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Biomedical subjects

A H Kadish

Publications and source records attributed to A H Kadish.

At least 73 records · Page 4Linked to original sources
PubMed1992

Spatial and temporal linking of epicardial activation directions during ventricular fibrillation in dogs. Evidence for underlying organization.

BACKGROUND: It remains controversial as to whether electrical activation during ventricular fibrillation (VF) is organized. To detect the presence of organization in VF, the direction of epicardial activation (EA) at multiple sites was examined by using vector mapping. If VF is not a random process, EA direction at a given site should be related to adjacent sites and prior beats. METHODS AND RESULTS: Thirteen dogs with healing myocardial infarction (MI) and four dogs without MI had VF induced by programmed stimulation. Using a plaque electrode array with a 2.5-mm interelectrode distance, 91 vector loops were created for each "beat" of VF. Direction of maximum EA was determined at each site for the first 10 consecutive beats of VF and for 10 consecutive beats recorded 5 seconds after VF was established. Spatial and temporal linking of EA directions was evaluated by the ability of activation direction at a given site to be predicted by activation directions at eight adjacent sites for the index beat and at eight adjacent sites and the site of interest for the preceding beat using stepwise linear regression. The strength of the model as reflected by the correlation coefficient (r) indicated the degree of linking. We determined 1) changes in the degree of linking over time during a given episode of VF (using a paired-difference t test), 2) differences in the degree of linking between the anterior and posterolateral walls in animals with (n = 4) and without (n = 4) MI (using two-way ANOVA), and 3) the effect of repeated inductions (n = 10) on the degree of linking (using one-way ANOVA with repeated measures). During 57 episodes of VF, r for each model ranged from 0.64 to 0.88 during the transition to VF to 0.39-0.78 during established VF (p < 0.0001 for the difference). The presence of MI, the site of recording, and repeated inductions did not affect the degree of linking. For each episode, spatial linking was more prominent than temporal linking. CONCLUSIONS: Electrical activation during VF is organized. The degree of linking of EA directions during VF is not affected by the presence of MI, the site of recording, or repeated inductions of VF. During the first 5 seconds of VF, the degree of linking decreases.

Animals↗
PubMed1991

Diagnosis and cure of the Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardias during a single electrophysiologic test.

BACKGROUND: We conducted this study to determine the feasibility of an abbreviated therapeutic approach to the Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardia, in which the diagnosis is established and radiofrequency ablation carried out during a single electrophysiologic test. METHODS: One hundred six consecutive patients were referred for the management of documented, symptomatic paroxysmal supraventricular tachycardias (66 patients) or the Wolff-Parkinson-White syndrome (40 patients). All agreed to undergo a diagnostic electrophysiologic test and catheter ablation with radiofrequency current. No patient had had such a test previously. RESULTS: Among the 66 patients with paroxysmal supraventricular tachycardias, the mechanism was found to be atrioventricular nodal reentry in 46 (70 percent) (typical in 44 and atypical in 2), atrioventricular reciprocating tachycardia involving a concealed accessory pathway in 16 (24 percent), atrial tachycardia in 2 (3 percent), and noninducible paroxysmal supraventricular tachycardia in 2 (3 percent). A successful long-term outcome was achieved in 57 of 62 patients (92 percent) with paroxysmal supraventricular tachycardia in whom ablation was attempted and in 37 of 40 patients (93 percent) with the Wolff-Parkinson-White syndrome. The only complications were one instance of occlusion of the left circumflex coronary artery, leading to acute myocardial infarction, and one instance of complete atrioventricular block. The mean (+/- SD) duration of the electrophysiologic procedures was 114 +/- 55 minutes. CONCLUSIONS: The diagnosis and cure of paroxysmal supraventricular tachycardia or the Wolff-Parkinson-White syndrome during a single electrophysiologic test are feasible and practical and have a favorable risk-benefit ratio. This abbreviated therapeutic approach may eliminate the need for serial electropharmacologic testing, long-term drug therapy, antitachycardia pacemakers, and surgical ablation.

Adolescent↗
PubMed1991

Comparison of the results of electrophysiologic testing after short-term and long-term treatment with amiodarone in patients with ventricular tachycardia.

