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Methods: It has been postulated that the statins may have beneficial affects on LV mass in the hypertensive population. We randomised 406 hypertensive patients with normal levels of serum cholesterol [...]

Wave intensity analysis (WIA) is a recently described non-invasive technique that provides information on the working state of the heart, wave reflections, and arterio-ventricular interaction. It is a measure of [...]

In spite of normal indices of LV chamber function, patients with LVH due to hypertension may have a depressed midwall systolic shortening (MWS). In order to assess the relationship between endocardial and MWS in normal subjects and those with LVH in our population we initially assessed using echocardiography 38 patients with previously untreated hypertensive LVH and 38 controls. In order to investigate the effects of treatment on midwall function 32 hypertensive patients underwent treatment with ramipril with the addition of felodipine and bendrofluazide, if required. Each underwent 2D echo at baseline, BP control and after a further 6 months of tight BP control. In the first part of the study the mean cardiac output, ejection fraction and endocardial fractional shortening were similar between the baseline groups (LVH 4.3 ± 0.2 l/min, 62 ± 2%, 35 ± 1.5%; control 4.5 ± 0.2 l/min, 66 ± 1%, 37 ± 0.8%) but MWS was significantly less in the LVH group (LVH 17.9 ± 1.1%, control 21.6 ± 0.6%, p < 0.01). When MWS was adjusted to take into account circumferential wall stress to compare stress-shortening relationships, these differences were maintained. In the treatment study, good BP control was achieved compared with baseline (143/86 ± 2.8/1.4 versus 174/103 ± 4.1/1.9 mm Hg; p < 0.01) with significant regression of LV mass index (124 ± 3.4 versus 145 ± 3.8 g/m2; p < 0.01). Endocardially assessed indices of LV systolic function were not significantly different. Cardiac output was 4.34 ± 0.19 l/min after 6 months compared with 4.48 ± 0.26 at baseline. MWS improved with regression of LVH (21.9 ± 0.84, 18.7 ± 1.19%; p < 0.05), post treatment MWS being similar to that of normal subjects. These results show that MWS is depressed in LVH compared with normal subjects. Depressed MWS has been shown to be an independent predictor of an adverse outcome in hypertensive subjects, particularly in those subjects with LVH so the improvement with therapy is an important observation.