In 47 male adult Wistar rats with 4-wk aortic coarctation (AC) and 39 age-m
atched sham-operated rats (SO) chronically instrumented for telemetry elect
rocardiogram recording, we investigated the mechanisms of arrhythmogenesis
in moderate cardiac hypertrophy, with an approach from "in vivo" toward the
cellular level, analyzing 1) stress-induced cardiac arrhythmias in all rat
s and 2) myocardial fibrosis in 35 animals and action potential duration an
d density of hyperpolarization-activated current in 19 others at the ventri
cular level. Aortic banding increased arterial blood pressure, cardiac weig
ht, and ventricular myocyte volume by 11, 25, and 14%, respectively (P< 0.0
01-0.05). Ventricular arrhythmias occurred at similar rates in AC and SO ra
ts throughout the stress procedure. Action potential duration and hyperpola
rization-activated current were about twice as great and myocardial fibrosi
s about four times greater in AC animals (P< 0.005-0.05). Electrocardiogram
data also revealed more supraventricular arrhythmias in AC rats during the
baseline period and after stress and fewer atrioventricular block episodes
after stress (P< 0.05). Thus stress-induced supraventricular and atriovent
ricular nodal, but not ventricular, arrhythmias were affected in moderate c
ardiac hypertrophy when ventricular morphofunctional alterations were evide
nt.