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PubMed1987

Chronic idiopathic idioventricular tachycardia caused by slow response automaticity.

A 22-year-old female, asymptomatic and without any evidence of cardiac disease, was found to have a persistent idioventricular tachycardia (IVT). Sinus rhythm and IVT rates were similar and showed parallel changes in successive resting electrocardiograms. Both IVT and sinus rhythm were transiently slowed or suppressed by vagal stimulation and accelerated by sympathetic stimulation. Long periods of atrial overdrive pacing, at a rate 62% faster than the spontaneous rate of IVT, depressed both ectopic and sinus activity. Fast channel blocking agents (lidocaine, disopyramide), and digoxin and amiodarone failed to modify IVT significantly. Verapamil, a calcium channel blocking drug, allowed total control of the arrhythmia. These electrophysiologic and pharmacologic responses suggest that the IVT may relate to the automatic activity of a ventricular focus of the "slow response" type, functionally resembling an "additional" sinus node with preserved innervation. During an 88-month follow-up, the patient continued to be asymptomatic, warning arrhythmias were never found and the features of IVT remained unmodified.

Adult↗
PubMed1990

Predictors of ventricular tachycardia inducibility in programmed electrical stimulation and the effectiveness of serial drug testing: Polish multicenter study.

In 100 patients with IHD and complex ventricular arrhythmias, programmed electrical stimulation was performed using up to three extrastimuli at sinus rhythm, and paced 100, 120 and 140 beats/min delivered from the RV apex, outflow tract or the LV with ventricular mapping to evaluate late potentials (LP) in 41 patients. Sustained monomorphic VT (SMVT) was provoked in 91% of 42 patients with a history of VT/VF, P less than 0.001, all five patients had SMVT in 24-hour ECG, P less than 0.005, and 91% of 21 patients with LV dyskinesis, P less than 0.01. After depolarizations were found in 62% of 21 patients with a history of VT, in 58% of 31 patients with inducible VT, P less than 0.01 and in five of six patients with LV dyskinesis. In patients with inducible VT, LP had a higher amplitude (105 +/- 35 vs 60 +/- 47 microV) and were more delayed (202 +/- 96 vs 133 +/- 75 msec) than in noninducible patients. In 17 patients, serial drug testing was performed after oral administration using mexilitene, disopyramide, chinidine, propafenone, sotalol, and amiodarone. If one drug was tested, the therapy efficacy was 25%, if two drugs-60%, and if three drugs-75%. In eight patients, VT was inducible in all tests, but in only one of these patients chronic antiarrhythmic therapy was not effective. We conclude that the most important predictors of VT inducibility are a history of VT or 24-hour ECG, and LV dyskinesis. Serial drug testing is efficient only when many drugs are tested, but even if VT is inducible, it does not exclude the possibility of a good clinical outcome in chronic therapy.

Adult↗
PubMed1991

Proarrhythmic response to antiarrhythmic drug as a risk factor for sudden cardiac death in patients with ischemic heart disease.

The prognostic significance of arrhythmogenic response to an antiarrhythmic drug was studied. In 782 patients with ischemic heart disease (IHD) and frequent and/or complex ventricular premature beats (VPBs), 1,041 drug tests guided by 24-hour Holter monitoring were conducted. The following drugs were assessed: beta blockers, disopyramide, mexiletine, amiodarone. Proarrhythmia was defined as: (1) greater than 4-fold increase in VPBs, (2) greater than 10-fold increase in repetitive forms, or (3) new occurrence of ventricular tachycardia or ventricular fibrillation (VT/VF). During a follow-up of 1-49 months (mean 22) patients were treated with antiarrhythmic drugs found to be safe in control Holter monitoring. Proarrhythmic effects were observed in 8.4% of patients. No drug was completely free of this type of reaction. In long-term observation, cardiac death and sudden death occurred in 53 and 32 patients, respectively. With actuarial analysis (Kaplan-Meier method, log-rank test) there was a significant difference in cardiac death (P less than 0.01) and sudden death rate (P less than 0.05) of proarrhythmia (+) compared with proarrhythmia (-) patients at 1 year (11% vs 4%, 7% vs 3%) and 3 years (24% vs 11%, 16% vs 7%). Proarrhythmic response was an independent risk factor apart from myocardial infarction, VT/VF, ejection fraction less than 40% and QTc greater than 440 msec. Arrhythmogenic response to antiarrhythmic drugs seems to be an additional predictor of sudden death in IHD.

