Protein A Reactivity of Lymphocytes from Some Patients with Chronic Lymphocytic Leukaemia Mediated by an Interaction with the F(ab')2 Region of Surface Immunoglobulin

Peripheral blood lymphocytes (PBL) from 15 of 38 patients with chronic lymphocytic leukaemia (CLL) were capable of forming rosettes with human erythrocytes coated with staphylococcal protein A (SpA-HRBC). PEL from seven patients also showed a marked proliferafive response after stimulation with Staphylocccus aureus bacteria strain Cowan I (Cowan Staph). The SpA-rosetling of CLL cells was inhibited by incubation with F(ab')₂ fragments of anli-immimoglobuiin (Ig) antibodies. In addition, incubation with these fragments inhibited the proliferative response of leukacmie B cells to Cowan Staph. The Cowan-Siaph-induced proliferation of CLL cells was also impaired by the addition of normal human IgG and human IgG F(ab')₂ fragments to the cultures, whereas non-immune rabbit IgG was not inhibitory, The inhibitory activity of human IgG F(ab')₂ fragments was retained hy a SpA-Sepharose column, and it was found in the material recovered from the same column by acid elution. These data indicate thai an interaction between SpA and a structure located in the F(ab')₂ region of surface Ig of different classes is responsible for either SpA-binding or the Cowan-Staph-induced proliferate response of PBL from some patients with CLL.     

Effect of Propranolol on Ventricular Rate During Atrial Fibrillation in the Wolff-Parkinson-White Syndrome

Atrial fibrillation was induced during an electrophysiology study in 10 patients with the Wolff-Parkinson-White (WPW) syndrome, after determination of baseline properties of the accessory atrioventricular (AV) connection; intravenous propranolol (0.2 mg/kg) was then administered. Atrial fibrillation terminated during the drug infusion in three patients, allowing determination of propranolol's effects on conduction and refractoriness during sinus rhythm, before atrial fibrillation was reinduced. In these three patients propranolol had no effect on refractoriness or conduction properties of the accessory AV connection during sinus rhythm. The mean ventricular rate during atrial fibrillation was slowed by 15–56 beats/min in six patients, had no effect on the mean rate in three patients, and markedly increased the ventricular rate (203 to 267 beats/min) in one patient. In this patient, 54% of QRS complexes during atrial fibrillation were narrow, compared to 0–25% in the other patients. Propranolol reduced the percentage of QRS complexes that were narrow from 13 ± 16% to 1 ± 2% (mean ± standard deviation, p < 0.05). We conclude that propranolol may slow the ventricular rate during atrial fibrillation in some patients with the WPW syndrome, probably by blockcing the effects of adrenergic activation. However, propranolol should not be used in patients with the WPW syndrome who have atrial fibrillation, if most QRS complexes during atrial fibrillation are preexcited. When a large percentage of QHS complexes are narrow, propranolol may increase the ventricular rate, probably by eliminating concealed retrograde conduction in the accessory AV connection.     

Paroxysmal Bundle Branch Block of Supraventricular Origin: A Possible Source of Misdiagnosis in Detecting Ventricular Tachycardia Using Time Domain Analyses of Intraventricular Electrograms

Current implantable antitachycardia devices use several methods for differentiating sinus rhythm (SR) from supraventricular tachycardia (SVT) or ventricular tachycardia (VT). These methods include sustained high rate, the rate of onset, changes in cycle length, and sudden onset. Additional methods for detecting VT include techniques based upon ventricular electrogram morphology. The morphological approach is based on the assumption that the direction of cardiac activation, as sensed by a bipolar electrode in the ventricle, is different when the patient is in SR as compared to VT. Whether paroxysmal bundle branch block of supraventricular origin (BBB) can be differentiated from VT has not been determined. In this study, we compared the morphology of the ventricular electrogram during sinus rhythm with a normal QRS (SRNIQRS) or SVT with a normal QRS (SVTNIQRS) with the morphologies of BBB and VT in 30 patients undergoing cardiac electrophysiology studies. Changes in ventricular electrogram morphology were determined using three previously proposed time domain methods for VT detection: Correlation Waveform Analysis (CWA), Area of Difference (AD), and Amplitude Distribution Analysis (ADA). CWA, AD, and ADA distinguished VT from SRNIQRS or SVTNIQRS in 16/17 (94%), 14/17 (82%), and 12/17 (71%) patients, and BBB from SRNIQRS or SVTNIQRS in 15/15 (100%), 13/15 (87%), and 6/15 (40%) patients, respectively. However, the ranges of values during BBB using these methods overlapped with ranges of values during VT in all cases for CWA, AD, and ADA. Hence, BBB may be a source of misdiagnosis in detecting VT when these time domain methods are used for ventricular electrogram analysis.     

