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Seventy-two patients with trifasicular disease were followed for an average of 40 months following permanent pacemaker insertion. The indications for pacemaker insertion were either electrocardiographic evidence of complete heart block with a wide QRS escape complex or a pattern of bifasicular block with either periods of Mobitz type II atrioventricular (A-V) block or a documented history of syncope. The patients were then divided into three groups depending on subsequent change in A-V conduction. There were 31 (43%) patients with no change in A-V conduction, 17 (24%) with increasing A-V block, and 24 (33%) with decreasing A-V block. The characteristics of these three groups, including age and sex distribution, were compared and found to be similar. The incidence of previous transmural myocardial infarction as determined by electrocardiographic criteria was higher in the group with decreasing block. Survival curves showed a significantly decreased probablity of surviving for those with decreasing block compared to both those with increasing block and those with no charge in conduction (P less than 0.03). We conclude that the probability of long-term survival was less in the group with decreasing block. This finding may be related to the greater prevalence of coronary heart disease in the patients.

One hundred and nineteen episodes of accelerated ventricular rhythm (less than 125/min) were noted in 37 patinets with acute myocardial infarction during a 1 year period. The incidence was 12.7 per cent. Twenty-seven episodes of fast ventricular tachycardia (less than 125/min) were noted in 16 of these patients. Eighteen patients had anterior myocardial infarction and 19 inferior myocardial infarction. The mechanism of onset of accelerated ventricular rhythm was classified as escape in 65 episodes. Ventricular premature beats were noted close to episodes of accelerated ventricular rhythm in 31 patients and fast ventricular tachycardia in 14 patients. The morphology of accelerated ventricular rhythm was similar to the ventricular premature beats in 27 patients and similar to the fast ventricular tachycardia in 12. In 11 patinets the morphology of ventricular premature beats, accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm is a relatively common complication of both anterior and inferior myocardial infarction. The high incidence of concomitant fast ventricular tachycardia, the frequency of ventricular premature beats with similar morphology and coupling time, and the instances of two arrhythmias having common rate multiples, suggest that at least in some instances accelerated ventricular rhythm may represent an ectopic focus with exit block.

Nadolol, a long-acting beta-adrenergic-blocking agent, was evaluated in 20 patients with chronic atrial fibrillation by means of a randomized, double-blind, crossover study. Patients were required either to demonstrate resting heart rates in excess of 80 bpm or to show a rate of 120 bpm or an increment of greater than 50 bpm during mild treadmill exercise provocation (3 minutes, 1.75 mph, 10% grade). With placebo the group averaged a heart rate of 92 +/- 19 bpm, determined by 24 hours of ambulatory ECG recordings; this rate was significantly reduced to 73 +/- 16 bpm (p less than 0.001) with nadolol (mean dosage, 87 +/- 43 mg/day). During standardized exercise testing, heart rates increased to 153 +/- 26 bpm with placebo and to 111 +/- 24 bpm with nadolol (p less than 0.001), representing 65% and 52% increments, respectively. Digoxin blood levels averaged 0.8 +/- 0.5 ng/ml with placebo and were similar with nadolol (0.9 +/- 0.4; p = NS). Total exercise time on a modified Bruce treadmill protocol was 466 +/- 143 seconds with placebo and was significantly decreased by nadolol (380 +/- 143; p less than 0.01). During initial dose titration with nadolol, one patient was dropped from study for intolerable fatigue and one for worsened claudication. No patients were dropped from the double-blind treatment periods, although two patients receiving nadolol and one patient receiving placebo complained of moderate fatigue. We conclude that nadolol is a safe and effective agent for the control of spontaneous and exercise-provoked heart rates in patients with chronic atrial fibrillation who were already receiving digoxin treatment.

Heart block was noted in 60 (35 complete and 25 second-degree) of 410 patients with acute inferior wall myocardial infarction. This group with heart block was compared to a control group of 30 patients with acute inferior wall infarction without heart block. The incidences of prior myocardial infarction and hypertension, in addition to the highest level of serum creatine phosphokinase and a maximum degree of ST-segment elevation in the inferior leads, were all greater in patients with heart block, as compared to the controls. The incidences of various complications, including dizziness and syncope, transient hypotension, cardiogenic shock, and congestive heart failure, were also higher in the group with heart block, while sinus nodal distrubances and atrial arrhythmias occurred with equal frequency. The mortality in those with heart block was 28 percent compared to 13 percent for the control. It is concluded that patients with heart block complicating acute inferior myocardial infarction have a greater amount of myocardial necrosis, a higher incidence of complications, and a higher mortality. Insertion of a temporary pacemaker should be considered when specific indications are present and not routinely.

