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Biomedical subjects

S Swiryn

Publications and source records attributed to S Swiryn.

At least 37 records · Page 2Linked to original sources
PubMed1989

Shortening of ventriculoatrial intervals with left bundle branch block during orthodromic reciprocating tachycardia in three patients with a right-sided accessory atrioventricular pathway.

Previous studies of the effects of bundle branch block on ventriculoatrial (VA) intervals during orthodromic reciprocating tachycardia have focused on the timing of the atrial electrograms. However, left bundle branch block importantly affects the timing of initial ventricular activation, and this effect would also be expected to affect VA intervals during orthodromic reciprocating tachycardia. Presented here are three patients with a single right-sided accessory atrioventricular pathway exhibiting left bundle branch block during orthodromic reciprocating tachycardia. Each had shortening of the VA interval by 10 to 30 ms during left bundle branch block beats. This shortening was accompanied by a nearly equal increase in the HV interval, with the His bundle to atrial interval remaining constant. It is concluded that the timing of ventricular as well as atrial electrograms impacts on the VA intervals with left bundle branch block beats during orthodromic reciprocating tachycardia. With left bundle branch block, delay in initial left septal activation results in later onset of the QRS complex and, with right ventricular activation occurring normally, shortening of the VA interval occurs in patients with a right-sided pathway.

Adolescent↗
PubMed1989

Lack of effectiveness of lidocaine for sustained, wide QRS complex tachycardia.

Records of 31 episodes of sustained, wide QRS complex tachycardia treated with IV boluses of lidocaine in 20 consecutive patients were reviewed. Most of the episodes were managed in the emergency department. Patient ages ranged from 18 to 91 years (mean +/- SD, 64 +/- 17), and 17 of 20 were men. All but three had coronary artery disease. Although 19 of 20 patients were admitted with a diagnosis of "rule out acute myocardial infarction," only two had this diagnosis confirmed. Seventeen patients had ventricular tachycardia, and three had wide QRS complex supraventricular tachycardia. Patients were given one to three boluses of lidocaine totaling 75 to 400 mg (127 +/- 64 mg). Termination of the tachycardia was temporally related to lidocaine administration in only six of 31 episodes (19%) occurring in five of 20 patients. In three of these five patients, lidocaine was given again for a recurrence of the tachycardia and was ineffective. A similarly low efficacy was seen in 20 episodes initially managed in the hospital compared with 11 episodes initially managed by paramedics. Thus, although lidocaine is widely considered the drug therapy of first choice for sustained wide QRS complex tachycardia, it was not usually effective in our study. Patients presenting to the ED with this rhythm disturbance rarely prove to have acute myocardial infarction. Although this small retrospective study should not be the basis for a change in standard medical practice, the recommendation of lidocaine as initial therapy for such patients should be reexamined.

Adolescent↗
PubMed1989

The coherence spectrum. A quantitative discriminator of fibrillatory and nonfibrillatory cardiac rhythms.

Previous work has suggested that a comparison of electrograms from two or more sites may best differentiate fibrillatory from nonfibrillatory rhythms. The coherence spectrum is a measure by which two signals may be compared quantitatively in the frequency domain. In the present study, the coherence spectrum was used to quantify the relation between spectral components of electrograms from two sites in either the atrium or ventricle during both fibrillatory and nonfibrillatory rhythms. Bipolar recordings of 35 rhythms from 20 patients were analyzed for coherence in the 1-59 Hz band. The 17 nonfibrillatory rhythms were sinus rhythm (six), paroxysmal supraventricular tachycardia (two), atrial flutter (four), and monomorphic ventricular tachycardia (five). The 18 fibrillatory rhythms were atrial fibrillation (12) and ventricular fibrillation (six). Nonfibrillatory rhythms exhibited moderate-to-high levels of coherence throughout the 1-59 Hz band, with peaks concentrated at the rhythm's fundamental frequency and its harmonics. Fibrillatory rhythms exhibited little coherence throughout the 1-59 Hz band, and harmonics were not evident. The mean magnitude-squared coherence (scale of 0 to 1) for the 1-59 Hz band ranged from 0.22 to 0.86 (mean +/- SD, 0.52 +/- 0.19) for nonfibrillatory rhythms and from 0.042 to 0.12 (0.067 +/- 0.021) for fibrillatory rhythms. Separation of fibrillatory and nonfibrillatory rhythms was possible whether signals were recorded by floating or fixed-electrode configurations. These findings indicate that comparison of two electrograms with magnitude-squared coherence measurements differentiates fibrillatory from nonfibrillatory rhythms. A recognition algorithm based on coherence spectra may provide a major variations in lead configuration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Worsening of ventricular tachycardia by amiodarone.

