{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T22:27:39Z","timestamp":1790720859954,"version":"4.1.0"},"reference-count":0,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2003,8,13]],"date-time":"2003-08-13T00:00:00Z","timestamp":1060732800000},"content-version":"vor","delay-in-days":834,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiovasc electrophysiol"],"published-print":{"date-parts":[[2001,5]]},"abstract":"\n Focal AF and Autonomic Nerves.<\/jats:bold>\n Introduction:<\/jats:italic>\n Focal paroxysmal atrial fibrillation (AF) was shown recently to originate in the pulmonary veins (PVs) and superior vena cava (SVC). In the present study, we describe an animal model in which local high\u2010frequency electrical stimulation produces focal atrial activation and AF\/AT (atrial tachycardia) with electrogram characteristics consistent with clinical reports.\n <\/jats:p>\n \n Methods and Results:<\/jats:italic>\n In 21 mongrel dogs, local high\u2010frequency electrical stimulation was performed by delivering trains of electrical stimuli (200 Hz, impulse duration 0.1 msec) to the PVs\/SVC during atrial refractoriness. Atrial premature depolarizations (APDs), AT, and AF occurred with increasing highfrequency electrical stimulation voltage. APD\/AT\/AF originated adjacent to the site of high\u2010frequency electrical stimulation and were inducible in 12 of 12 dogs in the SVC and in 8 of 9 dogs in the left superior PV (left inferior PV: 7\/8, right superior PV: 6\/8; right inferior PV: 4\/8). In the PVs, APDs occurred at\n 13 \u00b1 8 V<\/jats:styled-content>\n and AT\/AF at\n 15 \u00b1 9 V<\/jats:styled-content>\n (\n P < 0.01; n = 25<\/jats:styled-content>\n ). In the SVC, APDs were elicited at\n 19 \u00b1 6 V<\/jats:styled-content>\n and AT\/AF at\n 26 \u00b1 6 V<\/jats:styled-content>\n (\n P < 0.01; n = 12<\/jats:styled-content>\n ). High\u2010frequency electrical stimulation led to local refractory period shortening in the PVs. The response to high\u2010frequency electrical stimulation was blunted or prevented after beta\u2010receptor blockade and abolished by atropine. In vitro, high\u2010frequency electrical stimulation induced a heterogeneous response, with shortening of the action potential in some cells (from\n 89 \u00b1 35<\/jats:styled-content>\n msec to\n 60 \u00b1 22 msec; P < 0.001; n = 7<\/jats:styled-content>\n ) but lengthening of the action potential and development of early afterdepolarizations that triggered APD\/AT in other cells. Action potential shortening was abolished by atropine.\n <\/jats:p>\n \n Conclusion:<\/jats:italic>\n High\u2010frequency electrical stimulation evokes rapid ectopic beats from the PV\/SVC, which show variable degrees of conduction block to the atria and induce AF, resembling findings in patients with focal idiopathic paroxysmal AF. The occurrence of the arrhythmia in this animal model was likely due to alterations in local autonomic tone by high\u2010frequency electrical stimulation. Further research is needed to prove absolutely that the observed effects of high\u2010frequency electrical stimulation were caused by autonomic nerve stimulation.\n <\/jats:p>","DOI":"10.1046\/j.1540-8167.2001.00592.x","type":"journal-article","created":{"date-parts":[[2003,8,13]],"date-time":"2003-08-13T08:12:23Z","timestamp":1060762343000},"page":"592-599","source":"Crossref","is-referenced-by-count":184,"title":["Focal Atrial Fibrillation: Experimental Evidence for a Pathophysiologic Role of the Autonomic Nervous System"],"prefix":"10.1111","volume":"12","author":[{"given":"PATRICK","family":"SCHAUERTE","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"BENJAMIN J.","family":"SCHERLAG","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"EUGENE","family":"PATTERSON","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"MICHAEL A.","family":"SCHERLAG","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"KAGARI","family":"MATSUDARIA","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"HIROSHI","family":"NAKAGAWA","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"RALPH","family":"LAZZARA","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"WARREN M.","family":"JACKMAN","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2003,8,13]]},"container-title":["Journal of Cardiovascular Electrophysiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1046%2Fj.1540-8167.2001.00592.x","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/pdf\/10.1046\/j.1540-8167.2001.00592.x","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,11,19]],"date-time":"2023-11-19T09:31:24Z","timestamp":1700386284000},"score":1,"resource":{"primary":{"URL":"https:\/\/onlinelibrary.wiley.com\/doi\/10.1046\/j.1540-8167.2001.00592.x"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2001,5]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2001,5]]}},"alternative-id":["10.1046\/j.1540-8167.2001.00592.x"],"URL":"https:\/\/doi.org\/10.1046\/j.1540-8167.2001.00592.x","archive":["Portico"],"relation":{},"ISSN":["1045-3873","1540-8167"],"issn-type":[{"value":"1045-3873","type":"print"},{"value":"1540-8167","type":"electronic"}],"subject":[],"published":{"date-parts":[[2001,5]]}}}