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Biomedical subjects

W J Mandel

Publications and source records attributed to W J Mandel.

At least 19 recordsLinked to original sources
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↗
PubMed1988

Subthreshold atrial pacing in patients with a left-sided accessory pathway: an effective new method for terminating reciprocating tachycardia.

This study investigated the possibility of terminating reciprocating atrioventricular (AV) tachycardia using subthreshold atrial pacing. Ten patients with a left-sided accessory pathway and sustained AV tachycardia underwent subthreshold atrial pacing from the coronary sinus site closest to insertion of the accessory pathway. In seven of these patients, the tachycardia could be reliably terminated with subthreshold atrial overdrive pacing. When pacing at a cycle length of 80 +/- 23% of the tachycardia cycle length, the minimal subthreshold current that was effective in tachycardia termination was 64 +/- 14% of threshold current and the maximal ineffective current was 49 +/- 17% of threshold (p less than 0.05). In all cases, the tachycardia was terminated by one or two instances of atrial capture that resulted in a premature atrial impulse (20 +/- 4% advancement of the atrial cycle) that blocked the AV node limb of the tachycardia. Anterograde conduction over the accessory pathway never occurred, either during the tachycardia or during subthreshold pacing after a return to normal sinus rhythm. No instances of atrial fibrillation were provoked by subthreshold pacing. Possible explanations for the intermittent atrial capture with critically placed subthreshold impulses include supernormal atrial conduction or summation of impulses at the atrial insertion site of the accessory pathway. It is concluded that subthreshold pacing is effective in selected patients with AV tachycardia due to an accessory pathway. Furthermore, because neither atrial fibrillation nor anterograde conduction over the accessory pathway is seen with subthreshold pacing, this modality may hold significant promise for permanent antitachycardia pacing in these patients.

Adult↗
PubMed1988

Relation of monophasic action potential recorded with contact electrode to underlying transmembrane action potential properties in isolated cardiac tissues: a systematic microelectrode validation study.

Monophasic action potentials, recorded with contact non-suction electrodes, have been used both clinically and experimentally. However, to date no systematic microelectrode validation studies have been done to underlying myocardial cell populations from different myocardial regions with different transmembrane potential profiles. In the present study transmembrane action potential properties, recorded with standard microelectrodes, were compared with monophasic action potentials recorded with contact electrodes in three different (endocardium, epicardium, and free running Purkinje fibre) isolated canine preparations during pacing and during spontaneous automatic activity. The mean transmembrane durations at 50% and 90% repolarisations (APD50 and APD90) of 19-30 cells at a monophasic action potential recording site was not statistically significant from monophasic action potential duration in all three tissue preparations studied. However, in endocardial preparations, composed of superficial (1-2 cell layers) Purkinje fibres with deeper ventricular muscle cells, the APD50 (139(17) ms) and APD90 (181(26) ms) of monophasic action potentials more closely reflected (but not significantly different) the underlying deeper ventricular muscle cells (APD50 134(14) ms and APD90 167(15) ms) rather than the mean transmembrane action potential durations of the underlying most superficial Purkinje fibres (166(22) ms for APD50 and 210(30) ms for APD90) (p less than 0.025). Tetrodotoxin (TTX) at 1 x 10(-6) mol.litre-1 shortened Purkinje fibre action potential duration and slightly lengthened that of ventricular muscle. Simultaneously recorded monophasic action potential showed an intermediate change in action potential duration. Incremental pacing and applied single premature stimuli resulted in similar degrees of shortening of action potential duration for both monophasic action potential and transmembrane potential in all three preparations. In endocardial preparations, barium chloride (4 mmol.litre-1) superfusion induced early afterdepolarisations, and spontaneous phase 4 depolarisations (n = 6) in both Purkinje and ventricular muscle cells giving rise to spontaneous automatic activity. These abnormal automatic activities were accurately detected by simultaneous monophasic action potential recordings. Suppression of automaticity by verapamil (0.2-0.5 micrograms.ml-1) as confirmed by transmembrane action potential recordings were similarly detected by monophasic action potential recordings (ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1987

Effects of propafenone on sinus nodal and ventricular automaticity: in vitro and in vivo correlation.

