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In a patient with spells of paroxysmal supraventricular tachycardia of two types, the stimulation tests demonstrated a dual intranodal conduction responsible sometimes for "usual" reciprocal rhythms (slow anterograde pathway and rapid retrograde pathway), sometimes for "reversed" reciprocal rhythms (rapid anterograde pathway and slow retrograde pathway). The latter contrasted with the lack of discontinuity of the retrograde nodal function curve (V1-V2 versus A1-A2).

In a patient with the Wolff-Parkinson-White syndrome, the existence of dual accessory pathways, both right-sided, was suspected during ajmaline test and confirmed during electrophysiologic study. The first accessory pathway was manifest in sinus rhythm while the second was obscured and revealed during low right atrial pacing. Ajmaline abolished conduction over the first pathway which most probably had a long refractory period allowing manifestation of the second pathway which had a very short refractory period. A longer conduction time over the second accessory pathway was suggested to explain its concealment during sinus rhythm.

Late potentials occurring after the QRS complex were detected on the body surface using an advanced signal averaging technique. ECG waveforms were recorded from patients with and without recurrent ventricular tachycardia who had a damaged mass of ventricular tissue (left ventricular aneurysm or right ventricular dysplasia). The recorded analog data were digitized by a 10 bit A/D converter with a sampling rate of 1280 Hz onto digital magnetic tape. The digitized waveforms were averaged with a CDC-6600 computer using an advanced algorithm which employs a cross correlation function to extract fiducial synchronizing marks for the signal averaging. Waveforms were filtered with a digital bandpass filter with 30 Hz and 250 Hz low and high cut-off frequencies, respectively. Late potentials were detected in seven out of ten patients with left ventricular aneurysm (or right ventricular dysplasia) and recurrent ventricular tachycardia and in four out of five patients with left ventricular aneurysm (or right ventricular dysplasia) but without recurrent ventricular tachycardia. The delayed depolarizations, which were recorded, had an amplitude of 3.0-27.0 microV and extended a mean of 90 msec beyond the termination of the QRS complex. In three patients with left ventricular aneurysm the delayed waveforms were abolished by aneurysmectomy. In nine control subjects no late potentials were detected. We conclude that late potentials which represent late depolarization of a damaged mass of ventricular tissue can be detected in patients with and without recurrent ventricular tachycardia.

Patients with supraventricular or ventricular tachyarrhythmias resistant to antiarrhythmic drugs are candidates for surgical ablation of the bundle of His, and of accessory pathways or ventricular or atrial foci responsible for the arrhythmia. During the past 6 years closed-chest catheter techniques have been devised that allow electrical shock ablation of the atrioventricular junction, accessory pathways, or foci responsible for arrhythmias. The promising results of these ablative procedures (especially of the atrioventricular junction and posteroseptal accessory pathways) justify their trial in suitable patients before cardiac electrosurgery.

The effects of dantrolene sodium on occlusion and reperfusion ventricular arrhythmias (VA) were studied in a canine model. Transient ischemia was induced by a 10 min occlusion period of the left anterior descending coronary artery in 27 control dogs and 32 dogs pretreated with dantrolene sodium (2.5 mg/kg). In the control group, 14 (52%) dogs experienced VA during occlusion. Five of these had ventricular fibrillation, 3 of which were fatal. Eight of 24 control dogs which reached reperfusion experienced ventricular fibrillation during the first 30 sec of reperfusion. Dantrolene sodium did not lower the frequency of VA during occlusion 22/32 (69%). Moreover, the incidence of fatal ventricular fibrillation during occlusion was significantly (p less than 0.025) higher in the drug treated-group (12/32; 37.5%) than in the control group (3/27; 11%). Dantrolene sodium also significantly reduced the time that lasted from the commencement of occlusion to the appearance of ventricular fibrillation (240 +/- 1 sec versus 166 +/- 9 seconds, control and drug group, respectively p less than 0.05) without significantly altering either heart rate or blood pressure (169 +/- 4 b.p.m., and 170 +/- b.p.m.; 101 +/- 10 mmHg and 104 +/- 9 mmHg, before and after dantrolene sodium, respectively). These results indicate that dantrolene sodium might have an arrhythmogenic effect in the ischemic canine heart.