The case presented had an electrocardiographic pattern of complete right bundle branch block with alternating periods of left anterior hemiblock and left posterior hemiblock. During one of the periods of alternating hemiblock, an His bundle electrogram was recorded and the His Purkinje (H-V interval) conduction time was within normal limits. In a second episode of alternating hemoblock, periods of Mobitz type II second-degree A-V block were noted. It is postulated that this case provides clinical evidence that incomplete block of a fascicle may occur in spite of an electrocardiographic pattern of complete fascicular block. It is thought that the periods of alternating hemiblock result from a changing relationship between conduction velocity and refractory period.

A post hospital follow-up system based on predetermined antiarrhythmic strategies and telephone transmitters used to record ECGs was helpful in managing post hospital course and improved survival in patients with a history of out-of-hospital sudden death. All patients underwent therapy guided by serial electrophysiologic testing. Of the 47 patients, 19 used the telephone transmitter system and 28 did not. During follow-up, residual symptomatic and silent ventricular arrhythmia was documented in 78% of patients using telephone transmitters. Ventricular tachycardia was transmitted in six patients--all survived. During an average 15-month follow-up, 1 of 19 patients using the telephone transmitter system died vs 12 deaths among the 28 patients who did not use the system (p less than 0.005). These results were independent of ejection fraction, presence of congestive heart failure, amiodarone therapy, and the outcome on electrophysiologic therapy. Thus, patients with a history of out-of-hospital sudden death, discharged following electrophysiologic guided therapy, require repeated antiarrhythmic dose titration for side effects or residual ventricular arrhythmia. Prompt diagnosis and treatment of potentially fatal arrhythmia is crucial and feasible, especially with regular ECG checks through telephone transmission.

Thirty-eight patients with right bundle branch block and left anterior hemiblock who had undergone His bundle recordings were prospectively followed for development of heart block. Twenty-five were male and thirteen female. Their ages ranged from 35 to 92 with an average age of 74 years. The mean follow-up period was 28.5 months (range 2-52 months). The H-V interval was 55 msec or less in 17 patients (Group A), between 56 and 75 msec in 13 (Group B), and more than 75 msec in eight (Group C). Ten patients (26%) died during the follow-up period. Of these, three were in Group A (mortality rate 8% per year), three in Group B 10% per year), and four in Group C (21% per year). None of the deaths in Groups A and B were sudden, while one possible sudden death occurred in Group C. Mode of death in one patient each from Groups B and C remained unknown. Heart block was not seen in any patient from Group A and B, while two patients from Group C progressed to complete heart block during the follow-up period. It is concluded that patients with right bundle branch block and left anterior hemiblock with prolonged H-V intervals tend to show a higher mortality when compared to those with normal H-V intervals. A definite risk of heart block exists in patients with H-V intervals of more than 75 msec.

Since there is very little available systematic information on the psychological profile of patients with cardiac arrhythmia, a battery of 12 standardized personality inventories was administered to 102 patients ranging in age from 19 to 69 years. Thirty-eight patients with frequent ventricular premature beats (more than 30 per hour) without myocardial infarction were significantly more psychologically symptomatic than 34 age- and sex-matched general medical/surgical patients. The variables found to be significant portray the patient with frequent ventricular premature beats without myocardial infarction: high scores for hysteria, less moral orientation, more anxiety, depression and social alienation, and an inhibited and low respectful style. This combination of psychological variables produced a discriminant function (p less than 0.001) that accounted for 53 percent of the variance between the arrhythmia/no myocardial infarction group and the medical/surgical control group and could correctly predict group membership in 83.3 percent of cases. These results may have further implications in nonpharmacologic and psychotropic adjuncts to antiarrhythmic therapy.

