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Ajmaline was administered intravenously to six patients with the Wolff-Parkinson-White syndrome for the acute management of paroxysmal atrial flutter (three patients) or fibrillation (three patients) with a fast ventricular response (over the accessory pathway). Ajmaline increased refractoriness in the accessory pathway in all three patients with atrial flutter and stopped the flutter in one. The drug completely abolished preexcitation in two of the three patients with atrial fibrillation, decreasing the means ventricular rate of 240 and 300 beats/min to 110 and 180 beats/min, respectively. In the third patient with atrial fibrillation, ajmaline increased refractoriness over the accessory pathway, decreasing the mean ventricular rate of 300 beats/min to 160 beats/min. In two patients ajmaline was continued as an intravenous maintenance infusion until sinus rhythm was restored. It is concluded that ajmaline is an effective drug for the acute management of atrial flutter or fibrillation with a fast ventricular response in patients with the Wolff-Parkinson-White syndrome.

A 22-year-old woman with chronic atrial tachycardia following Mustard's operation for transposition of the great arteries presented with dizziness and ventricular tachycardia documented with dynamic 24-h electrocardiogram. During intracardiac electrophysiology study, programmed ventricular extrastimulation induced polymorphous ventricular tachycardia (torsades de pointes). This was prevented by intravenous administration of procainamide. We postulate that polymorphous ventricular tachycardia is a possible cause of death in patients with Mustard's operation. Postoperative electrophysiologic study may define those patients at risk to develop this potentially fatal arrhythmia.

The incidence, in-hospital evolution, and long-term follow-up were studied in patients who developed acute deviation of the mean (frontal) QRS axis to the right during an acute myocardial infarction (AMI). Among 3,160 patients evaluated, 13 (0.41 percent) developed left posterior hemiblock (LPHB) and 57 (1.8 percent) developed an incomplete form of LPHB, the right axis deviation group (RAD). Patients in the LPHB group had a statistically significant higher incidence of in-hospital morbidity (69 percent incidence of congestive heart failure) and mortality (38.5 percent). Follow-up revealed a statistically significant higher incidence of cardiac symptomatology (angina pectoris and congestive heart failure) in the RAD group than in the control group, mainly in patients in whom RAD persisted for more than 24 hours. Patients developing LPHB during AMI constitute a high risk population with a high incidence of morbidity and mortality. Patients developing RAD constitute an intermediate group (between the LPHB and the control group) characterized by a high incidence of cardiac symptoms at the time of follow-up.

Electrocardiographic assessment of the R/Q wave ratio (lead 2) of patients with a first acute inferior wall myocardial infarction (IWMI) offers important indirect quantitative information regarding the severity and extent of the myocardial damage. Eighty-eight consecutive patients with IWMI were investigated by echocardiography and radionuclear angiography. After measuring the R/Q ratio in lead 2 during the ST-wave stabilized stage of myocardial infarction, patients were separated into three groups--group 1 with an R/Q ratio greater than 2; group 2 with an R/Q ratio between 1 to 2; and group 3 with an R/Q ratio less than 1. Utilizing the information thus gathered from the electrocardiogram (ECG) offers a simple and efficient method for early prognosis which merits further investigation.

Amiodrone is a benytfuran derivative with class III anti arrhythmic effects. It has also been reported to convert atrial fibrillation and flutter to sinus rhythm and is highly effective for the prevention of atrial fibrillation (especially of the paroxysmal form) with an overall efficacy in the range of 70–50%. This high degree of efficacy was obtained in a majority of patients who had already failed various conventional anti arrhythmic agents. The mechanism of arrhythmia termination by intravenous amiodarone is not clear. The slowing in ventricular response, which most probably improves cardiac hemodynamics, has an indirect salutary effect. Despite the fact that none of the published reports on intravenous amiodarone used a placebo control group, these studies suggest that intravenous amiodarone has an important role in the acute treatment of atrial fibrilation with fast ventricular response.

Ten patients are described with two discrete discontinulties in AV nodal conduction curves suggesting triple antegrade AV nodal pathways. This represents approximately 6% of patients seen in this laboratory with dual AV nodal pathways. Patients ranged in age from 18 to 63 (mean ± Sd, 48 ± 15 years). Six of the 10 patients had organic heart disease and four did not. The effect of cycle length on triple pathways could be analyzed in 8 of 10 patients who had atrial extrastimulus testing at two or more cycle lengths. Three of these eight patients had triple pathways at all tested cycle lengths. Four patients had triple pathways only at shorter cycle lengths. One patient had triple pathways only at longer cycle lengths. Intact retrograde conduction was demonstrated in seven of ten patients, all of whom had atrial echoes (two patients) or inducible supraventricular tachycardia (SVT) (five patients). Echoes or SVT were induced on the slow pathway is all seven patients, but also on the intermediate pathway in three. However, sustained SVT usually reflected antegrade slow and retrograde fast pathway conduction. In conclusion. triple AV nodal pathways may be demonstrated in occasional patients during atrial extrastimulus testing. Thereby, functional longitudinal dissociation of the AV node is not limited to two pathways.

