Comparative effects of valsartan versus amlodipine on left ventricular mass and reactive oxygen species formation by monocytes in hypertensive patients with left ventricular hypertrophy.
OBJECTIVE
To compare the effects of the angiotensin receptor blocker (ARB) valsartan versus the calcium channel blocker amlodipine, reactive oxygen species (ROS) formation by monocytes, C-reactive protein (CRP), and left ventricular (LV) mass were studied in 104 hypertensive patients with left ventricular hypertrophy (LVH).


BACKGROUND
There is evidence that ARBs have blood pressure (BP)-independent effects on LV mass. Whether regression of LV mass by ARBs is correlated to ROS formation by monocytes and CRP is not fully understood yet.


METHODS
A cross-sectional and prospective study was performed. Participants were randomly assigned to either the 80-mg valsartan (n = 52) or 5-mg amlodipine (n = 52) group and were treated for eight months. The left ventricular mass index (LVMI) was calculated from two-dimensional M-mode echocardiography. Formation of ROS by monocytes was measured by gated flow cytometry. In addition, CRP, plasma renin activity, plasma aldosterone, and traditional risk factors were assessed.


RESULTS
Multiple regression analysis showed a significant correlation between LVMI and ROS formation by monocytes and between LVMI and CRP. Treatment reduced BP to a similar extent in both groups. Valsartan significantly reduced LVMI after eight months, but amlodipine had less effect (16% vs. 1.2%, n = 50, p < 0.01). Formation of ROS by monocytes was reduced to a greater extent with valsartan than with amlodipine (28% vs. 2%, n = 50, p < 0.01). Valsartan but not amlodipine reduced CRP levels. A significant correlation between changes in ROS formation by monocytes and LVMI or between CRP and LVMI was observed.


CONCLUSIONS
The ARB valsartan has BP-independent effects on LVH, ROS formation by monocytes, and CRP in hypertensive patients with LVH.
Yasunari
Kenichi
K
Department of General Medicine and Cardiology, Graduate School of Medicine, Osaka City University, Osaka, Japan. yasunari@med.osaka-cu.ac.jp
Maeda
Kensaku
K
Watanabe
Takanori
T
Nakamura
Munehiro
M
Yoshikawa
Junichi
J
Asada
Akira
A
D017311:Amlodipine / Q000008:administration & dosage / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D003430:Cross-Sectional Studies; D004311:Double-Blind Method; D004452:Echocardiography; D005260:Female; D005434:Flow Cytometry; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000188:drug therapy*; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism; D011446:Prospective Studies; D017382:Reactive Oxygen Species / Q000378:metabolism; D013777:Tetrazoles / Q000008:administration & dosage / Q000627:therapeutic use*; D016896:Treatment Outcome; D014633:Valine / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000627:therapeutic use*; D000068756:Valsartan
D000959:Antihypertensive Agents; D017382:Reactive Oxygen Species; D013777:Tetrazoles; D017311:Amlodipine; D000068756:Valsartan; D014633:Valine