Electrocardiograms and His bundle electrograms were reviewed in 28 patients with incomplete bilateral bundle-branch block complicating acute myocardial infarction. All had a His bundle electrogram at the time of pacemaker insertion; 10 had a second one. Of 23 patients with an initially abnormal HV interval (55 ms or greater), 15 died (65%), while only one died (20%) in the group of 5 with a normal HV interval. This difference is not statistically significant. Sequential His bundle electrograms were done in 6 of the 8 survivors with an initially abnormal HV interval, and 4 showed 10 to 15 ms decrease in HV interval. The disappearance of incomplete bilateral bundle-branch block occurred significantly more often in patients who survived (7 of 12) when compared with those who did not survive (2 of 16) (P less than 0.05). It is concluded that long-term survival is po-sible after incomplete bilateral bundle-branch block complicating acute myocardial infarction. The characteristics of the survivors include an initially normal HV interval, transient incomplete belateral bundle-branch block and a decreasing HV interval if it were initially abnormal.

A case report of a 29-year-old Hispanic male who developed an acute thrombocytopenic reaction immediately following a cardiac catheterization using Hypaque-M radiographic dye. Laboratory studies immediately post-catheterization revealed a platelet count of 11,000 with a subsequent further drop to a low of 4,000. A need for the prompt identification and possible causes of this unusual reaction are discussed. Recovery occurred following treatment with corticosteroids.

Four patients with different clinical conditions had transient cardiac standstill for periods of up to 22.5 seconds. All patients showed signs of cerebral ischemia and required cardiac resuscitation. In one patient, the standstill was thought to be the result of a transient increase in the vagal tone, and no long-term therapy was required. In the second patient, cardiac standstill occurred during hospitalization for impending myocardial infarction. Coronary arteriography followed by coronary artery surgery was performed, and there was no further episodes of standstill. In the third patient, standstill was probably related to long-term ingestion of propranolol hydrochloride, and was not observed after this medication was discontinued. In the fourth patient, standstill was the result of the sick sinus syndrome, and a permanent pacemaker was inserted. Standstill of both atria and ventricles may occur under different clinical settings, and management of arrhythmia should be guided by thf etiology of the arrhythmia.

The auscultatory features typical of myxoma were absent in a patient with nonprolapsing left atrial myxoma. Angiocardiographic and echocardiographic findings including B-mode cross-sectional scanning are presented.

The effects of digoxin priming dose of 0.04 mg/kg body weight followed by infusion of 0.02 mg/kg per min) on local tension and length characteristics of the nonischemic, border and ischemic left ventricular zones were studied in 30 dogs using Walton-Brodie strain gauge arches and mercury-in-Silastic segment length gauges. Total tension in the nonischemic zone increased to 130.9 plus or minus 5.3 percent (P smaller than 0.001) of the control level in association with parallel changes in preejection and ejection tension and rate of rise of tension when infusion of digoxin was instituted 15 to 30 minutes after ligation. Consistent increases in tension variables were noticed when infusion of digitalis was initiated 45 to 60 minutes or 2 to 3 hours after ligation. Segment length remained unchanged. In the border zone, total tension decreased to 68.9 plus or minus 5.9 percent (P smaller than 0.01) after infusion of digitalis. When infusion of digitalis was instituted 45 to 60 minutes or 2 to 3 hours after occlusion, similar increases in total tension and other tension variables were seen. Segment length again showed no significant changes. There was an increase in total tension in 5 of the 12 ischemic zones studied when digitalis was infused 15 to 30 minutes after coronary arterial ligation, whereas a consistent (3 to 5 percent) decrease in tension was observed when infusion of digitalis was instituted 45 to 60 minutes and 2 to 3 hours after coronary occlusion. There was no increase in segment length. In summary, digitalis uniformly increased contraction of the nonischemic and border zones after coronary arterial ligation, but the effects on contraction and aneurysmal bulging in the ischemic zone were minimal.

