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Biomedical subjects

S Swiryn

Publications and source records attributed to S Swiryn.

At least 73 records · Page 4Linked to original sources
PubMed1982

Exercise provocable right ventricular outflow tract tachycardia.

During the past 5 years, we have seen six patients who met inclusion criteria of exertional palpitations, reproducible treadmill (TM) provocable ventricular tachycardia (VT), and performance of electrophysiologic (EP) studies including isoproterenol (ISO) infusion. There were five males and one female, aged 15 to 55 years (mean +/- SD, 31 +/- 18 years). Three patients were trained athletes, two patients had mitral valve prolapse, three had enlarged right ventricular (RV) volumes (all trained athletes), and two had no evidence of organic heart disease. TM testing in all patients demonstrated reproducible exercise-provocable VT of at least 20 beats' duration. TM VT was characterized by left bundle branch block pattern ORS morphology and rates of 150 to 230 bpm (186 +/- 30 bpm). EP did not reproduce VT in five of six patients while ISO at a dose of 2 to 4 micrograms/min (2.5 +/- 0.8 micrograms/min) reproduced VT in all patients. ISO VT was characterized by QRS morphology identical to TM VT and rates of 165 to 230 bpm (191 +/- 26 bpm). Endocardial mapping of ISO VT revealed earliest activity in RV outflow tract. Serial TM testing revealed suppression of TM VT in all six patients on propranolol therapy. Responses to class I drugs were variable and less successful. In summary, we describe a group of patients with common clinical, ECG, and electrophysiologic features who may share a common pathophysiology of VT. Possible mechanisms are discussed.

Adolescent↗
PubMed1982

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↗
PubMed1982

Symptomatic spontaneous paroxysmal AV nodal block due to localized hyperresponsiveness of the AV node to vagotonic reflexes.

Two apparently healthy patients had recurrent syncope with documented paroxysmal AV block. In both patients the site of AV block was demonstrated to be in the AV node. Coronary angiography (in both patients) and sustained deep inspiration (one patient) reproducibly initiated episodes of paroxysmal AV nodal block (identical to spontaneous episodes). Atropine abolished further attempts of AV block induction. Vagal hyperresponsiveness was limited to the AV node, since the interventions provoking paroxysmal AV nodal block produced only appropriate sinus slowing. This syndrome reflects hyperresponsiveness of the AV node to vagotonic reflexes, and exists as a clinically significant entity producing recurrent syncope.

Adult↗
PubMed1982

Electrophysiologic study demonstrating triple antegrade AV nodal pathways in patients with spontaneous and/or induced supraventricular tachycardia.

Ten patients are described with two discrete discontinuities in AV nodal conduction curves suggesting triple antegrade AV nodal pathways. This represents approximately 6% of patients seen in this laboratory with dual AV nodal pathways. Patients ranged in age from 18 to 63 (mean +/- SD, 48 +/- 15 years). Six of the 10 patients had organic heart disease and four did not. The effect of cycle length on triple pathways could be analyzed in 8 of 10 patients who had atrial extrastimulus testing at two or more cycle lengths. Three of these eight patients had triple pathways at all tested cycle lengths. Four patients had triple pathways only at shorter cycle lengths. One patient had triple pathways only at longer cycle lengths. Intact retrograde conduction was demonstrated in seven of ten patients, all of whom had atrial echoes (two patients) or inducible supraventricular tachycardia (SVT) (five patients). Echoes or SVT were induced on the slow pathway is all seven patients, but also on the intermediate pathway in three. However, sustained SVT usually reflected antegrade slow and retrograde fast pathway conduction. In conclusion, triple AV nodal pathways may be demonstrated in occasional patients during atrial extrastimulus testing. Thereby, functional longitudinal dissociation of the AV node is not limited to two pathways.

Adolescent↗
PubMed1981

Retrograde dual atrioventricular nodal pathways.

