The electrophysiological effects of ouabain on sinus node and atrium in man.

Electrophysiological studies were performed in 16 patients before and 30 min after intravenous administration of ouabain (0.1 mg/kg). P-A interval (mean+/-SEM) was 40+/-2.1 ms before and 44+/- 1.5 ms after ouabain (P less than 0.001). Atrial effective and functional refractory periods (ERP and FRP) were measured in all patients during sinus rhythm and during driving at equivalent paced rates in 12 patients. The mean atrial ERP and FRP during sinus rhythm were, respectively, 244+/-10.5 and 307+/-11.0 ms before and 253+/-9.7 and 318+/-11.4 ms after infusion of ouabain (NS). Mean atrial ERP and FRP during driving were, respectively, 231+/-15.3 and 264+/-14.9 ms before and 266+/-18.6 and 296+/-19.7 ms after ouabain (P less than 0.01 and P less than 0.01). Mean sinus cycle length and sinus recovery times were, respectively, 887+/-31.2 and 1,113+/-38.7 ms before and 905+/-38.2 and 1,008+/-30.7 ms after infusion of ouabain (NS and P less than 0.005). Calculated sinoatrial conduction times before and after ouabain were 90+/-6.8 and 110+/-8.5 ms, respectively (P less than 0.005). In summary, ouabain produced depression of intraatrial conduction as manifested by increase in P-A interval and atrial effective and functional refractory periods. Ouabain significantly increased calculated sinoatrial conduction time without significant effect on spontaneous sinus cycle length.

Spontaneous arrhythmia detected on ambulatory electrocardiographic recording lacks precision in predicting inducibility of ventricular tachycardia during electrophysiologic study.

This study investigates the relation of spontaneous ventricular arrhythmia on ambulatory electrocardiographic (ECG) monitoring to the subsequent inducibility of ventricular tachycardia during programmed electrical stimulation. Eighty patients (65 men, 15 women), whose mean age was 58 years, presented with one of the following: sustained ventricular tachycardia (n = 54); sudden death requiring resuscitation (n = 4); ventricular fibrillation (n = 11); or syncope thought to be of cardiac origin (n = 11). All patients had 24 hour ambulatory electrocardiograms and programmed electrical stimulation while receiving no antiarrhythmic therapy. Programmed electrical stimulation resulted in inducible sustained ventricular tachycardia (defined as a rate of greater than or equal to 120 beats/min for greater than or equal to 1 minute or requiring intervention) in 53 of the 80 patients. There was no measure of frequency or complexity of spontaneous arrhythmia detected on ambulatory ECG that could identify the degree of subsequent ventricular tachycardia inducibility during programmed electrical stimulation. In fact, 25% of patients who had inducible sustained ventricular tachycardia had little or no spontaneous arrhythmia on ambulatory ECG. Furthermore, of the 53 patients with inducible sustained ventricular tachycardia, 28 and 55% had no couplets or nonsustained ventricular tachycardia, respectively, during ambulatory monitoring. The combination of a clinical presentation of sustained ventricular tachycardia, confirmed coronary artery disease and a left ventricular ejection fraction of less than 30% had a better positive predictive value than did any ambulatory ECG criterion in predicting the inducibility of sustained ventricular tachycardia.

Amiodarone pulmonary toxicity: prospective evaluation of serial pulmonary function tests.

Pulmonary toxicity developed in 15 (17%) of 89 patients treated with amiodarone during a follow-up period of 2 weeks to 54 (mean 20 +/- 15) months. Prospective evaluation of serial pulmonary function tests in 67 patients demonstrated both a significant decrease from baseline in three of six variables in patients with toxicity at the time of diagnosis and a significant difference compared with the same variables in patients without toxicity. The most significant of these was the diffusing capacity for carbon monoxide (DLCO). An individual decrease in DLCO greater than or equal to 15% gave an optimal sensitivity of 100% and a specificity of 89% for the diagnosis of pulmonary toxicity. However, a decrease in DLCO greater than or equal to 15% did not alone warrant a change in therapy in asymptomatic patients. Although higher maintenance doses of amiodarone appeared to be related to the development of this complication, an abnormal baseline DLCO (less than 60% of predicted) with or without an initial abnormal chest roentgenogram did not predispose to pulmonary toxicity.