Sixty-eight (17 per cent) of 380 patients with acute myocardial infarction had the bradycardia-hypotension syndrome (ventricular rate below 60/min and systolic blood pressure less than 100 mm Hg) during the first 24 hours of admission to a large general hospital. In 61 of the 68 patients, the administration of atropine significantly increased the heart rate (from 46 plus or minus 14 to 79 plus or minus 12/min) (p less than 0.01) and systolic blood pressure (from 70 plus or minus 15 to 105 plus or minus 13 mm Hg) (p less than 0.001). In 26 of the 68 patients, ventricular premature complexes decreased from 9.4 plus or minus 3/min to 2.4 plus or minus 0.7/min (p less than 0.001) after the administration of atropine. It is concluded that the bradycardia-hypotension syndrome is not an uncommon complication following acute myocardial infarction and that selected doses of atropine may have a beneficial effect without significant complications.

Serum, whole blood and red blood (intracellular) magnesium determinations were made in 52 patients, without other factors predisposing to hypomagnesemia, admitted to a coronary care unit. Acute uncomplicated myocardial infarction was documented in 31 and the serum cardiac enzymes as well as the electrocardiogram remained nondiagnostic in 21 patients. There was no significant difference in the serum magnesium level in the two groups. An increasing trend with time was noted in the serum (p less than 0.001) and whole blood magnesium (p less than 0.005) during the first 4 days postmyocardial infarction. The whole blood magnesium as well as the red blood (intracellular) magnesium was higher (p less than 0.01) in myocardial infarction patients. There was no significant difference in the hematocrit or other electrolytes during this time.

To evaluate changes in magnesium levels with treadmill exercise-induced coronary insufficiency, 59 consecutive patients were studied. In addition to electrocardiographic monitoring, hematocrit, total protein, whole blood, serum and red blood cell magnesium determinations were made before and after exercise testing. Fifteen patients had positive exercise test, 18 did not complete, and 26 had negative exercise test. There was no significant difference in the serum and red blood cell magnesium on the basis of stress test results for ischemia. Although whole blood magnesium, hematocrit, and total proteins increased (P less than .05) in both groups, we did not find a significant change in magnesium homeostasis.

To determine the factors affecting reproducibility of sinus node recovery time, the effects of basic pacing rate, pacing duration, milliamperage, vagal and beta-adrenergic stimulation, and sinud node injury, as well as its instantaneous and daily reproducibility, were studied in 36 anesthetized dogs. Corrected sinus node recovery time (CSNRT) showed a mean variation of 9.8 plus or minus 0.4 msec at an atrial pacing rate of 200 beats/min and 29.8 plus or minus 8 msec at an atrial pacing rate of 140 beats/min (P smaller than 0.05). CSNRT increased progressively from 55.4 plus or minus 10 msec to 103.7 plus or minus 13 msec with increase in pacing rate from 140 beats/min to 200 beats/min. It was reproducible when atrial pacing was carried out for 1-5 min, although a wide variation (10-30 msec) was seen from 7-60 minutes (P smaller than 0.05). This measurement was reproducible on two consecutive days and was unaffected by changes in milliamperage. Vagal stimulation consistently prolonged the CSNRT while beta-adrenergic stimulation decreased it from 132.9 plus or minus 34.5 msec to 50.0 plus or minus 6.5 msec. Sinus node injury consistently prolonged CSNRT at all paced rates. In summary, CSNRT is reproducible only if the same pacing rate and duration are utilized. Since vagal stimulation and sinus node injury prolong this measurement while beta-adrenergic stimulation shortens it, an "abnormal" CSNRT should be assessed in terms of the possible influence of the autonomic nervous system as well as sinus node dysfunction per se.

A total of 99 consecutive 24-hour Holter recordings with ventricular tachycardia were reviewed. Ventricular premature beats which occurred alone, and ventricular premature beats which initiated ventricular tachycardia were examined to determine which characteristics correlated with occurrence of ventricular tachycardia and which predicted rate and duration of ventricular tachycardia. The preceding R-R interval, the coupling interval, and a ratio of the two were examined. We found that ventricular tachycardia rate and duration increase with a shorter coupling interval, and the coupling interval/preceding R-R ratio was significantly different in single beats not initiating ventricular tachycardia. The ratio for the beat initiating ventricular tachycardia was smaller, indicating more prematurity.

A patient with the sick sinus syndrome accompanying mirror-image dextrocardia which was associated with double superior venae cavae and an absent inferior vena cava is presented. A permanent transvenous demand pacemaker was inserted because of repeated episodes of dizziness and a documented 31/2-second period of asystole. Precise knowledge of the venous system and the location of the apex of the right ventricle was necessary prior to permanent pacemaker implantation.

