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Biomedical subjects

A H Kadish

Publications and source records attributed to A H Kadish.

At least 55 records · Page 3Linked to original sources
PubMed1996

Local electrogram changes in response to a high-voltage intracardiac shock in humans.

INTRODUCTION: Transvenous defibrillators may have difficulty sensing ventricular fibrillation following an unsuccessful shock. This study was undertaken to characterize the changes that occur in intracardiac electrograms following a defibrillator shock that may contribute to the failure to redetect arrhythmias. METHODS AND RESULTS: Unipolar and bipolar electrogram recordings were made during sinus rhythm before and following monophasic and biphasic test shocks delivered in random order through a single lead defibrillator system in 15 patients. An additional 14 patients received only a biphasic shock. Electrogram amplitude, dV/dt, and activation recovery time were determined. Following biphasic shocks, unipolar electrogram amplitude decreased by a mean of 19.6% and the bipolar amplitude by a mean of 20.8% (P = NS). The mean dV/dt in the unipolar recordings decreased by 30.7% and in the bipolar recordings decreased by 33.0% (P = NS). Time constants for recovery were approximately 60 seconds. Reduction in dV/dt was greater when the shocking coil was closer to the distal sensing electrode. There was no significant influence of shock waveform (monophasic vs biphasic), recording type (unipolar vs bipolar), or clinical variables on the change in electrogram characteristics. CONCLUSION: Changes in intracardiac electrograms following defibrillator shocks through transvenous leads are seen with shocks delivered in sinus rhythm and may be related to the proximity of the shocking coil to the distal sensing electrode.

Aged↗
PubMed1996

Effect of graded increases in parasympathetic tone on heart rate variability.

INTRODUCTION: Time-and frequency-domain measurements of heart rate variability have been used as indices of parasympathetic tone. However, studies of the effect of parasympathetic stimulation on these indices in humans have yielded conflicting results. METHODS AND RESULTS: This study evaluated the effects of parasympathetic stimulation on heart rate variability. Twelve normal subjects (7 males, 5 females; age 24.8 +/- 3.4 years) were evaluated in the Clinical Research Center. Five-minute ECG recordings were obtained at baseline and during graded phenylephrine infusions (0.3 and 0.6 micrograms/kg per min). Recordings were made during spontaneous respiration and when breathing was timed with a metronome at 15 cycles/min. Heart rate variability analysis was performed using standard time- and frequency-domain parameters. Graded phenylephrine infusion resulted in a progressive increase in blood pressure and RR interval but no consistent changes in heart rate variability for the group. The results during normal versus metronome breathing were similar. Stepwise linear regression analysis revealed that the phenylephrine-induced changes in heart rate variability were inversely correlated with the baseline heart rate variability and not related to the baseline RR interval or the phenylephrine-induced change in RR interval. CONCLUSION: These findings suggest that the respiratory variation in "parasympathetic effect" typically observed at the sinus node can be either increased or decreased by parasympathetic stimulation, depending on the initial level of parasympathetic tone and the intensity of stimulation. This resolves the previously conflicting data. Thus, evaluation of parasympathetic tone using heart rate variability techniques should be cautiously undertaken.

Adrenergic alpha-Agonists↗
PubMed1995

Circadian variation in human ventricular refractoriness.