Surgical treatment of right atrial focal tachycardia in adults.

Although successful operative treatment of atrial focal tachycardia has been reported in children, there are only isolated reports of surgical treatment of this arrhythmia in adults. In this case series of eight patients (aged 10 to 53 years) with drug-resistant right atrial focal tachycardia, results of electrophysiologic studies, surgical techniques and long-term follow-up are described. Atrial focal tachycardia was reproduced during electrophysiologic study, and endocardial mapping localized the earliest onset of atrial activation in the right atrium in all patients. Epicardial mapping confirmed the location of atrial tachycardia foci in seven of eight patients whose tachycardia was inducible intraoperatively. Of four patients treated with epicardial cryoablation alone, two had recurrent tachycardia and required a second procedure. None have had arrhythmia recurrence. In all four patients after right atrial excision (two of whom had intraoperative recurrence of atrial focal tachycardia after epicardial cryoablation alone), there has been no recurrence during a clinical follow-up period of 11 to 67 months (mean 30). It is concluded that in adult patients 1) electrophysiologic study with endocardial and epicardial mapping permits successful surgical treatment of atrial focal tachycardia; 2) epicardial cryoablation alone may be associated with recurrence of atrial focal tachycardia either intraoperatively or postoperatively; and 3) subtotal right atrial resection appears to be a well tolerated procedure with no long-term recurrence of atrial focal tachycardia.

Importance of pacing site in entrainment of ventricular tachycardia.

Transient entrainment by pacing has been demonstrated during various tachyarrhythmias, including ventricular tachycardia. A patient is described who had two morphologically distinct forms of sustained ventricular tachycardia induced by programmed stimulation. Entrainment of both configurations of ventricular tachycardia was demonstrated. Evidence for entrainment included the presence of different degrees of fusion between paced and ventricular tachycardia complexes at different pacing cycle lengths, and the observation that the last entrained beat was always unfused and identical in configuration to the ventricular tachycardia complexes. Termination of ventricular tachycardia only occurred at pacing cycle lengths at which there was loss of fusion. Catheter endocardial mapping suggested a septal origin of both configurations of ventricular tachycardia. Demonstration of entrainment was dependent on pacing site, being seen only during pacing in the ventricle opposite from that showing earliest activation during ventricular tachycardia. Thus, when attempting to entrain ventricular tachycardia, multiple pacing sites in both ventricles should be used.

Permanent triggered antitachycardia pacemakers in the management of recurrent sustained ventricular tachycardia.

Permanent pacemakers capable of triggered ventricular stimulation were implanted in 28 patients with a history of sustained ventricular tachycardia or fibrillation. Noninvasive programmed ventricular stimulation was performed on 125 occasions during follow-up periods ranging from 1 to 25 months and was used to assess the efficacy of antiarrhythmic drug therapy, drug or dosage changes and left ventricular endocardial resection. Drug or dosage changes based on noninvasive programmed ventricular stimulation were made in 19 of the 28 patients. In addition, 126 episodes of spontaneous sustained ventricular tachycardia were terminated noninvasively in nine patients. It is concluded that a permanent pacemaker capable of triggered ventricular stimulation is useful in patients with ventricular tachycardia or fibrillation that is difficult to control.

Analysis of ambulatory electrocardiograms in 15 patients during spontaneous ventricular fibrillation with special reference to preceding arrhythmic events.

