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Do calcium antagonists (diltiazem, verapamil) or lidocaine alter conduction delay in the ischemic myocardium of anesthetized dogs?
Do calcium antagonists (diltiazem, verapamil) or lidocaine alter conduction delay in the ischemic myocardium of anesthetized dogs?
In a canine model of acute myocardial ischemia, slow channel blocking agents (diltiazem, verapamil) reduce ischemia-induced conduction delay, whereas lidocaine prolongs it.
Ca antagonists reduce while lidocaine increases ischemia-induced conduction delay in dogs; hypothesis-generating, should not yet inform clinical antiarrhythmic use.
Effects of calcium antagonists and lidocaine on the conduction delay observed in the ischemic myocardium were studied in 24 open-chest anesthetized dogs. Acute myocardial ischemia was produced by complete occlusion of the left anterior descending coronary artery (LAD) for 5 to 10 minutes. The conduction time was measured from the initial deflection of V waves on the His bundle electrograms to the major deflection of the bipolar electrograms recorded from the ischemic and non-ischemic subepicardium under a constant atrial pacing. LAD occlusion produced conduction delay in the ischemic zone (14.3 +/- 2.3 msec, p less than 0.001) with no effect on the normal zone. This ischemia-induced conduction delay was reversible and rate-dependently increased. Administration of lidocaine (2 mg/kg bolus, 4.3 mg/kg/hr constant infusion) prior to the second occlusion increased conduction delay by 12.9 +/- 1.9 msec (p less than 0.001) whereas diltiazem (0.4 mg/kg i.v.) and verapamil (0.3 mg/kg i.v.) reduced the ischemia-induced conduction delay by 12.7 +/- 4.9 msec (p less than 0.05) and 8.4 +/- 1.8 msec (p less than 0.001), respectively. These results indicate that slow channel blocking agents reduce the conduction delay induced by the myocardial ischemia, in contrast with the prolonging effect of lidocaine.
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Kitada et al. (1980) studied this question.
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