cardiac morbidity and mortality. In genetic hypertension (SHR) the   LVH is associated with the development of Hypertension. . In the same sense pharmacological treatment with different drugs   normalize the Blood Pressure and regress the LVH in this genetic model of hypertension    Several reports   suggest that LVH is not necessary to prevent cardiac failure, opening the possibility to inhibit his development . Objectives. Evaluate the  chronic therapeutic effects with different drugs on   hypertension 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 the different drugs administrate  in 1)L :(Losartan 30 mg kg/day) (n= 18) 2)H: (hydralazina 11mg kg/day (n=18) 3) R: (Rosuvastatina 10 mg kg/day )(n=18) 4) C : ( Carvedilol 20mg kg/day) (n=12) 5) G :( no drugs )(n=18) and 6) WKY : wistar kyoto (n=18)  as control normotensive  group. All the measures were done in awake conditions.  Systolic blood pressure (SBP) was periodically measured by tail-cuff plethysmography. 2). Echocardiograms (Aloka 550, 7.5 Mhz transducer) were obtained before  and at 6, 12 and 16 months of treatment. The echocardiography  transducer was positioned to obtain the long  and the short axis , the apical view of four chambers and five chambers(including aorta).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 Body Weight (LVM/BW), Left Ventricular End Diastolic Volume (LVDV) :(0,85 x DD3) , Left Ventricular End Systolic Volumes  (LVSV) :(0,85*SD3), Systolic Volume (SV) :( LVDV- LVSV), Cardiac Output (CO): (SV *HR) and Ejection Fraction (EF): (LVSV-LVSV/LVDV*100 were recorded. Euthanasia was practiced at the end of month 16. Left ventricular weights (LVW) were measured and they were corrected for BW (LVW/BW).  Results. Groups were indistinguishable according with BW. SBP values were (mmHg): 154 ±3 (L), 137 ±1 (H), 190 ±3 (R)*, 206 ±3 (SHR)*, 183 ±1 (C)*, 141 ±1 (WKY). P<0.05 vs.  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. Surprisingly high SBP values in C group were not followed with LVH . Conclusions. 1) The development of hypertension trough the life in this model of genetic hypertension induce Ventricular Hypertrophy and a deterioration of cardiac function 2) The normalization of blood pressure   either  Losartan  or Hydralazine was  followed by inhibition of ventricular hypertrophy and a preservation of cardiac function.-  3) The  light  antihypertensive effect of Rosuvastatin did not prevent either the ventricular depression in cardiac function or the hypertrophy 4) The  light  antihypertensive effect of Carvedilol , did not prevent  the ventricular depression in cardiac function but paradoxically inhibits the ventricular hypertrophy. This protective effect of carvedilol could be associated either  a beta blocker effect expressed trough reduction in the Heart rate and Cardiac Output or an antiproliferative effect.