Impact of frequent nocturnal hemodialysis on myocardial mechanics and cardiomyocyte gene expression.
BACKGROUND
Regression of left ventricular mass with nocturnal hemodialysis has been observed. The influence of nocturnal hemodialysis on myocardial mechanics and cardiomyocyte gene expression is unknown.


RESULTS
Forty-two patients (30 male:12 female; age, 44 ± 12 years [mean ± SD]) with end-stage renal disease were followed for 3.1 ± 1.8 years before and after conversion to nocturnal hemodialysis and were compared with 29 normal subjects (18 male:11 female; age, 48 ± 13 years). Myocardial mechanics were assessed by 2-dimensional velocity vector imaging. Uremic plasma (10%) was added to cultures of neonatal Sprague-Dawley rat ventricular myocytes. Total RNA was isolated from cell cultures and subjected to differential gene expression profiling with specific interest in genes affecting apoptosis and fibrosis. Left ventricular mass index and left atrial volume index decreased from 122.6 ± 42.6 to 98.5 ± 34.9 g/m(2) (P<0.001) and 25.9 ± 9.1 to 22.5 ± 9.6 cm(3)/m(2) (P=0.005), respectively. Left ventricular apical circumferential strain and basal rotation improved after conversion to nocturnal hemodialysis and approximated normal values. Nocturnal hemodialysis increased sessional dialysis dose and lowered parathyroid hormone levels (from 51 ± 67 to 24 ± 37 pmol/L, P<0.05) and phosphate. Under conventional hemodialysis conditions, there was an upregulation of genes leading to apoptosis and fibrosis in cardiomyocytes. The change in left ventricle rotation was associated with the change in parathyroid hormone values (r=0.37, P=0.02) and to the change in left ventricle mass (r=0.31, P=0.046).


CONCLUSIONS
Frequent hemodialysis is associated with improvement in myocardial mechanics and cardiac gene expression profile, which warrants prognostic validation.
Divisions of Nephrology and Cardiology, Department of Medicine, University Health Network, Toronto, Ontario, Canada. christopher.chan@uhn.on.ca
Christopher T
CT
Chan
Sara
S
Arab
Shemy
S
Carasso
Gil
G
Moravsky
Guo Hua
GH
Li
Peter P
PP
Liu
Harry
H
Rakowski
D000328:Adult; D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000235:genetics*; D002940:Circadian Rhythm; D015150:Echocardiography, Doppler / Q000379:methods*; D005260:Female; D005355:Fibrosis / Q000235:genetics*; D020869:Gene Expression Profiling; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000235:genetics* / Q000503:physiopathology / Q000517:prevention & control*; D007676:Kidney Failure, Chronic / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D032383:Myocytes, Cardiac; D010281:Parathyroid Hormone / Q000097:blood; D010710:Phosphates / Q000097:blood; D016133:Polymerase Chain Reaction / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D006435:Renal Dialysis / Q000379:methods*; D009418:S100 Proteins / Q000235:genetics*; D018709:Statistics, Nonparametric
D010281:Parathyroid Hormone; D010710:Phosphates; D009418:S100 Proteins; C110294:S100A1 protein