Pacemaker System Failure and Other Events in Children with Surgically Induced Heart Block

Of 1,193 consecutive pediatric (less than 18 years) patients undergoing intracardiac repair from 1975 to 1984, 38 (3.2%) developed surgically induced complete heart block and were treated by permanent pacemaker implantation. Anomalies included complete atrioventricular septal defect = 9 (24%), simple ventricular septal defect = 9 (24%), atrioventricular discordant connection = 8 (212), tetralogy of Fallot = 7 (182), and other complex anomalies = 5 (13%). There were no hospital deaths. follow-up was 100% complete. There were six late deaths = 16%. Actuarial survival was 79 + 9% at 10 years. None of the late deaths were related to disturbance of cardiac rhythm or pacemaker system failure. Twelve patients (32%), required 27 reoperations for various types of pacemaker system failure. Indications for reoperation included: lead failure (44%). Pulse generator failure (44%), and wound sepsis (12%). Actuarial freedom from any pacemaker related reoperation was 50 + 16% at 48 months and 25 + 15% at 96 months. Only first reoperation was found to be an incremental risk factor for subsequent reoperation (p = 0.03). Surgical heart block has been neutralized as a risk factor for hospital death after repair of congenital cardiac defects. The risk of the development of surgical heart block now approaches zero, as indicated by a decreased incidence (1 of 401 = 0.25%) in our institution from 1985 to 1987, as compared to the era 1975 to 1984 (p = 0.001).     

Identification of Ventricular Tachycardia Using Intracavitary Ventricular Electrograms: Analysis of Time and Frequency Domain Patterns

Tachycardia detection by implantable antitachycardia devices using rate alone has major limitations. Several alternative methods have been proposed to distinguish ventricular tachycardia or ventricular fibrillation from normal sinus rhythm using intracardiac electrograms. These methods have not been tested, however, for recognition of ventricular tachycardia in patients with abnormal surface QRS conduction during sinus rhythm or with antiarrhythmic drug therapy. In this study, three techniques for the indentification of ventricular tachycardia from intracavitary bipolar ventricular electrograms were examined and compared: correlation waveform analysis, amplitude distribution analysis, and spectral analysis using Fast Fourier transformation. Thirty episodes of induced monomorphic ventricular tachycardia were analyzed and compared sinus rhythm in four groups of patients with: I. Normal surface QRS conduction during sinus rhythm without antiarrhythmic drug therapy (five episodes); II. Intraventricular conduction delay or bundle branch block during sinus rhythm without antiarrhythmic drug therapy (nine episodes); III. Normal surface QRS conduction during sinus rhythm with antiarrhythmic therapy (six episodes); and IV. Intraventricular conduction delay or bundle branch block during sinus rhythm with antiarrhythmic drug therapy (ten episodes). Correlation waveform analysis had 100% sensitivity and specificity in distinguishing ventricular tachycardia from sinus rhythm, even in the presence of an intraventricular conduction delay, bundle branch block, and antiarrhythmic drug therapy. In contrast, amplitude distribution analysis differentiated 15/30 episodes (50.0%) of ventricular tachycardia from sinus rhythm, and a maximum of 18/30 episodes (60.0%) of ventricular tachycardia were identified by specal analysis using Fast Fourier transformation. Correlation waveform analysis appears to be a reliable technique to discriminate ventricular tachycardia from sinus rhythm using intracavitary ventricular electrograms. Its computational demands are modest, making it suitable for consideration in an implantable antitachycardia device.