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Biomedical subjects

W J Mandel

Publications and source records attributed to W J Mandel.

At least 37 records · Page 2Linked to original sources
PubMed1995

Cellular mechanisms of ventricular bipolar electrograms showing double and fractionated potentials.

OBJECTIVES: This study sought to determine the types of trans-membrane action potentials associated with bipolar electrograms that show double and fractionated potentials. BACKGROUND: The cellular correlates of ventricular bipolar electrograms showing double potentials and fractionated low amplitude potentials remain poorly defined. METHODS: A bipolar electrogram (1-cm interelectrode distance [6F, USCI]) and two transmembrane action potentials (within 1 mm of each pole) were recorded simultaneously in 12 isolated canine right ventricular endocardial preparations (2 x 1 cm, 2 mm thick). The long axis of the bipolar electrode was parallel to the long axis of the superficial endocardial fibers, and the recordings were made at 40 to 500 Hz. RESULTS: The following phenomena were associated with double potentials: 1) an increase in conduction time between the two poles of the bipole during a) the propagation of premature action potentials (7 of 12 tissues in 4 mmol/liter extracellular potassium ion concentration [K+]o); b) rapid pacing and premature stimuli (3 of 6 in 9 mmol/liter [K+]o); and c) the propagation of slow responses induced by barium chloride (4 mmol/liter). There was a positive correlation between conduction time (CT) and interspike interval (IPI) of the double potential (IPI [ms] = 0.5 x CT [ms] + 35) during early afterdepolarizations induced by barium chloride (4 mmol/liter) superfusion (three of six tissues). The following events were associated with fractionated electrograms: 1) propagation of induced graded responses (six tissues) in 4 mmol/liter [K+]o; 2) induced reentry at cycle lengths of 140 to 170 ms in 9 mmol/liter [K+]o (four of six tissues); and 3) asynchronous afterdepolarizations induced by 4 mmol/liter barium chloride (four of six tissues). CONCLUSIONS: Endocardial double potentials and fractionated electrograms seen on clinically used bipolar electrodes occur under conditions of slowed or discontinuous conduction and induced reentry and during asynchronous automatic firing initiated by afterdepolarizations. Caution must be exercised in interpreting such bipolar electrograms because more than one type of cellular action potential may cause these abnormal electrographic results.

Action Potentials↗
PubMed1994

Should every patient with atrial fibrillation have the rhythm converted to sinus rhythm?

Atrial fibrillation is the most common atrial tachyarrhythmia. Consideration for the potential conversion of atrial fibrillation and the subsequent maintenance of sinus rhythm may be related to underlying pathology. Typically, extra cardiac factors such as thyroid hyperactivity help to determine initial therapy. Intrinsic cardiac factors may also influence the clinician's decision regarding potential cardioversion and maintenance of sinus rhythm. Some acute events such as pericarditis and the effects of cardiac trauma may resolve and result in spontaneous restoration of sinus rhythm. Other cardiac events such as acute myocardial infarction with or without atrial ischemia, valvular disease, and others may result in the precipitation of atrial fibrillation. The major reasons to consider cardioversion, either medically or electrically, are ventricular rate control, hemodynamic improvement, sense of well being, and the avoidance of embolism. Certain clinical situations (e.g., Wolff-Parkinson-White syndrome) require urgent restoration of sinus rhythm in light of the potential for extremely rapid ventricular rates. It has been suggested that all antiarrhythmic drug administration should be initiated in the hospital setting, but the brief period of drug administration in an inpatient setting does not protect the patient from potential, late-onset proarrhythmic events. Both antiarrhythmic drug therapy and electric cardioversion are useful for restoration of sinus rhythm in both acute and chronic atrial fibrillation. The most important negative aspect of drug conversion of atrial fibrillation may be the potential development of a proarrhythmic drug effect. Although controversial, conversion (medical or electrical) is probably indicated in every patient with the first episode of persistent atrial fibrillation, even if the patient is asymptomatic.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1994

Transmyocardial impedance during single and multiple internal ventricular defibrillation shocks.

