Background: Triggered arrhythmias arise from delayed afterdepolarizations (DADs), with Ca2+ waves playing an important role in their formation. In ventricular hypertrophy, however, it remains unclear how Ca2+ waves change their propagation features and affect arrhythmogenesis. We addressed this important issue in a rat model of hypertrophy. Methods and Results: Rats were given a subcutaneous injection of 60 mg/kg monocrotaline (MCT-rats) or solvent (Ctr-rats). After 4 weeks, MCT-rats showed high right ventricular (RV) pressure and RV hypertrophy. Trabeculae were dissected from 36 right ventricles. The force was measured using a silicon strain gauge and regional intracellular Ca2+ ([Ca2+]i) was determined using microinjected fura-2. Reproducible Ca2+ waves were induced by stimulus trains (2 Hz, 7.5 s). MCT-rats showed a higher diastolic [Ca2+]i and faster and larger Ca2+ waves (P<0.01). The velocity and amplitude of Ca2+ waves were correlated with the diastolic [Ca2+]i both in the Ctr- and MCT-rats. The velocity of Ca2+ waves in the MCT-rats was larger at the given amplitude of Ca2+ waves than that in the Ctr-rats (P<0.01). The amplitude of DADs was correlated with the velocity and amplitude of Ca2+ waves in the Ctr- and MCT-rats. Conclusions: The results suggest that an increase in diastolic [Ca2+]i and an increase in Ca2+ sensitivity of the sarcoplasmic reticulum Ca2+ release channel accelerate Ca2+ waves in ventricular hypertrophy, thereby causing arrhythmogenesis.
- Ca waves
- Ventricular hypertrophy
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine