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. 1995 May;129(5):1021-5.
doi: 10.1016/0002-8703(95)90126-4.

Microwave ablation of canine atrial tachycardia induced by aconitine

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Microwave ablation of canine atrial tachycardia induced by aconitine

T H Rho et al. Am Heart J. 1995 May.

Abstract

We tested the efficacy of microwave-frequency energy for ablating atrial tachycardia in eight open-chest dogs. Five other dogs served as controls. Atrial tachycardia was induced by direct application of aconitine crystals to the epicardial atrial surface or by injection of aconitine solution (0.15 mg/ml) into the right or left atrial myocardium. Atrial tachycardias (n = 15) developed at a cycle length of 253 +/- 64 msec or within 245 +/- 116 sec after topical application or injection of aconitine. Catheter ablation was attempted on 10 atrial tachycardias in 8 experiment dogs by using continuous, unmodulated microwave energy from a 915 MHz frequency signal generator via a 7F helical or whip antenna catheter. Successful ablation was defined as conversion of atrial tachycardia to sinus rhythm during delivery of microwave energy and maintenance of sinus rhythm for > 5 minutes after termination of energy delivery. All 10 atrial tachycardias were successfully ablated by 2.3 +/- 1.6 applications of microwave energy for each atrial tachycardia induced. Forward microwave power level was 50.5 +/- 8.1 W, and the duration of energy application was 25.0 +/- 27.6 seconds. Sinus rhythm resumed 9.5 +/- 9.2 seconds after the onset of microwave energy application. After a mean follow-up of 10.4 minutes, seven atrial tachycardias recurred, most likely the result of diffusion of aconitine beyond the perimeter of rhe ablation lesions. Atrial tachycardia did not recur in 3 of 3 dogs that had larger ablation lesion. Gross examination revealed 10 demarcated round or oval transmural lesions in the right or left atrium, ranging from 12.6 to 105.6 mm2 in area.(ABSTRACT TRUNCATED AT 250 WORDS)

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