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Biomedical subjects

C R Wyndham

Publications and source records attributed to C R Wyndham.

At least 55 records · Page 3Linked to original sources

Concealed antidromic re-entrance during rapid atrial pacing in the Wolff-Parkinson-White syndrome.

In a patient with Wolff-Parkinson-White syndrome, rapid atrial pacing up to rates of 140/min resulted in A-H prolongation; increases in rate up to 200/min, however, failed to lengthen A-H further. The delta-H interval increased as rate rose to 120/min, but remained stable thereafter. These and other findings suggest retrograde activation of the His bundle via the accessory pathway at rates greater than 140/min. Such a phenomenon: 1) prevents initiation of PSVT with atrial pacing; 2) prevents one from determining the anterograde block rate of the AV node; 3) represents concealed antidromic re-entrance, which may theoretically lead to antidromic re-entrant PSVT.

Atrial Fibrillation↗

Sequential regional phase mapping of radionuclide gated biventriculograms in patients with sustained ventricular tachycardia: close correlation with electrophysiologic characteristics.

Radionuclide (RNA) gated studies were performed during sinus rhythm and during spontaneous or induced sustained ventricular tachycardia (VT) in six patients with clinical VT. Fourier analysis of time-activity variation was used to calculate a RNA phase value for each pixel in the image. Color coding of each pixel according to its calculated phase resulted in a RNA phase map of the ventricles. The following results were considered to be consistent with the known electrophysiology of VT: (1) the phase map correlated with QRS morphology and axis in most but not all tachycardias; (2) earliest phase usually demonstrated the VT origin to be at the border of the ventricular wall motion abnormality; (3) endocardial mapping (available in one patient) showed close correlation with RNA phase mapping; (4) in three patients with ischemic heart disease, VT with left bundle branch block (LBBB) pattern had earliest LV phase along the septum; and (5) for one patient imaged during two different VT morphologies, the tachycardias had earliest phase at different borders of the same wall motion abnormality with differing progression of phase across the ventricles. RNA phase mapping of VT is feasible and appears to provide data consistent with the electrophysiology of this arrhythmia.

Adult↗

Paroxysmal atrial fibrillation in the Wolff-Parkinson-White syndrome.

Eighty-eight patients with preexcitation were studied to determine how 30 patients with documented spontaneous paroxysmal atrial fibrillation differed from 58 patients without this arrhythmia. Inducible reentrant tachycardia was present in 23 (77 percent) of the 30 patients with, versus 28 (48 percent) of the 58 patients without, atrial fibrillation (p less than 0.025). Heart disease was present in 13 (43 percent) of the 30 patients with, versus 15 (26 percent) of the 58 patients without, atrial fibrillation (not significant). Inducible reentrant tachycardia or heart disease, or both, were significant). Inducible reentrant tachycardia or heart disease, or both, were present in 29 (97 percent) of the 30 patients with, versus 34 (59 percent) of the 58 patients without, atrial fibrillation (p less than 0.0005). Of 51 patients with inducible reentrant tachycardia, 23 patients with atrial fibrillation did not differ from 28 patients without this arrhythmia with respect to clinical features and atrial, sinus nodal, or anomalous pathway properties, or cycle length of induced reentrant tachycardia. Spontaneous degeneration of induced reentrant tachycardia to atrial fibrillation was observed in 6 (26 percent) of 23 patients with, versus none of 28 patients without, atrial fibrillation (p less than 0.025). In summary, patients with preexcitation and documented spontaneous paroxysmal atrial fibrillation almost always have inducible reentrant tachycardia or heart disease, or both. It is likely that in many patients with inducible reentrant tachycardia, spontaneously occurring reentrant tachycardia relates to induction of atrial fibrillation. However, it is unclear why some patients with inducible reentrant tachycardia have atrial fibrillation and others do not. In many patients with organic heart disease, atrial fibrillation could relate to hemodynamic changes.

Adolescent↗

Ventricular tachycardia: prediction of response to oral aprindine with intravenous aprindine.