Anti-Arrhythmia Agents↗
PubMed1993

Usefulness of fluoxetine hydrochloride for prevention of resistant upright tilt induced syncope.

Recurrent vasovagally mediated episodes of hypotension and bradycardia are a common cause of recurrent syncope that can be identified by head-upright tilt table testing. Although the use of beta blockers, transdermal scopolamine, disopyramide, and fludrocortisone may be helpful in preventing further episodes, some patients are intolerant of or respond poorly to each of these agents. Following anecdotal observations, we investigated the utility of fluoxetine (a serotonin re-uptake antagonist) in preventing head-upright tilt induced hypotension/bradycardia in patients unresponsive to or intolerant of standard therapy. Sixteen patients (7 men and 9 women, mean age 42 +/- 21 years) with recurrent syncope and positive head-upright tilt studies (refractory to normal therapy) were placed on fluoxetine and restudied 5-6 weeks afterward. Three patients were intolerant of the medication. Of the 13 patients who underwent repeat tilt studies, seven patients (53% of the patients retested or 44% of the total group) were rendered tilt table negative, and, over a mean follow-up period of 19 +/- 9 months, have remained asymptomatic. We conclude that fluoxetine may be an effective therapy in patients with recurrent vasovagally mediated syncope refractory to other forms of therapy.

Adult↗
PubMed1997

Neurally mediated syncopal syndromes: pathophysiological concepts and clinical evaluation.

The neurally mediated syncopal syndromes encompass a number of apparently related disturbances of reflex cardiovascular control characterized by transient inappropriate bradycardia and/or vasodilation of various arterial and venous beds. Certain of these syndromes (e.g., carotid sinus syndrome, postmicturition syncope) are encountered occasionally in clinical practice, whereas others are quite rare (e.g., swallow syncope). On the other hand, vasovagal syncope occurs so frequently, that as a group, the neurally mediated syncopal syndromes are among the most important causes of syncope. The pathophysiology of the neurally mediated syncopal syndromes is incompletely understood, but can be considered in terms of four basic elements: (1) the afferent limb; (2) central nervous system (CNS) processing; (3) the efferent limb; (4) feedback loops. The afferent limb consists of several peripheral and CNS trigger sites and the associated connections to medullary cardiovascular centers. CNS processing and efferent signals result in both bradycardia, which may be marked or relative, and vasodilatation. Failure of baroreceptor feedback controls to prevent hypotension is important in facilitating development of symptomatic hypotension. Head-up tilt table testing has become the diagnostic technique of choice for clinically assessing susceptibility to neurally mediated syncope, particularly of the vasovagal type. Most studies suggest that such testing discriminates relatively well between symptomatic patients and asymptomatic control subjects, of whom 10%-15% have a false-positive test results. Sensitivity of tilt table testing is more difficult to evaluate because there is no accepted diagnostic gold standard. However, sensitivity (measured against a classic presentation) has been estimated to range from 32%-85%, with most reports favoring the higher end of this range. Treatment strategies for neurally mediated syncope remain controversial. Many single episodes do not warrant treatment unless physical injury has occurred, or a high risk occupation or avocation is involved. Tilt test exposure alone may prove beneficial in educating patients with recurrent syncope to recognize warning signs of an imminent faint. Large controlled clinical studies have not been performed to test the efficacy of pharmacological therapy (e.g., beta-adrenergic blockers, disopyramide, serotonin reuptake blockers, vasoconstrictors) or pacing therapy. Such studies may be difficult to undertake due to the variable frequency of spontaneous symptoms and apparent long periods of remission. Nonetheless, many investigators and clinicians have come to rely on these agents, and on tilt testing to guide treatment decisions. Studies employing careful correlation of long-term clinical follow-up with results of early and perhaps later repeat tilt studies are still needed.

Afferent Pathways↗
PubMed1998

Atrial flutter with 1:1 atrioventricular conduction caused by propafenone.