Ten patients with Wolff-Parkinson-White syndrome underwent external His bundle recording using an advanced signal-averaging technique. Surface ECG waveforms were recorded and digitized at 1.28 kHz (10 bit resolution) and then averaged with a CDC-6600 computer. A cross-correlation function, operating in the frequency domain (using the Fast Fourier Transform algorithm) was employed to extract fiducial synchronizing marks for the waveform alignment. Using this technique, reliable His bundle activity could be recorded in nine of ten patients. There was a good correlation between the HQ and HV intervals obtained during external and internal His bundle recordings, respectively, in seven patients who underwent both recordings. Administration of ajmaline enabled to obtain the His bundle activity using a digital filter with low frequency cut-off of 30 Hz as compared to the cut-off of 150 Hz which was necessary during control to reduce the electrical activity of the delta wave. We conclude that using a computerized cross-correlation signal-averaging technique enables the external His bundle recording in patients with WPW syndrome.

The ability to detect coronary artery disease (CAD) in patients with normal, conventional electrocardiograms (ECG) was studied using high frequency electrocardiography and an advanced method of signal averaging in three groups of subjects. Group A consisted of ten healthy subjects under the age of 30; Group B of 15 patients with chest pains and normal coronary arteries; and Group C of 20 patients with chest pains and CAD. Four hundred ECG waveforms from leads V3, V4 and V5 were recorded, and the recorded analog data were digitized. The digitized waveforms were averaged using a cross-correlation function which operates in the frequency domain (fast-Fourier transform algorithm). The signals were filtered with a digital band pass filter with 150 and 250 Hz low and high cut-off frequencies, respectively. Zones of reduced amplitude in the envelope of the filtered QRS complex of at least two precordial leads were found more significantly in patients with CAD (75%) than in patients without CAD (12% for Groups A and B, p less than 0.00003). However, no significant difference was found between the voltage over the high frequency QRS complex and that of its envelope between the three groups. It is concluded that the morphology of the high frequency QRS complex as determined by this advanced method of analysis of the signal averaged ECG may be a useful indicator for the presence of CAD in patients with normal conventional ECG's.

The antiarrhythmic and haemodynamic effects of tiapamil, a new calcium antagonist, were studied in 28 anaesthetised open chest dogs. Tiapamil (2 mg X kg-1 intravenously over 5 min) was infused 15 min before a 20 min ligature of the left anterior descending coronary artery in 11 dogs. In 17 dogs physiological solution was given instead of tiapamil. In this control group, ventricular fibrillation developed during coronary occlusion in 14 (82%) dogs and after coronary reperfusion in seven of 9 (77%) dogs, which reached this stage. In contrast, in the dogs pretreated with tiapamil, ventricular fibrillation did not develop during coronary occlusion in any of the 11 dogs and did develop after coronary reperfusion in only one (9%). In addition, tiapamil appreciably decreased heart rate and blood pressure and increased cardiac output and stroke volume. These antiarrhythmic and haemodynamic effects of tiapamil suggest that this drug would be useful in the management of patients with coronary artery disease.

Adenosine triphosphate (ATP) and adenosine have strong negative chronotropic and dromotropic effects on the mammalian heart. The sensitivity of the sinus node and the atrioventricular node to ATP and adenosine manifests pronounced variability among species. For more than three decades, ATP has been used routinely in Europe in the acute therapy of paroxysmal supraventricular tachycardia. Preliminary clinical trials with adenosine in the United States suggest that this compound may have a similar therapeutic value. The exact mechanisms of action of ATP and adenosine on the mammalian heart are still not fully known. However, the vast clinical experience indicates that ATP, and probably also adenosine, can be safely and repetitively used in the acute therapy of paroxysmal supraventricular tachycardia.