Little is known about the transmyocardial impedance during internal ventricular defibrillation. In a canine model, using high rate on-line digitization, random shock delivery, and titanium electrodes, we determined the relationship among voltage, current, and impedance, delivered energy, and defibrillation success within the individual and within successive defibrillation shocks. Impedance decreased with repeated defibrillation in 10 of 11 dogs. Impedance always increased during trapezoidal discharges, whereas voltage decreased. Impedance was lower with high energy-voltage shocks in all dogs. Visually, voltage and current waveform did not show a phase shift. There was no difference in the total energy delivered and the energy converted into heat by the resistive part of the impedance. With a formula valid only for resistive loads, the capacitance of the defibrillator was calculated to be within the measurement accuracy and tolerance of the factory-provided value of 132 microF. Polarization voltage was consistently observed. Thus the transmyocardial impedance during defibrillation is primarily resistive, nonlinear voltage dependent, and declines with successive shocks. Defibrillation success was not influenced by these phenomena.

Animals↗
PubMed1994

Upper limit of vulnerability reliably predicts the defibrillation threshold in humans.

BACKGROUND: The upper limit of vulnerability is the stimulus strength above which electrical stimulation cannot induce ventricular fibrillation even when the stimulus occurs during the vulnerable period of the cardiac cycle. The purpose of this study was to test the hypothesis that the upper limit of vulnerability can accurately predict the defibrillation threshold in patients undergoing implantable cardioverter-defibrillator (ICD) implantation using nonthoracotomy lead systems. METHODS AND RESULTS: We studied 77 patients at the time of ICD implantation. Multiple endocardial-endocardial and endocardial-subcutaneous shock pathways were used. Two different protocols were used to test the upper limit of vulnerability. In protocol 1 (n = 17), the upper limit of vulnerability was tested with two shocks on the peak or the up-slope of the T wave of paced rhythm. The shocks were given randomly either at the peak and 20 milliseconds before the peak of T wave (n = 7) or at 20 and 40 milliseconds before the peak of T wave (n = 10). In protocol 2 (n = 60), the upper limit of vulnerability was tested with three shocks delivered at 0, 20, and 40 milliseconds before the peak of the T wave. The weakest shock that failed to induce ventricular fibrillation by a 5-J step-down or step-up method was defined as the upper limit of vulnerability. The defibrillation threshold was also determined by a 5-J step-down or step-up method. In protocol 1, the upper limit of vulnerability (9 +/- 6 J) was significantly lower than the defibrillation threshold (13 +/- 7 J) with a correlation coefficient of .87 and P < .001. In protocol 2, the upper limit of vulnerability (13 +/- 6 J) was not significantly different from the defibrillation threshold (13 +/- 6 J) with a correlation coefficient of .85 and P < .001. In 45 of the 60 patients, the upper limit of vulnerability was < or = 15 J; all had a defibrillation threshold of < or = 20 J. In 51 of the 60 patients, the upper limit of vulnerability was within 5 J of the defibrillation threshold. The upper limit of vulnerability overestimated the defibrillation threshold by > 10 J in 8 patients and underestimated the defibrillation threshold by > 10 J in only 1 patient. The overestimation and underestimation occurred only in patients with the upper limit of vulnerability > 15 J. CONCLUSIONS: When tested with three shocks on and before the peak of the T wave, the upper limit of vulnerability accurately predicted the defibrillation threshold in patients undergoing ICD implantation using nonthoracotomy lead systems. This method required either one or no episodes of ventricular fibrillation in most patients.

Aged↗
PubMed1993

Action potential alternans and irregular dynamics in quinidine-intoxicated ventricular muscle cells. Implications for ventricular proarrhythmia.

BACKGROUND: Cardiac cells display rate-dependent beat-to-beat variations in action-potential duration (APD), action potential amplitude (APA), and excitability during periodic stimulation. We hypothesized that quinidine causes a marked increase in the variability of APD, APA, and excitability of ventricular cells isolated from quinidine-toxic, arrhythmic ventricles. METHODS AND RESULTS: Action potentials were recorded from right ventricular endocardial tissues (2 x 1 cm, < 2 mm thick) isolated from dogs in which ventricular tachycardia and ventricular fibrillation (VT/VF) were induced with intravenous quinidine (80-100 mg/kg) over a 5-hour period in vivo (n = 7). As the basic cycle length (BCL) of stimulation was progressively shortened, rate-dependent variations in APD and APA occurred. The initial dynamic change was alternans of APD and APA that could be either in or out of phase between two cells. The magnitude of alternans was a function of the BCL and the strength of the stimulation current. At critically short BCLs, irregular APD and APA behavior emerged in the quinidine-intoxicated cells. In control cells (n = 16) isolated from three nontreated dogs, APD and APA remained constant at all BCLs tested (2,000-300 msec). Quinidine increased the slope of the APD restitution curve compared with control. The observed quinidine APD restitution curve was fitted with a biexponential equation, and computer simulation using the fitted restitution curve reproduced the aperiodic APD seen in the quinidine toxic cells during periodic stimulation. Thus, the observed irregular APD behavior was predictable from the restitution curve. CONCLUSIONS: Quinidine toxicity increases the temporal and spatial variability of APD and APA in the ventricle that may promote the initiation of reentrant VT/VF in vivo. The slope of the APD restitution curve provides a method to quantitate inhomogeneities in repolarization time and could be a useful marker for proarrhythmia.