BACKGROUND: The incidence of sudden cardiac death is highest in the morning hours. Although a circadian variation in myocardial ischemia may be responsible in part for this observation, other factors also may be contributory. It is not known whether a circadian variation in ventricular refractoriness exists that may be related to the increased morning incidence of sudden cardiac death. METHODS AND RESULTS: Nine subjects with primary conduction system disease, no evidence of structural heart disease, and permanent pacemakers were studied. Autonomic nervous system function as assessed by tilt table and baroreflex sensitivity testing was normal in all subjects. Using noninvasive programmed stimulation, ventricular effective refractory periods were measured hourly for 24 hours. Potassium, epinephrine, and norepinephrine levels also were measured hourly. In a subset of five subjects, ventricular refractory periods were again measured hourly over 24 hours during beta-blockade. A significant circadian variation in ventricular refractoriness was noted, with a mean difference between the shortest and longest refractory periods in individual subjects of 23 ms and 21 ms at drive cycle lengths of 600 ms and 400 ms, respectively. In eight subjects, the shortest refractory periods observed over 24 hours occurred within 2 hours of waking (random probability < 10(-8)). Adjustment of refractory period data according to the hour of waking resulted in a better correlation between ventricular refractory periods and time. Although a significant circadian variation was observed in potassium and catecholamine levels, neither was an independent predictor of refractory periods after adjustment for the hour of waking. The adjusted time of day was the only significant (P < .0001) independent predictor of refractory periods. beta-Blockade abolished the circadian variation in ventricular refractory periods. CONCLUSIONS: A significant circadian variation in ventricular refractory periods exists. Maximal shortening between hourly refractory periods as well as the shortest refractory periods occur in the early morning hours when the incidence of sudden cardiac death is greatest. Fluctuations in beta-adrenergic tone appear to be largely responsible for this phenomenon.

Adult↗
PubMed1995

Effect of increased drive-train stimulus intensity on dispersion of ventricular refractoriness.

BACKGROUND: Most studies evaluating the effects of high-intensity drive-train (S1) stimulation on the measurement of the ventricular effective refractory period (VERP) demonstrated a shortening of the VERP. Because this effect may be due to the local release of catecholamines, VERP shortening would be expected to occur only near the site of stimulation. Local shortening in the VERP should then result in an increased dispersion of refractoriness during high-intensity drive-train stimulation. Thus, this study evaluated the spatial distribution of the VERP shortening resulting from high-intensity S1 stimulation and its effect on dispersion of refractoriness. METHODS AND RESULTS: Three groups of patients were studied. In group 1, 10 subjects without structural heart disease had VERP determinations performed at the right ventricular apex (RVA) and outflow tract (RVOT) while the S1 site was changed to evaluate the effects of low-intensity S1 stimulation on the measured VERP. In group 2, the effect of high-intensity S1 stimulation on the VERP was studied 0, 7, 14, and 21 mm away from the S1 site to measure the spatial distribution of VERP shortening and the effect on dispersion of refractoriness; 10 additional subjects without structural heart disease made up group 2. Because increased dispersion of refractoriness may be deleterious in certain clinical situations, the effect of high-intensity S1 stimulation was studied in group 3, which comprised 10 subjects with chronically implanted transvenous defibrillators; noninvasive measurements of the VERP through the chronic lead were made while the S1 stimulus intensity was varied from low to high intensity. All VERP determinations were performed during continuous pacing by use of an incremental method and a low stimulus intensity for the extrastimulus. In group 1, the RVA VERPs were 218 +/- 9 and 214 +/- 10 ms when the S1 site was the RVA and RVOT, respectively (P = NS). The RVOT VERPs were also unchanged when the S1 site was changed from the RVOT to the RVA. In group 2, high-intensity S1 changed the VERP from 224 +/- 8 (at twice the threshold) to 203 +/- 10 ms (P < .01), 220 +/- 11 to 209 +/- 12 ms (P < .01), 222 +/- 12 to 221 +/- 12 ms, and 220 +/- 11 to 221 +/- 11 ms at 0, 7, 14, and 21 mm away from the S1 site, respectively. High-intensity S1 stimulation led to an increase in the dispersion of refractoriness from 13 +/- 4 to 22 +/- 9 ms (P = .006). In group 3, high-intensity S1 stimulation shortened the VERP from 309 +/- 23 to 285 +/- 30 ms (P = .0003). CONCLUSIONS: Low-intensity S1 stimulation has no significant effect on the VERP. High-intensity S1 stimulation shortens the refractory period maximally at the site of stimulation; the VERP shortening dissipates between 7 and 14 mm away from the site of S1 stimulation, resulting in an increased dispersion of refractoriness. The local VERP shortening with high-intensity stimulation is noted in patients with chronically implanted defibrillator leads, which may have implications for the mechanism of proarrhythmia during high-intensity stimulation.

