Is blood pressure the major determinant of left ventricular mass in subjects over 50 years of age?

The weak relation of systolic blood pressure to left ventricular (LV) mass in hypertension has frequently been regarded as evidence of non-hemodynamic stimuli to muscle growth. Anyway, left ventricular hypertrophy (LVH) is associated with a significantly increased risk for cardiovascular events. Data were obtained from M-mode echocardiograms in 10 normotensives and 58 hypertensives over 50 years (range 50-85 years); 18 hypertensives; were without (LVH -) and 40 were with LVH (LVH +) - when LV mass, normalized for body surface area, was calculated according to the Penn's Convention. Cardiac output was derived by Teicholz formula for LV volumes. End-systolic stress/end-systolic dimension ratio (ESS/ ESD r), an index of myocardial contractility, was calculated as previously validated in the literature. We found that, in subjects ranging from 50 to 85 years of age, the presence of LV hypertrophy is not necessarily associated with raised blood pressure levels. Systolic function was substantially preserved among the study groups, irrespective of their age, hypertensive condition and/or presence of LVH. The increased wall thickness in subjects with LVH was associated with a significant reduction in wall stress (thus suggesting an adequateness of the compensatory role of LVH - at least at the observed stage of the hypertrophy process) and with a significant decrease of the contractile performance. On the multivariate analysis, the observed relation of LV mass to blood pressure and myocardial contractility (r = 0.621, P < 0.001) may explain some apparently conflicting findings, such as the lack of LV hypertrophy in a number of hypertensive patients.

[Effects of intravenous administration of clarithromycin on plasma levels of gastrin and group I pepsinogen]. / Effetti della somministrazione venosa di claritromicina sui livelli plasmatici di gastrina e pepsinogeno del gruppo I.

Erythromycin and some of its derivatives have prokinetic gastrointestinal properties. In addition, erythromycin has been shown to stimulate isolated chief cells of the gastric mucosa, and to activate pepsin secretion. The above study was aimed at ascertaining in a group of dyspeptic patients whether clarithromycin, a structural analogue of erythromycin, is apt to modify certain functional parameters of gastric secretion, above all the patterns of gastrin and PG-I secretion. A 20-minute intravenous clarithromycin infusion (1.5 mg/kg) in fasting subjects has brought about a significant reduction (at 20 and 45 minutes from the start of infusion) of circulating gastrin (about 23%) and, after a meal, a 69% increase. No change of plasma PG-I level was observed either after placebo or after the active substance. These findings suggest that in vivo and at the doses used in our experiment clarithromycin has no influence on plasma PG-I release and is apt to modify the fasting and postprandial gastrin releasing pattern.