Action Potentials↗
PubMed1992

Selection of patients for programmed ventricular stimulation: a clinical decision-making model based on multivariate analysis of clinical variables.

OBJECTIVE: This study was conducted to assess the utility of clinical variables in predicting the inducibility of sustained ventricular arrhythmias in a heterogeneous group of patients undergoing programmed ventricular stimulation. METHODS: Variables were considered in a simulated chronologic order to determine the incremental information added by the signal-averaged electrocardiogram (ECG) and left ventricular ejection fraction. All patients undergoing baseline programmed ventricular stimulation for induction of ventricular tachyarrhythmia during a 30-month period were included in the study. Fourteen historical, ECG, signal-averaged ECG and left ventricular wall motion variables were evaluated for their ability in predicting inducibility of a sustained ventricular arrhythmia, a "positive" event, at programmed ventricular stimulation. RESULTS: On univariate analysis of the clinical variables, comparison between patients with positive or negative results showed significant differences in 10 of the 14 clinical variables: major cardiac diagnosis, history of ventricular tachycardia, myocardial infarction by history or ECG, all five signal-averaged ECG variables, left ventricular ejection fraction and presence of left ventricular aneurysm. On multivariate analysis, five independent variables were determined to be important: history of ventricular tachycardia, historical or ECG evidence of myocardial infarction, history of loss of consciousness, filtered QRS duration on the signal-averaged ECG and left ventricular ejection fraction. However, with sequential multivariate analysis, a model based only on historical and conventional ECG data was found to do as well as a model that included signal-averaged ECG and left ventricular ejection fraction data. CONCLUSIONS: Routinely available noninvasive historical, ECG, signal-averaged ECG and left ventricular wall motion variables can be used to accurately predict the outcome of programmed ventricular stimulation. The majority of the predictive power was obtained with the routine model, using only historical and ECG data. The signal-averaged ECG and left ventricular wall motion analysis added no significant incremental information.

Aged↗
PubMed1992

Phase plane plot of electrograms as a marker of ventricular electrical instability during acute ischemia: initial experimental results and potential clinical applications.

We used a phase plane plots method (a plot of voltage [V(t)] vs rate of change of voltage [dV/dt]) derived from nonlinear dynamics to transform a sinus rhythm strip into a geometric form. The geometric form thus obtained detects variations in the ECG over time and therefore may aid in identifying patterns of vulnerability to ventricular fibrillation (VF). The trajectories of consecutive ventricular depolarizations and repolarizations of sinus rhythm in dogs that evolve to VF showed characteristic differential band thickening (inhomogeneities) that were absent in the dogs that did not develop VF. This method of analysis can be a useful complementary tool to detect cardiac electrical instability, and with simple hardware, can easily be displayed in real time.

Animals↗
PubMed1992

Increased temporo-spatial dispersion of repolarization during double premature stimulation in the intact ventricle.

The degree of temporo-spatial variation of repolarization during single (S2) and double (S3) premature stimulation was evaluated in five closed-chest anesthetized dogs. Monophasic action potentials (MAP) were simultaneously recorded with contact electrode and MAP duration (MAPD) restitution curves constructed from right ventricular (RV) and left ventricular (LV) endocardial sites. At a given coupling interval, S3 was associated with significantly greater dispersion of MAPD then S2 (spatial dispersion, i.e., between RV and LV). Similarly, at a given diastolic interval, S3 at RV and LV sites, was associated with significantly greater dispersion of MAPD then S2 (temporal dispersion). It is concluded that S3 is associated with greater temporo-spatial dispersion of repolarization then S2.

Action Potentials↗
PubMed1992

Cellular mechanisms of differential action potential duration restitution in canine ventricular muscle cells during single versus double premature stimuli.