We describe a case of 1:1 atrial flutter in a patient with coronary disease taking propafenone. In atrial flutter, the atrial rate is usually about 300 beats/min with 2:1 AV conduction and a ventricular rate of 150 beats/min. Class IA antiarrhythmic drugs, especially quinidine and disopyramide, may cause 1:1 AV response because they reduce atrial rate and are vagolytic. However, propafenone is a Class IC agent and has no anticholinergic properties, and the occurrence of 1:1 AV conduction at a rate of about 250 beats/min is an important side effect that, although uncommon, should be recognized.

Anti-Arrhythmia Agents↗
PubMed1998

Treatment of malignant neurocardiogenic vasovagal syncope with a rate drop algorithm in dual chamber cardiac pacing.

A 29-year-old man with malignant vasovagal syncope presented with episodes of abrupt loss of consciousness associated with an aura, totaling more than 10 episodes over 3 months. Holter monitoring showed cardiac arrest with a duration of 15 seconds. Oral propranolol and disopyramide therapy failed to prevent the syncope. A dual chamber pacemaker with a rate drop response algorithm successfully prevented the syncope but not the aura. There may be multifactors involved in the mechanism of this syndrome. The patient has returned to a normal active life. This rate drop algorithm is an effective therapy for the prevention of syncope in malignant vasovagal syncope.

Adult↗
PubMed1993

Drug therapy for torsade de pointes.

Torsade de pointes is an uncommon and unique type of ventricular tachycardia. It differs from other forms of ventricular tachycardia by its morphological features, underlying mechanism, and modes of therapy. Recognizing torsade de pointes is of major clinical importance, as standard antiarrhythmic regimens might not only be ineffective in abolishing this life-threatening arrhythmia but may aggravate it. Torsade de pointes is most commonly precipitated by QT prolonging drugs, mainly type IA antiarrhythmic therapy such as quinidine and disopyramide, and other antiarrhythmic agents are reported to cause torsade de pointes as well. Predisposing factors known to increase the likelihood of developing torsade de pointes are: electrolyte imbalance (hypokalemia, hypomagnesemia, or both) and slow heart rate induced either by sinus bradycardia or heart block. Treatment of torsade de pointes is aimed at shortening the QT interval. By acceleration of the heart rate, the QT interval is shortened, thus preventing the recurrence of the arrhythmia. Treatment of torsade de pointes includes: isoproterenol infusion, cardiac pacing, and intravenous atropine. Intravenous magnesium sulfate, a relatively new mode of therapy for torsade de pointes, was proven to be extremely effective and is now regarded as the treatment of choice for this arrhythmia.

Action Potentials↗
PubMed1996

Pharmacologic therapy of atrial flutter.

Atrial flutter is a relatively rare but nonetheless important arrhythmia. Its mechanism and anatomy have been defined as right atrial macroreentry. It responds to treatment with a variety of antiarrhythmic agents but, in general, drug efficacy for acute termination is low. The addition of pacing to drug therapy markedly improves the success rate for restoration of sinus rhythm. Useful antiarrhythmic agents include amiodarone, sotalol, disopyramide, flecainide, and propafenone, but definitive efficacy studies have not been performed. The risk of provoking 1:1 AV conduction and a marked increase in ventricular response rate is always present. AV nodal blocking drugs (digoxin and verapamil) probably offer protection from this unwanted effect, but the prevalence of 1:1 conduction and the efficacy of AV nodal blockade remain to be established. When drug management fails, there is a place for radiofrequency ablation. Little is known about the thromboembolic risk of atrial flutter. As a consequence, the role of prophylactic anticoagulation is uncertain. Current interest in atrial flutter will ensure that these and other clinical questions are answered in the near future.

Animals↗
PubMed1997

Efficacy of midodrine hydrochloride in neurocardiogenic syncope refractory to standard therapy.