The details of worsening of ventricular tachycardia in 8 (4.1%) of 194 patients receiving treatment with amiodarone are reported. Two forms of amiodarone-induced tachycardia were recognized: first, the development of new tachycardias (three patients) and second, a change in the pattern of recurrence of clinical tachycardia (five patients). In retrospect, the time from the initiation of amiodarone to the initial documentation of worsening ranged from 1 to 23 days (mean +/- SD, 9.4 +/- 8.2 days) and the time from the initiation of therapy to the recognition of worsening ranged from 6 to 26 days (14.6 +/- 10.1 days). Seven patients survived the worsening of tachycardia and one died. The total dose of amiodarone received and the duration of administration did not correlate with time to manifestation or time to resolution of worsening. This report emphasizes that worsening of ventricular tachycardia as a result of amiodarone is often difficult to differentiate from inadequate drug loading or early recurrence of 2 patient's clinical tachycardia. Further, because of the pharmacokinetics of the drug, the manifestations of worsening may be prolonged. In the cases reported, it ranged from 2 to 26 days (7.9 +/- 8.3 days), which is longer than previously reported. Because of the potential for amiodarone to cause life-threatening worsening of ventricular tachycardia and in accordance with current results, a period of in-hospital monitoring of at least 10 days at the start of therapy with amiodarone is recommended.

Aged↗
PubMed1988

Ventricular response to atrial fibrillation: role of atrioventricular conduction pathways.

Irregularity of the ventricular rhythm is a hallmark of patients with atrial fibrillation, yet the genesis of the irregularity is not yet fully understood. The role of the atrioventricular (AV) node in determining the irregularity of the ventricular response to atrial fibrillation was investigated by comparing the frequency distributions of the atrial (AA) and the ventricular (RR) intervals. Atrial electrograms and surface electrocardiographic leads were recorded during sustained atrial fibrillation in 12 patients with conduction over the AV node. The scaling factor (mean RR interval/mean AA interval) quantified the ability of the conduction pathway to scale the atrial input to a slower ventricular response and ranged from 2.55 to 5.92 (mean +/- SD 3.77 +/- 0.92). The coefficient of variation (SD/mean) measured the relative variability of the AA and RR interval distributions. The atrial and ventricular coefficients of variation were not significantly different (0.20 +/- 0.04 versus 0.21 +/- 0.03, p greater than 0.27). Similar recordings were analyzed in six patients with conduction over a accessory AV pathway. The scaling factor ranged from 1.54 to 2.46 (2.02 +/- 0.39) and, as was the case for patients with conduction over the AV node, the atrial and ventricular coefficients of variation did not significantly differ (0.24 +/- 0.08 versus 0.27 +/- 0.10, p greater than 0.6). For both groups of patients, ventricular variability and the maximal RR intervals were predicted by the product of the scaling factor and either atrial variability or maximal AA intervals, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Computer discrimination of atrial fibrillation and regular atrial rhythms from intra-atrial electrograms.

Reliable detection of atrial fibrillation from intra-atrial data is an important requirement for automatic implantable anti-tachycardia devices. Simultaneous filtered and unfiltered intra-atrial electrograms were recorded from patients in regular rhythms (12 sinus rhythms and six regular atrial tachycardias) and atrial fibrillation (nine rhythms). Each rhythm was broken down into consecutive 4-second data segments for analysis by atrial rate calculation, power spectrum analysis and amplitude probability density function generation. Significant differences were found between regular rhythms and atrial fibrillation for atrial rate, for the percentage of the total power in the 4-9 hertz band and for amplitude probability density close to the isoelectric region. There was no overlap for any of these three parameters. For each method of analysis, algorithms were generated to discriminate individual data segments from regular rhythms and atrial fibrillation with high sensitivity and specificity. Comparable results were found when sinus rhythm was excluded from the analysis. Characteristics of intra-atrial recordings during atrial fibrillation were remarkably similar to previously published reports of intra-ventricular recordings during ventricular fibrillation. Each of the three methods of analysis may provide an algorithm for accurate detection of atrial fibrillation by anti-tachycardia devices.