BACKGROUND: We tested the hypothesis that action potential duration (APD) restitution of normal ventricular muscle cells is different during double premature stimuli (S3) compared with a single premature stimulus (S2). We propose a possible ionic mechanism for such a difference. METHODS AND RESULTS: Action potentials and isometric tension were recorded simultaneously from isolated canine right ventricular trabeculae (2 x 2 x 10 mm) (n = 35). APD and tension restitution curves (APD) and peak tension versus diastolic interval [DI] of S2 and S3 were constructed by the extrastimulus method during pacing at 1,500 msec. The following results were obtained. 1) The APD restitution curve of S2 was different from that of S3. During the restitution of S2, an early biphasic upward hump was present at short DIs. In contrast, a smooth exponential rise was consistently seen during S3 restitution. 2) Peak tension remained significantly (p less than 0.001) lower during the restitution of S2 than during S3 restitution at all DIs tested. 3) The variation of APD during the initial 100 msec of DI was significantly longer during S3 than S2 (22 +/- 5 msec versus 41 +/- 5 msec, p less than 0.001). 4) Caffeine (2 mM, n = 5) and ryanodine (10 microM, n = 5) blocked cyclic variations of tension, presumably by blocking cyclic variations of intracellular calcium ion concentrations ([Ca2+]i), and eliminated the differences in APD restitution between S2 and S3. 5) Nisoldipine at high (5 microM) but not at lower (2 microM, n = 5) concentration eliminated the differences in restitution of both APD and tension between S2 and S3. 6) BAY K 8644 (100 nM, n = 5) had no effect on this difference. CONCLUSIONS: Greater variations of APD occur during the restitution of S3 than during S2 at short DIs. These differences appear to be caused by cyclic variations in tension and thus in [Ca2+]i. Calcium-sensitive outward currents could explain these differences in APD restitution.

Action Potentials↗
PubMed1991

The role of enhanced vagal activity on ischemic ventricular tachycardia: pharmacologic basis of inefficiency.

The effects of pharmacologic modulation of vagal activity on ischemic ventricular tachycardia were evaluated in 21 conscious dogs after permanent left anterior descending coronary artery (LAD) occlusion. Studies were done on spontaneous ventricular tachycardia (cycle length 383 +/- 100 msec, n = 21), 24 to 72 hours after LAD occlusion, and on inducible sustained monomorphic ventricular tachycardia (cycle length 251 +/- 30 msec, n = 6), 4 to 7 days after LAD occlusion. Edrophonium (1 mg/kg intravenously), a cholinesterase inhibitor, and methacholine (0.1 to 1 mg intravenously), a muscarinic agonist, had no significant effect on the rate or QRS morphology of either type of tachycardia, despite severe slowing of the sinoatrial rate. Similarly, atropine (up to 60 micrograms/kg intravenously) had no effect on the rate and QRS morphology of either type of tachycardia. In an attempt to enhance myocardial drug delivery to the ischemic and infarcted left ventricle, edrophonium (1 mg/kg) and methacholine (0.1 to 0.2 mg) were injected retrogradely through the great cardiac vein. This did not impart any significant therapeutic advantage over the systemic intravenous route. Sympathetic beta blockade did not affect the therapeutic outcome (n = 5) with either edrophonium or methacholine. It is concluded that direct or indirect enhancement of cardiac vagal activity has no effect on ischemic ventricular tachycardia in this model of subacute myocardial infarction. The lack of efficacy appears to be independent of myocardial drug delivery to ischemic ventricular site(s) and background sympathetic activity. Such a lack of efficacy may be caused by ischemia-mediated degeneration of vagal nerve terminals, by altered responsiveness of muscarinic receptors at infarcted arrhythmogenic myocardial sites, or both.

Adrenergic beta-Antagonists↗
PubMed1991

Acute effects of intravenous propafenone on the internal ventricular defibrillation threshold in the anesthetized dog.