Aprindine was administered both intravenously and orally to 25 patients with ventricular tachycardia refractory to conventional antiarrhythmic agents to test the hypothesis that the response to intravenous aprindine predicts the response to oral aprindine. Ten patients had incessant ventricular tachycardia and 15 had paroxysmal sustained inducible ventricular tachycardia. Eleven patients (43 percent) had conversion to sinus rhythm with intravenous aprindine (nine with incessant and two with paroxysmal sustained ventricular tachycardia). Thirteen patients (all with paroxysmal sustained ventricular tachycardia) manifested slowing of the tachycardia without conversion, whereas in one patient with incessant ventricular tachycardia, the tachycardia became less frequent and nonsustained after intravenous aprindine. All 11 patients who had conversion to sinus rhythm with intravenous aprindine remained free of ventricular tachycardia during oral treatment with aprindine (at 2 weeks) and for a follow-up period of 2 to 38 months (mean 16 +/- 13). Of the 14 patients who did not have conversion to sinus rhythm with intravenous aprindine, 12 had spontaneous or inducible ventricular tachycardia, or both, at evaluation 1 to 2 weeks after initiation of oral aprindine. In conclusion, administration of intravenous aprindine to patients with ventricular tachycardia is helpful in predicting the subsequent response to oral aprindine. In addition, the pattern of ventricular tachycardia predicted the response to aprindine; patients with incessant ventricular tachycardia tended to respond, and those with paroxysmal sustained ventricular tachycardia tended not to respond.

Administration, Oral↗

Effects of oral disopyramide phosphate on induction of paroxysmal supraventricular tachycardia.

The effects of oral disopyramide phosphate on laboratory induction of paroxysmal supraventricular tachycardia (PSVT) were studied in 16 patients with clinical PSVT. After control electrophysiologic study to determine the inducibility and mechanism of PSVT, patients were given 200-300 mg (275 +/- 45 mg, mean +/- SD) of disopyramide for three to five doses over 24 hours and were then restudied. All patients had inducible, sustained PSVT during the control study. After disopyramide, PSVT was noninducible in eight patients (50%), including six of nine with atrioventricular nodal reentrance and two of seven with atrioventricular reentrance; inducible but nonsustained in two (12.5%) (both with atrioventricular reentrance); and inducible and sustained in six (37.5%). The benefit of disopyramide seemed predominantly to reflect depression of conduction in the retrograde limb of the circus movements, although effects upon the antegrade limb were also observed. In the eight patients with inducible PSVT before and after disopyramide, tachycardia cycle length increased from 348 +/- 33 to 404 +/- 29 msec (mean +/- SEM) (p less than 0.001). These results suggest that disopyramide would be effective in preventing recurrence of clinical PSVT in selected patients.

Administration, Oral↗

Significance of the HV interval in 517 patients with chronic bifascicular block.

In January 1975, we reported results of a prospective follow-up study (mean 538 +/- 42 days) of 119 patients with chronic bifascicular block (BFB), and concluded that BFB patients with normal and prolonged HV (NHV and PHV) had a similar incidence of atrioventricular (AV) block and mortality. In this report, we update these findings in 517 patients with a follow-up of 21 days to 9.8 years (mean 3.4 +/- 0.2 years). Three hundred nineteen patients (61%) had NHV and 198 (39%) had PHV (greater than 55 msec). The NHV and PHV groups were similar in regard to age (NHV vs PHV, 61 +/- 1 vs 62 +/- 1 years) and sex (80% male, 20% female vs 82% male and 18% female). The following were more common (p less than 0.05) in patients with PHV (percent of patients with finding in NHV vs PHV groups): angina (18% vs 27%), congestive failure (27% vs 42%), cardiomegaly (48% vs 66%), New York Heart Association functional class II-IV (34% vs 56%), premature ventricular complexes (20% vs 29%), and organic heart disease (OHD) (75% vs 85%). Spontaneous trifascicular block (TFB) developed in two patients (0.6%) with NHV and nine patients (4.5%) with PHV (p less than 0.05). Cumulative 7-year incidence of TFB was 3% with NHV and 12% with PHV (p less than 0.01). Seven-year cumulative cardiovascular mortality was 32% in NHV patients and 57% in PHV patients (p less than 0.005). In conclusion, PHV in patients with chronic BFB was associated with a greater incidence and severity of OHD, and higher total and sudden death mortalities. The risk of spontaneous TFB was small in patients with either NHV or PHV, although it was significantly higher in the latter.