The relationship of apparent steady-state serum concentrations of amiodarone and its metabolite, desethylamiodarone, to therapeutic and toxic effects was assessed in 127 patients who had treatment-resistant ventricular or supraventricular arrhythmias or were intolerant to other agents. After at least 2 months (mean, 9.8) of treatment with daily maintenance doses of 200 to 600 mg, arrhythmias were effectively suppressed in 78% of patients. Arrhythmias recurred in 47% of patients with serum amiodarone concentrations of less than 1.0 mg/L, whereas only 14% of patients with higher concentrations had recurrences (p less than 0.005). Side effects, most of them mild, occurred in 57%; only 9 patients required discontinuation of drug therapy. The risk of developing adverse reactions was related to serum amiodarone concentrations (p less than 0.0001). Adverse reactions were common in patients with serum values exceeding 2.5 mg/L, although pulmonary complications did occur at lower concentrations. Monitoring serum amiodarone concentrations may differentiate failure of drug therapy from suboptimal dosing and reduce the incidence of concentration-related side effects.

A 49-year-old man with a silent remote postero-inferior wall myocardial infarction exhibited recurrent episodes of sustained ventricular tachycardia which was hemodynamically well tolerated. Ventricular tachycardia was neither terminated nor prevented by therapy with multiple class I and class III antiarrhythmic drugs. In contrast, ventricular tachycardia was repeatedly terminated within a few minutes following intravenous administration of 10 mg verapamil and did not recur during oral therapy with verapamil (360 mg daily). Electrophysiologic study suggested that ventricular tachycardia was due to a reentrant mechanism rather than to triggered or abnormal automaticity. Thus, in contrast to previous reports, findings in this patient indicate that verapamil may be very effective and safe in certain types of ventricular tachycardia occurring late after a myocardial infarction.

Transcatheter electrical shock ablation of a concealed posteroseptal accessory pathway was performed on a 57-year-old man with drug-refractory paroxysmal supraventricular tachycardia. A single 300-joules shock delivered at the ostium of the coronary sinus abolished conduction in the accessory pathway and resulted in long-term cure of the arrhythmia. No complications were observed during the procedure.

In a series of 48 patients undergoing electrophysiological investigation for attacks of reciprocating tachycardia related to concealed or overt Wolff-Parkinson-White syndrome in sinus rhythm, 4 patients were found to have duality of nodal conduction. This association was responsible for several tachycardia circuits: in 2 patients the activation passed constantly retrogradely through the accessory pathway and then either through the slow nodal pathway or the rapid nodal pathway in the anterograde direction. In the other two patients, in addition to classical orthodromic tachycardia, purely intranodal reciprocating rhythms giving rise to sustained tachycardia in one case and to simple echos in the other, were observed.

The electrophysiologic effects of adenosine triphosphate (ATP) and adenosine and the modification of these effects by atropine, propranolol, vagotomy, dipyridamole and aminophylline were studied in a canine model. Both ATP and adenosine exerted transient, dose-dependent negative chronotropic and dromotropic effects on the sinoatrial and atrioventricular nodes, respectively. At all doses tested, the effects of ATP were more pronounced. Treatment with either atropine or propranolol plus bilateral cervical vagotomy attenuated the effects of ATP but not of adenosine. In the presence of propranolol plus vagotomy, both the negative chronotropic and dromotropic effects of ATP and adenosine were enhanced and attenuated in a similar manner by dipyridamole and aminophylline. Thus, when ATP and adenosine are injected rapidly into the right atrium of the intact canine heart, vagal involvement in the mechanism of action of ATP but not of adenosine is mainly responsible for the difference in the magnitude of the electrophysiologic effects of these 2 compounds, and only a small part of the electrophysiologic effects of ATP are the result of its degradation to adenosine.