INTRODUCTION: Some patients with neurocardiogenic syncope continue to have recurrent syncope or presyncope despite the use of currently available drug therapy. The purpose of this study was to determine whether midodrine hydrochloride, a selective adrenergic agonist, could be effective in patients resistant to, or intolerant of, currently used medications in the treatment of neurocardiogenic syncope. METHODS AND RESULTS: Eleven patients with a history of recurrent syncope or presyncope in whom hypotension with syncope or presyncope could be provoked during head-up tilt testing were included. There were 4 men and 7 women with a mean age (+/-SD) age of 34 +/- 13 years. In all patients, standard therapy with beta-adrenergic receptor blocking agents, ephedrine, theophylline, disopyramide, fludrocortisone, and sertraline hydrochloride, was either ineffective, poorly tolerated, or contraindicated. Midodrine was initially administered orally at a dose of 2.5 mg three times daily. After adjustment of dosage over 2 to 4 weeks, patients were followed-up clinically. Midodrine was discontinued in one patient because of side effects. Frequency of syncope or presyncope during the 3 months prior to starting treatment was compared during a mean follow-up of 17 +/- 4 weeks after starting treatment with midodrine. There was significant (P < 0.01) reduction in syncopal and presyncopal episodes on midodrine. Five patients had complete resolution of symptoms, while four patients had significant improvement. Symptoms did not improve in one patient. CONCLUSIONS: Midodrine hydrochloride can be effective in preventing recurrent symptoms in selected patients with neurocardiogenic syncope unresponsive to, or intolerant of, standard drug therapy.

Administration, Oral↗
PubMed1998

Sinus tachycardia with atrioventricular block: an unusual presentation during neurocardiogenic (vasovagal) syncope.

INTRODUCTION: Neurocardiogenic (vasovagal) syncope is characterized by hypotension and bradycardia. The presence of sinus tachycardia along with AV block during syncope in patients with neurocardiogenic syncope has not been described previously. METHODS AND RESULTS: Two female patients (18 and 16 years old) with recurrent syncope and documented sinus tachycardia at the time of syncope are described. Patient 1 had recurrent episodes of syncope. During one of these episodes, which occurred while she was being monitored, sinus tachycardia along with high-grade AV block was seen at the time of syncope and hypotension. Patient 2 had a history of recurrent syncope and seizure. During one of these episodes, she was documented to have ventricular asystole lasting for about 39 seconds. The sinus rate was 480 msec at the beginning, before slowing down to 960 msec prior to restoration of sinus rhythm with 1:1 AV conduction. The same scenario was repeated during head-up tilt testing. Both patients were treated successfully with oral disopyramide and, during a follow-up of 28 months and 9 months, have remained symptom-free. CONCLUSION: Sinus acceleration along with high-grade AV block during syncope and hypotension can occur in some patients with neurocardiogenic syncope. The exact mechanism of this phenomenon is unclear.

Adolescent↗
PubMed1998

Recurrent supine syncope: an unusual manifestation of the neurally mediated faint.

INTRODUCTION: Syncope occasionally may occur in the supine patient due to severe brady- or tachyarrhythmia. However, recurrent syncope upon assumption of the supine position as a result of a neurally mediated reflex mechanism has not been reported previously. METHODS AND RESULTS: Two young patients, both of whom had significant systemic illnesses, experienced recurrent episodes of presyncope and/or syncope shortly after assuming the supine position. During ambulatory ECG monitoring, symptoms were provoked only by lying down and were associated with transient bradycardia. Head-up tilt table testing was undertaken as part of the syncope evaluation and was nondiagnostic in both cases. However, both patients exhibited a transient cardioinhibitory response with reproduction of typical symptoms upon return of the table to the supine position ("reverse tilt"). During follow-up (8 and 14 months), both patients improved with pharmacologic treatment (disopyramide in one case and midodrine in the other). CONCLUSION: Presyncope or syncope upon lying down can be an unusual manifestation of the neurally mediated faint.

Adult↗
PubMed2006

Na"Fuzzy space": does it exist, and is it important in ischemic injury?

Work is reviewed which provides evidence for the presence of a subsarcolemmal microdomain, in which the [Na(+)] is influenced by Na(+) influx via the Na(+) channel and the activity of the Na pump. The sarcolemma adjacent to this microdomain, which has been referred to as "Na(+) fuzzy space," appears to include Na-Ca exchangers, and thus alterations of [Na(+)] in this space may influence Ca(2+) influx and efflux, and thus Ca(2+) loading, more directly than do alterations of bulk cytoplasmic [Na(+)]. The degree of Ca(2+) loading is an important determinant of contractility in heart muscle, and therefore alterations in fuzzy space [Na(+)] may be important in mediating the positive inotropic effects of Na pump inhibitors, such as digitalis, and the negative inotropic effects of Na(+) channel blockers such as disopyramide. During ischemia, myocyte Ca(2+) overload can contribute to ATP depletion by activation of Ca(2+)-dependent ATPases and by induction of the mitochondrial permeability transition, and thus is an important contributor to myocyte dysfunction and injury. Hypoxia associated with ischemia can induce Na(+) influx via a persistent opening of the Na(+) channel. It is likely that this Na(+) influx elevates [Na(+)] in the fuzzy space, and thus increases Ca(2+) influx via Na-Ca exchange, and increases Ca(2+) loading. Inhibition of the persistent Na(+) current with a resulting decrease in Ca(2+) loading by drugs such as tetrodotoxin (TTX) and ranolazine may be a mechanism by which these agents produce a cardio-protective effect during ischemia.

