Search

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.

The purpose of this study was to evaluate ST-segment elevation induced by regional myocardial stretch without myocardial ischemia in canine hearts. A strain gauge arch (TH-601T) was sutured to the left ventricular epicardium, parallel to the short axis, to shorten the end-diastolic length of the myocardium beneath the arch (stretch zone; SZ) and to produce regional myocardial stretch in each of 6 dogs. An increase in preload caused by altering the height of a saline-filled reservoir affected prolongation or shortening of the myocardium both in the SZ and outside the arch (normal zone; NZ) to increase myocardial stretch. An epicardial electrocardiogam was recorded in both the SZ and the NZ. After suture of the strain gauge arch, the ST segment was elevated in the SZ. An increase in preload augmented stretch during systole in the SZ, resulting in additional ST-segment elevation. These results suggest that regional myocardial stretch itself plays an important role in ST-segment elevation. (Jpn Circ J 1997; 61: 921 - 926)

We report a patient with Brugada syndrome who developed sustained monomorphic ventricular tachycardia (SMVT). The patient was a 29-year-old man who experienced recurrent episodes of palpitation and syncope after drinking alcohol. Electrocardiogram showed right bundle branch block and ST-segment elevation in precordial leads V1-3 without Q-Tc prolongation. Organic heart disease and coronary artery disease were excluded by noninvasive and invasive tests. Ventricular fibrillation was induced by the application of a single extra-stimulus to the right ventricular outflow tract. During isoproterenol infusion, SMVT of left bundle branch block morphology (240/min) was induced by the application of a single extrastimulus to the right ventricular apex. SMVT also developed spontaneously. Pace mapping disclosed that SMVT originated at the free wall of the right ventricular outflow tract. Head-up tilt test and an alcohol provocation test both induced similar SMVT that was associated with hypotension and near syncope. SMVT was not terminated by intravenous administration of lidocaine, procainamide or adenosine triphosphate (10 mg), but was terminated by propranolol. Thus, a beta-adrenoceptor-mediated mechanism appears to play an important role in SMVT in this patient. The site of origin of SMVT might be closely related to the lesion that causes ST-segment elevation.