Prevention of hypertensive hypertrophy by medical therapy: effects on systolic wall stress and systolic function.

Left ventricular (LV) hypertrophy and LV systolic pumping function of spontaneously hypertensive rats (SHR) treated for 40 weeks with hydralazine (n = 8), metoprolol (n = 8) and both metoprolol and hydralazine (n = 9) were compared with those of 25 age-matched untreated SHR. LV pressure (PLV), peak systolic wall stress (SWS), cardiac index (CI), LV ejection fraction (EF), LV muscle mass to body weight ratio (LV/BW) and the mass volume ratio (M/V) were determined. In the rats treated with hydralazine and metoprolol and hydralazine combined PLV was 28.7% (129 +/- 19 mm Hg) and 31.5% (124 +/- 17 mm Hg) lower compared to the untreated control group (181 +/- 18 mm Hg). In spite of the same amount of blood pressure reduction, LV hypertrophy was less expressed after treatment with metoprolol and hydralazine than after hydralazine only (LV/BW: 2.48 +/- 0.17 versus 2.67 +/- 0.24 mg/g, p less than 0.01; M/V: 2.43 +/- 0.59 versus 3.09 +/- 0.47 mg/microliter, p less than 0.05 respectively). In the group treated with metoprolol and hydralazine LV systolic ejection function parameters (CI, EF) did not differ from those untreated due to an unchanged LV afterload as demonstrated by identical systolic wall stress values (169 +/- 43.4 X 10(3) versus 171 +/- 26.0 X 10(3) dyn/cm2, ns). The identical systolic wall stress values indicate that cardiac hypertrophy had regressed in proportion to the reduced LV peak systolic pressure. Following hydralazine therapy systolic wall stress was even lower (140 +/- 26.5 X 10(3) dyn/cm2) in comparison to the untreated group (171 +/- 26.0 X 10(3) dyn/cm3, p less than 0.05). This reflects an inappropriate low muscle mass reduction in relation to blood pressure reduction. In conclusion (I) antihypertensive therapy with an arteriolar vasodilator in combination with a beta-receptor blocker is more effective in preventing cardiac hypertrophy than therapy with a vasodilator only. (II) Myocardial working capacity remained unaltered after prevention of cardiac hypertrophy as well as LV pumping function.