Angina Pectoris↗

Chronic nonparoxysmal junctional tachycardia.

We describe an adult with chronic (three years' duration) acquired nonparoxysmal junctional tachycardia, a previously undescribed rhythm. Ambulatory monitoring revealed junctional rates ranging from 75 to 110 beats/min. Electrophysiologic studies demonstrated intact atrioventricular and ventriculoatrial conduction with a normal H-V interval (43 msec) and narrow QRS. Underlying sinus node function appeared to be normal (recovery time of 900 msec). Junctional rate increased with administration of atropine and isoproterenol, suggesting that the junctional pacemaker was located in the proximal His bundle. Electrocardiographic and electrophysiologic observations suggested that this case of chronic nonparoxysmal junctional tachycardia was benign, not necessitating therapy.

Aged↗

Serial electrophysiologic testing of multiple drugs in patients with atrioventricular nodal reentrant paroxysmal tachycardia.

Serial electrophysiologic testing of multiple drugs was performed in 21 patients with recurrent atrioventricular (AV) nodal reentrant paroxysmal supraventricular tachycardia (PSVT). All patients had reproducible sustained PSVT induced before drug administration. Serial daily PSVT induction was attempted after administration of i.v. ouabain (0.01 mg/kg) (16 patients), i.v. propranolol (0.1 mg/kg (17 patients), i.v. ouabain + propranolol (same dosages) (12 patients), i.v. procainamide (600-1000 mg) (17 patients) and oral quinidine (1600-2400 mg/day) (nine patients). In two of 21 patients (10%), no tested drug prevented induction of sustained PSVT. In 19 of 21 patients (90%), one or more drugs prevented induction of sustained PSVT: ouabain--seven patients, propranolol--seven patients, ouabain + propranolol--seven patients, procainamide--11 patients, quinidine--seven patients. The site of action of ouabain and/or propranolol was either the antegrade limb or the retrograde limb (RL) of the circus movement. The site of action of procainamide or quinidine was always the RL. These 19 patients were treated with oral drugs, based on results of serial testing. Eighteen patients were successfully followed for 6-50 months. In 13 of these 18 patients PSVT did not recur. Two patients (11%) had > 95% reduction in frequency of PSVT recurrences, and three (17%) did not respond to chosen oral drugs. Serial electrophysiologic testing of multiple drugs is feasible in patients with AV nodal reentrant paroxysmal tachycardia. Drug responses are variable. In most but not all patients, serial electrophysiologic testing defines effective prophylactic drug therapy. This method of defining prophylactic drug therapy appears most suitable for patients with poorly tolerated tachycardias that occur only sporadically.

Administration, Oral↗

Successful surgical excision of focal paroxysmal atrial tachycardia. Observations in vivo and in vitro.

A 41-year-old man had chronic, recurrent, drug-resistant paroxysmal right atrial tachycardia. Electrophysiologic studies revealed features suggesting atrial reentrance, including induction and termination of tachycardia with rapid atrial pacing and atrial extrastimuli. Endocardial catheter mapping localized the origin of tachycardia to the right atrial appendage. Intraoperative epicardial mapping refined the localization to the posterolateral rim of the appendage. The appendage was excised and the tachycardia was permanently cured. Microelectrode studies on the excised tissue revealed an inducible rhythm localized to a small area of the atrial endocardium, characterized by rapid pacing induction, rhythmicity generated from a suprathreshold afterdepolarization, low maximum diastolic potential, low overshoot potential and a smooth transition from phase 4 to phase 0, suggesting triggered automaticity. This is the first observation in man of probable triggerable atrial automaticity, which may be a direct counterpart of the clinical arrhythmia. The successful surgical outcome indicates that a focal atrial tachycardia can be excised in selected patients.

Adult↗