MECHANICAL MODULATION OF STRETCH-INDUCED PREMATURE VENTRICULAR BEATS - INDUCTION OF A MECHANOELECTRIC ADAPTATION PERIOD

Objective: Mechanoelectric Feedback, a mechanical intervention inducin g an electrical change, is gaining credence as a cause of cardiac arrh ythmia in the clinical situation. However, the precise mechanism is un known. To elucidate this we investigated mechanical and chemical modul ation of stretch-induced premature ventricular beats. Methods: We posi tioned a balloon in the left ventricle of an isolated heart (New Zeala nd White rabbit), perfused by the Langendorff technique. Balloon infla tion regularly produces premature ventricular beats. Monophasic action potentials, ECG's and pressure recordings monitored changes during me chanical intervention. The hearts were subjected to (i) variations in the degree of preload and duration of inflation, and (ii) cytoskeletal disrupters, colchicine and cytochalasin-B. Results: Mechanical dilati on of the left ventricle can not only induce premature ventricular bea ts, but also induce a period during which premature beats cannot be re -induced on a subsequent inflation, i.e. a mechanoelectric adaptation period. The trigger for the mechanoelectric adaptation period seems to occur immediately on balloon inflation and required up to 60 s to rec over. This period started with an undershoot in the diastolic componen t of the monophasic action potential as well as in the peak systolic p ressure, with return to control levels within the period. Deflation pr oduced an overshoot (rather than undershoot) in the monophasic action potential duration, but this also returned to control levels within th e period. Changes in preload, duration of inflation and disruption of the cytoskeleton failed to modulate the mechanically induced premature beats, or the mechanoelectric adaptation period. Conclusions: Transie nt ventricular stretch produces arrhythmia, followed by an antiarrhyth mic adaptive period. Possible mechanisms are related to a mechanical i nfluence on stretch-activated channels, changes in ionic concentration or diffusion, or second messenger systems, which influence membrane p otential. The arrhythmic adaptation does not appear to be related to t he mechanical properties of the cytoskeleton. Final elucidation of the mechanism of the mechanoelectric adaptation period demonstrated, may prove important in determining the mechanism of stretch-induced premat ure ventricular beats and consequently arrhythmia management. (C) 1998 Elsevier Science B.V.