This 68 year old man had recurrent episodes of paroxysmal atrial tachycardia, probably due to chronic pericarditis, persisting over a 7 year period. These episodes were resistant to all conventional medical therapy and at times produced ischemic chest pain. There was no evidence of Wolff-Parkinson-White syndrome either on the standard electrocardiogram or on the His bundle electrogram performed with atrial pacing. Rapid atrial pacing at a rate of 200/min was found to promptly terminate the tachycardia and restore normal sinus rhythm. Because of the refractoriness of the patient's tachycardia, in addition to the presence of ischemic chest pain during these episodes, a permanent radio frequency triggered atrial pacemaker was inserted which enables him to initiate rapid atrial pacing by pressing an external control. The patient has been maintained on antiarrhythmic medications in an attempt to decrease the frequency of these episodes; during an 8 month follow-up period, he has done well with approximately one episode of tachycardia each month requiring radio frequency atrial pacing for termination.

The hospital course and serial vectorcardiograms of 56 consecutive patients with acute inferior wall myocardial infarction were reviewed. Left anterior hemiblock (LAH) complicating inferior wall myocardial infarction was diagnosed by vectorcardiographic criteria. Seven patients (12.5%) developed LAH between the first and third hospital day, while 49 patients did not. There was no significant difference between these two groups when compared for age, sex, incidence of congestive heart failure, atrial and ventricular arrhythmias, atrioventricular (A-V) block, hospital mortality, and previous hypertension, diabetes mellitus, and myocardial infarction. We conclude that LAH is a relatively common complication of acute inferior wall myocardial infarction, with no apparent effect on the clinical course.

This report describes 16 patients with block within the His bundle seen over a period of 55 months. Ten were women and 6 men, with an average age of 76 years, range, 42 to 98 years. All patients had His bundle recordings showing split His bundle potentials (H and H) (13 patients) or narrow QRS with block distal to the His bundle potential (3 patients). Of the 16 patients, 10 had complete heart block, 4 second degree AV block (2 patients with Mobitz type II, and 2 with 2:1), and 2 first degree AV block. Ten patients had a narrow QRS in the conducted beats or escape rhythms. Intravenous atropine (1 to 2 mg) had a variable effect on AV conduction and the rate of the escape rhythm. Twelve patients have had a permanent pacemaker implanted. During the follow-up period, 10 patients died 1 to 31 months from the time of initial examination. The remaining 6 patients (5 with pacemaker) are alive 3 to 58 months later.

The presence of nocturnal angina and congestive heart failure within the month prior to admission was evaluated in the 174 patients with acute myocardial infarction. Heart size was evaluated radiographically at the time of admission. Twenty-three patients (13 per cent) experienced nocturnal angina. The incidence of nocturnal angina was significantly higher in those with anterior myocardial infarction (p less than 0.005) and subendocardial infarction (p less than 0.02) when compared with patients with inferior MI. Congestive heart failure was more common prior to admission in those with nocturnal angina (9/23) as opposed to those without (3/141) (p less than 0.001). Cardiomegaly was seen in 9/23 patients with nocturnal angina and 22/141 without (p less than 0.02). We conclude that the presence of nocturnal angina in those who develop MI increases the likelihood that the infarction will be either anterior or subendocardial rather than inferior. The association of nocturnal angina and congestive heart failure to anterior myocardial infarction is probably due to more severe and probably significant left coronary artery disease.

His bundle electrocardiography was performed on a patient with accidental hypothermia on whom the standard electrocardiogram (ECG) showed absent P waves, prominent J waves and a slightly irregular rhythm. Sino-ventricular conduction and a prolonged AH interval not responsive to atropine were found. These abnormalities reversed with rewarming.

The case report demonstrates another case of hypomagnesemia with electrocardiographic evidence of acute myocardial ischemia due to coronary spasm. The patient was successfully treated with intravenous, followed by oral, magnesium sulfate. Magnesium therapy may be justified especially in patients with prolonged QT intervals, cardiac arrhythmias and hypokalemia with hypomagnesemia.