Nicotine increases ventricular vulnerability to fibrillation in hearts with healed myocardial infarction

Masaaki Yashima, Toshihiko Ohara, Ji Min Cao, Young Hoon Kim, Michael C. Fishbein, William J. Mandel, Peng-Sheng Chen, Hrayr S. Karagueuzian

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

The vulnerability of the infarcted hearts to ventricular fibrillation (VF) was tested in in situ canine hearts during nicotine infusion. The activation pattern was mapped with 477 bipolar electrodes in open-chest anesthetized dogs (n = 8) 5-6 wk after permanent occlusion of the left anterior descending coronary artery. Nicotine (129 ± 76 ng/ml) lengthened (P <0.01) the pacing cycle length at which VF was induced from 171 ± 8.9 to 210 ± 14.7 ms. Nicotine selectively amplified the magnitude of conduction time and monophasic action potential (MAP) amplitude and duration (MAPA and MAPD, respectively) alternans in the epicardial border zone (EBZ) but not in the normal zone. With critical reduction of the MAPA and MAPD in the EBZ, conduction block occurred across the long axis of the EBZ cells. Block led immediately to reentry formation in the EBZ with a mean period of 105 ± 10 ms, which, after one to two rotations, degenerated to VF. Nicotine widened the range of diastolic intervals over which the dynamic MAPD restitution curve had a slope > 1. We conclude that nicotine facilitates conduction block, reentry, and VF in hearts with healed myocardial infarction by increasing the magnitude of depolarization and repolarization alternans consistent with the restitution hypothesis of vulnerability to VF.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume278
Issue number6 47-6
StatePublished - Jun 2000
Externally publishedYes

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Ventricular Fibrillation
Nicotine
Myocardial Infarction
Canidae
Coronary Vessels
Electrodes
Thorax
Dogs

Keywords

  • Action potential restitution
  • Alternans
  • Conduction block
  • Mapping
  • Teentry

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Yashima, M., Ohara, T., Cao, J. M., Kim, Y. H., Fishbein, M. C., Mandel, W. J., ... Karagueuzian, H. S. (2000). Nicotine increases ventricular vulnerability to fibrillation in hearts with healed myocardial infarction. American Journal of Physiology - Heart and Circulatory Physiology, 278(6 47-6).

Nicotine increases ventricular vulnerability to fibrillation in hearts with healed myocardial infarction. / Yashima, Masaaki; Ohara, Toshihiko; Cao, Ji Min; Kim, Young Hoon; Fishbein, Michael C.; Mandel, William J.; Chen, Peng-Sheng; Karagueuzian, Hrayr S.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 278, No. 6 47-6, 06.2000.

Research output: Contribution to journalArticle

Yashima, Masaaki ; Ohara, Toshihiko ; Cao, Ji Min ; Kim, Young Hoon ; Fishbein, Michael C. ; Mandel, William J. ; Chen, Peng-Sheng ; Karagueuzian, Hrayr S. / Nicotine increases ventricular vulnerability to fibrillation in hearts with healed myocardial infarction. In: American Journal of Physiology - Heart and Circulatory Physiology. 2000 ; Vol. 278, No. 6 47-6.
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