Circulation, Vol 86, 968-978, Copyright © 1992 by American Heart Association
MR Franz, R Cima, D Wang, D Profitt and R Kurz
BACKGROUND. Although the existence of myocardial mechanoelectrical feedback
is well established, the mechanism of arrhythmia induction by ventricular
dilatation or stretch remains insufficiently defined. In particular,
controversy exists when comparing the arrhythmogenic potential of chronic
versus acute myocardial stretch. Also, assessment of cellular
electrophysiological effects of myocardial stretch has been incomplete.
METHODS AND RESULTS. To evaluate the electrophysiological and
arrhythmogenic effects of slow versus rapid ventricular wall stretch, we
developed an isolated Langendorff-perfused rabbit heart model in which left
ventricular (LV) volume can be changed by a computer-controlled servopump.
Cellular electrophysiological effects and premature ventricular excitations
(PVEs) and their origin produced by the volume increases were assessed by a
multiple-site monophasic action potential (MAP) recording system and by
volume-conducted ECGs obtained by immersing the entire preparation in a
saline-filled tank. Volume was increased either gradually with slow volume
ramps (0.1 ml/sec) or suddenly by volume pulses of varying pulse waveforms
(three different amplitudes and five different rise velocities) applied
randomly 250-350 times to each of eight hearts. Gradual LV volume loading
caused gradual decreases in MAP resting and action potential amplitude,
whereas rapid, transient volume pulses caused transient depolarizations.
Despite similar membrane potential effects of stretch, gradual volume
increases rarely (11%) produced PVEs, even with large volume loads, whereas
rapid volume pulses of moderate amplitudes regularly triggered PVEs
(45-100% of interventions). Logistic regression analysis showed that the
probability of PVE occurrence increased independently with both the
amplitude and the velocity of the volume increase, with the greatest
sensitivity to stretch velocity exhibited at low and intermediate pulse
amplitudes. Faster volume pulse rise velocities triggered PVEs at a lower
instantaneous pulse amplitude than lower rise velocities, further
corroborating the dependence of stretch-activated arrhythmias on the
velocity of stretch. In contrast, an increase in the basic ventricular
volume had no effect on the probability of PVE occurrence during the volume
pulses. The MAP recordings demonstrated spatial variability in the extent
of local depolarizations and site of PVE origin; transient depolarizations
occurred, and PVEs originated most often in the posterolateral region of
the left ventricle. CONCLUSIONS. Membrane depolarization is caused by both
gradual and rapid ventricular stretch, but PVEs are more easily elicited by
rapid stretch. Regions of greater myocardial compliance that experience
greater relative stretch may act as "foci" for stretch- activated
arrhythmias during dynamic ventricular loading. These whole- heart data
corroborate the existence of stretch-activated membrane channels in
ventricular myocardium and may help explain ventricular ectopy under
conditions of differential ventricular loading, as in ventricular
dyskinesia, or regional muscle traction, as in mitral valve prolapse
syndrome.
ARTICLES
Electrophysiological effects of myocardial stretch and mechanical determinants of stretch-activated arrhythmias [published erratum appears in Circulation 1992 Nov;86(5):1663]
Cardiology Division, Stanford University, Calif.
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