Thirty-one (3.5 percent) of 887 studied patients had retrograde dual atrioventricular (A-V) nodal pathways, as manifested by discontinuous retrograde A-V nodal conduction curves (29 patients) or by two sets of ventriculoatrial (V-A) conduction intervals at the same cycle length (2 patients). All patients had A-V nodal reentrant ventricular echoes of the unusual variety induced with ventricular stimulation (25 patients had single, 2 patients had double and 4 patients had more than three ventricular echoes). The weak link of the reentrant circuit was always the retrograde slow pathway. Eleven of the 31 patients also had anterograde dual A-V nodal pathways (bidirectional dual pathways). Eight patients (26 percent) had spontaneous as well as inducible A-V nodal reentrant paroxysmal supraventricular tachycardia (of the unusual type in three and the usual type in five). In addition, three patients (10 percent) had only inducible supraventricular tachycardia (two of the unusual and one of the usual type). Retrograde dual A-V nodal pathways are uncommon. They are associated with the finding of at least single A-V nodal reentrant ventricular echoes (all patients), anterograde dual pathways (one third of patients) and A-V nodal reentrant paroxysmal supraventricular tachycardia of the usual and unusual variety (one third of patients).

Adult↗
PubMed1981

Procainamide-induced polymorphous ventricular tachycardia.

Seven cases of procainamide-induced polymorphous ventricular tachycardia are presented. In four patients, polymorphous ventricular tachycardia appeared after intravenous administration of 200 to 400 mg of procainamide for the treatment of sustained ventricular tachycardia. In the remaining three patients, procainamide was administered orally for treatment of chronic premature ventricular contractions or atrial flutter. These patients had Q-T prolongation and recurrent syncope due to polymorphous ventricular tachycardia. In four patients, the arrhythmia was rapidly diagnosed and treated with disappearance of further episodes of the arrhythmia. In two patients, the arrhythmia degenerated into irreversible ventricular fibrillation and both patients died. In the seventh patient, a permanent ventricular pacemaker was inserted and, despite continuation of procainamide therapy, polymorphous ventricular tachycardia did not reoccur. These seven cases demonstrate that procainamide can produce an acquired prolonged Q-T syndrome with polymorphous ventricular tachycardia.

Administration, Oral↗
PubMed1981

Electrophysiologic effects of ouabain in patients with preexcitation and circus movement tachycardia.

Effects of intravenous ouabain were evaluated in 19 patients with an anomalous conduction pathway (14 with manifest and 5 with concealed preexcitation (utilizing intracardiac stimulation and recording. Anterograde conduction through the anomalous pathway was present in all 14 patients with manifest preexcitation at a maximal atrial paced rate of 140 to 250 beats/min (mean +/- standard error of the mean 214 +/- 7.2) before and at 150 to 240 beats/min (mean 206 +/- 7.1) after ouabain (difference not significant [NS]). The anterograde effective refractory period of the anomalous pathway, measured at an equivalent atrial paced rate in 10 patients, was 250 to 450 ms (mean 309 +/- 19.7) before and 260 to 450 ms (mean 300 +/- 17.2) after ouabain (NS). Retrograde conduction through the anomalous pathway was possible at maximal ventricular paced rates (17 patients) of 160 to 250 beats/min (mean 222 +/- 6.6) before and 190 to 250 beats/min (mean 221 +/- 4.4) after ouabain (NS). Sustained atrioventricular (A-V) reentrant paroxysmal supraventricular tachycardia was inducible in all 19 patients before and in 17 patients (89 percent) after ouabain (tachycardia could not be induced in two patients because of increased A-V nodal refractoriness). The mean cycle length of tachycardia in the 17 patients was 320 +/- 6.7 ms before and 340 +/- 8.1 ms after ouabain (p < 0.01). In conclusion, ouabain has no significant effect on either anterograde or retrograde anomalous pathway refractoriness. Although ouabain slightly increases the cycle length of tachycardia, it does not interfere with induction of tachycardia in most patients with preexcitation. Oral cardiac glycosides alone would appear to be of limited value in patients with preexcitation and recurrent supraventricular tachycardia.