The results of electrophysiologic testing after short-term and long-term treatment with amiodarone were compared in 71 patients with ventricular tachycardia. Electrophysiologic testing was performed in the baseline state after 11 +/- 3 days of treatment with 1.2 to 2.4 gm/day of amiodarone, and after 13 +/- 4 weeks of therapy with a daily amiodarone dose of 400 mg. After short-term therapy, 62% of the patients had an adequate response to amiodarone. In 27 patients who were hemodynamically unstable, ventricular tachycardia was induced and became noninducible or hemodynamically stable after combination therapy with a class I agent. Among 18 patients who did not have inducible ventricular tachycardia after short-term therapy, eight (44%) had inducible, hemodynamically unstable ventricular tachycardia after long-term treatment with amiodarone. On the other hand, six of the 27 patients who had hemodynamically unstable ventricular tachycardia after short-term therapy had an adequate response after long-term treatment with amiodarone. Therefore an adequate electrophysiologic response after short-term therapy does not guarantee a similar response after long-term treatment, and an inadequate response after short-term therapy does not always predict a similar response after long-term therapy.

Aged↗
PubMed1991

The effect of quinidine and mexiletine on the adaptation of ventricular refractoriness to an increase in rate.

The purpose of this study was to determine the effects of quinidine and mexiletine on the adaptation of ventricular refractoriness to a change in heart rate. The ventricular effective refractory period was measured at a basic drive cycle length of 500 msec with basic drive train durations of two beats, eight beats, 20 beats and 3 minutes. The ventricular refractory periods were measured in the baseline state and after oral treatment with quinidine or mexiletine in 20 subjects each. In the baseline state, there was progressive shortening of the ventricular refractory period as the drive train duration increased from two beats to 3 minutes. Quinidine prolonged refractoriness by 5% (p less than 0.001) at each drive train duration. Mexiletine did not affect the ventricular effective refractory period at any of the drive train durations. In a control group of 20 subjects, there were no significant differences between two determinations of refractoriness at each basic drive train duration. In conclusion, neither quinidine nor mexiletine affect the adaptation of ventricular refractoriness to an increase in rate. Although the ventricular effective refractory period measured with a conventional basic drive train duration of eight beats is often more than 20 msec longer than the actual ventricular effective refractory period measured with a drive train duration of 3 minutes, the effects of quinidine and mexiletine on the conventionally measured ventricular effective refractory period accurately reflect the effects of these drugs on the actual ventricular effective refractory period.

Adaptation, Physiological↗
PubMed1991

Differences in QRS configuration during unipolar pacing from adjacent sites: implications for the spatial resolution of pace-mapping.

To examine the spatial resolution of unipolar pace-mapping, 12 lead electrocardiograms (ECGs) recorded during pacing from each of the poles of a quadripolar catheter (5 mm interelectrode distance) were examined. Unipolar pacing was performed from each of the poles at late diastolic threshold, twice threshold and 10 mA at a cycle length of 500 ms. In 15 patients, pacing was performed at the right ventricular apex and in 14 at various left ventricular sites. Pacing from the distal catheter pole at threshold (index ECG) was used to simulate the site of origin of ventricular tachycardia, and all other ECGs were compared with the index ECG. Electrocardiograms were evaluated by two independent observers for 1) minor configuration differences (notch, new small component, change in the amplitude of individual components or change in QRS shape); 2) major differences in configuration (new large component, marked change in the amplitude of an existing component or two minor changes); and 3) peak to peak changes in amplitude. Minor differences in configuration were seen in a mean 2.4 +/- 1.9, 4.6 +/- 2.4 and 4.4 +/- 2.9 leads during pacing at 5, 10 and 15 mm from the distal electrode (index site). Major differences in configuration were seen in a mean of 0.3 +/- 0.5, 2.1 +/- 2.1 and 3.7 +/- 2.3 leads during pacing at 5, 10 and 15 mm from the index site. Differences in amplitude were seen in a mean of 3.1 +/- 2.2, 5.6 +/- 2.5 and 6.8 +/- 3.0 leads per ECG during pacing at 5, 10 and 15 mm from the index ECG pacing site, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1991

Effect of antiarrhythmic drug therapy on the incidence of shocks in patients who receive an implantable cardioverter defibrillator after a single episode of sustained ventricular tachycardia/fibrillation.