Algorithms↗
PubMed1988

Effects of procainamide on intra-atrial [corrected] electrograms during atrial fibrillation: implications [corrected] for detection algorithms.

The effects of antiarrhythmic drugs on electrograms have implications for arrhythmia-detection algorithms in implantable antitachycardia devices. Filtered and unfiltered intra-atrial electrograms were analyzed in eight patients who received procainamide (50 mg/min iv, up to 1000 mg) during 11 episodes of atrial fibrillation. Continuous recordings were made before, during, and after the infusion. The recordings were digitized, divided into 4.27 sec segments, and analyzed for atrial rate, median frequency and amplitude probability density function. Significant differences were noted before and after infusion of procainamide for atrial rate (498 +/- 97 vs 356 +/- 146 beats/min; p less than .005), median frequency (5.50 +/- 1.22 vs 4.24 +/- 0.99 Hz; p less than .0005), and density (58.3 +/- 13.9% vs 69.1 +/- 15.0%; p less than .005). Pre- and postprocainamide values were compared with published criteria for detection of atrial fibrillation. Before procainamide, only 2.3%, 5.7%, and 3.4% of the data segments failed to meet criteria for atrial fibrillation by rate, frequency content, and density, respectively. In contrast, after procainamide, 50%, 36.4%, and 28.4% of the data segments failed to meet these same criteria, despite electrograms still meeting morphologic criteria for atrial fibrillation. Thus procainamide resulted in changes sufficient to cause failure of published criteria for detection of atrial fibrillation. These findings have broad implications for the function of antitachycardia devices in patients receiving antiarrhythmic drug therapy.

Adult↗
PubMed1986

Long-term therapy with disopyramide phosphate: side effects and effectiveness.

In this study, the safety and efficacy of long-term therapy with disopyramide phosphate were evaluated in 40 patients with documented, recurrent, symptomatic tachyarrhythmias. Twenty-one (53%) of the patients had organic heart disease, and nine of these patients had compensated congestive heart failure. The tachyarrhythmias which were treated were paroxysmal supraventricular tachycardia (21 patients), paroxysmal atrial fibrillation (six patients), and paroxysmal ventricular tachycardia (13 patients). In each patient there was evidence, from continuous ECG monitoring or electrophysiologic testing, that disopyramide would be effective therapy, and each patient was able to tolerate disopyramide (no side effects or tolerable side effects) during an initial trial period of 1 to 2 weeks. Dosages of disopyramide were 400 to 1600 mg/day (994 +/- 320 mm/day). During long-term therapy, side effects were reported by 28 (70%) of the patients. The side effects were usually anticholinergic, and were usually a continuation of side effects noted during the initial trial period. None of the patients had idiosyncratic reactions to disopyramide. Most of the patients found side effects to be tolerable; however, in seven patients it was necessary to discontinue disopyramide after 1 to 8 (6 +/- 3) months. Actuarial incidence of intolerable side effects was 21 +/- 7% at 12 months. Nine (22%) of the 40 patients had symptomatic recurrences of tachyarrhythmia after 3 to 32 (15 +/- 9) months of therapy. Actuarial incidence of drug ineffectiveness was 32 +/- 10% at 24 months. Disopyramide was both effective and tolerated in 24 (60%) of the patients, who were followed for 2 to 64 (23 +/- 16) months.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Tachyarrhythmias in young athletes.

