SUMMARY Forty-three subjects with uncomplicated primary hypertension and without echocardtographic left ventricular hypertrophy and 54 normotensive volunteers were studied by two-dimensional targeted M-mode echocardiography to evaluate systolic function and contractility before the development of compensatory hypertrophy. The ratio of peak systolic pressure to end-systolic dimension was used to assess left ventricular performance and was divided for either posterior wall thickness or cross-sectional area to generate hypertrophy-independent indices of inotropic state. Fractional shortening was normal in the hypertensive group, despite the increase in end-systolic stress. Systolic pressure/dimension ratio was higher in hypertensive subjects (p< 0.001), as were hypertrophy-independent indices of inotropic state (p< 0.005), which were inversely correlated to left ventricular mass (p<0.001). Values in 11 hypertensive subjects were above the upper confidence limit of the normal shortening/stress relation, which provides a load-independent measure of inotropic state. They showed high hypertrophy-independent indices of inotropic state (p<0.01), while the other hypertensive subjects did not. High fractional shortening, wall stress, and systolic pressure (p<0.01) were found in the subgroup with supernormal performance, while left ventricular mass was not different from that of other subgroups, depicting inadequate left ventricular hypertrophy. The duration of hypertension was the same in the subgroups. Supernormal inotropic state could be considered one form of primary adaptation to high wall stress that serves to maintain systolic ventricular performance. (Hypertension 11: 457-463, 1988) KEY WORDS • contractility • arterial hypertension • systolic function T HE role of left ventricular (LV) contractility in the maintenance of pump function during hypertensive disease is still under investigation. Some evidence suggests that performance is enhanced in subjects with primary hypertension, 1 " 3 but its mechanism of action is unclear. An increase in cardiac performance can be due to either improved inotropic state or an increase in the amount of myocardium available for contraction. Although enhancement of contractile force has been thought to be associated with increased LV mass,
SUMMARYLoad changes were obtained in 7 females with untreated primary hypertension by means of controlled intravenous infusion of sodium nitroprusside (0.2mg/ml), in order to assess variations in the more usual indexes of left ventricular (LV) contractility to different loads and to verify that those indexes were independent of load. 2D-controlled Mmode echocardiograms were performed at baseline and when systolic blood pressure (SBP) had been reduced by 7, 16 and 23% for at least 5 min. Heart rate did not change during the test; decrease in SBP was associated with either decreases in both end-systolic dimension (LVIDs) and end-systolic stress (ESS), or an increase in systolic function. SBP/ LVIDs, SBP/end-systolic volume (ESV) and ESS/LVIDs ratios were examined and compared as indexes of contractile state. SBP/ESV and ESS/LVIDs ratios showed great variation at all stages as compared to baseline values, while the SBP/LVIDs ratio did not change. The percent variation between the baseline values and the last stage of the test was 51% for the ESS/LVIDs ratio, 37% for the SBP/ESV and 5% for the SBP/ LVIDs ratio. Best-fitting regression showed that a linear relationship existed only between SBP and LVIDs. Echocardiographic two-dimensional (as ESS) or three-dimensional derivations (as ESV) should be carefully employed when the contractile state is studied, while the SBP/LVIDs ratio can be easily used as a baseline value, as it is insensitive to changes in load.Additional Indexing Words: Afterload Contractility Primary hypertension ENGTH-TENSION relationships are employed to assess left ventricular (LV) contractility, as changes in these relationships, relatively independ-
There is evidence in the literature that calcium entry blockers are able to affect calcium-dependent hormone secretion and therefore can influence sodium and calcium metabolism. We have studied in 18 mild to moderate hypertensives (27-65 yrs) the effects of chronic treatment with nicardipine, a dihydropyridine derivative, vs placebo on: 1) renin-angiotensin-aldosterone axis; 2) parathyroid hormone and calcium metabolism; 3) daily sodium and calcium urinary excretion. After a 2-week placebo wash-out when any antihypertensive treatment was withdrawn, patients were kept on a well balanced normocaloric diet without salt intake restriction. Blood pressure, plasma renin and serum aldosterone after a 1-hour standardized walk, serum PTH, serum and 24-hour urinary Na, K, Ca, P, Mg were measured. Thereafter patients were randomly and blindly given nicardipine 20 mg tid or placebo tablet tid for 2 months. At the end of this period the same measurements were repeated. Blood pressure significantly dropped during nicardipine (from 165/96 +/- 19/9 vs 150/88 +/- 16/9 mm Hg P less than .05) without change in heart rate. No change was observed on placebo. Plasma renin, serum aldosterone, serum parathyroid hormone and serum and urinary electrolytes did not change during active and placebo treatment. The results of this study suggest that chronic nicardipine does not affect hormone secretion.
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