Thirty-four cases of ventricular tachyarrhythmia characterized by polymorphy of the QRS complexes with changing R-R intervals and a heart rate of 150 to 300 beats/min, termed polymorphous ventricular tachycardia, are described. The factors involved in the appearance of this arrhythmia were the administration of antiarrhythmic drugs (quinidine 22 patients, procainamide 5 patients, ajmaline 1 patient), antianginal drugs (prenylamine [Synadrin] 4 patients) and antidepressant drugs (thioridazine 1 patient). Twenty-one patients were treated for premature ventricular complexes, three for chronic recurrent ventricular tachycardia, six for atrial flutter and fibrillation, three for anginal pain and one patient for mental depression. All patients except one had a drug-induced prolonged corrected Q-T interval before the appearance of polymorphous ventricular tachycardia. Most of the patients with this arrhythmia were considered to have severe myocardial disease. Lidocaine and electric cardioversion were administered to all patients, but were effective only in seven patients whose tachycardia occurred in short, single episodes. The most effective treatment (17 patients) was temporary ventricular pacing at rates ranging from 100 to 140 beats/min. Intravenous isoproterenol proved to be successful in another 10 cases. It is concluded that patients with severe myocardial involvement receiving antiarrhythmic drugs for premature ventricular complexes, especially the multiform variety, are at high risk for the development of polymorphous ventricular tachycardia.

Sixty-five patients with dual pathway atrioventricular (A-V) nodal reentrant paroxysmal tachycardia were studied. Of these 65 patients, 11 (17 percent) had a short P-R interval (0.12 second or less) and 3 (5 percent) had a short A-H interval (53 ms or less) during sinus rhythm, suggesting the Lown-Ganong-Levine syndrome. Frequency distribution analyses of P-R and A-H intervals in the 65 patients demonstrated continuous unimodal functions, suggesting a continuum of A-V nodal properties. Regression analyses of P-R and A-H (fast pathway) intervals versus cycle length of paroxysmal tachycardia revealed an r value of 0.11 and 0.10, respectively (not significant). The cycle length of paroxysmal tachycardia did not differ between the 11 patients with a short P-R interval (370 +/- 20 ms) and the 54 patients without a short P-R interval (382 +/- 11 ms). Regression analysis of the slow pathway A-H interval versus cycle length of paroxysmal tachycardia revealed an r value of 0.68 (p less than 0.001). The cycle length of dual pathway A-V nodal reentrant paroxysmal tachycardia is a function of the slow pathway A-H interval and not the P-R or A-H interval during sinus rhythm. Identification of short P-R intervals in patients with A-V nodal reentrant paroxysmal tachycardia has little significance.

A patient with clinically silent mitral valve prolapse experienced an episode of out-of-hospital cardiac arrest due to ventricular fibrillation. This arrhythmia was easily replicated in the electrophysiology laboratory and despite treatment with amiodarone alone and amiodarone in combination with propranolol. Amiodarone in combination with quinidine prevented the induction of ventricular fibrillation and proved effective during a 3-year follow-up period. Even though a clear-cut relationship between the arrhythmias and mitral valve prolapse cannot be established, this case suggests that sudden death can occur in patients with mitral valve prolapse but without the known risk factors for the development of sudden death.

The pathologic substrate for sudden death in the middle-aged or elderly adult is usually ischemic heart disease. In contrast, few data are available regarding the pathology of sudden death in teenagers. This report describes three teenagers without clinically suspected heart disease dying suddenly. Patient 1 (age 15, male) was known to have right ventricular premature ventricular beats. Postmortem examination revealed marked premature aging, sclerosis of the cardiac skeleton extending to the right side of the summit with fibrosis of the left and right bundle branches. Patient 2 (age 17, male) was a trained athlete who died during football scrimmage. Autopsy revealed moderate mitral valve prolapse and marked premature aging, sclerosis of the left side of the cardiac skeleton, which extended to the right ventricular side, and secondary involvement of the trifascicular conduction system with mononuclear cell infiltration. Patient 3 (age 19, female) died suddenly at home. Autopsy revealed mitral valve prolapse, thrombosis of the sinoatrial (SA) node artery, and premature aging, sclerosis of the left side of the cardiac skeleton, with involvement of the ventricular septum more on the right ventricular side and involvement of the atrioventricular bundle and trifascicular conduction system. In conclusion, unexpected deaths in three teenagers occurred with demonstrable pathologic findings in the heart. Two of the three patients had mitral valve prolapse, one of whom also had thrombosis or embolism of the sinoatrial node artery. All three had sclerosis of not only the left side but also the right side of the ventricular septum with involvement of the conduction system. The anatomic substrate demonstrated in these three patients could relate to lethal bradyarrhythmia or tachyarrhythmia, or both.

We used programmed ventricular stimulation to test intravenous bretylium tosylate in 10 consecutive patients with inducible sustained ventricular tachycardia (usually refractory to type I antiarrhythmic agents). These 10 patients had previously documented sustained ventricular tachycardia and/or ventricular fibrillation complicating stable heart disease. Following control inductions of sustained ventricular tachycardia, bretylium 10 mg/kg was infused over 30 minutes. Thirty minutes after this infusion, sustained ventricular tachycardia could be induced in 9 of the 10 patients (one of these nine patients also had bretylium-potentiated spontaneous ventricular tachycardia). Tachycardia induced in the nine patients after bretylium was similar to control tachycardia with respect to morphology and cycle length (333 +/- 16 msec after bretylium versus 330 +/- 16 msec during control). However, five of the nine patients tolerated induced tachycardia less well after bretylium (exacerbated hypotension). In one patient, ventricular tachycardia could not be induced after intravenous bretylium.