Fifteen patients sustained ventricular fibrillation during ambulatory electrocardiographic recording in a period of 3.5 years over which time 16,500 ambulatory electrocardiograms were analyzed (prevalence = 0.09% or 1/1,100). Eight patients died, and seven survived cardiopulmonary resuscitation. Quantitative analysis of hourly ventricular arrhythmias prior to ventricular fibrillation revealed an increased frequency of premature ventricular beats and ventricular tachycardia, especially in the 2 hours immediately before ventricular fibrillation. Ventricular fibrillation was initiated by ventricular tachycardia in all 15 cases. These runs of ventricular tachycardia were characterized by their unusual length (mean = 560 +/- 536 beats) and their rapid rate (241 +/- 45 beats/min). Although an R on T premature ventricular beat initiated ventricular tachycardia and ventricular fibrillation occasionally, the mean prematurity index of the initiating premature ventricular beat was not early (mean = 1.27 +/- 0.28). QT prolongation was present in only 3 of the 15 patients (mean QTc interval = 0.42 +/- 0.06). Left ventricular dysfunction (mean left ventricular ejection fraction = 34.9 +/- 9.9%) and coronary artery disease were nearly always present. The cardiac medications most frequently associated with these patients at the time of ventricular fibrillation were digitalis and quinidine.

Sudden death in patients with chronic bifascicular block.

Prospective follow-up studies of 277 patients with chronic bifascicular block showed that 30 patients developed sudden cardiac death (SCD). Cumulative one-, two-, and three-year SCD mortality was computed. The patients that developed SCD were compared with the remaining patients (209 alive and 38 dead). The groups were similar in regard to age, sex, AH, and HV intervals. The following were more frequent in the SCD group (P less than .05): angina, previous myocardial infarction, heart failure, cardiomegaly, left bundle-branch block, premature ventricular beats, and ventricular tachycardia. Ventricular fibrillation was the cause of death in four cases of SCD where terminal ECG documentation was available. We concluded that SCD is a major cause of mortality in patients with chronic bifascicular block. The association of SCD with coronary disease and ventricular dysrhythmia suggested ventricular fibrillation as a frequent mechanism.

Role of invasive electrophysiologic testing in the management of life-threatening ventricular arrhythmias.

Electrophysiologic studies are indicated in patients with sustained paroxysmal ventricular tachycardia, ventricular fibrillation or aborted sudden death. These studies allow determination of mechanism and reproducibility of initiation as well as pacing termination of ventricular tachycardia, against which the effects of pharmacologic or nonpharmacologic therapies can be tested. Such studies are also indicated in certain patients with syncope in whom a strong suspicion exists for an arrhythmic cause. The content and conduct of electrophysiologic testing in these patients require attention to the physiology of the conduction system and systematic programmed stimulation of the right ventricle. The stimulation protocol should include, if necessary, twice-threshold stimulation at 2 sites at 3 or more cycle lengths, with up to 3 extrastimuli. Sufficient variability exists in electrophysiologic testing as in other clinical methods calling for careful attention to the reproducibility of tachycardia induction in a given patient, lest chance alone mimic beneficial or deleterious effects of antiarrhythmic regimens. Mapping-directed surgery for ventricular tachycardia remains the most effective therapy in patients with sustained monomorphic ventricular tachycardia with a mortality similar to other forms of medical therapy.

Sinus nodal responses to atrial extrastimuli in patients without apparent sinus node disease.

In 36 patients without sinus node disease scanning with an atrial extrastimulus (A2) was performed during sinus rhythm with the sinus cycle length measured in milliseconds. Zones of nonreset due to interference, reset, interpolation and sinus echoes were defined by noting the timing of the first response after A2. Zones were defined in terms of their longest and shortest A1-A2 coupling intervals (in milliseconds). A zone of nonreset was found in 12 of 12 patients in whom A2 was delivered late. The mean cycle length in these 12 patients was 779 msec, with a mean zone of nonreset of 779 to 585 msec (25 percent of cycle length). All 36 patients (100 percent) had a zone of reset. The mean cycle length in these 36 patients was 803 msec with a zone of reset from 692 to 319 msec (46 percent of cycle length). Seven of 36 patients (19 percent) had a zone of interpolation. The mean cycle length in these seven patients was 754 msec, with a mean zone of interpolation of 344 to 279 (9 percent of cycle length). Four of 36 patients (11 percent) had a zone of sinus echoes. The mean cycle length in these four patients was 870 msec, with a mean zone of echoes from 350 to 313 msec (4 percent of cycle length). Calculated sinoatrial conduction time ranged from 40 to 153 msec (mean +/- standard deviation 92 +/- 30 msec). Shortening of the cycle length with atrial pacing increased the number of patients with zones of interpolation and echoes. In conclusion, zones of nonreset and reset are found in all patients with normal sinus nodal function, whereas zones of interpolation and echoes are much less common. Sinoatrial conduction time is surprisingly long in patients without apparent sinus node disease.