We describe a newborn infant with concealed ventricular preexcitation in sinus rhythm on the early ECGs, and who developed recurrent episodes of preexcited reciprocating tachycardia. Manifestation of the ventricular preexcitation and initiation of the tachycardias were dependent on the presence of severe conduction disturbances in the normal atrioventricular pathway, probably in the atrioventricular node.

The effects of verapamil and bepridil on occlusion and reperfusion ventricular arrhythmias including ventricular fibrillation (VF) were studied in a canine model. The control group consisted of 27 dogs. 30 dogs received intravenous verapamil (0.2 mg/kg/3 min followed by a continuous infusion of 0.01 mg/kg/min for 15 min). 18 dogs received bepridil (0.5 mg/kg/min for 10 min). The left anterior descending coronary artery was occluded in one step 8 min after the commencement of verapamil administration and 5 min after the termination of bepridil infusion. The incidence of ventricular arrhythmias during the occlusion period was 14 (VF, 5/14), 13 (VF, 0/13) and 14 (VF, 9/14) in the control, verapamil and bepridil groups, respectively. The frequencies of reperfusion VF were 8/24 (33%), 4/30 (13.3%) and 0/13 (0%), respectively. It was concluded that (a) verapamil effectively prevents occlusion but not reperfusion VF and (b) bepridil has an arrhythmogenic effect in the ischemic canine heart but reduces the incidence of reperfusion VF.

A fetal tachyarrhythmia was discovered at the thirty-second week of gestation of a 22-year old woman. Fetal echocardiography revealed atrial fibrillation with rapid ventricular rate, without any other demonstrable cardiac abnormality. In spite of therapeutic maternal blood levels of digoxin, the fetal ventricular rate and cardiac size increased, which prompted us to perform cesarean section at the thirty-fourth week of gestation. A baby with a Wolff-Parkinson-White syndrome but no other cardiac anomaly was delivered. Recurrent episodes of nonsustained atrial fibrillation with conduction over the accessory pathway occurred in the first hours of life. The Wolff-Parkinson-White pattern was not present on subsequent ECG recordings. The use of echocardiography in the diagnosis and management of this rare fetal tachyarrhythmia is emphasized.

This article reviews current information on the clinical pharmacology, therapeutic utility, and adverse reactions of amiodarone, with emphasis on guidelines for its rational use.

9 patients (6 males and 3 females, age 5-69 years) with ventricular tachycardia induced by supraventricular beats are reported. 3 patients had had previous myocardial infarction, 1 patient had mitral valve prolapse and in 5 patients no organic heart disease could be demonstrated. Ventricular tachycardia was initiated by a single atrial premature beat in 4 patients, double atrial premature beats in 3 patients (in 1 of them following exercise), by nonsustained AV nodal tachycardia in 1 patient, by rapid atrial pacing in 3 patients and exercise-related ectopic atrial tachycardia in 1 patient. Programmed ventricular stimulation induced ventricular tachycardia in all patients in whom the tachycardia was induced by atrial stimulation. Verapamil abolished sustained ventricular tachycardia in 1 of the 3 patients in whom this drug was administered. Hypotheses are made on the electrophysiological mechanisms of the arrhythmias and clinical implications are listed.

Programmed ventricular stimulation was performed in a patient with sarcoidosis who exhibited an episode of sustained ventricular tachycardia. Sustained rapid ventricular tachyarrhythmias requiring cardioversion for termination were induced by double right ventricular apical extrastimuli during control, and treatment with disopyramide, quinidine, and fluocortolone. In contrast, only four repetitive ventricular complexes were induced during combined therapy with quinidine, mexiletine and amiodarone. While receiving the latter regimen, the patient has been asymptomatic during 28 months of follow-up.

