{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,9]],"date-time":"2025-10-09T16:53:55Z","timestamp":1760028835136},"reference-count":39,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2007,4,29]],"date-time":"2007-04-29T00:00:00Z","timestamp":1177804800000},"content-version":"vor","delay-in-days":4623,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiovasc electrophysiol"],"published-print":{"date-parts":[[1994,9]]},"abstract":"<jats:p>Mechanism\u2010Specific Action of Levcromakalim. <jats:italic>Introduction:<\/jats:italic> The hypothesis that levcromakalim. a potassium channel (I<jats:sub>K\u2010ATP<\/jats:sub>.) activator with antihypertensive properties, has a mechanism\u2010specific antiarrhythmic action against repolarization\u2010dependent ventricular tachycardias (VTs) was tested in dogs.<\/jats:p><jats:p> <jats:italic>Methods and Results:<\/jats:italic> A low dose of leveromakalim (0.01 mg\/kg) was selected, which decreased blood pressure by 25% but had almost no electrophysiologic effect on AV nodal or ventricular conduction or effective refractory period. In dogs with chronic AV block, the antiarrhythmic action of this dose of levcromakalim was evaluated in three models of abnormal impulse formation: (I) dsotalol (2 mg\/kg) induced torsades de pointes VT, initiated by early afterdepolarizations (EADs). (2) sustained ouabain\u2010induced VTs, which are dependent on delayed after depolarizations (DADs), and (3) VT occurring 24 hours after left anterior descending coronary artery occlusion, which are likely based on abnormal automaticity. Levcromakalim abolished d\u2010sotalol induced U waves, ventricular ectopic beats, and self\u2010terminating bouts of torsades de pointes. Induction of torsades de pointes by pacing was also completely prevented. The cycle length of the idioventricular rhythm, which was lengthened after d\u2010sotalol from 1490 \u00b1 515 to 1700 \u00b1 610 msec (P &lt; 0.05), remained similar after levcromakalim (1655 \u00b1 580 msec). The QT(U) duration, which was increased after d\u2010sotalol from 410 \u00b1 55 to 550 \u00b1 40 msec (P &lt; 0.05), normalized to 405 \u00b1 70 msec (P &lt; 0.05). Lcvcromakulim did not suppress but rather enhanced ouabain\u2010induced VT by decreasing the cycle length slightly from 315 \u00b1 35 to 290 \u00b1 35 msec (P &lt; 0.05). Pretreatment with a beta Mocker prevented this acceleration in rate. Finally, levcromakalim had no effect on VT 24 hours after infarction.<\/jats:p><jats:p> <jats:italic>Conclusion:<\/jats:italic> A low dose of levcromakalim has specific antiarrhythmic properties against repolarization\u2010dependent arrhythmias, but it does not affect VTs based on other mechanisms of abnormal impulse formation.<\/jats:p>","DOI":"10.1111\/j.1540-8167.1994.tb01196.x","type":"journal-article","created":{"date-parts":[[2007,5,14]],"date-time":"2007-05-14T01:44:16Z","timestamp":1179107056000},"page":"731-742","source":"Crossref","is-referenced-by-count":9,"title":["Mechanism\u2010Specific Antiarrhythmic Effects of the Potassium Channel Activator Levcromakalim Against Repolarization\u2010Dependent Tachycardias"],"prefix":"10.1111","volume":"5","author":[{"given":"MARC A.","family":"VOS","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"ANTON P.M.","family":"GORGELS","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"GYORGYI C.","family":"LIPCSEI","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.H. 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