Recent studies indicate that oral administration of mexiletine is useful in the therapy of recurrent ventricular tachycardia (VT). To further define the clinical usefulness of this drug, mexiletine was administered to 13 men and 4 women with a mean age ± standard deviation of 62 ± 8 years who had drug-refractory paroxysmal sustained VT associated with chronic ischemic heart disease in 14, valvular heart disease in 1, and primary myocardial disease in 1. One patient had no heart disease. All 17 patients had inducible sustained VT during the control electrophysiologic study and during serial electrophysiologic study on conventional drugs. Eleven patients tolerated a mean maximal daily dose of 1,073 ± 149 mg of mexiletine and underwent programmed ventricular stimulation; sustained VT was inducible in 10 patients and nonsustained VT in 1. in 10 patients with inducible sustained VT on mexiletine, the VT cycle length was longer during mexiletine therapy than during control (mean ± standard error of the mean, 342 ± 22 versus 268 ± 14 ms, respectively) (p

Five patients with acute myocardial infarction had ventricular fibrillation as a complication of indicated temporary pacing. All five patients had evidence of right ventricular infarction (three patients with postmortem confirmation). The presence of right ventricular infarction seems to be a contributing mechanism involved in the induction of ventricular fibrillation during temporary pacing for bradyarrhythmia complicating acute myocardial infarction.

Thirty-one (3.5 percent) of 887 studied patients had retrograde dual atrioventricular (A-V) nodal pathways, as manifested by discontinuous retrograde A-V nodal conduction curves (29 patients) or by two sets of ventriculoatrial (V-A) conduction intervals at the same paced cycle length (2 patients). All patients had A-V nodal reentrant ventricular echoes of the unusual variety induced with ventricular stimulation (25 patients had single, 2 patients had double and 4 patients had more than three ventricular echoes). The weak link of the reentrant circuit was always the retrograde slow pathway. Eleven of the 31 patients also had anterograde dual A-V nodal pathways (bidirectional dual pathways). Eight patients (26 percent) had spontaneous as well as inducible A-V nodal reentrant paroxysmal supraventricular tachycardia (of the unusual type in three and the usual type in five). In addition, three patients (10 percent) had only inducible supraventricular tachycardia (two of the unusual and one of the usual type). Retrograde dual A-V nodal pathways are uncommon. They are associated with the finding of at least single A-V nodal reentrant ventricular echoes (all patients), anterograde dual pathways (one third of patients) and A-V nodal reentrant paroxysmal supraventricular tachycardia of the usual or unusual variety (one third of patients).

We report on twelve patients with alternating Wenckebach periods (AWP) occurring during an acute inferior myocardial infarction (AIMI). There were nine males and three females, with a mean age of 61 years (range, 43 to 75). AWP appeared during the first 48 hours of the AIMI in 10 patients and on the fourth day of hospitalization in two patients. AWP occurred spontaneously in nine patients and following the administration of atropine in the remaining three patients. Mean systolic blood pressure significantly decreased during AWP as compared to the period preceding or following the bradyarrhythmia (93 +/- 42 mmHg vs 123 +/- 37 mmHg, p less than 0.02). Killip functional class was significantly higher during AWP as compared to the period preceding or following the bradyarrhythmia (2.1 +/- 1.2 vs 1.5 +/- 0.8, p less than 0.02). Pacemaker therapy was initiated prophylactically in two patients, because of syncope in six, because of hemodynamic deterioration in two, and for syncope and hemodynamic deterioration in two. Three patients died in cardiogenic shock despite pacemaker therapy. No evidence of right ventricular infarction was seen in the patients. Atropine administration during AWP significantly increased the sinus rate and significantly decreased the ventricular rates and the systolic blood pressure. In addition, three patients developed long bouts of paroxysmal AV block. Isoproterenol administration improved AV conduction in one patient, caused no change in two patients and induced non-sustained ventricular tachycardia in three patients. In conclusion, AWP occurring during AIMI is a symptomatic bradyarrhythmia associated with hemodynamic deterioration.(ABSTRACT TRUNCATED AT 250 WORDS)

Anterograde and retrograde fast pathway properties were analyzed in 160 patients with anterograde dual atrioventricular (A-V) nodal pathways, with or without A-V nodal reentrant tachycardia. A-H intervals (reflecting anterograde fast pathway conduction) ranged from 46 to 234 ms (mean ± standard deviation 91 ± 30). The longest atrial paced cycle lengths at which block occurred in the anterograde fast pathway ranged from 231 to 857 ms (435 ± 112). Regression analysis of these cycle lengths versus A-H intervals revealed a correlation coefficient (r) value of 0.41 (p < 0.01). Retrograde fast pathway conduction was present (at a ventricular paced cycle length slightly shorter than sinus rhythm) in 84 of 125 patients: 15 of 16 with an A-H interval of less than 60 ms, 44 of 58 with an interval of 60 to 90 ms, 20 of 41 with an interval of 91 to 130 ms and 5 of 10 with an A-H Interval of more than 130 ms (p < 0.01). Retrograde fast pathway conduction was intact at a cycle length of 375 ms in 41 of 124 patients: 11 of 16 with an A-H interval of less than 60 ms, 22 of 57 with an interval of 60 to 90 ms, 7 of 41 with an interval of 91 to 130 ms and 1 of 10 with an A-H interval of more than 130 ms (p

