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NDT Advance Access originally published online on February 16, 2005
Nephrology Dialysis Transplantation 2005 20(4):760-767; doi:10.1093/ndt/gfh611
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org


Original Article

Atherosclerosis and vascular calcification are independent predictors of left ventricular hypertrophy in chronic haemodialysis patients

Alaattin Yildiz1, Esat Memisoglu2, Huseyin Oflaz3, Halil Yazici1, Hamdi Pusuroglu1, Vakur Akkaya1, Faruk Erzengin3 and Savas Tepe2

Division of 1 Nephrology and 3 Cardiology, Istanbul School of Medicine, Department of Internal Medicine and 2 TEST Tani Merkezi, Radiology Center, Istanbul, Turkey

Correspondence and offprint requests to: Alaattin Yildiz, MD, Istanbul University, Istanbul School of Medicine, Department of Internal Medicine, Division of Nephrology, Millet Caddesi, 34390, Capa, Topkapi, Istanbul, Turkey. Email: alaattiny{at}hotmail.com or yildiza{at}istanbul.edu.tr

Background. Accelerated atherosclerosis and vascular calcification are common in chronic haemodialysis (HD) patients. In this study, we aimed to investigate the relationship between left ventricular hypertrophy (LVH) in HD patients and atherosclerosis and vascular calcification measured by electron beam computed tomography (EBCT).

Methods. In a cohort of 118 HD patients (52 male, 66 female, mean age: 46±13 years), we measured biochemical parameters, including BUN, creatinine, albumin, haemoglobin, C-reactive protein and fibrinogen levels, and performed echocardiography, high-resolution B-mode carotid ultrasonography and EBCT in 85 of them. The degree of stenosis was measured at four different sites (communis, bulbus, interna and externa) in both carotid arteries. Carotid plaque scores were calculated by summing the degrees of stenosis measured at all locations.

Results. LVH was detected in 89 of the patients (75%). Plaque-positive patients had higher left ventricular mass index (LVMI) than plaque-negative patients (175±59 vs 143±46 g/m2, P = 0.003). LVMI was correlated with systolic blood pressure (r = 0.62, P<0.001), pulse pressure (r = 0.58, P<0.001), haemoglobin levels (r = – 0.25, P = 0.008), carotid plaque score (r = 0.32, P = 0.001) and coronary (CACS) and aortic wall calcification score (AWCS) (r = 0.34, P = 0.002 and r = 0.43, P<0.001, respectively). Multiple linear regression analysis (model r = 0.76) showed the independent factors related to LVMI to be systolic blood pressure, pulse pressure, CACS and presence of carotid plaques.

Conclusion. Extra-coronary atherosclerosis and vascular calcification are associated with LVH in HD patients. Whether the treatment of atherosclerosis or vascular calcification may cause regression of or even prevent LVH in HD patients remains to be seen.

Keywords: carotid atherosclerosis; haemodialysis; left ventricular hypertrophy; pulse pressure; vascular calcification


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