Adult↗
PubMed1995

Electrical activation during ventricular fibrillation in the subacute and chronic phases of healing canine myocardial infarction.

BACKGROUND: Little information is available regarding the effects of myocardial infarction on the characteristics of ventricular fibrillation (VF). Epicardial activation during VF can be characterized by the cycle length and by the characteristics of activation wave fronts. METHODS AND RESULTS: VF was induced by programmed stimulation in 6 dogs with subacute healing (1 week) myocardial infarction (MI), 5 dogs with chronic (8 week) healing MI, and 6 dogs without MI. Using a plaque electrode array with a 2.5-mm interelectrode distance, 112 electrograms were recorded and 91 vector loops were created for each cycle of VF from either the anterior (infarcted) or lateral (noninfarcted) wall. Direction of maximum epicardial activation was determined at each site for the first 10 cycles of VF (early) and for 10 cycles after 5 seconds of VF (late). Wave front size was determined based on a similarity in epicardial activation directions within a given area and by a statistical analysis that determined the degree of spatial linking at varying distances over the recording plaque. VF cycle length was defined as the mean interval of 10 consecutive local activation times. Differences among groups and differences between the anterior and posterolateral walls were determined by ANOVA. The mean wave front area was significantly larger in the presence of subacute MI (97 +/- 4 mm2, early; 78 +/- 3 mm2, late) or chronic MI (94 +/- 5 mm2, early; 78 +/- 5 mm2, late) than in noninfarcted animals (73 +/- 5 mm2, early; 61 +/- 3 mm2, late). The degree of linking of epicardial activation directions was similar in the three groups at distances of 2.5 and 5.0 mm but was lower at a distance of 7.5 mm among animals without infarction, confirming a smaller wave front size and suggesting less organization of activation. VF cycle length was significantly longer in the presence of infarction (98 +/- 5 ms, normal control animals; 121 +/- 13 ms, subacute MI; 127 +/- 13 ms, chronic MI). VF cycle length was significantly longer over the anterior than the lateral wall in the presence of subacute MI (131 +/- 8 ms, anterior; 109 +/- 5 ms, lateral) or chronic MI (136 +/- 9 ms, anterior; 119 +/- 6 ms, lateral) but not in noninfarcted animals (99 +/- ms, anterior; 97 +/- 5 ms, lateral). The prolongation of VF cycle length among animals with infarction was associated with slower estimated conduction velocities during VF. CONCLUSIONS: During VF, in animals with subacute or chronic healing MI, (1) the size of activation wave fronts is larger, (2) the cycle length of VF is longer, (3) the conduction velocities are slower, and (4) the degree of organization is greater than in control animals. Thus, the characteristics of VF throughout the heart are altered by the presence of regional myocardial infarction. The implications of these findings for the initiation and maintenance of VF in the presence of different underlying myocardial substrates require further study.

Animals↗
PubMed1995

Sudden cardiac death and polymorphous ventricular tachycardia in patients with normal QT intervals and normal systolic cardiac function.

This study delineates the clinical spectrum of 15 patients with polymorphic ventricular tachycardia and normal QT intervals in the absence of apparent structural heart disease, adverse drug effects, or electrolyte disturbances. Patients presented with either palpitations (n = 2), presyncope (n = 5), syncope (n = 4), no symptoms (n = 1), or aborted sudden death (n = 3). Mean age was 41 years (range 20 to 64), and mean follow-up 38 months (range 4 to 109). Left ventricular function was normal as determined by either echocardiogram (n = 9) or left ventriculography (n = 9). Episodes of polymorphic ventricular tachycardia (VT) were analyzed in terms of the preceding interval, and the relation of the initiating coupling interval to the QT interval (coupling interval/QT interval = polymorphic VT index). The mean QT for the group as a whole was 0.41 +/- 0.02 second. Patients could be separated into 3 distinct groups. Four patients had polymorphic VT reproducibly induced by exercise and initiated by late-coupled beats (mean polymorphic VT index 1.27 +/- 0.21). Isoproterenol induced polymorphic VT in 3 of 4 patients, and all 4 responded to chronic beta blockade. Two patients had polymorphic VT during episodes of coronary artery spasm, and both responded to calcium channel blockade. Polymorphic VT unrelated to exertion or coronary vasospasm occurred in 9 patients. Tachycardia onset was initiated by closely coupled beats (mean polymorphic VT index 0.95 +/- 0.16), and was preceded by a pause in 4 patients, and no pause in 5 patients. Sudden death occurred in 5 of 9 patients with the shortest polymorphic VT indexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effects of autonomic stimulation and blockade on signal-averaged P wave duration.

