Damage induced arrhythmias: Mechanisms and implications

H. E.D.J. Ter Keurs, Ming Zhang Ying Ming Zhang, A. W. Davidoff, P. A. Boyden, Y. J. Wakayama, M. Miura

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)


Little is known about the role played by non-uniform myocardial stress and strain distributions and by non-uniform excitation contraction coupling in mechanisms underlying the premature beats that initiate an arrhythmia. We will review the evidence in support of a mechanism in which both non-uniform contraction and increased Ca2+ load of cells adjacent to acutely damaged cells are essential in the "spontaneous" generation of Ca2+ transients during the relaxation phase of the electrically driven twitch. The putative mechanism of initiation of the propagating Ca2+ waves involves feedback of rapid length (or force) changes to dissociation of Ca2+ from the contractile filaments. A novel aspect of this concept is that these mechanically elicited Ca2+ transients induce propagating Ca2+ waves that travel into the adjacent normal myocardium and cause after-depolarizations, which, in turn, may cause premature action potentials. These premature action potentials will further load the cells with Ca2+, which promotes the subsequent generation of propagating Ca2+ transients and leads to triggered arrhythmias. The damage-induced premature beats may also initiate re-entry arrhythmias in non-uniform myocardium. These observations strongly support the concept that abnormal cellular Ca2+ transport plays a crucial role in the initiation of arrhythmias in damaged and non-uniform myocardium.

Original languageEnglish
Pages (from-to)73-81
Number of pages9
JournalCanadian Journal of Physiology and Pharmacology
Issue number1
Publication statusPublished - 2001


  • Ca
  • Cardiac muscle
  • Damage
  • Et arrhythmias
  • Excitation-contraction coupling


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