title: Impact of concomitant diabetes and chronic kidney disease on preload-induced changes in left ventricular diastolic filling in hypertensive patients.
abstract: OBJECTIVE
  Concomitant diabetes and/or chronic kidney disease (CKD) in hypertensive patients may portend additive deleterious effects on active left ventricular relaxation. We investigated the effect of a passive leg lifting (PLL) maneuver, a means of increasing preload, on left ventricular filling to assess the relationship of concomitant diabetes mellitus (DM) and/or CKD with diastolic function in hypertensive patients.
  
  
  METHODS
  A total of 155 asymptomatic essential hypertensive patients underwent Doppler echocardiography to compare the echocardiographic indices at baseline and during PLL. In 51 patients, the effect of physiological saline infusion was also examined.
  
  
  RESULTS
  The changes in echocardiographic indices, including deceleration time of early diastolic filling (EDT) and the ratio of transmitral early left ventricular filling velocity to early diastolic Doppler tissue imaging of the mitral annulus (E/E') by saline infusion showed a good correlation with those induced by PLL (Bland-Altman plot and linear regression). We next divided the total participants into four groups according to the presence/absence of diabetes and/or CKD [DM(-)/CKD(-); n = 48, DM(+)/CKD(-); n = 25, DM(-)/CKD(+); n = 43, and DM(+)/CKD(+); n = 39)] and found that the changes in EDT (F = 15.92, P < 0.01) as well as those in E/E' (F = 8.87, P < 0.01) were significantly different among the subgroups. Multiple logistic regression analysis revealed that these complications were independent predictors of EDT less than 150 ms [DM, odds ratio (OR): 2.82; CKD, OR: 2.18, P < 0.05, respectively] as well as E/E' ratio at least 15.0 during PLL (DM, OR: 4.78; CKD, OR: 3.32, P < 0.05, respectively).
  
  
  CONCLUSIONS
  This simple preloading test unmasks latent progression of left ventricular dysfunction in essential hypertension; that is, these complications potentially cause deterioration of left ventricular compliance and preload reserve even in the early stages of diastolic dysfunction.
authors.affiliation: Division of Hypertension and Nephrology, Department of Medicine, National Cardiovascular Center, Osaka, Japan.
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Iwashima
authors.forename: Takeshi
authors.initials: T
authors.lastname: Horio
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Takashi
authors.initials: T
authors.lastname: Takagi
authors.forename: Kei
authors.initials: K
authors.lastname: Kamide
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Ohishi
authors.forename: Toshio
authors.initials: T
authors.lastname: Ogihara
authors.forename: Junichi
authors.initials: J
authors.lastname: Yoshikawa
authors.forename: Yuhei
authors.initials: Y
authors.lastname: Kawano
authors.forename: Hiromi
authors.initials: H
authors.lastname: Rakugi
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D048909:Diabetes Complications / Q000150:complications / Q000503:physiopathology*; D003971:Diastole; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000150:complications / Q000503:physiopathology*; D008875:Middle Aged