OBJECTIVES: This study sought to evaluate the effects of autonomic stimulation and blockade on the signal-averaged P wave duration. BACKGROUND: Signal-averaged P wave duration has been shown to have prognostic implications for patients prone to develop atrial fibrillation, but autonomic influences on the signal-averaged P wave duration have not been studied. METHODS: In 14 healthy volunteers (8 men, 6 women; mean [ +/- SD] age 28.5 +/- 4.8 years, range 22 to 38), signal-averaged P wave duration was measured on day 1 at baseline, during sympathetic stimulation with infusions of epinephrine (50 ng/kg body weight per min) and isoproterenol (50 ng/kg per min), beta-blockade with propranolol (0.2 mg/kg) and autonomic blockade with propranolol followed by atropine (0.04 mg/kg). On a second day, 10 of the 14 subjects returned for repeat baseline recordings and recordings during parasympathetic blockade with atropine (0.04 mg/kg). Signal averaging was performed using a P wave template. Both unfiltered and filtered (least-squares fit filter with 100-ms window) P wave durations were measured. Day to day and interobserver variability were assessed by calculation of intraclass correlation coefficients. RESULTS: The mean ( +/- SD) baseline filtered P wave duration on day 1 was 141 +/- 10 ms. Isoproterenol infusion significantly shortened the P wave duration to 110 +/- 16 ms (p < 0.001), and epinephrine resulted in significant prolongation to 150 +/- 10 ms (p < 0.05). Beta-adrenergic blockade increased the P wave duration to 153 +/- 10 ms (p < 0.005). Autonomic blockade shortened the P wave duration to 143 +/- 16 ms (p < 0.05 vs. beta-blockade). On the second day, the mean baseline P wave duration was slightly longer (144 +/- 10 ms, p < 0.02). Parasympathetic blockade with atropine resulted in mild shortening of the P wave duration to 136 +/- 15 ms (p < 0.1). Interobserver reproducibility was excellent (intraclass correlation coefficient 0.99). Day to day reproducibility was good (intraclass correlation coefficient 0.56). CONCLUSIONS: The signal-averaged P wave duration is not a fixed variable because it may change significantly under different autonomic conditions. This has important implications for the application of this test to the heterogeneous population susceptible to atrial fibrillation.

Adult↗
PubMed1994

Atrial and accessory pathway activation direction in patients with orthodromic supraventricular tachycardia: insights from vector mapping.

