The purpose of this prospective randomized study was to compare the safety and efficacy of the cephalic approach versus a contrast-guided extrathoracic approach for placement of endocardial leads. Despite an increased incidence of lead fracture, the intrathoracic subclavian approach remains the dominant approach for placement of pacemaker and implantable defibrillator leads. Although this complication can be prevented by lead placement in the cephalic vein or by lead placement in the extrathoracic subclavian or axillary vein, these approaches have not gained acceptance. A total of 200 patients were randomized to undergo placement of pacemaker or implantable defibrillator leads via the contrast-guided extrathoracic subclavian vein approach or the cephalic approach. Lead placement was accomplished in 99 of the 100 patients randomized to the extrathoracic subclavian vein approach as compared to 64 of 100 patients using the cephalic approach. In addition to a higher initial success rate, the extrathoracic subclavian vein medial approach was determined to be preferable as evidenced by a shorter procedure time and less blood loss. There was no difference in the incidence of complications. In conclusion, these results demonstrate that lead placement in the extrathoracic subclavian vein guided by contrast venography is effective and safe. It was also associated with no increased risk of complications as compared with the cephalic approach. These findings suggest that the contrast-guided approach to the extrathoracic portion of the subclavian vein should be considered as an alternative to the cephalic approach.

Long-chain acylcarnitines (LCACs) increase rapidly within minutes after the onset of ischemia in vivo or hypoxia in vitro and produce a time-dependent reversible reduction in gap junctional conductance in isolated myocyte pairs. The present study was performed to assess whether LCACs contribute to cellular uncoupling in response to ischemia in isolated bloodperfused rabbit papillary muscles by use of simultaneous measurements of transmembrane action potentials, extracellular electrograms, extracellular K', and tissue LCACs and ATP. LCACs increased threefold in response to 20 minutes of no-flow ischemia from 127±5 to 397±113 pmol/mg protein (P<.01), concomitant with the onset of cellular uncoupling, extracellular K' accumulation, and a marked reduction in conduction velocity and action potential duration. To assess whether inhibition of the accumulation of LCACs modified the electrophysiological alterations during ischemia, muscles were pretreated with either sodium 2-(5-(4-chlorophenyl)-pentyl)-oxirane-2-carboxylate (POCA, 10 gmol/L) or oxfenicine (100 ,umol/L), inhibitors of carnitine acyltransferase I. Both POCA S udden cardiac death in the setting of acute myocardial ischemia usually results from spontaneous ventricular tachycardia degenerating into ventricular fibrillation.1,2 Spontaneous malignant arrhythmias occur within minutes of the onset of ischemia in vivo and are primarily due to conduction delay and block leading to intramural reentry.3,4 Changes in membrane excitability and cell-to-cell uncoupling are likely to represent the basic electrophysiological alterations leading to disturbances in propagation. As shown previously, a decrease in excitability occurs immediately after coronary occlusion,5 whereas the onset of electrical cell-to-cell uncoupling occurs with a delay of 10 to 15 minutes.6 At present, the metabolic events that initiate cellular uncoupling are unknown. The blood-perfused papillary muscle preparation is an attractive system in which to evaluate precisely how discrete biochemical events contribute to the electrophysiological derangements induced by myocardial ischemia. MO 63110. and oxfenicine completely prevented the increase in LCACs even with 40 minutes of ischemia (138±37 and 56±4 pmol/mg protein, respectively), associated with a marked delay in the onset and progression of cellular uncoupling and ischemic contracture. Although POCA and oxfenicine did not affect either the initial early rise in extracellular K' or the initial fall in conduction velocity, both agents markedly delayed the secondary rise in extracellular K' as well as the secondary fall in conduction velocity, independent of the level of tissue ATP. Thus, LCACs accumulate during myocardial ischemia and contribute substantially to the initiation of cell-to-cell uncoupling. Inhibition of carnitine acyltransferase I and prevention of the increase in LCACs markedly delays cellular uncoupling and development of ischemic contracture in response to ischemia. (Circ Res. 1994;74:83-95.) Key Words * rabbit papillary mus...

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In patients with atrial flutter, conventional RF ablation may not result in complete isthmus block. This prospective, randomized study tested the hypothesis that the cooled RF ablation is safe and facilitates the achievement of isthmus block with fewer RF applications than with standard ablation for typical atrial flutter. Isthmus ablation was performed in 59 patients (40 men, 64 +/- 14 years) with type I atrial flutter using standard RF (n = 31) or cooled RF (n = 28) catheters with crossover after 12 unsuccessful RF applications. The endpoint was bidirectional isthmus block or a total of 24 unsuccessful RF applications. After the first 12 RF applications, 17 (55%) of 31 standard RF and 22 (79%) of 28 cooled RF patients had bidirectional isthmus block (P < 0.05). After the remaining patients crossed over to the alternate RF ablation system and underwent up to 12 more RF applications, bidirectional isthmus block had been demonstrated in 27 (87%) of 31 standard RF and 25 (89%) of 28 cooled RF patients (P = NS). Isthmus block was not achieved within 24 RF applications in four standard and three cooled RF patients. Mean measured tip temperatures for cooled RF were lower than for standard RF (38.5 degrees C +/- 6.98 degrees C vs 57.2 degrees C +/- 7.42 degrees C, P < 0.0001). Peak temperatures were also lower for cooled RF compared to standard RF (45.7 degrees C +/- 22.7 degrees C vs 63.4 degrees C +/- 9.87 degrees C, P < 0.0001). Importantly, mean power delivered was significantly higher for cooled than for standard RF (42.3 +/- 9.48 vs 34.0 +/- 14.0 W, P < 0.0001). There were no serious complications for either ablation system. During a 12.8 +/- 3.76-month follow-up, there were two atrial flutter recurrences in the cooled RF group and four in the standard RF group (P = NS). In patients with type I atrial flutter, ablation with the cooled RF catheter is as safe as, and facilitates creation of bidirectional isthmus block more rapidly than, standard RF ablation.