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Ectopic ventricular tachycardia sensitive to calcium antagonists in acute myocardial infarction in dogs
The effects of antiarrhythmic agents on automatic ventricular tachycardia (VT), which emerged in the early stage of acute myocardial infarction (AMI), were examined in 30 closed-chest mongrel dogs. Antiarrhythmic agents were administered intravenously when the rate of VT became almost equal to sinus rate (5.6 +/- 1.4 hours). VT was slowed significantly by verapamil (0.15 or 0.3 mg/kg), diltiazem (0.2 or 0.4 mg/kg), propranolol (0.1 mg/kg) and amiodarone (5 mg/kg), but not by procainamide (20 mg/kg), lidocaine (2 or 4 mg/kg), nifedipine (0.01 mg/kg) and nicorandil (0.03 mg/kg). The number of ventricular premature complexes was reduced most effectively by verapamil. The significant suppressive effects of calcium antagonist drugs (verapamil and diltiazem) and propranolol indicate that an inward calcium current during diastole may play a critical role in the abnormal enhancement of ventricular automaticity in the early stage (4 to 8 hours) of AMI.
The effects of antiarrhythmic agents on automatic ventricular tachycardia (VT), which emerged in the early stage of acute myocardial infarction (AMI), were examined in 30 closed-chest mongrel dogs. Antiarrhythmic agents were administered intravenously when the rate of VT became almost equal to sinus rate (5.6 +/- 1.4 hours). VT was slowed significantly by verapamil (0.15 or 0.3 mg/kg), diltiazem (0.2 or 0.4 mg/kg), propranolol (0.1 mg/kg) and amiodarone (5 mg/kg), but not by procainamide (20 mg/kg), lidocaine (2 or 4 mg/kg), nifedipine (0.01 mg/kg) and nicorandil (0.03 mg/kg). The number of ventricular premature complexes was reduced most effectively by verapamil. The significant suppressive effects of calcium antagonist drugs (verapamil and diltiazem) and propranolol indicate that an inward calcium current during diastole may play a critical role in the abnormal enhancement of ventricular automaticity in the early stage (4 to 8 hours) of AMI.