OBJECTIVES: The purpose of this study was to utilize vector mapping to investigate atrial and accessory pathway activation direction during orthodromic supraventricular tachycardia. BACKGROUND: Although advances have been made in the electrophysiologic evaluation and management of accessory pathways, our understanding of accessory pathway anatomy and physiology remains incomplete. Vector mapping has been validated as a method of studying local myocardial activation. METHODS: In 28 patients with a left-sided or posteroseptal accessory atrioventricular (AV) pathway referred for ablation, atrial and accessory AV pathway activation direction was determined during ventricular pacing or orthodromic supraventricular tachycardia, or both, by summing three orthogonally oriented bipolar electrograms recorded from the coronary sinus to create three-dimensional vector loops. Atrial and accessory AV pathway activation direction was determined in all patients from the maximal amplitude vectors of the vector loops. Because of beat to beat variability in the directions of the vector loops, data from 8 of 28 patients could not be analyzed. RESULTS: At 81 of 83 sites, atrial activation direction along the long axis of the coronary sinus corresponded with the direction suggested by activation time mapping. Activation direction along the anteroposterior and inferosuperior axes was variable, potentially due to variations in the level of the atrial insertion of the accessory AV pathway and in the depth or angling of pathway fibers in the AV fat pad. In eight patients, at least one recording was obtained at the site of an accessory AV pathway potential. Accessory AV pathway activation proceeded superiorly and to the right in seven of eight patients; in one patient with a posteroseptal pathway, accessory AV pathway activation proceeded superiorly and to the left. CONCLUSIONS: 1) Vector mapping is a useful technique for localizing accessory AV pathways; 2) left-sided accessory AV pathways angle from left to right as they traverse the AV groove; and 3) variable activation directions of the atrial myocardium adjacent to the coronary sinus suggest that accessory AV pathway insertion into the atrium differs from patient to patient.

Adult↗
PubMed1994

Antidromic tachycardia utilizing decremental, latent accessory atrioventricular fibers: differentiation from adenosine-sensitive ventricular tachycardia.

OBJECTIVES: We studied two patients with latent, decremental atrioventricular (AV) fibers in whom pre-excitation could be demonstrated only during wide complex tachycardia. BACKGROUND: The presence of decremental AV fibers participating in antidromic AV reentrant tachycardia is usually suspected by the presence of pre-excitation either in sinus rhythm or during atrial pacing. METHODS: Two patients were referred for evaluation and treatment of wide complex tachycardia whose configuration suggested ventricular tachycardia that could be terminated with adenosine infusion. They underwent standard electrophysiologic studies. RESULTS: Baseline AH and HV intervals were normal. No pre-excitation was noted with atrial overdrive at multiple sites or during atrial extrastimulation. Retrograde conduction was present with a sequence compatible with AV node conduction. Sustained wide complex tachycardia was induced with ventricular overdrive pacing. Late atrial premature depolarizations during tachycardia pre-excited the subsequent ventricular activation. Earlier atrial premature depolarizations delayed the subsequent ventricular activation. In one patient, early atrial premature depolarizations terminated the tachycardia without activating the ventricle. In the other patient, spontaneous tachycardia termination was accompanied by ventriculoatrial block. The earliest ventricular activation was at the annulus in the posteroseptal region in one patient and at the left posterior region in the other. Atrioventricular node reentry and atrial tachycardia with bystander AV fibers were also excluded. These findings establish the diagnosis of antidromic AV reentrant tachycardia utilizing a slow, decrementally conducting AV pathway. CONCLUSIONS: This is the first report describing the presence of latent, decremental accessory AV pathways in which conduction was manifest only during antidromic AV reentrant tachycardia. To differentiate these wide complex tachycardias from adenosine-sensitive ventricular tachycardia, we recommend that atrial premature depolarizations be applied during tachycardia to rule out the presence of a latent, decremental AV fiber even in patients who do not otherwise have pre-excitation with atrial pacing techniques.

Adenosine↗
PubMed1994

Effect of physiologic and pharmacologic adrenergic stimulation on heart rate variability.