In 10 treated and 2 control dogs, the short-term effects of intravenous propafenone (2 mg/kg/10 minutes, followed by 1 mg/min [n = 2] or 25 micrograms/kg/min [n = 8]) on the internal ventricular defibrillation energy requirements (DER) were investigated. Multiple stored energy levels were randomly tested and the percent successful defibrillation was plotted against the stored energy, and the raw data were fit by logistic regression. The energy at 50% (E50) and 80% (E80) defibrillation success increased after propafenone by a mean of 75% (8.4 +/- 2.4 to 14.7 +/- 5.9 joules, p less than or equal to 0.05) and 59% (11.1 +/- 3.5 to 17.6 +/- 6.7 joules, p less than or equal to 0.05), respectively. Plasma propafenone levels ranged from 778 to 2554 ng/ml (1495 +/- 592 ng/ml) at the beginning to 833 to 2193 ng/ml (1297 +/- 389 ng/ml) at the end of the defibrillation trials. Two dogs served as controls and received Ringer's solution instead of propafenone and showed the temporal stability of the preparation. In conclusion, intravenous propafenone increases the internal ventricular DER in this canine model. This may have important clinical implications in patients with automatic implantable cardioverter-defibrillators (AICDs) receiving concomitant antiarrhythmic drug therapy and in patients undergoing therapy with intravenous propafenone.

Animals↗
PubMed1991

Syncope of unknown origin: clinical, noninvasive, and electrophysiologic determinants of arrhythmia induction and symptom recurrence during long-term follow-up.

Ninety-one consecutive patients with syncope of unknown origin underwent electrophysiologic studies (EPS). Univariate analysis identified the following variables: age, + signal-averaged ECG (SAECG), left ventricular ejection fraction (LVEF), history of myocardial infarction, coronary artery disease, left ventricular aneurysm, and history of sustained monomorphic ventricular tachycardia (SMVT) on Holter; multivariate analysis identified +SAECG, LVEF, and history of SMVT as risk factors for induction of SMVT at EPS. All patients were followed up for 19.0 +/- 8.3 months and 17 had recurrence of syncope. Patients were divided into empiric, EP-guided, and no therapy groups. The EP-guided therapy group included all patients with SMVT at EPS. Recurrence rates among all three groups were similar. We conclude that: (1) Patients who have inducible SMVT at EPS can be identified using certain clinical and noninvasive variables. When these patients undergo EP-guided therapy, their rate of recurrence of syncope becomes compatible with that of patients who had no arrhythmia induced at EPS. (2) Empiric therapy does not offer any benefit over no therapy in reducing the rate of recurrent of scope.

Aged↗
PubMed1991

The role of diastolic outward current deactivation kinetics on the induction of spiral waves.

The mechanism of induced reentry in an initially homogeneous repolarization matrix still remains undefined. In the present study we hypothesized that the slow deactivation rate of the delayed outward current (dIo/dt), which occurs during diastole after complete repolarization, can cause activation failure and facilitate reentry. We modeled the excitation-recovery process using the modified FitzHugh-Nagumo equations in a two-dimensional medium of 128 by 128 cells using the Connection Machine (CM-2), a massively parallel computer that is highly suitable for this class of problem. The model was one cell thick, uniformly excitable, and isotropic. When the rate of Io deactivation was slowed to yield action potential duration (APD) restitution curves similar to experimentally observed arrhythmic ventricular muscle cells ADP restitution curves, premature stimulation (S2) induced nonstationary double spiral waves (Figure 8 reentry). A decrease in dIo/dt increased the radius of the circle around which the tip of the spiral waves rotates and decreased its angular velocity. Wave fronts propagated through areas where the residual diastolic Io was fully inactivated and blocked in areas where its amplitude was high. No such dynamics of wave front propagation could be induced when S2 was applied after the completion of Io deactivation. We conclude that the kinetics of deactivation of the Io during diastole has a profound influence on the dynamics of two-dimensional wave front propagation. The similarities of the APD restitution curve implemented in the computer model with slow deactivation of Io and that observed in our canine model of quinidine induced ventricular tachyarrhythmias suggest that Io deactivation kinetics may play an important role in arrhythmogenesis in the intact ventricle.

Action Potentials↗
PubMed1990

Benefit and risks of long-term amiodarone therapy for sustained ventricular tachycardia/fibrillation: minimum of three-year follow-up in 145 patients.

