Echocardiographic left ventricular hypertrophy as related to arterial pressure and plasma norepinephrine concentration in arterial hypertension. Reversal by atenolol treatment

Abstract

We tried to assess relationships between echocardiographic left ventricular hypertrophy (LVH), arterial pressure levels, and plasma norepinephrine concentration (NE) in 20 previously untreated stable hypertensive patients with LVH, and in 11 healthy normotensive control subjects. Interventricular septal (IVS) thickness, posterior wall (PW) thickness, and left ventricular mass index (LVMI) were related to arterial pressure levels and to NE by unvariate and multivariate regression analyses. In addition, after 18 months of monotherapy with atenolol (carried out in 9 of 20 patients), the relationship between echocardiographic changes and degree of pressure reduction was tested. Before treatment, PW thickness weakly correlated with systolic (r = 0.55; p <0.01) and mean (r = 0.50; p <0.05) arterial pressure. IVS thickness weakly correlated with NE (r = 0.53; p <0.05). On this relatively small sample, multivariate regression analysis showed an association of both IVS thickness (R = 0.57; p <0.05) and PW thickness (R = 0.58; p <0.05) with mean arterial pressure (MAP) and NE. After atenolol, there was a reduction in IVS thickness (1.15 to 1.02 cm; p <0.01), PW thickness (1.08 to 0.99 cm; p <0.01), and LVMI (136.3 to 113.8 g/m2; p <0.01), besides a significant reduction in blood pressure and heart rate. The degree of pressure reduction induced by treatment did not correlate the change in IVS or PW thickness. In contrast, the change in diastolic and mean arterial pressure positively correlated the change in LVMI (r = 0.72 and r = 0.75, respectively; both p <0.05). These findings suggest that both arterial pressure levels and NE could influence the degree of LVH in stable arterial hypertension with LVH, and that IVS and PW thickness seem more sensitive indicators of LVH, than LVMI, in the research of subtle relationships with hypothetical pathogenetic factors. In contrast, LVMI seems more suitable than the thickness of either wall in the overall assessment of LVH regression during antihypertensive drug treatment when a possible relationship with pressure reduction is being investigated.