OBJECTIVES: The aim of this study was to evaluate and compare the effects of physiologic and pharmacologic sympathetic stimulation on time and frequency domain indexes of heart rate variability. BACKGROUND: Measurements of heart rate variability have been used as indexes of sympathetic tone. To date, the effects of circulating catecholamines on heart rate variability have not been evaluated. METHODS: Fourteen normal subjects (eight men, six women, mean [+/- SD] age 28.5 +/- 4.8 years) were evaluated. Five-minute electrocardiographic recordings were obtained in triplicate after physiologic and pharmacologic sympathetic stimulation: during upright tilt, after maximal exercise, during epinephrine and isoproterenol infusions at 50 ng/kg body weight per min, during beta-adrenergic blockade and during combined beta-adrenergic and parasympathetic blockade. RESULTS: Beta-adrenergic stimulation resulted in a significant decrease in time domain measures of heart rate variability. The frequency domain indexes showed variable responses, depending on the individual stimulus. Tilt caused an increase in low frequency power and in the ratio of low to high frequency power. These changes were not necessarily observed with other conditions of beta-adrenergic stimulation. Double blockade suppressed baseline heart rate variability, but beta-adrenergic blockade had no significant effect. Time domain measures of heart rate variability demonstrated excellent reproducibility over the three recordings, but the frequency domain variables demonstrated fair to excellent reproducibility. CONCLUSIONS: These findings suggest that different modes of beta-adrenergic stimulation may result in divergent heart rate variability responses. Thus, current heart rate variability techniques cannot be used as general indexes of "sympathetic" tone. Studies utilizing heart rate variability to quantify sympathetic tone need to consider this.

Adrenergic Agents↗
PubMed1994

Effect of stimulus intensity on atrial refractoriness and sinus node recovery.

INTRODUCTION: Prior studies of sinus node function in man stated that the stimulus intensity of overdrive pacing has no effect on the response of the sinus node to overdrive suppression; however, data documenting these statements were lacking. Previous studies have also suggested that drive train stimulus intensity can alter ventricular refractoriness, but similar studies have not been performed on the human atrium. The purpose of this study was to evaluate the effects of drive train stimulus intensity on atrial effective refractory period and sinus node recovery time. METHODS AND RESULTS: The effect of drive train stimulus intensity on atrial effective refractory period and sinus node recovery time was studied in 42 patients undergoing clinical electrophysiologic tests. The atrial effective refractory period was shorter at 10 mA (221 +/- 20 msec) and 5 mA (232 +/- 25 msec) than at a drive train stimulus intensity of 1.5 times late diastolic threshold (248 +/- 24 msec, P < 0.05 for pairwise comparison). The sinus node recovery time did not demonstrate a similar effect in the baseline state, following beta-adrenergic blockade, or following combined parasympathetic and beta-adrenergic blockade. However, following isolated parasympathetic blockade with atropine, the corrected sinus node recovery time shortened from 88 +/- 51 msec at 1.5 times late diastolic threshold to 48 +/- 55 msec at 10 mA (P < 0.05). Significant variability was present in sinus node recovery time measurements at baseline and following beta blockade; this variability decreased following parasympathetic blockade. CONCLUSION: These data suggest that drive train stimulus intensity can affect the electrophysiologic properties of sinus node and atrial tissue. This effect appears to be mediated by local catecholamine and acetylcholine release and provides further evidence that the interaction between pacing stimuli and the cardiac autonomic system may need to be considered in evaluating electrophysiologic effects.

Adolescent↗
PubMed1994

Dissociation of heart rate variability from parasympathetic tone.

Time and frequency domain measurements of heart rate variability have been used as indexes of parasympathetic tone. This study evaluates the effects of parasympathetic stimulation on these indexes. Ten normal subjects (5 females, 5 males; age 27.4 +/- 5.1 yr) were evaluated in the Clinical Research Center. Five-minute electrocardiographic recordings were obtained at baseline and during 1) combined alpha-adrenergic stimulation with baroreflex-increased cardiac parasympathetic activity produced by phenylephrine infusion; 2) parasympathetic blockade (atropine 0.04 mg/kg); and 3) isolated alpha-adrenergic stimulation produced by phenylephrine infusion after parasympathetic blockade. The infusion rate of phenylephrine was titrated to increase the systolic blood pressure by 20-30 mmHg. Heart rate variability analysis was performed using standard time and frequency domain parameters. Phenylephrine infusion resulted in a decrease in the time domain measures and in the high-frequency power. After parasympathetic blockade, alpha-adrenergic stimulation had no significant effect on the heart rate variability parameters. These findings suggest that the heart rate variability parameters traditionally associated with parasympathetic tone do not always reliably measure parasympathetic tone, since they decrease with baroreflex parasympathetic stimulation.

