In this study we evaluated the possibility of initiating long-lasting ventricular tachycardias acutely, using isolated porcine hearts and thus avoiding an open-chest operation model. This set-up was designed especially to investigate defibrillating or antitachycardiac pacing devices, which terminate these malignant arrhythmias if medical treatment fails.
The experiments were performed on 42 pigs, weighing 20–25 kg. After thoracotomy their hearts were removed and adapted to a Langendorff perfusion system. Supplied with their own blood, beating hearts were manipulated in three different ways: direct current impulses (4.5 V, 750 ms) or programmed ventricular stimulation, creation of a small myocardial infarction, and application of antiarrhythmic drugs (ajmalin, lidocaine, sotalol). Out of all possibilities the combination of ajmalin (mean concentration 0.041 µg/ml) and a small anteroapical myocardial infarction (3–6 cm2) along with direct current impulses (4.5 V), led to sustained ventricular tachycardias in the highest proportion (93%) of trials (P < 0.001). The heart rate was 251 beats per minute on average. Lidocaine trials were less successful (53%), while programmed ventricular stimulation and sotalol failed to induce ventricular tachycardias. This study supports the evidence that the combination of ajmalin and a small myocardial infarction with direct current impulses is a reliable model for sustained ventricular tachycardias in isolated pig hearts. Although it is a rather artificial organ model, tachycardias can be induced acutely without any long-term pretreatment. Animal models based on chronic myocardial infarctions will therefore be unnecessary for the investigation of defibrillating systems and antitachycardiac pacing devices.
Ventricular tachycardia Antiarrhythmic drug Isolated pig heart Langendorff perfusion
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Bardy GH, Smith WM, Ungerleider RM, Cox JL, Gallagher JJ, Ideker RE (1984) Identification of reproducible ventricular tachycardia in a canine model. Am J Cardiol 53:619–625PubMedGoogle Scholar
Davis J, Glassman R, Wit AL (1982) Method for evaluating the effects of antiarrhythmic drugs on ventricular tachycardias with different electrophysiologic characteristics and different mechanisms in the infarcted canine heart. Am J Cardiol 49:1176–1184PubMedGoogle Scholar
El-Sherif N, Scherlag BJ, Lazzara R, Hope RR (1977) Reentrant ventricular arrhythmias in the late myocardial infarction period. 1. Conduction characteristics in the infarction zone. Circulation 55:686–704PubMedGoogle Scholar
Garan H, Fallon JT, Ruskin JN (1981) Nonsustained polymorphic ventricular tachycardia induced by electrical stimulation in 3-week-old canine myocardial infarction. Am J Cardiol 48:280–286PubMedGoogle Scholar
Hoffman BF, Rosen MR (1981) Cellular mechanisms for cardiac arrhythmias. Circ Res 49:1–15PubMedGoogle Scholar
Hope RR, Scherlag BJ, El-Sherif N, Lazzara R (1977) Continuous concealed ventricular arrhythmias. Am J Cardiol 40:733–738PubMedGoogle Scholar
Janse MJ, Kleber AG (1981) Electrophysiologic changes and ventricular arrhythmias in the early phase of regional myocardial ischemia. Circ Res 49:1069–1081PubMedGoogle Scholar
Kaplinski E, Yahini JH, Neufeld HN (1972) On the mechanism of sustained ventricular arrhythmias associated with acute myocardial infarction. Cardiovasc Res 6:135–142PubMedGoogle Scholar
Karaguezian HS, Fenoglio JJ Jr, Weiss MB, Wit AL (1979) Protracted ventricular tachycardia induced by premature stimulation of the canine heart after coronary artery occlusion and reperfusion. Circ Res 44:833–846PubMedGoogle Scholar
Michelson EL, Spear JF, Moore EN (1980) Electrophysiologic and anatomic correlates of sustained ventricular tachyarrhythmias in a model of chronic myocardial infarction. Am J Cardiol 45:583–590PubMedGoogle Scholar
Michelson EL, Spear JF, Moore EN (1981) Initiation of sustained ventricular tachyarrhythmias in a canine model of chronic myocardial infarction: Importance of the site of stimulation. Circulation 63:776–784PubMedGoogle Scholar
Schmid C, Nitsch J, Funke HD, Kirchhoff PG (1987) Potentialverteilung bei intra- und extrakardialer Defibrillation. Thorac Cardiovasc Surgeon 35:255–258Google Scholar
Sherlag BJ, Kabell G, Brachmann J, Harrison L, Lazzara R (1983) Mechanisms of spontaneous ventricular arrhythmias in the 24-hour infarcted dog heart. Am J Cardiol 51:207–213PubMedGoogle Scholar
Vaughan Williams EM (1970) Classification of antiarrhythmic drugs. In: Sandoe E, Flensted-Jensen E, Olesen KH (eds) Cardiac arrhythmias. AB Astra, Elsinore, p 449Google Scholar
Wit AL, Bigger JT Jr (1975) Possible electrophysiological mechanisms for lethal arrhythmias accompanying myocardial ischemia and infarction. Circulation 51/52 [Suppl III-96–III-115]Google Scholar
Wolff GA, Veith F, Lown B (1968) A vulnerable period for ventricular tachycardia following myocardial infarction. Cardiovasc Res 2:111–121PubMedGoogle Scholar