Adolescent↗
PubMed1981

Assessment of left ventricular function by radionuclide angiography during induced supraventricular tachycardia.

Electrocardiographically synchronized radionuclide angiography was performed before, during and after induced paroxysmal supraventricular tachycardia in 13 patients. Data were acquired with a computer-interfaced Anger camera in a left anterior oblique projection. No data were acquired during tachycardia until tachycardia had been sustained for 1 minute. Patients ranged in age from 20 to 64 years (mean +/- standard deviation 42 +/- 14.5). Three patients had organic heart disease and 10 did not. Baseline and tachycardia heart rates (beats/min) were 59 to 99 (73 +/- 11) versus 141 to 228 (157 +/- 22). Baseline and tachycardia left ventricular measurements (mean +/- standard error) were as follows: ejection fraction 64 +/- 2 versus 62 +/- 4 percent (not significant), ejection rate 3.0 +/- 0.1 versus 4.3 +/- 0.4 mean ventricular counts/s (p less than 0.001), normalized end-diastolic counts 72.7 +/- 7.8 versus 48.7 +/- 6.7 X 10(3) counts (p less than 0.001), normalized stroke counts 37.1 +/- 3.4 versus 23.3 +/- 2.7 X 10(3) counts (p less than 0.001) and normalized count cardiac output 2,717.5 +/- 273.0 versus 3,620.2 +/- 403.7 X 10(3) counts/min (p less than 0.005). Although ejection fraction for the whole group did not change significantly, it decreased during tachycardia by 5 percentage points or more in five patients. These were the three patients with heart disease and the two normal patients with the fastest heart rate during tachycardia (228 and 214 beats/min, respectively). In summary, paroxysmal supraventricular tachycardia was characterized by a marked decrease in left ventricular end-diastolic and stroke volumes but increased ejection rate and cardiac output without significant change in ejection fraction. Heart disease or rapid heart rate during tachycardia appeared to have a deleterious effect on ejection fraction.

Adult↗
PubMed1981

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↗
PubMed1981

Tricuspid insufficiency detected by equilibrium gated radionuclide study.

The results of a gated radionuclide cardiac study are reported in a patient with biventricular failure and tricuspid insufficiency demonstrated by clinical evaluation, M-mode and 2-D sector echocardiography, and cardia catheterization. The processed gated radionuclide cardiac study showed a left ventricular/right ventricular stroke volume ratio of 0.5; expansion of the hepatic blood pool demonstrated by hepatic time activity curve and calculation of an "'expansion fraction"; and synchronous changes of count rate of the atrial and hepatic regions detected by phase analysis (similar phase shifts).

Echocardiography↗
PubMed1981

Natural history of chronic second-degree atrioventricular nodal block.

This report details our experience with documented chronic second-degree atrioventricular (AV) nodal block (proximal to His [H]) in 56 patients. Forty-six men (82%) and 10 women (18%), ages 18-87 years, were studied. Nineteen of the patients (34%) had no organic heart disease (including seven trained athletes) and 37 (66%) had organic heart disease. ECGs in all patients demonstrated episodes of type I second-degree block; five patients also had periods of 2:1 block. Prospective follow-up patients with no organic heart disease (157-2280 days, mean 1395 +/- 636 days) revealed one patient with clear indication for permanent pacing because of bradyarrhythmic symptoms (permanently placed on day 220 of follow-up). Two patients died nonsuddenly. In patients with organic heart disease (prospective follow-up of 60-2950 days, mean 1347 +/- 825 days), pacemakers were implanted in 10 patients, primarily for treatment of congestive heart failure in eight and syncope in two. Sixteen patients died -- three suddenly, seven with congestive heart failure, two of an acute myocardial infarction and four of causes unrelated to cardiac disease. In summary, chronic second-degree AV nodal block has a relatively benign course in patients without organic heart disease. In patients with organic heart disease, prognosis is poor and related to the severity of underlying heart disease.

Adolescent↗
PubMed1981

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↗