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Triggered Activity As a Possible Mechanism for Arrhythmias in Ventricular Hypertrophy
Author(s) -
CHARPENTIER FLAVIEN,
BAUDET STÉPHANE,
MAREC HERVÉ
Publication year - 1991
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/j.1540-8159.1991.tb02756.x
Subject(s) - medicine , afterdepolarization , stimulation , muscle hypertrophy , right ventricular hypertrophy , repolarization , cardiology , endocrinology , contraction (grammar) , electrophysiology , ventricle
To study the cellular mechanisms of arrhythmias occurring in cardiac hypertrophy, we performed standard microelectrode studies on pupillary muscles isolated from control (group N) and hypertrophied ferrets right ventricles. Different stages of hypertrophy, induced by pulmonary banding, were studied: 10–22 days (group H1), 4–6 weeks (H2), and 5 1/2 –6 months (H3). During the development of hypertrophy, under p‐adrenergic stimulation, triggered activity (TAJ induced by delayed afterdepolurizalions appeared in 2 of 5 muscles in group H1 and 8 of H in group H2. This arrhythmia was absent in N muscles, as well as in H3, despite a pronounced prolongation of the action potentials at 50% (100 ± 9.3 msec in group H3 vs 67 ± 5.7 msec in H2; P < 0.01) and 90% of repolarization (225 ± 8.7 in H3 vs 185 ± 7.4 msec in H2; P < 0.02). The presence of TA was associated with an increase in the intracellular calcium activity (144 ± 60 nM in H2 vs 47 ± 9 nM in N; P < 0.05). TA properties were as follows. Triggering frequency increased as p‐adrenergic stimulation increased, as pacing cycle length (PCL) decreased, and as duration of the prestimulative pause increased. The duration of salvos of TA increased as duration of the prestimulative pauses increased (NS). The coupling interval of the first triggered beat decreased as PCL decreased (P < 0.001). The minimal cycle length of salvos of TA was not modified by these parameters. It is concluded that delayed afterdepolarizations‐induced TA may occur under β‐adrenergic stimulation during the first stages of ventricular hypertrophy. This could partly explain the occurrence ofadrenergic‐dependent arrhythmias in ventricular hypertrophy.