Seventy-four patients (16 women, 58 men, age 58 +/- 11 years, mean +/- standard deviation) who received an implantable cardioverter defibrillator (ICD) after experiencing a single episode of ventricular tachycardia or ventricular fibrillation were followed to determine if antiarrhythmic drug therapy affects the incidence of ICD discharges. Thirty-three patients (group A) were treated with an antiarrhythmic drug that was either untested or previously demonstrated during electropharmacological testing to be ineffective in suppressing the induction of ventricular tachycardia. Forty-one patients (group B) were not treated with an antiarrhythmic drug. There were no significant differences between the two groups in regards to age, sex, incidence of coronary artery disease, left ventricular function or the type of ICD pulse generator used. During a mean follow-up of 14 months for the entire cohort, 15 patients (46%) in group A and 18 patients (44%) in group B experienced at least one ICD shock. The time to the first appropriate shock (5 +/- 5 months in both groups) and the frequency of ICD shocks (0.3 +/- 0.2/month in group A vs 0.4 +/- 0.5/month in group B) were similar in both groups. The incidence of syncope at the time of ICD discharge was higher in group A than group B patients (31% vs 5%, P less than 0.05). In conclusion, antiarrhythmic drugs that are untested or have failed electropharmacological testing do not appear to reduce the probability of ICD discharge over a short-term (mean 14 months) follow-up in patients who have had only one clinical episode of VT/VF and may increase the risk of syncope during ICD discharge.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1991

Variability in the measurement of human ventricular refractoriness.

The degree of variability in ventricular refractoriness and factors potentially affecting this variability were evaluated in 80 patients undergoing an electrophysiological study. Each of seven variables (stimulation current, coupling interval of the basic drive train to spontaneous rhythm, pause between determinations, bipolar pacing configuration, bipolar vs unipolar pacing, atrioventricular synchrony, and autonomic tone) was evaluated in a group of ten patients to determine its effects on the reproducibility of refractoriness. Measurements were repeated ten times in every patient under each of two conditions. Five variables had significant effects on the reproducibility of measurements. Pacing at 10 mA was associated with less variability in the determination of ventricular refractoriness than pacing at twice threshold (within-subject variance component 4.5 vs 10.1 msec; P less than 0.001). The mean difference between the longest and shortest determinations of refractory periods (range) was 6.2 msec at 10 mA and 8.6 msec at twice threshold. The use of a conditioning period of pacing and continuous trains (eight beats with a 3-sec pause) rather than a variable pause between serial trials reduced the mean within-subject variance component from 16.5 to 3.3 (P less than 0.001) and the mean range of refractory period determinations from 10.8 to 4.8. The use of the distal rather than the proximal pole as the cathode decreased the mean within-subject variance component from 9.4 to 3.3 (P less than 0.001) and the range of determinations from 6.4 to 5.8 msec. Unipolar pacing was associated with less variability than bipolar pacing (mean within-subject variance component 4.6 vs 6.4; P less than 0.05, mean range 5.0 vs 7.6 msec).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1991

A comparison of QRS complexes resulting from unipolar and bipolar pacing: implications for pace-mapping.

UNLABELLED: To examine differences in QRS configuration produced by bipolar versus unipolar pacing, 12-lead electrocardiograms recorded during bipolar (distal cathode) pacing with 5- and 10-mm interelectrode distances were compared to electrocardiograms recorded during unipolar cathodal pacing from the distal catheter pole. Pacing was performed at a cycle length of 500 msec using each of the two bipolar configurations at current strengths equal to late diastolic threshold, twice threshold and 10 mA. The pacing site was at the right ventricular apex in 15 patients and at various left ventricular locations in 14 patients. The electrocardiograms recorded during bipolar and unipolar pacing were compared by two independent observers for minor QRS configuration changes, major configuration changes and amplitude changes. Minor configuration differences between unipolar and bipolar pacing occurred occasionally when the interelectrode distance during bipolar pacing was 5 mm (mean +/- S.D. 0.5 +/- 1.2 leads per electrocardiogram). However, when the interelectrode distance was 10 mm, minor configuration differences were seen more commonly (1.3 +/- 2.0 leads per electrocardiogram; P less than 0.05 vs 5-mm distance). Major configuration differences were uncommon with either configuration at all current strengths. Pacing at 10 mA produced a larger number of configuration differences than pacing at either threshold or twice threshold (P less than 0.05). Amplitude differences were seen in a mean of 1.9 +/- 2.1 leads per electrocardiogram with the 5-mm interelectrode distance and a mean of 2.9 +/- 2.1 leads using the 10-mm interelectrode distance (P less than 0.05). IN CONCLUSION: (1) bipolar ventricular pacing can result in QRS complexes that are different from those obtained with unipolar pacing at the same catheter location, presumably due to an anodal contribution during bipolar pacing; (2) increasing the interelectrode distance and stimulus intensity increases these differences; and (3) because the proximal electrode's contribution to depolarization can alter the QRS configuration during pacing in a variable way, the use of bipolar pace-mapping to localize sites of origin of ventricular tachycardia may result in less spatial resolution than unipolar pace-mapping.

