Effect of alacepril on 24-hour blood pressure in elderly hypertensive patients.

The effect of administration of an angiotensin-converting enzyme inhibitor, alacepril, on 24-hour blood pressure in the elderly hypertensive patients was investigated. Thirteen elderly hypertensive patients (mean age 71 +/- 5; 6 male and 7 female) participated in the present study. After 2 weeks of control period alacepril was administered 25-50 mg/day for 8 weeks. Ambulatory blood pressure monitoring with cuff-oscillometric method was performed at the end of both control and treatment periods. Alacepril administration for 8 weeks significantly decreased 24-hour blood pressure while it had little effect on heart rate. Daytime blood pressure was significantly decreased from 154 +/- 10/91 +/- 5 mmHg to 145 +/- 8/85 +/- 5 mmHg, while the change in nocturnal blood pressure was not significant: from 137 +/- 17/79 +/- 7 mmHg to 130 +/- 15/75 +/- 9 mmHg. Hyperbaric area of systolic blood pressure was also significantly decreased (from 295 +/- 185 mmHg x hour/day to 172 +/- 111 mmHg x hour/day), indicating that pressure load to the heart was effectively reduced. Administration of alacepril did not cause tachycardia in response to the decrease in blood pressure. Acrophase of both blood pressure and heart rate was changed to 11:00 a.m. These findings indicate that blockade of the renin-angiotensin system in the elderly hypertensive patients decreased blood pressure effectively without causing tachycardia or deterioration of diurnal variations of blood pressure. These hemodynamic changes produced by alacepril administration are favorable for the treatment of the elderly patients with cardiovascular disease.

[A case of idiopathic orthostatic hypotension manifesting sick sinus syndrome due to sympathetic nervous dysfunction].

A 67-year-old woman with idiopathic orthostatic hypotension was presented. The patient started to experience faintness on standing since 1993. During a physical examination, her systolic blood pressure fell from 148 to 50 mmHg on standing. Blood pressure responses to the mental arithmetic test and hyperventilation stress were normal. However, cold pressor test failed to increase blood pressure. These observations, with the finding that phase IV response on Valsalva's maneuver was absent, indicate afferent sympathetic nervous dysfunction. Peripheral neuropathy including diabetes mellitus and involvement of central nervous system such as multiple system atrophy were excluded. Holter ECG examination revealed a 3.9 second sinus arrest and bradycardia (total beats 88901/day). the blunted responses of the heart rate to atropine as well as isoproterenol further suggested the presence of sick sinus syndrome. Amezinium administration significantly improved her orthostatic hypotension and eliminated sinus arrest. These findings indicate that sympathetic nervous dysfunction could account for at least a part of the sick sinus syndrome in this patient.

Left ventricular mass index negatively correlates with heart rate variability in essential hypertension.

To investigate the relationship between alterations of the autonomic nervous activity and left ventricular mass index in essential hypertensive patients, 24-h power spectral analysis of R-R intervals was performed using Holter electrocardiography. Fifty-three patients (mean age, 58.0 +/- 13.1 years; 30 men and 23 women) participated. The urinary excretions and plasma levels of catecholamines were also determined. Power spectral analysis of R-R interval was performed every 10 min by the maximum entropy method to obtain the low frequency band (LFB; 0.04 to 0.15 Hz), which is an index of both parasympathetic and sympathetic nervous activities, and the high frequency band (HFB; 0.15 to 0.4 Hz), which reflects parasympathetic nervous activity. LFB and HFB were averaged every hour to obtain hourly LFB and HFB levels. Total LFB and HFB were calculated as the summation of 24-h LFBs and HFBs. Left ventricular mass index showed a significant negative correlation with total LFB (r = -0.466, P < .001) and total HFB (r = -0.319, P < .02). These findings suggest that the level of end-organ damage correlates with neuronal alteration in essential hypertension.

Glucose intolerance exaggerates left ventricular hypertrophy and dysfunction in essential hypertension.

The influence of glucose intolerance, the preclinical stage of diabetes mellitus, on the progression of left ventricular hypertrophy and left ventricular dysfunction in essential hypertension, was assessed with two-dimensional M-mode echocardiography in age- and sex-matched essential hypertensive patients with (n = 28) or without (n = 44) glucose intolerance, and normotensive control subjects (n = 29). Left ventricular mass index in hypertensive patients with glucose intolerance was significantly higher than that in hypertensive patients without glucose intolerance (mean +/- SD, 115.6 +/- 28.2 v 102.1 +/- 22.1 g/m2; P < .05). Left ventricular diastolic function as reflected by peak lengthening rate was reduced in glucose-intolerant hypertensive patients than in hypertensive patients without glucose intolerance (2.68 +/- 0.71 v 3.16 +/- 0.82/sec; P < .05). End-systolic wall stress/left ventricular end-systolic volume index, an index of left ventricular contractility, was reduced more in glucose-intolerant hypertensive patients than in hypertensive patients without glucose intolerance (2.75 +/- 0.55 v 3.13 +/- 0.55 10(3) dyn.m2/cm2.mL-1; P < .01). These findings suggest that glucose intolerance accelerates progression of left ventricular hypertrophy and deteriorates left ventricular diastolic function and contractility in essential hypertension.