TY - JOUR
T1 - Effect of ramipril on left ventricular mass in normotensive hemodialysis patients
AU - Yu, Wen Chung
AU - Lin, Yao Ping
AU - Lin, I. Feng
AU - Chuang, Shao Yuan
AU - Chen, Chen Huan
N1 - Funding Information:
Support: This work was supported in part by grants from the National Science Council (NSC 90-2314-B-010-024 and NSC 91-2314-B-010-011), and a grant from Aventis Pharma, Co., Ltd., Taiwan. Potential conflicts of interest: None.
PY - 2006/3
Y1 - 2006/3
N2 - Background: Normotensive hemodialysis patients may still have left ventricular hypertrophy in the absence of significant pressure or volume overload. We examined the hypothesis that treatment with an angiotensin- converting enzyme inhibitor could be beneficial in the reversal of left ventricular hypertrophy in these patients. Methods: Forty-six normotensive patients with end-stage renal disease on regular hemodialysis therapy were randomly assigned to administration of ramipril, 2.5 mg 3 times/wk, or placebo for 1 year. Left ventricular mass index and parameters of cardiovascular structure and function were evaluated noninvasively by means of echocardiography and arterial tonometry at baseline, 6 and 12 months after treatment, and 1 month after washout. Results: In the ramipril group, blood pressure decreased significantly at 6 and 12 months after treatment. There were no significant within-group or between-group differences in left ventricular mass index at entry, 6 and 12 months after treatment, and 1 month after washout. There were no significant differences in left atrial dimension, left ventricular size and wall thickness, left ventricular ejection fraction, aortic dimension, intima-media thickness, elastic modulus and augmentation index of the common carotid artery, and aortic pulse wave velocity between the ramipril and placebo groups at entry, 6 and 12 months after treatment, and 1 month after washout. Conclusion: A 12-month treatment with ramipril did not cause significant regression of left ventricular hypertrophy in normotensive hemodialysis patients. Results may suggest that the renin-angiotensin system has little role in the pathogenesis of mild left ventricular hypertrophy in these patients.
AB - Background: Normotensive hemodialysis patients may still have left ventricular hypertrophy in the absence of significant pressure or volume overload. We examined the hypothesis that treatment with an angiotensin- converting enzyme inhibitor could be beneficial in the reversal of left ventricular hypertrophy in these patients. Methods: Forty-six normotensive patients with end-stage renal disease on regular hemodialysis therapy were randomly assigned to administration of ramipril, 2.5 mg 3 times/wk, or placebo for 1 year. Left ventricular mass index and parameters of cardiovascular structure and function were evaluated noninvasively by means of echocardiography and arterial tonometry at baseline, 6 and 12 months after treatment, and 1 month after washout. Results: In the ramipril group, blood pressure decreased significantly at 6 and 12 months after treatment. There were no significant within-group or between-group differences in left ventricular mass index at entry, 6 and 12 months after treatment, and 1 month after washout. There were no significant differences in left atrial dimension, left ventricular size and wall thickness, left ventricular ejection fraction, aortic dimension, intima-media thickness, elastic modulus and augmentation index of the common carotid artery, and aortic pulse wave velocity between the ramipril and placebo groups at entry, 6 and 12 months after treatment, and 1 month after washout. Conclusion: A 12-month treatment with ramipril did not cause significant regression of left ventricular hypertrophy in normotensive hemodialysis patients. Results may suggest that the renin-angiotensin system has little role in the pathogenesis of mild left ventricular hypertrophy in these patients.
KW - Arterial stiffness
KW - Left ventricular function
KW - Left ventricular mass
KW - Ramipril
KW - Renal failure
UR - http://www.scopus.com/inward/record.url?scp=32844469027&partnerID=8YFLogxK
U2 - 10.1016/j.cap.2005.11.044
DO - 10.1016/j.cap.2005.11.044
M3 - Article
C2 - 16490627
AN - SCOPUS:32844469027
SN - 0272-6386
VL - 47
SP - 478
EP - 484
JO - American Journal of Kidney Diseases
JF - American Journal of Kidney Diseases
IS - 3
ER -