Nonischemic ST-segment elevation induced by negative inotropic agents

Megumi Shimada, Yoshiro Nakamura, Shiro Iwanaga, Keiko Asakura, Shingo Hori, Shigehiko Hattori, Masando Takahashi, Satoshi Ogawa

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)


The present study investigated whether regional ventricular dyskinesia (ie, systolic bulging) is a direct cause of ST-segment elevation in canine hearts in vivo. Regional ventricular dyskinesia was induced in 33 anesthetized open-chest dogs by injection of negative inotropic agents into the left anterior descending coronary artery (LAD) without disruption of coronary blood flow. Regional myocardial contraction was assessed in terms of the percent systolic shortening (%SS) and percent systolic bulging (%bulging), which were measured using ultrasonic crystals. The ST-segment elevation of the LAD-perfused area was measured with a unipolar electrode. Lidocaine, a sodium channel blocker, nicorandil, a potassium channel opener, propranolol, a beta-adrenergic blocker, or verapamil, a calcium channel blocker, was administered by intracoronary injection during maximal vasodilation induced by adenosine. All drugs induced dose-dependent ST- segment elevation in association with a parallel reduction in %SS and a parallel increase in %bulging. The absence of myocardial ischemia was confirmed by the absence of NADH fluorescence. It was concluded that regional ventricular dyskinesia had an important role in ST-segment elevation not associated with myocardial ischemia.

Original languageEnglish
Pages (from-to)610-616
Number of pages7
Issue number8
Publication statusPublished - 1999 Aug


  • Myocardial ischemia
  • Negative inotropic agents
  • Regional ventricular dyskinesia
  • ST-segment elevation

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine


Dive into the research topics of 'Nonischemic ST-segment elevation induced by negative inotropic agents'. Together they form a unique fingerprint.

Cite this