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2014 ; 25
(12
): 2812-21
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Pathogenesis of arrhythmias in a model of CKD
#MMPMID24854269
Hsueh CH
; Chen NX
; Lin SF
; Chen PS
; Gattone VH 2nd
; Allen MR
; Fishbein MC
; Moe SM
J Am Soc Nephrol
2014[Dec]; 25
(12
): 2812-21
PMID24854269
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Patients with CKD have an increased risk of cardiovascular mortality from
arrhythmias and sudden cardiac death. We used a rat model of CKD (Cy/+) to study
potential mechanisms of increased ventricular arrhythmias. Rats with CKD showed
normal ejection fraction but hypertrophic myocardium. Premature ventricular
complexes occurred more frequently in CKD rats than normal rats (42% versus 11%,
P=0.18). By optical mapping techniques, action potential duration (APD) at 80% of
repolarization was longer in CKD rats (78±4ms) than normal rats (63±3 ms, P<0.05)
at a 200-ms pacing cycle length. Calcium transient (CaT) duration was comparable.
Pacing cycle length thresholds to induce CaT alternans or APD alternans were
longer in CKD rats than normal rats (100±7 versus 80±3 ms and 93±6 versus 76±4 ms
for CaT and APD alternans, respectively, P<0.05), suggesting increased
vulnerability to ventricular arrhythmia. Ventricular fibrillation was induced in
9 of 12 CKD rats and 2 of 9 normal rats (P<0.05); early afterdepolarization
occurred in two CKD rats but not normal rats. The mRNA levels of TGF-?,
microRNA-21, and sodium calcium-exchanger type 1 were upregulated, whereas the
levels of microRNA-29, L-type calcium channel, sarco/endoplasmic reticulum
calcium-ATPase type 2a, Kv1.4, and Kv4.3 were downregulated in CKD rats. Cardiac
fibrosis was mild and not different between groups. We conclude that cardiac ion
channel and calcium handling are abnormal in CKD rats, leading to increased
vulnerability to early afterdepolarization, triggered activity, and ventricular
arrhythmias.
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