Ajmaline test (50 mg intravenously over 1 minute) and ergometric exercise test were performed in 24 patients with the Wolff-Parkinson-White syndrome. The effects of both tests on the conduction in the accessory pathway (AP) were correlated with the anterograde effective refractory period (ERP) of the AP. Ajmaline caused transient anterograde block in the AP in 15 patients, 14 with an ERP of more than 250 ms and 1 with an ERP of 250 ms. Ajmaline failed to abolish preexcitation in 9 patients, all with ERP of the AP of 250 ms or less. Exercise testing caused anterograde block in the AP in 5 patients, in 2 during exercise (ERP of 340 and 360 ms) and in the remaining 3 patients during the recovery phase (ERP of 600, 520 and 460 ms). Of the 10 patients with an ERP of 250 ms or less, ajmaline did not abolish preexcitation in 9 and exercise did not abolish it in any of them. Of the 7 patients with an ERP of 330 ms or more, ajmaline abolished preexcitation in 7 and exercise abolished it in 5 patients. Of the 7 patients with ERP of the AP more than 250 ms but less than 330 ms, ajmaline but not exercise abolished preexcitation in all. Thus, ajmaline and exercise testing can detect patients with short and long ERPs of the AP, respectively, and the effects of ajmaline and exercise tests combined may be useful in the noninvasive assessment of various ranges of ERP of the AP.

The influence of aminophylline, a competitive antagonist of adenosine, on the chronotropic and dromotropic effects of adenosine and adenosine triphosphate was studied in pentobarbital anaesthetised dogs under various modifications of the autonomic nervous tone. Adenosine and adenosine triphosphate (3 mumol.kg-1 each) were rapidly (greater than or equal to 1 s) injected into the right atrium during both sinus rhythm and right atrial pacing (cycle length 300 ms) before and after infusion of aminophylline (5 mg.kg-1) (n = 21) as well as after increasing doses of aminophylline (n = 10). Some dogs underwent either muscarinic blockade with atropine (0.2 mg.kg-1) (n = 10), or beta adrenergic blockade with propranolol (1 mg.kg-1) (n = 10), or complete autonomic blockade with atropine and propranolol (n = 10). Aminophylline (5 mg.kg-1) antagonised the negative chronotropic and dromotropic effects of adenosine triphosphate and adenosine in dogs pretreated with atropine or atropine plus propranolol but did not affect them in autonomically intact dogs. In addition, the electrophysiological effects of adenosine were antagonised by only the highest doses of aminophylline in autonomically intact dogs and by aminophylline (5 mg X kg-1) in dogs pretreated with propranolol. It was concluded that (a) alteration of the electrophysiological effects of adenosine triphosphate and adenosine by aminophylline is appreciably influenced by the autonomic nervous tone and (b) autonomic blockade is required for the manifestation of the antagonism by aminophylline of the electrophysiological action of adenosine and adenosine triphosphate.

Simultaneous AV nodal reentrant and ventricular tachycardias were observed during the course of an electrophysiological study in a 51-year-old patient who suffered from recurrent attacks of sustained ventricular tachycardia. Occurrence of simultaneous tachycardias was facilitated by the fact that both tachycardias had a similar cycle length. Ventricular tachycardia was most probably initiated by AV nodal tachycardia previously induced by atrial extrastimulation following the administration of atropine.

