Key Points
- Investigate the in vivo and cellular electrophysiological mechanisms underlying stress-induced arrhythmogenesis during moderate cardiac hypertrophy triggered by pressure overload.
- Studied 47 adult male Wistar rats undergoing 4-week aortic coarctation and 39 age-matched sham-operated controls instrumented for telemetry electrocardiogram recording.
- Evaluated stress-induced cardiac arrhythmias in all rats, quantified ventricular myocardial fibrosis in 35 animals, and measured action potential duration alongside hyperpolarization-activated current density in 19 animals.
- Aortic banding elevated arterial blood pressure by 11%, cardiac weight by 25%, ventricular myocyte volume by 14%, and myocardial fibrosis fourfold (P < 0.05 to P < 0.001).
- Action potential duration and hyperpolarization-activated current density roughly doubled in banded rats (P < 0.05), yet ventricular arrhythmia rates during stress were similar between groups.
- Banded rats exhibited significantly higher rates of supraventricular arrhythmias at baseline and post-stress, along with fewer post-stress atrioventricular block episodes (P < 0.05).
Structured PICO
PPopulation86 male adult Wistar rats (47 with 4-week aortic coarctation and 39 age-matched sham-operated)
IInterventionAortic coarctation (AC) for 4 weeks to induce moderate cardiac hypertrophy
CComparatorAge-matched sham operation (SO)
OOutcomeStress-induced cardiac arrhythmiassurrogate
In a rat model of moderate cardiac hypertrophy, stress-induced supraventricular and atrioventricular nodal arrhythmias are altered, but ventricular arrhythmias are not increased despite significant morphofunctional remodeling.