Cardiac Catheterization↗
PubMed1990

Cost of catheter versus surgical ablation in the Wolff-Parkinson-White syndrome.

In this retrospective study of 22 patients with the Wolff-Parkinson-White (WPW) syndrome, the cost of catheter ablation in 11 patients was compared with that of surgical ablation in another 11 patients. All patients in the catheter ablation group had a posteroseptal accessory pathway; in the surgical group, 5 patients had a left lateral accessory pathway, 3 had a left lateral and posteroseptal accessory connection and 3 had a right-sided pathway. Catheter ablation was successful in 8 of 11 patients (73%). In the surgical group, the accessory pathway was interrupted successfully in all patients (100%). The mean duration (+/- standard deviation) of hospitalization was 6 +/- 2 days in the catheter ablation group and 8 +/- 4 days in the surgical group. The mean cost/patient, expressed in 1988 dollar values, was +14,116 +/- 4,493 in the catheter ablation group and +34,175 +/- 5,434 in the surgical ablation group (p less than 0.0001). The mean time lost from work or school was 10 +/- 5 days in the catheter ablation group and 60 +/- 16 days in the surgical group (p less than 0.01). Catheter ablation is significantly less expensive than surgical ablation of accessory pathways. Assuming that all patients in whom catheter ablation is unsuccessful subsequently undergo successful surgical ablation, the mean cost of definitive therapy in the catheter ablation group (+24,382 +/- 4,741) is still significantly lower than the cost in the surgical group (+34,175; p less than 0.001). An additional economic advantage of catheter ablation is that the mean time lost from work or school is 10 days compared to 60 days with surgical ablation.

Adolescent↗
PubMed1990

Effect of basic drive cycle length on the yield of ventricular tachycardia during programmed ventricular stimulation.

The yield of sustained, monomorphic ventricular tachycardia (VT) induced by programmed ventricular stimulation was compared, using basic drive trains of 400 ms, 600 ms and sinus rhythm, to identify the most efficient sequence of basic drive trains to use during programmed stimulation. Fifty-five patients with coronary artery disease and inducible sustained monomorphic VT not requiring countershock to terminate underwent 81 electrophysiology tests in which 1 to 3 extrastimuli were introduced during sinus rhythm and after basic drive trains of 600 and 400 ms. In 72 electrophysiology tests, sustained, monomorphic VT was induced at the right ventricular apex. The yield of VT using a drive cycle length of 400 ms was 63 of 72 (88%), compared to 46 of 72 (64%) when the drive cycle length was 600 ms, and 23 of 72 (32%) when the extrastimuli were introduced during sinus rhythm (p less than 0.001 for all pairwise comparisons). In 14 electrophysiology tests in which VT was not induced using a 400 ms basic drive cycle length at the apex, the yield of VT was higher using a 400 ms drive cycle length at a second right ventricular site (12 of 14) than with a 600 ms drive cycle length (3 of 12) or sinus rhythm (4 of 12) at the apex (p less than 0.05). The yield of sustained, monomorphic VT induced by 1 to 3 extrastimuli increases as the basic drive cycle length shortens. Whereas programmed stimulation is conventionally started during sinus rhythm or with a drive cycle length of 600 ms, the present results suggest that starting with a drive cycle length of 400 ms may be more efficient.

Cardiac Pacing, Artificial↗
PubMed1990

Magnitude and time course of beta-adrenergic antagonism during oral amiodarone therapy.

To examine the presence and time course of beta-adrenergic antagonism produced by amiodarone, the heart rate, QT interval and arrhythmia frequency in response to graded doses of isoproterenol were evaluated in eight patients treated with oral amiodarone for sustained ventricular tachycardia. Measurements were made before and every 2 days after beginning oral amiodarone therapy (600 mg twice daily). Isoproterenol was given in doses of 12.5, 25 and 50 ng/kg body weight per min. The mean heart rate at rest decreased from 73.1 +/- 17.8 beats/min on day 0 to 57.8 +/- 15.0 beats/min after 12 days of amiodarone therapy. A significant linear decline in heart rate at rest was observed until day 6 (p less than 0.05 for all comparisons). On all days isoproterenol produced a progressive increase in heart rate that reached 115.5 +/- 20.2 beats/min on day 0 and 94.2 +/- 18.5 beats/min on day 12. Amiodarone blunted the heart rate increase produced by isoproterenol on days 2 to 12 (p less than 0.05 versus day 0). This effect was present by day 2 and did not change significantly thereafter. The mean corrected QT (QTc) interval increased from 430 +/- 30 ms on day 0 to 449 +/- 63 ms on day 12. A significant linear increase in QTc interval was observed until day 6 (p less than 0.05 for all comparisons). There was no systematic effect of isoproterenol on the QTc interval. Five of eight patients had a significant number of isoproterenol-induced premature ventricular complexes. Ventricular ectopic activity in response to isoproterenol was abolished after 4 days of amiodarone therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

Effect of the intertrain pause on the ventricular effective refractory period measured by the extrastimulus technique.

