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Arrhythmogenesis in Heart Failure
Author(s) -
JANSE MICHIEL J.,
VERMEULEN JESSICA T.,
OPTHOF TOBIAS,
CORONEL RUBEN,
WILMSSCHOPMAN FRANCIEN J. G.,
RADEMAKER HAN M. E.,
BAARTSCHEER ANTONIUS,
DEKKER LUKAS R. C.
Publication year - 2001
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1046/j.1540-8167.2001.00496.x
Subject(s) - medicine , heart failure , cardiology , afterdepolarization , volume overload , heart rate , pressure overload , sinus rhythm , endoplasmic reticulum , anesthesia , blood pressure , atrial fibrillation , electrophysiology , repolarization , cardiac hypertrophy , biochemistry , chemistry
Arrhythmogenesis in Heart Failure. In a rabbit model of heart failure produced by combined pressure and volume overload, nonsustained ventricular tachycardias developed in 15 of 23 failing rabbits. Sinus rate was increased in rabbits dying suddenly, but was decreased in survivors. This also was true in isolated preparations. Microelectrode recordings from ventricular trabeculae both from patients with end‐stage failure and from failing rabbits showed that in half of the preparations, delayed afterdepolarizations and triggered activity occurred, but only in the presence of norepinephrine and a lowered extracellular K + concentration of 3 mM. This was due to spontaneous release of Ca 2+ from the sarcoplasmic reticulum.