Stretch-induced arrhythmias in the isolated canine ventricle. Evidence for the importance of mechanoelectrical feedback.

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Abstract
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.