YOU ARE NOW CONNECTED TO THE TOXLINE (1981 FORWARD, NON-ROYALTY) FILE. ==VENTRICLE HYPERTROPHY== 2 AUTHOR Machnig T AUTHOR Henneke KH AUTHOR Engels G AUTHOR Pongratz G AUTHOR Schmalzl M AUTHOR Gellert J AUTHOR Bachmann K TITLE Nitrendipine vs. captopril in essential hypertension: effects on circadian blood pressure and left ventricular hypertrophy. SOURCE Cardiology; VOL 85, ISS 2, 1994, P101-10 ABSTRACT Both nitrendipine and captopril have been shown to reverse left ventricular hypertrophy in hypertensive patients. So far, no study allowed a true comparison of these drugs in this regard and with respect to their potential of reducing circadian blood pressure. Therefore, a total of 86 patients with newly diagnosed arterial hypertension and echocardiographic evidence of left ventricular hypertrophy underwent randomized treatment with captopril (n = 43) or nitrendipine (n = 43). Eighteen patients had to be put on a combination therapy of nitrendipine and captopril during the course of the study to control blood pressure effectively. Before and after the 6th and 38th weeks of treatment all patients underwent ambulatory 24-hour blood pressure monitoring, M-mode echo assessment of left ventricular mass and Doppler evaluation of left ventricular filling. The 24-hour blood pressure data were smoothed with a Fourier series and then compared with a normotensive reference profile with respect to blood pressure load and variability. The daytime and nighttime mean and the office blood pressure were also analyzed. Substance-specific profiles of action were obtained by subtracting the smoothed profiles after therapy from the profiles before therapy. After 38 weeks ambulatory blood pressure had decreased from 152 +/- 11/101 +/- 7 to 137 +/- 13/87 +/- 10 mm Hg on nitrendipine and from 147 +/- 11/99 +/- 6 to 134 +/- 13/89 +/- 9 mm Hg on captopril. The substance-specific profiles calculated for captopril and nitrendipine showed a balanced antihypertensive effect throughout the day and the night. The mean percentage decreases in left ventricular muscle mass under nitrendipine was 15% and did not differ significantly from the decrease of 21% under treatment with captopril (p < 0.001). There is no significant association between the reduction in blood pressure and the regression of left ventricular hypertrophy. In patients with disturbances of left ventricular diastolic function the early-to-late diastolic left ventricular flow ratio and the isovolumetric relaxation time were improved independent of the drug used. It is concluded that a long-term therapy with captopril and nitrendipine leads to a comparable degree of circadian blood pressure reduction and regression of hypertensive left ventricular hypertrophy. 5 AUTHOR Agabiti-Rosei E AUTHOR Muiesan ML AUTHOR Rizzoni D AUTHOR Zulli R AUTHOR Calebich S AUTHOR Beschi M AUTHOR Castellano M AUTHOR Muiesan G TITLE Reduction of left ventricular hypertrophy after longterm antihypertensive treatment with doxazosin. SOURCE J Hum Hypertens; VOL 6, ISS 1, 1992, P9-15 ABSTRACT The aim of this study was to evaluate the effect of antihypertensive treatment with doxazosin on left ventricular anatomy and function. Therefore, after 4 weeks of washout with placebo (phase 1), doxazosin (dosage range from 1 to 16 mg, plus hydrochlorothiazide when necessary) was given to 11 essential hypertensive patients (6 M, 5 F, age range 34-63 years) for 8 weeks (phase 2) in order to achieve diastolic blood pressure values less than 90 mmHg; this dosage was then maintained for a further 20 weeks up to the end of the study (phase 3). Blood pressure was significantly reduced (Anova P less than 0.05), while heart rate did not change. A significant reduction of left ventricular mass index (from 128.5 +/- 26 to 114 +/- 23 g/m2, at the end of phase 1 and 3 respectively, P less than .001)) was observed. Before and during treatment left ventricular systolic function, both at rest and during stress (handgrip and cold pressor tests), evaluated by fractional shortening as related to end-systolic stress, in every case within 95% confidence limits, was calculated in normal subjects. Diastolic function, as evaluated by the ratio between peak early and atrial velocities of transmitral flow examined by pulsed doppler was significantly improved. Plasma catecholamine concentrations, plasma renin activity and plasma aldosterone did not change. A significant reduction of plasma cholesterol concentration was observed. These results confirm that doxazosin is a well tolerated and effective antihypertensive drug, with a favourable effect on blood lipids and they indicate that its longterm administration can induce a significant reduction of left ventricular mass. 6 AUTHOR Senda Y AUTHOR Tohkai H AUTHOR Kimura M AUTHOR Shida Y AUTHOR Tutumi S AUTHOR Koshiyama H AUTHOR Tanaka T AUTHOR Shimaji Y AUTHOR Nogita T TITLE ECG-gated cardiac scan and echocardiographic assessments of left ventricular hypertrophy: reversal by 6-month treatment with diltiazem. SOURCE J Cardiovasc Pharmacol; VOL 16, ISS 2, 1990, P298-304 ABSTRACT Serial changes of left ventricular (LV) mass and LV function were evaluated in nine patients with essential hypertension and LV hypertrophy (LVH) after administration of diltiazem (180 mg/day). LV mass and LV function were determined at baseline and at 6 months of therapy by electrocardiogram-gated cardiac CT (ECG-gated CCT) scanning and two-dimensional-guided M-mode echocardiography. At baseline measurements, ECG-gated cardiac scanning clearly showed LVH in two patients in whom no LVH was observed by echocardiography. The systolic and diastolic blood pressures were reduced significantly after 6 months of drug therapy (189-156 mm Hg; p less than 0.01, 111-96 mm Hg; p less than 0.01, respectively). Sequential ECG-gated cardiac scanning revealed a marked reduction in thickness of the interventricular septum (IVS), LV anterior wall (AW), and LV posterior wall (PW) (15.0-12.1 mm; p less than 0.01, 12.5-9.7 mm; p less than 0.01, 10.7-8.3 mm; p less than 0.05, respectively). Simultaneous echocardiographic measurements revealed a reduction in LV mass in six of these patients and a significant reduction in thickness of the IVS (12.1-11.0 mm; p less than 0.05). ECG-gated cardiac scanning demonstrated significant reductions in the thickness of the LVAW, which are difficult to detect by echocardiography. Diltiazem had no effect on the ejection fraction (EF) measured by both methods. In conclusion, ECG-gated cardiac scanning allowed more accurate diagnosis and quantitation of LVH than conventional echocardiography, and LVH in patients with essential hypertension could be reversed by the administration of diltiazem.