title: Atherosclerosis and vascular calcification are independent predictors of left ventricular hypertrophy in chronic haemodialysis patients.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Istanbul School of Medicine, Department of Internal Medicine, Millet Caddesi, 34390, Capa, Topkapi, Istanbul, Turkey. alaattiny@hotmail.co
authors.forename: Alaattin
authors.initials: A
authors.lastname: Yildiz
authors.forename: Esat
authors.initials: E
authors.lastname: Memisoglu
authors.forename: Huseyin
authors.initials: H
authors.lastname: Oflaz
authors.forename: Halil
authors.initials: H
authors.lastname: Yazici
authors.forename: Hamdi
authors.initials: H
authors.lastname: Pusuroglu
authors.forename: Vakur
authors.initials: V
authors.lastname: Akkaya
authors.forename: Faruk
authors.initials: F
authors.lastname: Erzengin
authors.forename: Savas
authors.initials: S
authors.lastname: Tepe
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D050197:Atherosclerosis / Q000150:complications*; D002114:Calcinosis / Q000150:complications*; D002340:Carotid Artery Diseases / Q000150:complications*; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D006435:Renal Dialysis / Q000009:adverse effects*