Nineteen young athletes with documented symptomatic tachyarrhythmia were systematically evaluated. There were 15 men and 4 women, aged 14 to 32 years (mean 22 +/- 6). Documented tachyarrhythmias were paroxysmal atrial fibrillation in five patients, paroxysmal supraventricular tachycardia in five, paroxysmal ventricular tachycardia in eight (sustained in five, nonsustained in three) and ventricular fibrillation in one patient. Abnormal substrates were demonstrated in 15 (79%) of the 19 athletes: 5 had an anomalous atrioventricular (AV) pathway and 10 had heart disease (mitral valve prolapse in 9 patients and dilated cardiomyopathy in 1 patient). In 13 (68%) of the 19 athletes, all spontaneous attacks of tachyarrhythmia had started during strenuous exercise. Tachyarrhythmia that closely resembled clinical arrhythmia was induced by programmed cardiac stimulation in 13 athletes (68%) and was reproducibly provoked by treadmill exercise in 8 athletes (42%). In four of seven athletes with ventricular tachycardia, tachycardia closely resembling clinical arrhythmia was provoked by infusion of isoproterenol. In summary: young athletes can have any of several tachyarrhythmias; abnormal substrates can be demonstrated in many athletes with symptomatic tachyarrhythmia; and tachyarrhythmias in young athletes frequently occur during exercise.

Adolescent↗
PubMed1985

Computer detection of atrioventricular dissociation from surface electrocardiograms during wide QRS complex tachycardias.

Differentiation of wide QRS complex tachycardias on surface electrocardiograms is difficult for physicians and computers due in part to their inability to identify atrial activity, specifically atrioventricular (AV) dissociation. We studied 20 examples of AV associated rhythms and 17 examples of AV dissociated ventricular tachycardia. We applied an algorithm consisting of subtraction of a mean beat from each individual beat in leads II and V1 to generate remainder electrocardiograms. The remainder electrocardiograms were visually inspected for the presence of P wave candidates and then autocorrelated. AV dissociated P wave candidates were evident on visual inspection of remainder electrocardiograms in none of 20 AV associated and 15 of 17 AV dissociated rhythms. Atrial cycle length and the presence of AV dissociation were automatically detected by applying a peak selection algorithm to the autocorrelation function. AV association was detected in all 20 AV associated rhythms and AV dissociation was detected for 11 of 17 AV dissociated rhythms (sensitivity 65%, specificity 100%, positive and negative predictive accuracy 100%, 77%). The correlation coefficient of detected vs true atrial cycle length for the 11 correctly detected AV dissociated rhythms was r = .98. Visual inspection of the remainder electrocardiograms along with the original electrocardiogram may increase the ease with which human readers can identify the presence of AV dissociation and thus diagnose ventricular tachycardia. Computer diagnosis of wide QRS complex tachycardias should be significantly improved by use of this algorithm.

Atrioventricular Node↗
PubMed1984

Torsade de pointes due to quinidine: observations in 31 patients.

We performed a mail solicitation and obtained the records of 31 patients with documented torsade de pointes (TDP) due to quinidine. All 31 patients had heart disease: ischemic = 11 patients (36%), rheumatic = five patients (16%), hypertensive = four patients (13%), cardiomyopathic = four patients (13%), other = seven patients (22%). Quinidine was administered to these patients for the following reasons: atrial fibrillation or flutter = 22 patients (71%), ventricular premature beats = six patients (19%), ventricular or supraventricular tachycardia = three patients (10%). The 31 patients were receiving quinidine, 650 to 2400 (mean 1097) mg/day, and 14 patients had serum quinidine levels of 1.4 to 10.6 (mean 3.7) micrograms/ml. TDP occurred within 1 week of initiation of quinidine therapy in 23 (74%) of the patients. Twenty-eight (90%) of the 31 patients were receiving digoxin, and 5 (24%) of 21 patients had hypokalemia at the time of TDP. Off of quinidine therapy, corrected QT (QTc) intervals in 24 patients ranged from 390 to 580 (mean 470) msec and were prolonged in 17 patients (71%). On quinidine therapy, QTc intervals in 23 patients ranged from 390 to 630 (mean 510) msec and were prolonged in 21 patients (91%). In summary, patients with TDP due to quinidine usually had heart disease complicated by atrial fibrillation, were receiving digoxin, and were receiving moderate dosages of quinidine for less than 1 week prior to TDP. Approximately two thirds of patients with TDP due to quinidine had long QT intervals while off of quinidine.

Adolescent↗
PubMed1984

Sinus node function and dysfunction.

The wide range of normal sinus node function makes identification of dysfunction difficult. Emphasis is placed upon real time correlation of ECG bradyarrhythmia with typical symptoms. A spectrum of atrial electrical dysfunction is described which includes abnormalities of the sinus and AV nodes as well as failure of escape pacemakers and atrial tachyarrhythmias.

Adolescent↗