Animals↗
PubMed1985

Prazosin binding to human alpha 1-acid glycoprotein (orosomucoid), human serum albumin, and human serum. Further characterization of the 'single drug binding site' of orosomucoid.

The plasma protein binding of the alpha 1-adrenergic blocking agent prazosin was investigated by means of circular dichroism (CD) and equilibrium dialysis (ED) measurements. The interaction of prazosin with human alpha 1-acid glycoprotein (alpha 1-AGP) results in pronounced negative extrinsic Cotton effects at 255 nm and a smaller negative band at 285 nm which are associated with the binding of prazosin to only one site of the protein. Various basic drugs, and warfarin also, at 50 microM displace prazosin 10 microM from its binding site on alpha 1-AGP and reduce the CD-spectra at 255 nm by 26% (disopyramide), 52% (mepivacaine), about 70% (verapamil, biperiden), and 90-100% (trihexyphenidyl, warfarin). (+/-)-Propranolol reduces the CD-spectra by 76%, its (-)-isomer by 89%, and the (+)-isomer by 65%. ED experiments indicated that the binding of prazosin to alpha 1-AGP is saturable with an association constant of 48 000 M-1 and 0.85 binding sites per protein molecule. Displacement of prazosin from alpha 1-AGP by the same drug as used for the CD experiments at displacer/prazosin ratios of 5 resulted in comparable reductions of the fraction bound as obtained by the CD experiments. Prazosin was also highly bound to human serum albumin (600 microM) with about 80-85% bound at prazosin concentrations from 1-100 microM. Since prazosin binding to human serum is only slightly higher (80-90%) it is concluded that prazosin binding in serum is largely mediated by the albumin fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Binding Sites↗
PubMed1990

Comparative drug exsorption in the perfused rat intestine.

The factors affecting drug exsorption into the gastrointestinal tract are uncertain. In this study, the intestinal clearance (CLi) of compounds which vary in their lipophilicity, serum protein binding, molecular weight and ionic charge at physiological pH, has been measured. Male Sprague-Dawley rats with ligated bile ducts were infused with the test compounds through the jugular vein. The small intestine was intubated and perfused with Tyrode solution at 20 mL h-1. The CLi of the compounds investigated (urea, polyethylene glycol, inulin, albumin, dextran, barbituric acid, salicylic acid, thiobarbital, thiopental, thioseconal, theophylline, S-disopyramide and quinidine) was determined under anaesthesia by dividing the rate of a component's appearance rate in the perfusate by its carotid arterial concentration. Serum protein binding of the compounds was determined by equilibrium dialysis. The n-octanol-water partition coefficients of the compounds were measured as indices of lipophilicity. The CLi values of dextran, albumin, inulin, polyethylene glycol and urea were 0.56, 1.03, 4.5, 4.8 and 12.0 mL h-1, respectively. The larger the molecular weight of a compound, the smaller its CLi. The molecular weight is apparently one of the major determinants of CLi. Thiobarbital, thiopental and thioseconal are compounds of similar structure with increasing lipophilicity and serum protein binding. The CLi of thiobarbital, thiopental and thioseconal was proportional to the unbound fraction in serum. The unbound clearance (CLui) of three thiobarbiturates were similar (approximately 11 mL h-1). The unbound fraction of drug in serum appears to be a factor determining their CLi. Barbituric acid and salicylic acid, two acidic compounds, showed a low CLi (less than 1 mL h-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1992

Concentration-dependent exsorption of quinidine in the rat intestine.

