RESUMO
The purpose of this study was to detect the anatomical and functional response of the left ventricle in essential, uncomplicated hypertension. Fifty outpatients, whose hypertension (DBP greater than 95 mmHg on three separate visits) had been documented from few weeks to a maximum of 5 years, showing neither electrocardiographic abnormalities nor other signs referable to target organ damage, underwent an M-mode, computerised echocardiographic study. Twenty-seven patients has never been treated, and 23 patients were withdrawn from previous treatments for at least one month. Echocardiographic data of the left ventricle were compared with those of 38 normals, matched by sex, age and body surface area. Hypertensives showed a significant increase in both LV mass index (p less than 0.001) and relative wall thickness (p less than 0.001), a pattern of concentric hypertrophy, which prevented an inappropriate rise in wall tension. Twenty-four patients, whose LV mass was above the mean normal value plus two standard deviations, were considered to have left ventricular hypertrophy. The remaining 26 patients were classified as non hypertrophic, for their mass resulted lower than the mean value of controls plus 2 SD: left ventricular mass was 152 +/- 32 g/m2 and 97 +/- 19 g/m2, respectively (p less than 0.001). Systolic performance was enhanced in both subgroups of hypertensives, since their values of fractional shortening and those of mean-Vcf were both above the line which represents the normal relationship with end-systolic stress. Diastolic relaxation, evaluated by means of time to peak filling rate, was impaired only in the hypertensive subjects with increased LV mass (p less than 0.001 vs. normotensive), being retained in the non-hypertrophic patients. In the whole hypertensive group, LV mass index poorly correlated with casual systolic blood pressure (r = 0.31; p less than 0.05), while time to peak filling rate showed a good correlation with LV mass index (r = 0.76; p less than 0.001). We conclude that: 1) in essential hypertension without electrocardiographic abnormalities or target organ damage, echocardiographic left ventricular hypertrophy is a rather frequent finding; 2) the pattern of concentric hypertrophy, by reducing the increase in wall tension due to pressure load, contributes to the retained, or enhanced, systolic performance seen in our series; 3) on the other hand, left ventricular filling seems to be impaired in relation to the degree of myocardial hypertrophy.