Adult↗
PubMed1994

Assessment of effects of autonomic stimulation and blockade on the signal-averaged electrocardiogram.

BACKGROUND: Signal-averaged ECG is a noninvasive test designed to detect "late potentials." The effects of alterations in autonomic tone on the signal-averaged ECG have not been evaluated systematically. METHODS AND RESULTS: The effects of autonomic stimulation and blockade on the signal-averaged ECG were evaluated in 14 healthy subjects (8 men and 6 women; age, 28.5 +/- 4.8 years) on 2 separate days. The signal-averaged ECG was recorded at baseline and after physiological and pharmacologic beta-adrenergic stimulation (tilt, exercise, and epinephrine and isoproterenol infusions), sequential and combined beta-adrenergic and parasympathetic blockade, and alpha-adrenergic stimulation before and after parasympathetic blockade. Analysis was performed with a bidirectional filter (40-Hz high-pass). Significant changes in the signal-averaged QRS duration from baseline (105.1 +/- 12.0 milliseconds) were noted with tilt (96.8 +/- 8.8 milliseconds), tilt after double blockade (97.5 +/- 9.0 milliseconds), epinephrine (110.5 +/- 11.8 milliseconds), and isoproterenol (99.6 +/- 12.6 milliseconds). Changes in the root-mean-square voltage of the terminal 40 milliseconds and the low-amplitude (< 40 microV) signal duration paralleled the changes in the QRS duration. CONCLUSIONS: The signal-averaged ECG does not measure only "fixed" parameters but rather is altered under a variety of physiological and pharmacologic conditions. Upright tilt leads to shortening of the QRS duration before and after autonomic blockade; thus, the decrease in QRS duration with tilt may be related to factors other than changes in autonomic tone. These findings have implications for interpretation of the results of signal-averaged ECG.

Adult↗
PubMed1993

Successful radiofrequency energy ablation of automatic junctional tachycardia preserving normal atrioventricular nodal conduction.

Automatic junctional tachycardia is frequently refractory to medical management and difficult to treat with nonpharmacological methods. A 12-year-old female with symptomatic, refractory automatic junctional tachycardia is reported. Earliest atrial activation during supraventricular tachycardia was in the posterior portion of the intraatrial septum. The patient underwent electrophysiological study and successful radiofrequency current ablation of the ectopic automatic focus within the atrioventricular junction. Normal atrioventricular junctional conduction was maintained, and at 7-month follow-up the patient has been free of tachycardia.

Atrioventricular Node↗
PubMed1993

The response of paroxysmal supraventricular tachycardia to overdrive atrial and ventricular pacing: can it help determine the tachycardia mechanism?

INTRODUCTION: Standard electrophysiologic techniques generally allow discrimination among mechanisms of paroxysmal supraventricular tachycardia. The purpose of this study was to determine whether the response of paroxysmal supraventricular tachycardia to atrial and ventricular overdrive pacing can help determine the tachycardia mechanism. METHODS AND RESULTS: Fifty-three patients with paroxysmal supraventricular tachycardia were studied. Twenty-two patients had the typical form of atrioventricular (AV) junctional (nodal) reentry, 18 patients had orthodromic AV reentrant tachycardia, 10 patients had atrial tachycardia, and 3 patients had the atypical form of AV nodal reentrant tachycardia. After paroxysmal supraventricular tachycardia was induced, 15-beat trains were introduced in the high right atrium and right ventricular apex sequentially with cycle lengths beginning 10 msec shorter than the spontaneous tachycardia cycle length. The pacing cycle length was shortened in successive trains until a cycle of 200 msec was reached or until tachycardia was terminated. Several responses of paroxysmal supraventricular tachycardia to overdrive pacing were useful in distinguishing atrial tachycardia from other mechanisms of paroxysmal supraventricular tachycardia. During decremental atrial overdrive pacing, the curve relating the pacing cycle length to the VA interval on the first beat following the cessation of atrial pacing was flat or upsloping in patients with AV junctional reentry or AV reentrant tachycardia, but variable in patients with atrial tachycardia. AV reentry and AV junctional reentry could always be terminated by overdrive ventricular pacing whereas atrial tachycardia was terminated in only one of ten patients (P < 0.001). The curve relating the ventricular pacing cycle length to the VA interval on the first postpacing beat was flat or upsloping in patients with AV junctional reentry and AV reentry, but variable in patients with atrial tachycardia. The typical form of AV junctional reentry could occasionally be distinguished from other forms of paroxysmal supraventricular tachycardia by the shortening of the AH interval following tachycardia termination during constant rate atrial pacing. CONCLUSIONS: Atrial and ventricular overdrive pacing can rapidly and reliably distinguish atrial tachycardia from other mechanisms of paroxysmal supraventricular tachycardia and occasionally assist in the diagnosis of other tachycardia mechanisms. In particular, the ability to exclude atrial tachycardia as a potential mechanism for paroxysmal supraventricular tachycardia has important implications for the use of catheter ablation techniques to cure paroxysmal supraventricular tachycardia.