Summary The purpose of this study was to investigate the correlation between the origin of premature ventricular contractions (PVC's) appearing during acute myocardial infarction (AMI) and the location of the infarction as determined by the electrocardiogram (ECG). The PVCs were termed acute or chronic according to the time of their appearance. The origin of the PVCs, located at the left ventricle (anterior or posterior wall) or the right ventricle, was determined by ECG criteria. In 82 out of 91 cases of acute PVCs (90.2%), the PVCs presented an origin similar to the AMI location (p≤.001). In 23 cases with chronic PVCs, this correlation was not observed. In all 13 cases of primary ventricular fibrillation in which the PVCs origin was determined prior to the event, the PVCs were acute coming from the same location as the AMI. The effectiveness of lidocaine treatment on PVCs was also determined. Out of 44 cases with acute PVCs, 38 responded to lidocaine, with 37 of them showing an origin similar to the AMI location (p≤.001); 5 non-responders showed an origin different from the AMI location. No response was observed in 20 out of 23 cases with chronic PVCs. These results show a good correlation between the origin of the acute PVCs and the location of the AMI. It is concluded that the determination of the origin of PVCs appearing during AMI provides further clinical information as to the location of AMI, its prognosis in relation to serious arrhythmias and the resistance of certain PVCs to lidocaine treatment.

Two distinct electrocardiographic patterns of ventricular fibrillation (VF) complicating acute myocardial infarction (AMI) were observed in 34 patients during the first 24 hours from initial symptoms. Type 1 (seven patients) was characterized by fast disorganized ventricular activity, small voltage, and no clear identifiable QRS complexes (fine VF). Type 2 (27 patients) was defined as multiform QRS configuration (>300/min) with marked changes in the amplitude (polymorphous VF). Type 1 rhythm was seen mostly during the hyperacute ischemic phase, probably associated with total coronary vessel occlusion; type 2 was observed when Q waves were already present in the electrocardiogram.

We have reviewed all available noninvasive diagnostic studies for the evaluation of syncope of suspected cardiovascular origin. This eight-step diagnostic approach covers the majority of available syncopal etiologies. In patients evaluated for syncope, we believe a complete noninvasive evaluation should be performed (if clinically indicated) before performing invasive electrophysiologic studies.

Eighteen patients with a first AMI, who during the acute ischemic phase did not develop ST segment elevation, but only positive or peaked T waves, are described. Patients who do not develop ST segment elevation during evolving anterior AMI represent a subgroup with a high probability of total obstruction of the LAD artery with retrograde filling via collateral vessels and a small degree of left ventricular dysfunction. We assume that during the period of total obstruction there was preexisting adequate collateral circulation in order to prevent transmural ischemia, which explains the absence of ST segment elevation.

Four cases of longitudinal dissociation of the atrioventricular node, with dual pathways developing during the acute phase of an inferior wall myocardial infarction (three cases) or during acute ischemia (one case), are presented. In all four cases, two grossly different P-R intervals were recorded, and in two cases, studies of the His bundle confirmed the location of the dissociation within the atrioventricular node. In one case, premature atrial depolarization caused a bidirectional shifting of P-R intervals, while in the remaining three cases, premature ventricular depolarization (spontaneous or pacemaker-induced) was responsible for this phenomenon. In all cases, evidence of longitudinal dissociation of the atrioventricular node appeared during the acute phase of the infarction or ischemia, and in all of them the phenomenon was transient. This favors the assumption that this phenomenon is of a functional nature, most probably related to the ischemic lesion of the atrioventricular node.

We have retrospectively examined data from 41 patients studied in our laboratory for symptomatic ventricular arrhythmia in order to test whether any clinical or electrophysiologic variables could be identified which would predict the patient's response to class I antiarrhythmic drugs. All patients had (1) clinically documented paroxysmal sustained ventricular tachycardia (VT) or ventricular fibrillation remote from acute myocardial infarction, (2) inducible sustained VT during control electrophysiologic study (EPS), and (3) EPS after one or more of the following class I antiarrhythmic drugs: intravenous procainamide (36 patients), oral quinidine (30 patients), and oral disopyramide (36 patients). Initially, patients were divided into those who had noninducible or only nonsustained VT after any of the tested drugs (responders), and those who continued to have inducible sustained VT after all tested drugs (nonresponders). A logistic regression technique demonstrated no independent contribution to drug response by any of the following variables: sex, arteriosclerotic heart disease, cardiomegaly, age, time since the initial episode of VT, and cycle length of VT during control study. The number of antiarrhythmic drugs the patient had received prior to study was found to be a significant independent contributor ( p

There is an apparent correlation between the severity and duration of skeletal muscle involvement, cardiac manifestations and the extent of conduction system disease in polymyositis. Cardiac involvement during the course of polymyositis has been recognized as one of the typical features of skeletal muscle myositis. We report a patient with polymyositis in whom bifascicular block, prolonged P-R interval and congestive heart failure appeared three years before any clinical or laboratory evidence of active skeletal muscle myositis. To the best of our knowledge, this is the first report of polymyositis where cardiac manifestations preceded those of skeletal muscle myositis.

