Laser ablation of normal and diseased human ventricle.

The feasibility and safety of laser photoablation in patients with ventricular tachycardia (VT) and accessory pathways are currently being examined. We studied the qualitative and quantitative effects of argon laser radiation on normal and diseased human ventricle to determine the relationship between the size of tissue lesion and delivered energy. Twenty-nine human ventricle segments (normal ventricle = 10; diseased ventricle = 19) were excised from patients during mapping-guided subendocardial resection for VT (seven patients), mitral valve replacement (five patients), or immediately at autopsy (three patients). Lasing was performed with a 15 W argon laser coupled to a 300 micron optical fiber. Incremental laser discharges from 10 to 1000 J were delivered in air and saline with the optical fiber 5 mm from the endocardial surface. Gross and microscopic damage was quantified and correlated with laser discharges at low (10 to 100 J), intermediate (101 to 300 J), and high (greater than 300 J) energies. Histologic examination of laser-induced lesions in both normal and diseased human ventricle in either medium showed focal thermal injury with crater formation, vacuolization, and coagulation necrosis of endocardium and myocardium. In normal ventricle, mean lesion diameter and depth in air increased with increasing energies up to 300 J. Over 300 J, tissue perforation was frequently observed. In saline, the mean lesion depth was significantly reduced (p less than 0.02) at comparable energies. In diseased ventricle, mean lesion diameter and depth in air and saline also increased with increasing laser discharge energies up to 300 J. Higher energy laser discharges did not increase mean lesion dimensions or result in tissue perforation.(ABSTRACT TRUNCATED AT 250 WORDS)

A prospective randomized study of the clinical efficacy and safety of transvenous cardioversion for termination of ventricular tachycardia.

The clinical efficacy and safety of transvenous cardioversion for termination of sustained ventricular tachycardia (VT) were examined by a prospective randomized study design in 22 patients (19 men, three women; mean age 64 +/- 9 years) with organic heart disease and sustained VT. Patients were randomly assigned to undergo an incremental low-energy protocol from 0.03 to 2.2 J (group A, 11 patients) or an incremental high-energy protocol from 0.5 to 10.0 J (group B, 11 patients). Transvenous cardioversion was performed during electrophysiologic studies in the control (drug-free) state and during serial antiarrhythmic drug testing in all patients. Both groups were comparable for demographic, disease and functional status, and electrophysiologic parameters. A total of 77 episodes of VT (group A, 45; group B, 32) were analyzed. The overall efficacy of transvenous cardioversion for termination of VT was 62% (group A 56% vs group B 72%; p less than .01). Antiarrhythmic drug therapy did not significantly enhance efficacy of transvenous cardioversion (control 59% vs drug 65%; p greater than .2). Stepwise discriminant analysis correlated successful transvenous cardioversion with longer VT cycle length (p less than .0005), higher energy (p less than .025), lower energy waveform tilt (p less than .025), shorter time to initial cardioversion attempt (p less than .025), and shorter QRS duration in sinus rhythm (p less than .05). Acceleration of VT was frequent (8% incidence per delivered shock). Thirty-one percent of all incremental shock protocols were terminated because of this complication. After cardioversion, transient arrhythmias were common (bradyarrhythmias 23%, supraventricular tachyarrhythmias 12%). Displacement of electrode catheters after transvenous cardioversion was uncommon (3%).(ABSTRACT TRUNCATED AT 250 WORDS)

Studies on left ventricular function during sustained ventricular tachycardia.

The acute effects of rapid ventricular pacing and sustained ventricular tachycardia on left ventricular function were examined in patients with recurrent sustained ventricular tachycardia. Programmed electrical stimulation and left ventricular hemodynamic measurements were performed in 20 patients (19 men and 1 woman), with an age range of 49 to 79 years (mean 63 +/- 9). Indexes of left ventricular function that were analyzed included left ventricular peak systolic pressure, end-diastolic pressure, first derivative of peak left ventricular pressure (dP/dt) and negative left ventricular dP/dt. Measurements were obtained during sinus rhythm, after paced premature ventricular depolarizations, during rapid ventricular pacing (cycle lengths 600 to 250 ms) and immediately after induction of sustained ventricular tachycardia. Mean left ventricular peak systolic blood pressure was 123 +/- 19 mm Hg during sinus rhythm, decreased to 77 +/- 23 mm Hg (p less than 0.05) at the induction of ventricular tachycardia and remained decreased during arrhythmia (p less than 0.01). Mean left ventricular end-diastolic pressure was 22 +/- 5 mm Hg during sinus rhythm, did not change after arrhythmia induction (22 +/- 9 mm Hg, p greater than 0.2) and remained unchanged during sustained ventricular tachycardia (p greater than 0.2). Mean peak left ventricular dP/dt was 1,400 +/- 620 mm Hg/s in sinus rhythm, decreased to 810 +/- 580 mm Hg/s (p less than 0.05) at ventricular tachycardia induction and remained decreased during sustained ventricular tachycardia (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)