Circulation, Vol 81, 1094-1105, Copyright © 1990 by American Heart Association
DE Hansen, CS Craig and LM Hondeghem
Alterations in loading conditions and muscle length influence the
electrophysiology of ventricular myocardium and may play a role in
arrhythmogenesis in globally dilated or dyskinetic ventricles. To test the
hypothesis that stretch can initiate arrhythmias in normal myocardium, the
response to graded mechanical stretch was studied in seven isolated
blood-perfused canine ventricles. After eight conditioning contractions
produced by His bundle pacing (2 Hz), global stretch of the ventricle was
produced by a servocontrolled pump that abruptly increased ventricular
volume by a precise amount (delta V) during early diastole and then
returned ventricular volume to the initial holding volume (Vi). Ventricular
premature contractions were readily produced; ventricular couplets and
short runs of ventricular tachycardia were occasionally elicited. The
probability of a stretch- induced arrhythmia was determined from multiple
alternating sequences in which a stretch of known amplitude (delta V) or no
stretch was delivered. As delta V was increased, the probability of a
stretch- induced arrhythmia was low initially, increased sharply after a
threshold was exceeded, and approaching 100% with physiological volumes.
With Vi set to a standard value of 20 ml, corresponding to end- diastolic
pressure of 5.3 +/- 5.2 mm Hg (mean +/- SD), the delta V resulting in a 50%
chance of a stretch-induced arrhythmia (delta V50) was 15.0 +/- 1.6 ml. A
decline in delta V50 was consistently observed when Vi was increased. While
delta V50 values were remarkably similar (10.7% coefficient of variation),
the pressure at the time the ventricular premature depolarization was
triggered was highly variable for different ventricles; this finding
suggests that myocardial strain is more important than absolute level of
wall stress in the initiation of these arrhythmias. These results
demonstrate that myocardial stretch predictably initiates arrhythmias and
that the susceptibility to stretch-induced arrhythmias is enhanced by
ventricular dilatation. Thus, ventricular ectopy in patients with
regionally or globally dilated hearts may arise, in part, by a mechanism of
myocardial stretch.
ARTICLES
Stretch-induced arrhythmias in the isolated canine ventricle. Evidence for the importance of mechanoelectrical feedback
Department of Medicine and Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.
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