Of a population of 400 patients treated with amiodarone, 97 underwent thyroid function evaluation. Of these, 20 patients proved to be thyrotoxic and 16 hypothyroid. In thyrotoxic patients, symptoms developed 2 to 36 months after starting treatment with amiodarone, the most specific laboratory finding being a high total T3 (TT3). No antithyroid treatment proved useful. Thyroid function returned to normal 3 to 7 months after stopping amiodarone therapy. In the hypothyrold group, a high thyroid-stimulating hormone was the most specific laboratory finding. These patients were treated with substitute therapy with or without withdrawal of amiodarone. The iodine content of the thyroid gland in part of this population taking amiodarone was measured by in vivo x-ray fluorescence. Patients in whom thyrotoxicosis developed showed especially high Iodine contents. During treatment with amiodarone, patients at high risk of thyrotoxocosis were recognized by increasing TT3 values and higher iodine thyroid levels. A reduction in maintenance dose should be considered in this specific population.

Of 139 consecutive patients with a first inferior acute myocardial infarction, 26 (19%) had advanced atrioventricular (AV) block and 113 (81%) did not. All were evaluated by 2-dimensional echocardiography (2-D echo) and radionuclide angiography. Patients with advanced AV block had lower radionuclide left ventricular (LV) ejection fraction (51 +/- 10 vs 58 +/- 11%, p less than 0.01), higher LV wall motion score on 2-D echo (5.6 +/- 2.6 vs 3.1 +/- 2.7, p less than 0.001), lower radionuclide right ventricular (RV) ejection fraction (32 +/- 15 vs 39 +/- 16%, p less than 0.001) and higher RV wall motion score on 2-D echo (3.4 +/- 1.7 vs 1.5 +/- 2, p less than 0.002) than did patients without AV block. The incidence rate of RV dysfunction was higher in patients with advanced AV block (78 vs 40%, p less than 0.02), and the mortality rate was also higher (although not significantly) in patients with advanced AV block (15 vs 6%). In conclusion, patients with inferior acute myocardial infarction and advanced AV block have larger infarct sizes (as seen on radionuclide angiography and 2-D echo) and lower RV and LV function than patients without AV block. This finding may explain the higher mortality rate observed in this group.

Electrophysiological studies in a patient with paroxysmal supraventricular tachycardia disclosed anterograde dual atrioventricular nodal pathways, and a concealed left-sided anomalous atrioventricular pathway which was used as the retrograde limb of two circus movement tachycardias. Tachycardia No.1, reflecting anterograde fast pathway conduction, was characterised by functional left bundle-branch block and a stable cycle length of 330 ms. Paroxysmal loss of bundle-branch block resulted in tachycardia No.2, which reflected anterograde slow pathway conduction, and was characterised by narrow QRS and a stable cycle length of 355 ms. Tachycardia No.2 had a longer cycle length than tachycardia No.1 because the increment in AH interval (slow pathway instead of fast pathway condition) more than compensated for the decrement in ventriculoatrial interval (narrow QRS instead of bundle-branch block).

We observed sinoatrial block due to chronic amiodarone administration in a 5-year-old boy with primary cardiomyopathy, Wolff-Parkinson-White syndrome and supraventricular tachycardia. Reduction in the dosage of amiodarone resulted in the disappearance of the sinoatrial block and the persistence of asymptomatic sinus bradycardia.

A 27-year-old trained athlete with recurrent syncope of suspected vaso-vagal origin was evaluated. A 60 degrees head-up tilt table test reproducibly triggered the patient's spontaneous symptoms and allowed the investigation of different modalities of therapy (medical and pacing) in preventing syncopal episodes. The head-up tilt table test may be a useful tool in the evaluation of syncope of vaso-vagal origin, helping to determine the initial precipitating vagal event and the effect of therapy.

A 52-year-old man had longstanding hypertension and asymemtric septal hypertrophy and normal major coronary arteries. His acute anterior wall ischemia gave rise to transient Q waves and septoapical dyskinesia, complicated by mural thrombus formation. Follow-up revealed a gradual and complete recovery of echocardiographic left ventricular function with total disappearance of mural thrombi and of electrocardiographic Q waves. Acute myocardial ischemia can cause prolonged electrical and mechanical stunning which can lead to mural thrombus formation.

In a patient with the sick sinus syndrome and near syncope a prolonged sinus pause was documented and reproduced thereafter during sustained deep inspiration. Administration of intravenous atropine abolished this phenomenon, most probably indicating a hyperresponsiveness of the sinus node and AV junction to a vagotonic reflex.