Adult↗
PubMed1992

Relation between QT and RR intervals during exercise testing in atrial fibrillation.

The ability to predict the RR-QT relation over a range of heart rates was evaluated in 10 patients with atrial fibrillation (AF) and in 10 control subjects in sinus rhythm. The data from each subject were fitted by regression into 3 QT prediction formulas (the square root formula of Bazett, the cube root formula of Fridericia and the exponential formula of Sarma) applied in standard form and modified with a weighted average of the preceding 5 RR intervals. The goodness-of-fit of each formula was evaluated using mean square residual and Akaike information criterion. For AF, the mean square residuals did not differ among the 3 standard QT prediction formulas (Bazett 624 +/- 274, Fridericia 625 +/- 274 and Sarma 611 +/- 267) and among the 3 modified QT prediction formulas (Bazett 507 +/- 325, Fridericia 496 +/- 255 and Sarma 495 +/- 328). The weighted average modification produced a significant decrease in mean square residuals for all 3 equations (p less than 0.05) in all patients. These findings were confirmed by Akaike information criterion. Goodness-of-fit in sinus rhythm was similar to previously published reports, and significantly better than the fit for AF (p less than 0.0001). For 9 of the 10 patients with AF, sinus rhythm electrocardiograms were obtained and the above regression equations were used to predict QT intervals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Efficacy and risks of moricizine in inducible sustained ventricular tachycardia.

OBJECTIVE: To assess the efficacy and toxicity of moricizine in treating patients with serious ventricular arrhythmias and inducible sustained ventricular tachycardia. DESIGN: Uncontrolled clinical trial. SETTING: The intensive care and telemetry units of Northwestern Memorial Hospital, St. Francis Hospital and Medical Center, and Lenox Hill Hospital. PATIENTS: Twenty-six patients with sustained ventricular arrhythmias or hemodynamically significant nonsustained ventricular tachycardia, most of whom failed therapy with at least one class I antiarrhythmic agent. INTERVENTION: Patients were treated with moricizine, 400 to 1000 mg/d. MEASUREMENT: Efficacy was assessed by the results of programmed ventricular stimulation done during moricizine therapy. MAIN RESULTS: Seven of the 26 patients (27%) developed life-threatening ventricular proarrhythmia during moricizine loading. Three patients had incessant sustained ventricular tachycardia, two had incessant nonsustained ventricular tachycardia, one had new sustained ventricular tachycardia, and one had new cardiac arrest. One of these patients died of intractable ventricular fibrillation. No clinical or electrophysiologic variables clearly identified those at risk for proarrhythmia. Only 3 of 26 patients (12%) became noninducible on moricizine. CONCLUSION: Moricizine has a low rate of efficacy and carries a considerable risk for life-threatening proarrhythmia in patients with serious ventricular arrhythmias and inducible ventricular tachycardia who have failed therapy with other class I antiarrhythmic agents.

Adult↗