Nonischemic ST-segment elevation induced by negative inotropic agents

Jpn Circ J. 1999 Aug;63(8):610-6. doi: 10.1253/jcj.63.610.


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.

MeSH terms

  • Adenosine / pharmacology
  • Animals
  • Depression, Chemical
  • Dogs
  • Dyskinesia, Drug-Induced / complications*
  • Dyskinesia, Drug-Induced / physiopathology
  • Electrocardiography / drug effects*
  • Electrocardiography / methods
  • Female
  • Hemodynamics
  • Lidocaine / pharmacology
  • Male
  • Myocardial Contraction / drug effects*
  • Myocardial Ischemia / etiology
  • Myocardium / metabolism
  • Nicorandil / pharmacology
  • Nitroglycerin / pharmacology
  • Ventricular Dysfunction, Left / chemically induced


  • Nicorandil
  • Lidocaine
  • Nitroglycerin
  • Adenosine