Two apparently healthy patients had recurrent syncope with documented paroxysmal AV block. In both patients the site of AV block was demonstrated to be in the AV node. Coronary angiography (in both patients) and sustained deep inspiration (one patient) reproducibly initiated episodes of paroxysmal AV nodal block (identical to spontaneous episodes). Atropine abolished further attempts of AV block induction. Vagal hyperresponsiveness was limited to the AV node, since the interventions provoking paroxysmal AV nodal block produced only appropriate sinus slowing. This syndrome reflects hyperresponsiveness of the AV node to vagotonic reflexes, and exists as a clinically significant entity producing recurrent syncope.

In this study, the safety and efficacy of long-term therapy with disopyramide phosphate were evaluated in 40 patients with documented, recurrent, symptomatic tachyarrhythmias. Twenty-one (53%) of the patients had organic heart disease, and nine of these patients had compensated congestive heart failure. The tachyarrhythmias which were treated were paroxysmal supraventricular tachycardia (21 patients), paroxysmal atrial fibrillation (six patients), and paroxysmal ventricular tachycardia (13 patients). In each patient there was evidence, from continuous ECG monitoring or electrophysiologic testing, that disopyramide would be effective therapy, and each patient was able to tolerate disopyramide (no side effects or tolerable side effects) during an initial trial period of 1 to 2 weeks. Dosages of disopyramide were 400 to 1600 mg/day (994 +/- 320 mm/day). During long-term therapy, side effects were reported by 28 (70%) of the patients. The side effects were usually anticholinergic, and were usually a continuation of side effects noted during the initial trial period. None of the patients had idiosyncratic reactions to disopyramide. Most of the patients found side effects to be tolerable; however, in seven patients it was necessary to discontinue disopyramide after 1 to 8 (6 +/- 3) months. Actuarial incidence of intolerable side effects was 21 +/- 7% at 12 months. Nine (22%) of the 40 patients had symptomatic recurrences of tachyarrhythmia after 3 to 32 (15 +/- 9) months of therapy. Actuarial incidence of drug ineffectiveness was 32 +/- 10% at 24 months. Disopyramide was both effective and tolerated in 24 (60%) of the patients, who were followed for 2 to 64 (23 +/- 16) months.(ABSTRACT TRUNCATED AT 250 WORDS)

It is the thesis of this presentation, that electrophysiologic evaluation of proposed antiarrhythmic agents is mandatory. The purposes of this evaluation are as follows: 1) Electrophysiologic study provides part of the pharmacologic profile of an antiarrhythmic drug, which is generally biologically important information necessary about a drug and its properties. 2) Electrophysiologic study may allow prediction of drug toxicity, in regard to the cardiac conduction system. 3) Data arrived from electrophysiologic evaluation, may in part predict sites of action and possible mechanisms of effectiveness of antiarrhythmic drugs. 4) Electrophysiologic study may allow direct demonstration of effectiveness of an antiarrhythmic agent (for example, the demonstration that an antiarrhythmic drug prevents induction of paroxysmal supraventricular tachycardia in a patient with this arrhythmia).

The effect of intravenous (IV) amiodarone (300 mg) on heart rate was investigated in 22 patients with acute myocardial infarction (18) or ischemia (4) and sinus tachycardia. There were 11 men and 11 women (age range, 48 to 83 years; mean, 63.5). Amiodarone IV slowed the mean heart rate from 109 +/- 14 beats/min to 94 +/- 15 beats/min (p less than 0.0005). There was a linear correlation between the initial heart rate (preamiodarone) and the final heart rate (postamiodarone), (r = 0.6930, p less than 0.0005). Most of the patients with initial heart rates higher than the mean maintained relatively high heart rates (above the mean), while most patients with lower initial heart rates showed low heart rates (below the mean) after amiodarone administration. Patients in Killip class 1 showed a significant reduction in heart rate after receiving amiodarone, from a mean of 105 +/- 10 to 88 +/- 11 beats/min (p less than 0.01). Patients in Killip class 2 also had reduced heart rates (118 +/- 14 to 81 +/- 39 beats/min), but these changes were not statistically significant. Of the three patients in Killip class 3 to 4, the heart rate slowed by 10 beats/min in one, while in the remaining two no changes were observed. There were no significant side effects from the administration of amiodarone.

Nine patients are presented who had polymorphous ventricular tachycardia (PMVT) occurring during atrioventricular (AV) block. There were five men and four women with a mean age of 80 +/- 9 years. Five patients had organic heart disease and the remaining four had primary conduction disease (bundle branch block). AV block was complete in four patients (2:1 in three, and paroxysmal in two). The mean ventricular cycle length (of the AV block rhythm) was 1567 +/- 203 ms. The mean QT interval was 0.64 +/- 0.09 s and the mean QTc was 0.51 +/- 0.06 s. When compared to a similar control group with AV block but without PMVT, the ventricular cycle length was similar but the QT and QTc were significantly longer. PMVT was usually of short duration (eight beats to 12 s) and in seven of these nine patients, frequent premature ventricular beats (PVBs) were recorded at various times from the occurrence of PMVT. This is in contrast to the control patients in whom PVBs were detected in one patient only. In conclusion, patients with AV block who develop PMVT usually have longer QT intervals and have detectable PVBs on routine ECGs, unlike similar patients with AV block but without PMVT. In a patient with AV block, a QT interval above 0.60 s and PVBs on the ECG seem to indicate an increased risk for the development of PMVT.

