Circulation, Vol 90, 2786-2796, Copyright © 1994 by American Heart Association
GM London, B Pannier, AP Guerin, SJ Marchais, ME Safar and JL Cuche
BACKGROUND: We wished to assess the respective roles of the
antihypertensive and blood pressure (BP)-independent effects of
antihypertensive drugs on arterial hemodynamics and left ventricular
hypertrophy (LVH) in end-stage renal disease (ESRD) patients. METHODS AND
RESULTS: In a double-blind study, 24 ESRD patients with LVH were randomized
to 12 months' administration of either the angiotensin- converting enzyme
(ACE) inhibitor perindopril (n = 14) or the calcium channel blocker
nitrendipine (n = 10). Repeated measurements of the following parameters
were performed: BP (mercury sphygmomanometry), left ventricular mass (LVM,
echocardiography), cardiac output (aortic cross-section and velocity
integral), total peripheral resistance (cardiac output and mean BP), aortic
and large-artery compliance (pulse wave velocity, Doppler flowmeter), and
arterial wave reflections (augmentation index, applanation tonometry).
Radioimmunoassay was used to determine plasma renin activity, aldosterone,
and plasma catecholamine levels. Two-way (time-treatment) ANOVA for
repeated measures was used for statistical analysis. Perindopril and
nitrendipine induced significant and similar decreases in BP, total
peripheral resistance (P < .001), aortic and arterial pulse wave
velocities (P < .001), and arterial wave reflections (P < .01). At
baseline, the two groups had LVH mostly due to increased LV end- diastolic
diameter (LVEDD) (perindopril, 54.3 +/- 1.4 and nitrendipine, 54.3 +/ 2.4
mm) with near-normal mean LV wall thickness (perindopril, 11.4 +/- 0.3 and
nitrendipine, 11.2 +/- 0.4 mm). A decrease in LVM was observed only in
patients receiving perindopril (from 317 +/- 18 to 247 +/- 21 g)
(time-treatment interaction, P = .036). Nitrendipine had no significant
effect on LVM (314 +/- 29 versus 286 +/- 32 g). The decrease in LVM
observed with perindopril was associated with a reduction in LVEDD (49.9
+/- 1.6 versus 54.3 +/- 1.4 mm after 12 months) (time-treatment
interaction, P = .04), while the mean LV wall thickness was unchanged (11.4
+/- 0.3 versus 10.5 +/- 0.5 mm). Cardiac alterations were not correlated
with changes in BP or with alterations in plasma renin activity or
aldosterone or catecholamine levels. CONCLUSIONS: In ESRD patients with
LVH, ACE inhibition decreases LVM independently of its antihypertensive
effect and of associated alterations in arterial hemodynamics. The decrease
in LVM was due primarily to a decrease in LV volume, which may have
resulted in these patients from chronic volume overload.
ARTICLES
Cardiac hypertrophy, aortic compliance, peripheral resistance, and wave reflection in end-stage renal disease. Comparative effects of ACE inhibition and calcium channel blockade
Centre Hospitalier F.H. Manhes, Fleury-Merogis, France.
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