protein and iso-mRNA levels in cultured cardiac myocytes were quantified during hypertrophy stimulated by the a,-adrenergic agonist, norepinephrine (NE). fl-MHC iso-protein content was increased 3.2-fold vs. control (P < 0.001), whereas a-MHC isoprotein content was not changed significantly (1.4-fold vs. control, P = NS). MHC iso-mRNA levels were quantified by nuclease Si analysis, using a single oligonucleotide probe. NE increased fl-MHC iso-mRNA content by 3.9-fold

Electrophysiologic studies were performed in 172 consecutive patients for evaluation of documented sustained ventricular tachyarrhythmias. One hundred thirteen patients presented with sustained ventricular tachycardia that was hemodynamically stable, and 59 patients presented with cardiac arrest. Seventy-one patients without previously documented or suspected ventricular arrhythmias were also studied to determine the specificity of our electrophysiologic study protocol. have demonstrated inducible tachycardias in 65% to 95%`6 of patients with recurrent sustained ventricular tachycardia (VT) and in 63% to 81% of patients with cardiac arrest.7 The purpose of the present study was to evaluate whether the use of triple extrastimuli in the electrophysiologic study protocol would (1) increase the likelihood of induction of tachycardia in patients presenting with documented sustained VT or cardiac arrest, (2) be more frequently associated with induction of faster and/or polymorphic tachycardias than observed when using two or fewer extrastimuli and rapid pacing, and (3)

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Previous canine experiments suggested that transvenous catheters placed in the coronary sinus could be used to deliver limited energy shocks, resulting in fibrosis in the atrial wall and coronary sulcus with sparing of the coronary artery. From the distribution of the fibrosis, it appeared that this approach could be used for attempted ablation of accessory pathways in patients with the Wolff-Parkinson-White syndrome. Eight patients with symptomatic Wolff-Parkinson-White syndrome underwent electrophysiologic testing with attempted ablation of 10 accessory pathways. Shocks were limited to 40 to 80 J, except in one patient who received shocks of 100 and 150 J. From 2 to 26 shocks were given to each accessory pathway. All the accessory pathways were blocked completely immediately after the shocks. Subsequently, evidence of accessory pathway conduction recurred in each patient. Three had early promise of long-term improvement after the procedure, with prolongation of the refractory periods of the accessory pathways during the remainder of the initial hospitalization. Several weeks later, however, there was evidence of return toward original values in two of these. Another patient who appeared not to benefit during her initial hospitalization returned 7 weeks later with very depressed accessory pathway conduction, possibly due to developing fibrosis. The only significant complication occurred in the patient receiving shocks of 100 and 150 J; he had apparent rupture of the coronary sinus requiring pericardial drainage. In two patients in whom nonsurgical ablation was not successful, intraoperative mapping showed that the accessory pathway was located in an area of fibrosis at the site of the attempted ablation. In summary, nonsurgical electrical ablation of accessory pathways via the coronary sinus may be successful using limited energy levels in a few patients. The procedure remains experimental, and widespread application must await more effective means of delivering the shocks.

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