Thirty-two consecutive patients who initially had horizontal or downward-sloping ST segment depression confined to the precordial leads were studied. Patients were divided into two groups: group A included 21 patients with horizontal or downward-sloping ST depression with peaked positive T waves, and group B comprised 11 patients with peaked negative T waves and downward or horizontal ST depression. The incidence of acute myocardial infarction (AMI) was similar (group A 38.1% vs group B 36.4%; p greater than 0.05). In-hospital mortality was much more significant in group B (p = 0.03). Coronary arteriography was performed in 31 patients. Of the 10 patients in group B who were catheterized, seven (70%) had left main occlusion. Of the 21 patients in group A, none had a significant left main lesion (p = 0.001), although eight (38.1%) had single-vessel disease (p = 0.05). Thus the ECG pattern of horizontal or downward-sloping ST depression passing into a peaked negative T wave identifies a subgroup of high-risk patients in whom the prognosis is poor once AMI occurs. Early catheterization is recommended when this ischemic pattern is apparent on the ECG.

We report on a patient with myotonic muscular dystrophy in whom mitral valve prolapse associated with prolonged PR interval and left anterior hemiblock was documented 3 years before any clinical evidence of myotonia, muscle weakness or wasting. One year after diagnosis had been established, he developed atrial flutter with 1:1 atrioventricular conduction, an arrhythmia that in addition to complete heart block and ventricular arrhythmias may account for the occurrence of syncope and sudden death in this group of patients.

Three patients presented to the emergency room with atrial fibrillation and fast ventricular response with wide preexcited QRS complexes (Wolff-Parkinson-White syndrome). All three patients received intravenous verapamil (5-10 mg). The first patient developed ventricular fibrillation requiring several defibrillations; the second patient developed severe hemodynamic deterioration requiring urgent cardioversion; in the third patient a marked increment in the ventricular response was noted, however, there was no hemodynamic impairment. Verapamil may cause detrimental results when given to patients with the Wolff-Parkinson-White syndrome and atrial fibrillation. Its administration should therefore be considered as an absolute contraindication in these patients.

Thirteen patients with acute myocardial infarction with multiform accelerated idioventricular rhythm (AIVR) occurring during the first 12 hours of monitoring in the coronary care unit are described. This arrhythmia, similar to the more common uniform AIVR, was intermittent, did not cause hemodynamic compromise, and was not related to more serious ventricular arrhythmias. There was no correlation between the bundle branch block pattern of the multiform AIVR and the electrocardiographic location of the myocardial infarction, but there was a perfect correlation between the frontal plane electrical axis of the multiform AIVR and the electrocardiographic location of the myocardial infarction. The presence of fusion beats between the different forms of AIVR suggests multifocality rather than multiformity. Intravenous verapamil (3 to 5 mg bolus) was administered to 6 patients with multiform AIVR in whom the arrhythmias were persistent enough to allow the evaluation of the effect of verapamil on the arrhythmia. Verapamil caused no change in the rate of AIVR in 1 patient, but in a second patient it decreased the rate by 20 beats/min. In 4 patients, verapamil abolished the arrhythmia: in 2 patients carotid sinus pressure (induced sinus slowing) allowed the emergence of the AIVR at a lower rate, and in the remaining 2 patients the arrhythmia was not observed.

The presence of accelerated idioventricular rhythm (AIVR) in its multiform variant in two patients with acute myocardial infarction is described. No difference was noted in the clinical evolution of this arrhythmia and the more commonly observed unifocal AIVR.

Serial section of the conduction system and both atrioventricular (A-V) rims was performed in three patients who died with known preexcitatlon and idiopathic myocardial hypertrophy with fibroelastosis proved at autopsy. All three patients had type B preexcitation and a leftward and inferior 20 ms vector, suggesting a right free wall anomalous pathway. Patient 1 had no arrhythmia, Patient 2 died suddenly and Patient 3 had recurrent paroxysmal supraventricular tachycardia. Electrophysiologic study in Patients 1 and 3 revealed a bidirectionally conducting anomalous pathway with short refractoriness. Patient 1 had no, and Patient 3 had easily inducible A-V reentrant paroxysmal supraventricular tachycardia. Electrophysiologic study in Patient 3 revealed an anterior right free wall or anteroseptal anomalous pathway, manifested by the shortest stimulus-delta interval with pacing of the right anterior atrium. No electrophysiologic studies were performed in Patient 2. In Patient 1 serial section revealed a large right free wall anomalous pathway with myocardial disarray on the ventricular side of the anomalous pathway. In Patient 2, there were two small anomalous pathways in the right free wall. In Patient 3, no anomalous pathway was found in the right free wall; however, the right atrium was connected to the infundibular septum anterior to the membranous septum. This anomalous pathway had continuity with an anterior A-V nodal-like structure. In summary, (1) all three patients anatomically had a right-sided anomalous pathway (as predicted on electrocardlography in all three and electrophyBiologically in Patients 1 and 3). (2) In Patient 2, myocardial disarray in the Kent bundle may have prevented paroxysmal supraventricular tachycardia. (3) In Patient 3, histologic study revealed an anterior septal anomalous pathway on the right side with an anterior A-V nodal-like structure. Because the anomalous pathway did not show any A-V nodal properties, the significance of this structure is not clear. (4) The relation of the right-sided anomalous pathway to the left-sided fibroelastosis is not known.

