Improvement of repolarization abnormalities by a K+ channel opener in the LQT1 form of congenital long-QT syndrome

Wataru Shimizu, Takashi Kurita, Kiyotaka Matsuo, Kazuhiro Suyama, Naohiko Aihara, Shiro Kamakura, Jeffrey Towbin, Katsuro Shimomura

Research output: Contribution to journalArticle

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Abstract

Background - This study used monophasic action potential (MAP) to examine the effect of nicorandil, a K+ channel opener, on repolarization abnormalities induced by epinephrine in the LQT1 form of congenital long-QT syndrome in which the KvLQT1 mutation underlies the defect in the channel responsible for the slowly activating component of the delayed rectifier potassium current. Methods and Results - MAPs were recorded simultaneously from two or three sites on the right ventricular and left ventricular endocardium in 6 patients with a congenital form of LQT1 syndrome with KvLQT1 defect (17 sites) and 8 control patients (24 sites). In LQT1 patients, epinephrine infusion prolonged the QT interval and 90% MAP duration (MAPD90) and increased the dispersion of MAPD90. Epinephrine also induced early afterdepolarizations (EADs) as well as ventricular premature complexes (VPCs) in 2 of the 6 patients. Nicorandil during epinephrine infusion abbreviated the QT interval and MAPD90, decreased the dispersion of MAPD90, and abolished the EADs as well as the VPCs in 1 patient. Addition of propranolol completely reversed the effect of epinephrine in prolonging the QT interval and MAPD90 and increasing the dispersion and eliminated the EADs and VPCs in another patient. In control patients, the effect of epinephrine and that of additional nicorandil and propranolol on repolarization parameters were much less than in the LQT1 patients. Conclusions - Our results suggest that nicorandil, a K+ channel opener, improves repolarization abnormalities in the LQT1 form of congenital long-QT syndrome with KvLQT1 defect.

Original languageEnglish (US)
Pages (from-to)1581-1588
Number of pages8
JournalCirculation
Volume97
Issue number16
DOIs
StatePublished - Apr 28 1998

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Long QT Syndrome
Nicorandil
Epinephrine
Ventricular Premature Complexes
Propranolol
Action Potentials
Endocardium
Potassium
Mutation

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Shimizu, W., Kurita, T., Matsuo, K., Suyama, K., Aihara, N., Kamakura, S., ... Shimomura, K. (1998). Improvement of repolarization abnormalities by a K+ channel opener in the LQT1 form of congenital long-QT syndrome. Circulation, 97(16), 1581-1588. https://doi.org/10.1161/01.CIR.97.16.1581

Improvement of repolarization abnormalities by a K+ channel opener in the LQT1 form of congenital long-QT syndrome. / Shimizu, Wataru; Kurita, Takashi; Matsuo, Kiyotaka; Suyama, Kazuhiro; Aihara, Naohiko; Kamakura, Shiro; Towbin, Jeffrey; Shimomura, Katsuro.

In: Circulation, Vol. 97, No. 16, 28.04.1998, p. 1581-1588.

Research output: Contribution to journalArticle

Shimizu, W, Kurita, T, Matsuo, K, Suyama, K, Aihara, N, Kamakura, S, Towbin, J & Shimomura, K 1998, 'Improvement of repolarization abnormalities by a K+ channel opener in the LQT1 form of congenital long-QT syndrome', Circulation, vol. 97, no. 16, pp. 1581-1588. https://doi.org/10.1161/01.CIR.97.16.1581
Shimizu, Wataru ; Kurita, Takashi ; Matsuo, Kiyotaka ; Suyama, Kazuhiro ; Aihara, Naohiko ; Kamakura, Shiro ; Towbin, Jeffrey ; Shimomura, Katsuro. / Improvement of repolarization abnormalities by a K+ channel opener in the LQT1 form of congenital long-QT syndrome. In: Circulation. 1998 ; Vol. 97, No. 16. pp. 1581-1588.
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AU - Suyama, Kazuhiro

AU - Aihara, Naohiko

AU - Kamakura, Shiro

AU - Towbin, Jeffrey

AU - Shimomura, Katsuro

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N2 - Background - This study used monophasic action potential (MAP) to examine the effect of nicorandil, a K+ channel opener, on repolarization abnormalities induced by epinephrine in the LQT1 form of congenital long-QT syndrome in which the KvLQT1 mutation underlies the defect in the channel responsible for the slowly activating component of the delayed rectifier potassium current. Methods and Results - MAPs were recorded simultaneously from two or three sites on the right ventricular and left ventricular endocardium in 6 patients with a congenital form of LQT1 syndrome with KvLQT1 defect (17 sites) and 8 control patients (24 sites). In LQT1 patients, epinephrine infusion prolonged the QT interval and 90% MAP duration (MAPD90) and increased the dispersion of MAPD90. Epinephrine also induced early afterdepolarizations (EADs) as well as ventricular premature complexes (VPCs) in 2 of the 6 patients. Nicorandil during epinephrine infusion abbreviated the QT interval and MAPD90, decreased the dispersion of MAPD90, and abolished the EADs as well as the VPCs in 1 patient. Addition of propranolol completely reversed the effect of epinephrine in prolonging the QT interval and MAPD90 and increasing the dispersion and eliminated the EADs and VPCs in another patient. In control patients, the effect of epinephrine and that of additional nicorandil and propranolol on repolarization parameters were much less than in the LQT1 patients. Conclusions - Our results suggest that nicorandil, a K+ channel opener, improves repolarization abnormalities in the LQT1 form of congenital long-QT syndrome with KvLQT1 defect.

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