During intravenous infusion, the luminal concentration of quinidine was higher than the plasma concentration. The intestinal clearance (CLi) of the drug was measured by dividing the rate of appearance of the drug in the intestinal luminal perfusate by the plasma concentration. The CLi of quinidine was therefore much higher than the rate of luminal perfusion. Over the infusion dose range of 0.1-2 mg h-1, the CLi of quinidine decreased with increasing plasma concentration of quinidine. Adding quinidine into the luminal perfusate had little effect on the CLi of quinidine. Co-administration of quinidine with other agents intravenously did not alter the CLi of salicylic acid and urea, while the same treatment decreased the CLi of theophylline and S-disopyramide. In-vitro experiments on brush-border membrane vesicles showed that quinidine decreased the rate of Na+ uptake and H+ efflux. The inhibition was significant at quinidine concentrations above 20 microM. Quinidine was a more potent inhibitor than amiloride. At quinidine infusion rates less than 2 mg h-1, quinidine concentration in plasma or in the luminal perfusate was at the lower limit of the inhibitory concentration. Microclimate pH at the intestinal surface was also measured. At mid-jejunum, the microclimate pH increased 0.3 pH units by infusing 2 mg h-1 of quinidine, while the microclimate pH at most other measuring sites was not significantly altered by quinidine infusion. It was concluded that quinidine is exsorbed from blood into the intestinal lumen by a carrier-mediated pathway in addition to the passive diffusion. At high plasma concentration, quinidine exsorption becomes saturated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Properties of the block of single Na+ channels in guinea-pig ventricular myocytes by the local anaesthetic penticainide.

1. The blocking mechanism of a disopyramide derivative Penticainide (2-alkyl-(4-(dialkylamino)-2-)pyridyl-butyramide) on cardiac Na+ channels has been studied using single-channel analysis in cell-attached and inside-out patches from guinea-pig ventricular cells. Penticainide was applied in concentrations between 3 and 100 microM. The S-enantiomer of DPI 201-106 (5 microM) was used as a tool to slow the inactivation, improve the time resolution by prolonging the mean open time, and to increase the number of openings per depolarization of the channel. 2. When in cell-attached or inside-out patch experiments up to 100 microM-Penticainide was applied to the bathing solution no significant effect was observed on the probability of the channel being open or on the mean open time. 3. In cell-attached patch experiments with 100 microM-Penticainide in the pipette, the open-state probability of the Na+ channel was much lower than in the absence of Penticainide. No significant changes were found in the potential of half-maximum activation or in the slope of the activation curve. The maximum open-state probability was reduced by a factor five in the presence of Penticainide. The single-channel conductance was not affected by the drug. 4. The decrease in the probability of the channel being open was mainly due to an increased probability of observing sweeps with no activity ('nulls'). 5. A dramatic relief from the block was observed when pauses were interposed into the normal activation pattern, or when the pacing rate was reduced. 6. The distribution of the open times of the bursting Na+ channel could be fitted with two exponentials. Penticainide in the patch pipette reduced the mean open time. Also the contribution of the number of long openings to the total number of openings was reduced. 7. Closed-time distribution was also fitted with two exponentials. Penticainide in the patch pipette prolonged the long mean closed time. The contribution of the number of short closings to the total number of closings was decreased. 8. Penticainide in the patch pipette did not significantly change the time constant of the decay of the ensemble-averaged currents measured at -30 mV. Because of the close correlation between the burst duration and the time constant of inactivation (Nilius, Vereecke & Carmeliet, 1988b), we conclude that no striking effect of Penticainide on the burst duration can be expected.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1984

Pharmacological observations in patients with nodoventricular pathways.

Three patients with accessory nodoventricular pathways and re-entry tachycardia are reported. In all three patients the accessory nodoventricular pathway formed the anterograde limb of the re-entry circuit while the His-Purkinje-atrioventricular node axis formed the retrograde limb of the tachycardia in two of the patients and a concealed accessory pathway formed the retrograde limb in the remaining patient. All three patients also manifested dual anterograde atrioventricular nodal pathways with conduction through the accessory nodoventricular pathways being associated with the atrioventricular nodal fast pathway. Type I antiarrhythmic drugs, especially disopyramide and quinidine, were effective for the treatment of the re-entry tachycardia because of their depressive action on the nodoventricular pathway. Beta blockers were also effective because of their action on the atrioventricular nodal portion of the re-entry circuit in one patient and most probably due to atypical (atrioventricular nodal like) properties of a retrogradely conducting accessory pathway in a second patient.

Adolescent↗