The efficacy, electrophysiologic effects, and side effects of adenosine triphosphate (ATP) and verapamil in the short-term management of paroxysmal reciprocating junctional tachycardia (PRJT) were compared in 20 patients. All patients had inducible sustained PRJT during control electrophysiologic study. Fourteen patients had PRJT involving a retrograde accessory pathway, and six patients had atrioventricular (AV) nodal reentrant tachycardia ("slow-fast" type). ATP, which has a very short half-life, was first administered (10 mg iv over 1 sec) during sustained PRJT. If PRJT did not terminate within 2 min, a bolus of 20 mg ATP was given. Verapamil (5 mg iv over 15 sec) was subsequently administered during sustained PRJT, and if the latter did not terminate within 3 min another bolus of 5 mg verapamil was given. The cycle lengths of PRJT before administration of 10 or 20 mg ATP and 5 mg verapamil were similar. The 10 mg dose of ATP terminated PRJT in 17 of the 20 patients, and 20 mg ATP was required to terminate PRJT in the three remaining patients. The 5 mg dose of verapamil terminated PRJT in 15 patients, whereas an additional bolus of 5 mg terminated PRJT in one of the remaining five patients. The overall efficacy of ATP (20/20, 100%) was significantly greater than that of verapamil (16/20, 80%) (p less than .05); however, there was no significant difference between the conversion rate of PRJT after administration of 10 mg ATP (17/20) and 5 mg verapamil (15/20). ATP terminated PRJT more quickly than verapamil (mean 24 sec vs mean 51 sec; p less than .01). Termination of PRJT by either ATP or verapamil was mainly related to a block in the AV node in patients with accessory pathways and to a block in the antegrade slow pathway in patients with AV nodal reentry. Cycle length alternans before termination of tachycardia was observed more frequently after verapamil than after ATP (7/16 vs 1/20; p less than .01). The total incidence of transient second-degree AV nodal block and various cardiac supraventricular and ventricular arrhythmias was higher after termination of PRJT by ATP than after verapamil (17/20 vs 5/16; p less than .001). A higher incidence of transient but frequently uncomfortable noncardiac side effects was observed after ATP. We conclude that ATP (10 to 20 mg) is more effective and more rapid than verapamil (5 or 5 + 5 mg) in terminating PRJT but results in a higher incidence of cardiac and noncardiac side effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Transcatheter shock ablation of ventricular tachycardia was attempted in seven patients who had drug-resistant ventricular tachycardia and in one patient in whom ventricular tachycardia was electrophysiologically induced during therapy with multiple antiarrhythmic drugs. Seven patients had previous myocardial infarction and five of them were high risk candidates for surgical therapy. One patient without organic heart disease had repetitive ventricular tachycardia manifesting two different patterns of left bundle branch block. After endocardial mapping, synchronized unipolar 250 to 300 J shocks (one to six) were delivered between the pole recording the earliest endocardial activity during ventricular tachycardia (40 to 200 ms before the onset of the QRS complex) and a body surface electrode. Immediate complications included severe but reversible cardiogenic shock (one patient), nonclinical ventricular tachycardia (two patients, requiring cardioversion in one), transient atrioventricular and intraventricular conduction disturbances (three patients) and permanent left bundle branch block (one patient). A late complication in one patient, left heart failure, occurred 3 days after delivery of five intracardiac shocks. In two patients, left ventricular ejection fraction markedly decreased and in one of them new ventricular contraction abnormalities appeared. Clinical ventricular tachycardia did not recur in five of the seven post-myocardial infarction patients after 7 to 17 months, and it was not inducible in the four patients undergoing late electrophysiologic study. In the patient with idiopathic ventricular tachycardia, one of the configurational types of ventricular tachycardia recurred.(ABSTRACT TRUNCATED AT 250 WORDS)

We tested the effect of disopyramide on reperfusion arrhythmias in mongrel dogs. The control group consisted of 27 dogs. Twenty-nine dogs received two intravenous doses of disopyramide (total: 5.3 mg/kg) before and during the occlusion of the left anterior descending coronary artery. The blood levels of disopyramide averaged 3.95 +/- 0.95 micrograms/ml and 5.9 +/- 1.1 micrograms/ml, 2.5 and 9.5 min after the ligation. The incidence of reperfusion arrhythmias was significantly (p less than 0.05) lower in the treated group (7.5%) than in the control group (33.3%). Disopyramide also lowered the incidence of arrhythmias during the occlusion period (14% vs. 52%, p less than 0.01). Both groups showed a correlation between the incidence of arrhythmias during the occlusion period and on reperfusion.