Thirty cases in which transient left anterior hemiblock (LAHB) obscured the diagnosis of right bundle branch block (RBBB) appearing during the first days of an acute myocardial infarction (AMI) are presented. Twenty-eight of the patients with AMI had a clear septal wall involvement, while the remaining two had an anterolateral and lateral wall AMI, respectively. These intraventricular conduction defects developed 2-120 hours (mean 64.9 +/- 26 hours) after the acute event, and persisted for 24 hours to 7 days (mean 63.1 +/- 35 hours). The ECG was characterized by a pure LAHB with wide QRS complexes and the presence of RBBB was shown by recording high V1 and right-sided chest leads. The vectorcardiogram was also useful in several cases. The clinical course of this type of bifascicular block was transient and benign, with an in-hospital mortality of 6.7%. No patient developed trifascicular or complete atrioventricular block and, therefore, we conclude that prophylactic installation of a temporary pacemaker is not indicated in this type of bifascicular block. The possible role of extracellular potassium released during acute myocardial necrosis in the pathophysiological mechanism of these blocks is discussed.

A patient in whom Wenckebach phenomenon was observed to coexist in the three distal branches of the specialized ventricular conduction system, with an intermittent trifascicular block producing a second degree A-V block, is described. Surface electrocardiogram demonstrated the presence of this phenomenon in the right bundle branch (RBB) and the anterior division of the left bundle branch (LBB). Evidence of the presence of Wenckebach phenomenon in the remaining fascicle was provided by His bundle recording.

Surgical cure of right ventricular tachycardia (RVT) has been recently described in patients with "arrhythmogenic right ventricular dysplasia," a disease characterized by abnormal electrical activation of the right ventricle and localized or generalized angiographic right ventricular (RV) wall motion abnormalities (WMA). In search of a selective RV cardiomyopathy complicated by chronic recurrent RVT, 38 consecutive patients (mean age 30.5 +/- 12 years) with RVT and no ischemic heart disease were studied clinically, noninvasively, and by cardiac catheterization including left and right ventriculography. RV volumes were as follow: end-systolic volume ranged from 23 to 103 (mean +/- SD, 45.8 +/- 20) cc/m2 and was abnormal in 14 patients (37%); end-diastolic volume ranged from 57 to 138 (90.5 +/- 26) cc/m2 and was abnormal in 15 patients (39%); ejection fraction (EF) ranged from 0.18 to 0.64 and was decreased in five patients (13%). Seventeen patients (45%) had abnormal RV volume, EF, and/or pressures (RVD), five (13%) of whom had abnormal LV volume, EF, and/or pressures (LVD), and 12 (32%) patients with RVD had no LVD. Twenty-one patients (55%) had no RVD, two of whom had LVD. Only two of the 17 patients had RV regional WMA, one with and one without LVD. Most patients with LVD five of seven (71%) also had RVD while 12 of 31 patients (39%) with no LVD had RVD. In conclusion, less than one half of patients with RVT had selective RV cardiomyopathy and more than one half of patients with RVT had normal RV hemodynamics and angiography.

Of 760 consecutive cases with anterior acute myocardial infarction (AMI), 55 developed acute bundle-branch block (BBB), fascicular block, or high-degree atrioventricular block during the hyperacute ECG stage of AMI. According to the direction of the ST segment during the acute ischemic episode, patients were divided into two groups. Group A consisted of 32 patients who developed BBB during ST-segment elevation, positive T wave, and absent or minimal Q wave. Group B consisted of 23 patients who developed BBB during ST-segment depression and evolved into anterior AMI. Group A was characterized by a higher incidence of right BBB and left anterior hemiblock [91% vs. 26% and 56% vs. 13%, respectively (p

The coronary angiographic findings and the in-hospital prognosis of unstable angina pectoris presenting with T wave positivization only (group A: 32 patients) or with additional ST segment elevation (group B: 27 patients) were evaluated. Clinical data and haemodynamic parameters before and during unstable anginal events showed no significant statistical difference, indicating blood flow reduction as the probable mechanism of ischaemia in both groups. The incidence of hospital myocardial infarction was higher in patients of group B (group A 6.24% vs group B 31%; P less than 0.02). Death due to haemodynamic deterioration occurred in 2 patients of group B. This finding can be partially explained by more developed collateral circulation in patients with T wave changes only (25 of 65 obstructed arteries in group A vs 8 out of 48 obstructed arteries in group B; P less than 0.05). Left ventricular function was comparable between the two groups. The extent, severity and location of coronary artery disease was similar in the groups. Thus, the electrocardiographic pattern of T wave changes only, in patients with unstable angina pectoris (group A) define a subgroup who have a favourable prognosis and development similar to patients with chronic stable angina pectoris. Urgent measures may be delayed in this group.