Our experience with amiodarone therapy in 145 consecutively referred patients with medically refractory sustained ventricular tachycardia and/or fibrillation treated for at least 3 years was reviewed. Ninety-seven had sustained ventricular tachycardia; the remaining 48 patients were survivors of sudden cardiac death. The patients had a mean of 3.7 +/- 1.4 unsuccessful anti-arrhythmic drug trials before initiation of amiodarone. The initial doses of amiodarone averaged 845 +/- 258 mg for the first 2 weeks and 56% of all patients received a type I antiarrhythmic drug in addition to amiodarone during the initial phase of therapy. The average maintenance dose of amiodarone was 410 +/- 187 mg per day. All patients were followed for a minimum of 3 years or until death or withdrawal from therapy. The maximum follow-up was a period of 8 years. Thus, the average duration of amiodarone therapy was 39 +/- 26 months, representing 472 patient years of therapeutic time on amiodarone. The incidence of deaths either caused by a documented ventricular tachyarrhythmia or presumed to result from an arrhythmic cause was 5.5% in the first year and 3.4% in each of the second and third years of follow-up. During the entire period of follow-up, 56 patients died of all causes (38.6% of the study population). Survival over the follow-up period was influenced significantly by left ventricular function, as judged by either New York Heart Association Functional Class or objective assessment of left ventricular ejection fraction, which was available in 102 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Nonhomogeneous local atrial activity during acute atrial fibrillation: spectral and dynamic analysis.

Atrial fibrillation (A Fib) has been categorized into four different types (I-IV) based on the morphology of the epicardial bipolar electrogram. In the present study, we hypothesized that these same types of A Fib also exist at endocardial sites. Simultaneous high, mid, and low right atrial endocardial bipolar electrograms were analyzed during acute A Fib induced by a rapid train of stimuli (20-40 Hz) for 1-3 seconds in anesthetized closed-chest dogs (N = 7, total of 72 episodes). A Fib lasted between 3 seconds and a few minutes (22.3 +/- 22.8 sec). During A Fib, bipolar electrograms (0.5-500 Hz) were both discrete (types I and II) on electrograms recorded at one site and at the same time irregular (type III) on electrograms recorded at another site. The three simultaneously recorded electrograms encompassed all combinations of the four types of A Fib. When A Fib had a discrete electrogram morphology (types I and/or II), the mean rate of the A Fib was 494 +/- 93 beats/min. At a given site, electrogram morphology also changed type over time. Fast Fourier transform (FFT) of the digitized electrograms (8-10 sec, 800 Hz digitization) showed peaks mostly below 15 Hz (range 0-30 Hz), that were either discrete (narrow band) with clear harmonic components, or had continuous (broad band) spectra, that changed in a time and site dependent manner. Phase plane plots (PPP), a plot of voltage versus rate of change of voltage, varied with respect to time and location. However, the morphology of these PPP often inscribed well defined structure suggesting dynamics compatible with deterministic chaos, rather than random dynamics.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1990

Nonlinear dynamic analysis of temporally heterogeneous action potential characteristics.

Rate-dependent bifurcations and aperiodic changes in action potential duration and amplitude were observed in periodically stimulated cardiac Purkinje and ventricular muscle cells isolated from dogs with quinidine-induced ventricular fibrillation and ventricular tachycardia. The slope of the action potential duration restitution curve was higher in the quinidine intoxicated fibers than in normal untreated fibers. Aperiodicity and bifurcations in action potential duration (APD) could not be observed in normal untreated cardiac fibers. The data suggest that induction of reentrant ventricular fibrillation and ventricular tachycardia could be brought about not by fixed but rather by changing alterations in cellular electrical activity. Theory based on nonlinear dynamics seems to provide a quantitative basis for such an analysis. This could have important implications in the issue of sudden cardiac death, a major problem in cardiology.

Action Potentials↗
PubMed1988

Utility of the signal-averaged electrocardiogram in patients presenting with sustained ventricular tachycardia or fibrillation while on an antiarrhythmic drug.

The utility of the signal-averaged electrocardiogram (SAECG) for predicting ventricular tachycardia (VT) induction in patients presenting with sustained VT or ventricular fibrillation (VF) while on an empirically chosen antiarrhythmic agent was assessed in 17 patients. At the time of presentation with a malignant arrhythmia, 12 patients were taking quinidine, three patients were taking procainamide, and two patients were taking flecainide. All patients underwent programmed ventricular stimulation when not taking antiarrhythmic drugs; 12 patients had no inducible sustained VT and five patients had inducible sustained monomorphic VT. The SAECG done in the control state without antiarrhythmic agents was negative for late potentials in 11 of 12 patients in the noninducible group and positive for late potentials in four of five patients in the inducible group (sensitivity = 80% and specificity = 92%). We conclude that in patients presenting with life-threatening ventricular arrhythmias while taking an antiarrhythmic drug, the SAECG distinguishes patients with possible proarrhythmic events from those who have the substrate for inducible sustained VT.

Adult↗