{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T14:44:30Z","timestamp":1774449870692,"version":"3.50.1"},"reference-count":29,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2007,4,20]],"date-time":"2007-04-20T00:00:00Z","timestamp":1177027200000},"content-version":"vor","delay-in-days":2422,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiovasc electrophysiol"],"published-print":{"date-parts":[[2000,9]]},"abstract":"<jats:p>Chirality and Repolarization. <jats:italic>Introduction<\/jats:italic>: Two hypotheses have been proposed to explain the mechanisms of vulnerability and related failure of defibrillation therapy: the cross\u2010field\u2010induced critical point hypothesis and the virtual electrode\u2010induced phase singularity hypothesis. These two hypotheses predict the opposite effect of preshock repolarization on the chirality (direction of rotation) of shock\u2010induced reentry. The former suggests its reversal upon reversal of repolarization, whereas the latter suggests its preservation. The aim of this study was to determine, by reversing the repolarization sequence, which of the mechanisms is responsible for internal shock\u2010induced arrhythmia in the Langendorff\u2010perfused rabbit heart.<\/jats:p><jats:p> <jats:italic>Methods and Results<\/jats:italic>: We used high\u2010resolution optical mapping to assess the chirality of postshock reentry in 11 hearts. Hearts were paced at a coupling interval of 300 msec at various sites around the field of view (13.5 \u00d7 13.5 to 16.5 \u00d7 16.5 mm). Cathodal monophasic implantable cardioverter defibrillator shocks (\u2010100 V, 8 msec) were applied during the T wave from a 10\u2010mm coil electrode placed into the right ventricular cavity. We used 3.5 \u00b1 0.8 different pacing sites per heart. Change in direction of repolarization did not result in change of chirality. Chirality was constant in all 11 hearts despite the complete reversal of activation and repolarization patterns. However, the position of resulting vortices depended on transmembrane polarization gradient \u03b4V<jats:sub>m<\/jats:sub> and amplitude of negative polarization V<jats:sub>m<\/jats:sub> (deexcitation). Stronger gradients and deexcitation produced earlier epicardial break excitation (P = 0.04 and P &lt; 0.0001, respectively).<\/jats:p><jats:p> <jats:italic>Conclusion<\/jats:italic>: Virtual electrode\u2010induced phase singularity mechanism underlies internal shock\u2010induced arrhythmia in this model.<\/jats:p>","DOI":"10.1111\/j.1540-8167.2000.tb00172.x","type":"journal-article","created":{"date-parts":[[2007,4,20]],"date-time":"2007-04-20T13:10:15Z","timestamp":1177074615000},"page":"998-1007","source":"Crossref","is-referenced-by-count":24,"title":["Reversal of Repolarization Gradient Does Not Reverse the Chirality of Shock\u2010Induced Reentry in the Rabbit Heart"],"prefix":"10.1111","volume":"11","author":[{"given":"YUANNA","family":"CHENG","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"VLADIMIR","family":"NIKOLSKI","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"IGOR 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