The electrophysiologic effects of the new antiarrhythmic drug, propafenone, were evaluated in anesthetized closed-chest dogs and on isolated cardiac tissues with the microelectrode technique. Propafenone (2 to 4 mg/kg intravenously) had no effect on sinus rate or on sinus nodal recovery time, but caused a dose-dependent significant decrease in the rate of idioventricular rhythm and increased the duration of ventricular overdrive suppression in dogs (n = 8) with complete atrioventricular block. On isolated canine Purkinje fibers (n = 8) manifesting automaticity with resting membrane potential less negative than -70 mV, propafenone reduced the slope of phase 4 depolarization and reduced the rate of automatic impulse initiation in a concentration-dependent manner (10(-6) M-4.10(-5) M). At these concentrations, propafenone had no effect on rabbit sinus nodal automaticity (n = 8) or on sinoatrial conduction. However, significant depression of sinus nodal automaticity occurred with propafenone concentrations above 5.10(-6) M in the presence of cholinergic or complete autonomic blockade with atropine (10(-6) M) and propranolol (5.10(-5) M). Propafenone caused a concentration-dependent decrease in the disparity of Purkinje fiber-ventricular muscle action potential duration (APD), mainly by shortening Purkinje fiber APD. We conclude: that propafenone suppresses idioventricular rhythm in the intact dog, most likely by depressing Purkinje fiber automaticity; the depressant effect of propafenone on sinus nodal automaticity is evident only during cholinergic receptor blockade; and the antiarrhythmic properties of propafenone may include removal of APD disparity by selective shortening of Purkinje fiber and not of ventricular muscle APD.

Animals↗
PubMed1987

Acute and chronic effects of amiodarone on delayed afterdepolarization and triggered automaticity in rabbit ventricular myocardium.

The effects of amiodarone on delayed afterdepolarization (DAD) and triggered automaticity induced by low potassium (0.5 mEq/L) were evaluated on isolated rabbit right ventricular muscles, by means of standard microelectrode techniques. Triggered automaticity was induced in 6 of 10 muscles in the control group, in four of eight in the amiodarone-superfused group, and in three of four in the Tween 80-pretreated group. In contrast, triggered automaticity could be induced in only 2 of 10 of amiodarone-pretreated muscles (n = 10) (20 mg/kg intraperitoneally, daily for 4 weeks; p less than 0.05 compared to control and amiodarone-superfused groups). The amplitude of DAD was significantly lower in muscles isolated from rabbits pretreated with amiodarone compared to those from nontreated control rabbits (n = 17). The degree of reduction was significant during all three cycle lengths of stimulation tested (800, 600, and 400 msec), that is, 2.5 +/- 1.8 vs 5.1 +/- 1.8, 2.4 +/- 2.1 vs 5.5 +/- 2.3, and 3.3 +/- 3.4 vs 9.3 +/- 4.3, respectively (values are in millivolts of mean +/- SD). Superfusion with amiodarone (3 micrograms/ml; n = 8) significantly (p less than 0.05) reduced the amplitude of DAD at 800 msec cycle length, but had no significant effect at cycle lengths of 600 and 400 msec. Tissue concentrations of amiodarone in the pretreated group were significantly (p less than 0.05) lower than those in the superfused group (10 +/- 6.8 vs 21 +/- 3.1 micrograms/gm).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1987

Failure of episodic high-dose oral verapamil therapy to convert supraventricular tachycardia: a study of plasma verapamil levels and gastric motility.

The practicality of administering large oral doses of verapamil tablets to terminate supraventricular tachycardia (SVT) was investigated in 10 patients. A pilot study in four patients showed that unexpectedly low plasma levels (less than 40 ng/ml) were obtained 60 minutes after administering 160 mg or 240 mg of verapamil during SVT. Nuclear studies in the six other patients showed that fractional liquid gastric emptying times (T) were significantly prolonged in SVT compared to sinus rhythm (SR), p less than 0.05 from T 1/3 onward. Further verapamil absorption studies (200 to 360 mg) performed during SVT and SR in five of six patients showed that peak verapamil levels in four patients in SVT were 23% to 71% lower than in sinus rhythm, where they had peaked at greater than 250 ng/ml 60 minutes post verapamil ingestion, and areas under the plasma concentration time curves were 26% to 100% (mean 67%) less in SVT than in SR for all five patients. SVT was terminated by verapamil in one patient after 40 minutes and the rate of SVT was slowed after 90 minutes in two other patients. Thus plasma verapamil levels are considerably reduced during SVT as compared to SR, and changes in gastric emptying are likely a contributing cause. Since SVT was converted to sinus rhythm in only 1 of 10 patients within 1 hour, large oral doses of verapamil tablets appear unsatisfactory for the episodic treatment of SVT.

Administration, Oral↗