This study determined the effect of the duration of the intertrain pause on the ventricular effective refractory period (VERP) measured by the extrastimulus technique using conventional eight-beat basic drive trains. In 50 subjects, the VERP was measured using a basic drive train cycle length of 500 msec, 2-msec steps in the extrastimulus coupling interval, and intertrain pauses of 0, 1, 4, 8, 20, 40, 60, or 180 seconds. The VERP increased significantly with each stepwise increment in the intertrain pause up to 20 seconds, then reached a plateau. The VERP measured with an intertrain pause of 20 seconds was a mean of 13 msec longer than when measured with a conventional 4-second pause. The results of this study demonstrate a direct relationship between the VERP and the duration of the pause separating the eight-beat basic drive trains used to measure the VERP. When the cycle length of the basic drive train is 500 msec, the VERP lengthens as the duration of the intertrain pause increases from 1 to 20 seconds, demonstrating that the basic drive trains exert a cumulative effect on the VERP when the intertrain pause is shorter than 20 seconds. A cumulative effect of the basic drive trains on the VERP is lost when the intertrain pause is 20 seconds or more.

Action Potentials↗
PubMed1990

The ventricular excitability-interval relationship in early diastole in humans: the influence of the electrode configuration during bipolar stimulation.

The purpose of this study was to determine the relationship between ventricular excitability and the extrastimulus (S2) coupling interval in early diastole in humans. The influence of the electrode configuration during bipolar stimulation was examined. Ventricular strength-interval curves were constructed using an eight beat drive train at a cycle length of 600 msec, 2-msec decrements in the S2 coupling interval, and 0.2-mA increments in the current intensity of S2 at each coupling interval. A transient dip in the excitation threshold was observed in early diastole during bipolar pacing when the distal electrode was the anode in six of 17 patients (35%). In contrast, this type of dip was not observed when the distal electrode was the cathode. The excitation threshold at the trough of the dip ranged from 1.0 to 2.2 mA. Unipolar strength-interval curves indicated that a dip occurred with anodal but not cathodal pacing. We postulated that the dip might interfere with the accurate determination of the ventricular effective refractory period by resulting in transient loss of ventricular capture during decremental scanning of diastole with S2. A gap in ventricular capture was produced in all six patients who demonstrated a dip in the bipolar strength-interval curve by selecting an S2 current intensity that fell within the dip. In conclusion, the bipolar strength-interval curve may display an early diastolic dip in the excitation threshold, depending on the electrode configuration.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed1990

The effect of rate on prolongation of ventricular refractoriness by quinidine in humans.

In this study, the rate dependent effect of quinidine on the ventricular effective refractory period (VERP) was evaluated in 30 patients undergoing electropharmacological testing with quinidine. The VERPs were measured in the baseline state and after at least 2 days of treatment with 1,458-2,044 mg/day of quinidine gluconate (mean plasma quinidine concentration 2.2 +/- 0.7 mcg/mL). In 20 patients, the VERP was measured using conventional basic drive trains of 8 beats and basic drive cycle lengths of 600, 500, 400, and 350 msec. In another 10 patients, the VERP was measured after 3 minutes of continuous ventricular pacing at cycle lengths of 600 and 400 msec, and compared to the VERPs measured at the same basic drive cycle lengths using basic drive train durations of 2 and 8 beats. In the baseline state and after treatment with quinidine, the VERP shortened progressively as the basic drive train cycle length decreased and as the drive train duration increased to 3 minutes (P less than 0.001). Quinidine consistently prolonged the VERP by 9%-11% (P less than 0.001), regardless of the basic drive train cycle length. Quinidine's effect was also not affected by the basic drive train duration. In conclusion, the effect of quinidine on VERP in humans is independent of the rate of the basic drive train, both when measured using conventional 8-beat basic drive trains and when a three minute drive train duration is used in order to attain the maximum effect of the basic drive train cycle length on the VERP.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