title: Quatrefoil reentry in myocardium: an optical imaging study of the induction mechanism.
abstract: BACKGROUND
  The "critical point hypothesis" for induction of ventricular fibrillation has previously been extended to infer the coexistence of four critical points, and hence four simultaneous spiral reentries or a quatrefoil reentry, resulting from only one premature stimulus delivered to the same location as the pacing stimulus. An optical imaging technique was used to explore its existence and to study the induction mechanism of this peculiar reentry pattern.
  
  
  RESULTS
  In 16 isolated, Langendorff-perfused rabbit hearts, high-speed optical imaging at 133 or 267 frames/sec was performed to observe the induced response with a unipolar point electrode. A novel quatrefoil-shaped reentry pattern consisting of two pairs of opposing rotors was created by delivering long stimuli during the vulnerable phase. Successful induction occurred in a narrow range of coupling intervals. A dogbone pattern of virtual electrodes was established during the premature stimulus. Propagating wavefronts launched from the virtual anodes immediately after the termination of S2. The alternating blocking and conducting effects of the virtual electrodes, as well as the boundary between virtual cathode and virtual anode, provided the necessary pathways for quatrefoil reentry. Propagation directions of the reentrant spiral wavefronts reversed with a reversal in S2 polarity. Quatrefoil reentries were not sustained and lasted 1 to 4 complete cycles.
  
  
  CONCLUSIONS
  The initiation of quatrefoil reentry followed anodal- or cathodal-break stimulation as a result of local symmetrical enhancement of the dispersion of tissue excitability. The "critical point hypothesis" provides the minimum topology required for this type of reentry; the "graded response hypothesis" can be viewed as providing a more detailed explanation of how this topology is actually realized. Triggering mechanisms due to the "break" mode of stimulation also posits a new mechanism for defibrillation.
authors.affiliation: Department of Physics & Astronomy, Vanderbilt University, Nashville, Tennessee, USA. linsf@ctrvax.vanderbilt.edu
authors.forename: S F
authors.initials: SF
authors.lastname: Lin
authors.forename: B J
authors.initials: BJ
authors.lastname: Roth
authors.forename: J P
authors.initials: JP
authors.lastname: Wikswo
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004195:Disease Models, Animal; D004558:Electric Stimulation; D005336:Fiber Optic Technology; D005711:Gallopamil / Q000494:pharmacology; D006329:Heart Conduction System / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology; D066298:In Vitro Techniques; D007834:Lasers; D008564:Membrane Potentials; D009200:Myocardial Contraction / Q000187:drug effects; D010477:Perfusion; D011817:Rabbits; D013611:Tachycardia, Atrioventricular Nodal Reentry / Q000175:diagnosis* / Q000503:physiopathology
chemical_list: D002121:Calcium Channel Blockers; D005711:Gallopamil