Background-Percutaneous approaches for radiofrequency ablation of ventricular tachycardia (VT) in the left ventricle are typically transarterial retro-aortic, antegrade transmitral via an interatrial septal puncture, or epicardial. However, all 3 approaches may be contraindicated in certain cases. We describe 2 cases of VT ablation in which aortic and mitral valve replacements did not permit utilization of any of these techniques. Methods and Results-Direct access to the left ventricular cavity was achieved with a percutaneous puncture through the intercostal space overlying the apex in the first case and through a left minithoracotomy in the second. A sheath was then inserted via the Seldinger technique, allowing catheter access for mapping and ablation of the VT. After successful ablation, the sheaths were withdrawn and hemostasis was achieved. A large left hemothorax occurred from the left ventricular apical puncture in the first case. Direct closure with a purse-string suture in the second case achieved hemostasis. Conclusions-Direct

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Background— Sudden arrhythmic death after myocardial infarction (MI) is most frequent in the first month. Early programmed ventricular stimulation (within 1 week) post-MI has been able to identify long-term ventricular tachycardia (VT) occurrence. We aimed to determine the timing of development and stabilization of VT circuits after MI and how the evolution of the underlying substrate differs with VT inducibility. Methods and Results— MIs were induced in 36 sheep. The 21 survivors underwent serial electroanatomic mapping and programmed ventricular stimulation. Animals were classified as VT pos (inducible VT) or VT neg (noninducible VT) at day 8. Forty-three percent of MI survivors were VT pos on day 8 (9/21), and all remained inducible on day 100 with 1.5 (1.0–2.0) and 1.0 (1.0–2.0) morphologies per animal on days 8 and 100, respectively. Twelve-lead electrocardiogram matched in 15 of 19 VTs between days 8 and 100. The earliest presystolic ventricular activations during VT circuits were in similar locations at the 2 time points. The 12 VT neg animals remained noninducible on day 100. There was no difference in voltage or velocity substrate with time or inducibility. The area with fractionated signals increased with time and VT inducibility. VT pos animals had more linear regions of slowed conduction forming conducting channels. Conclusions— The inducibility and earliest presystolic endocardial activation sites of VT as well as voltage and velocity substrate on day 8 predicted those on day 100 postinfarct, indicating early formation and stabilization of the arrhythmogenic substrate. VT inducibility was influenced by the distribution of conducting channels and increased complex fractionated signals.

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