ince the publication of Pardee's study, 1 ST-segment elevation on an electrocardiogram (ECG) has been considered one of the most useful markers of acute myocardial infarction (MI). During myocardial ischemia, electrical changes, such as shortening of the action potential duration, depolarization of the resting membrane potential and a decrease in the amplitude of the action potential, cause an abnormal injury current from the normal to the ischemic myocardium, resulting in ST-segment elevation. 2 However, persistent ST-segment elevation after the infarcted myocardium heals is thought to be a sign of left ventricular aneurysm. 3 In addition, an exercise or dobutamine stress-test sometimes induces ST-segment elevation in patients with an old anteroseptal MI, probably due to asynergy. 4,5 These findings suggest that regional ventricular dyskinesia is a possible mechanism for ST-segment elevation unrelated to myocardial ischemia.We investigated the role of regional ventricular dyskinesia in ST-segment elevation not associated with ischemia in a canine model of regional ventricular dyskinesia produced with negative inotropic agents.
Methods
Surgical PreparationsThirty-three mongrel dogs of either sex weighing 15-25 kg were sedated with an intramuscular injection of 1.0-1.5 mg/kg of body weight of droperidol and anesthetized with intravenous injection of 25-30 mg/kg of pentobarbital.Respiration was controlled with a Harvard pump (Harvard Apparatus Inc, South Natick, MA, USA) using a mixture of room air and 1.0 L/min of oxygen. A thoracotomy was performed via the left fifth intercostal space, and the pericardium was opened. The left anterior descending artery (LAD) isolated just distal to the first diagonal branch was cannulated and perfused with autologous arterial blood from the left subclavian artery through a bypass circuit made of silicone tubing with anticoagulant properties. An electromagnetic flow probe (Nihon Kohden Co, Tokyo, Japan) was placed in the bypass circuit to measure bypass blood flow (coronary blood flow). A catheter was inserted through the right femoral vein for intravenous infusions. Aortic pressure was monitored using a catheter inserted via the right femoral artery. Left ventricular (LV) pressure was measured through a short catheter inserted into the LV cavity from the apex. A pair of ultrasonic dimension crystals (Nihon Kohden Co) was inserted into the subendocardium perfused via the bypass circuit to measure serial changes of regional myocardial contraction. The epicardial ECG was monitored using a contact electrode placed at the center of the region perfused via the bypass circuit, and using Wilson central terminal as the indifferent electrode (Fig 1). The data were recorded on a polygraph (Nihon Kohden Co) at a paper speed of 25 and 100 mm/s. The heart was allowed to beat at its spontaneous rate without pacing.
Experimental ProtocolAfter documentation of sufficient reactive hyperemia and stabilization of hemodynamic parameters, we administered a continous intracoronary infusion of adenosin...