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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The automatic implantable cardioverter-defibrillator (AICD) has been shown to reduce the mortality rate of patients with malignant ventricular tachyarrhythmias. This report describes experience with implantation of 36 automatic implantable cardioverter-defibrillators (AID-B and AID-BR models) in 22 persons over a 44 month patient follow-up period (mean 19.6 months). There were five deaths: two patients died suddenly 22 and 29 months, respectively, after their second implant, one died of congestive heart failure, one died of respiratory failure and one died of catheter sepsis. Although 11 (50%) of the 22 patients never received a countershock for a ventricular tachyarrhythmia and are still alive, the other 11 received one or more spontaneous countershocks. Nine patients (41%) experienced spurious shocks during the follow-up period. Assuming that the first shock for presumed ventricular tachyarrhythmia prevented death, the hypothetical cumulative survival of patients at 42 months would have been 34 +/- 14.1% in the absence of an automatic implantable cardioverter defibrillator rather than the actual survival rate of 59 +/- 16.8%. The cumulative device survival of the 36 AID-B units was 92 +/- 5.62% at 15 months but diminished to 37 +/- 14.4% by 20 months. No unit lasted longer than 22 months. There were 12 battery depletions. The number of shocks emitted did not influence unit longevity. The manufacturer's elective replacement indicator is of uncertain validity. Six units remained active 7 to 17 months after surpassing their replacement indicator. The automatic implantable cardioverter-defibrillator prolongs the life of many patients with otherwise intractable arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

This double-blind, randomized, placebo crossover study was used to evaluate the effects of a cholinesterase inhibitor--slow-release pyridostigmine (180 mg orally every 12 hours)--on the anticholinergic and antiarrhythmic properties of disopyramide. Quantitative side effects questionnaire scores were used to guide disopyramide administration in 20 men with ventricular tachycardia. Disopyramide was given to each patient both with placebo and with active pyridostigmine. The maximal administered dose for each regimen was used in conjunction with corresponding questionnaire scores to calculate an index or estimate of the maximal tolerable dose of disopyramide. Additional evaluations performed at baseline and at each maximal administered dose regimen included tear and saliva quantitation, 24 hour electrocardiogram (ECG), exercise testing and programmed ventricular stimulation. Results showed that the maximal administered dose of disopyramide was greater with active pyridostigmine than with placebo: 295 +/- 75 versus 245 +/- 100 mg every 6 hours (p less than 0.05). The calculated maximal tolerable dose was substantially greater in the presence of pyridostigmine: 355 +/- 90 versus 260 +/- 115 mg every 6 hours (p less than 0.001). Maximal side effects questionnaire scores also reflected decreased anticholinergic activity in the presence of pyridostigmine compared with placebo: 101.9 +/- 2.2 versus 104.6 +/- 2.8, respectively (p less than 0.005). Baseline tear and saliva production was significantly reduced during disopyramide therapy, but was restored toward normal by the addition of pyridostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)