Electrophysiologic demonstration of bilateral anomalous pathways in a patient with Wolff-Parkinson-White syndrome (type B preexcitation).

Pre- and postoperative electrophysiologic studies are described that were suggestive of two (right- and left-sided) anomalous atrioventricular (A-V) connections in a patient with type B Wolff-Parkinson-White syndrome and intractable arrhythmias, who underwent epicardial mapping and successful surgical ablation of the right-sided anomalous pathway. The presence of the right-sided anomalous pathway capable of both antegrade and retrograde conduction was suggested by the following observations: (1) Type B preexcitation on the surface electro-cardiogram; (2) maximal preexcitation and minimal stimulus-delta with low lateral right atrial pacing; (3) epicardial mapping of the atria and ventricles; and (4) disappearance of ventricular preexcitation after surgical ablation of the right-sided anomalous pathway. The presence of an additional left-sided anomalous pathway capable of only retrograde conduction (concealed on the surface electrocardiogram) was sugg-sted by the following observations: (1) Left to right retrograde atrial activation sequence during reentrant tachycardia and ventricular pacing at rapid rates and with coupled ventricular pacing postoperatively; (2) spontaneous conversion of wide ORS tachycardia utilizing the anomalous pathway for antegrade conduction to narrow QRS tachycardia with significant slowing in rate; and (3) smooth antegrade A-V nodal conduction curves with echo zone postoperatively. The demonstration of bilateral anomalous pathway in patients with preexcitation has important electrophysiologic and surgical implications.

Assessment of left ventricular function by radionuclide angiography during induced supraventricular tachycardia.

Electrocardiographically synchronized radionuclide angiography was performed before, during and after induced paroxysmal supraventricular tachycardia in 13 patients. Data were acquired with a computer-interfaced Anger camera in a left anterior oblique projection. No data were acquired during tachycardia until tachycardia had been sustained for 1 minute. Patients ranged in age from 20 to 64 years (mean +/- standard deviation 42 +/- 14.5). Three patients had organic heart disease and 10 did not. Baseline and tachycardia heart rates (beats/min) were 59 to 99 (73 +/- 11) versus 141 to 228 (157 +/- 22). Baseline and tachycardia left ventricular measurements (mean +/- standard error) were as follows: ejection fraction 64 +/- 2 versus 62 +/- 4 percent (not significant), ejection rate 3.0 +/- 0.1 versus 4.3 +/- 0.4 mean ventricular counts/s (p less than 0.001), normalized end-diastolic counts 72.7 +/- 7.8 versus 48.7 +/- 6.7 X 10(3) counts (p less than 0.001), normalized stroke counts 37.1 +/- 3.4 versus 23.3 +/- 2.7 X 10(3) counts (p less than 0.001) and normalized count cardiac output 2,717.5 +/- 273.0 versus 3,620.2 +/- 403.7 X 10(3) counts/min (p less than 0.005). Although ejection fraction for the whole group did not change significantly, it decreased during tachycardia by 5 percentage points or more in five patients. These were the three patients with heart disease and the two normal patients with the fastest heart rate during tachycardia (228 and 214 beats/min, respectively). In summary, paroxysmal supraventricular tachycardia was characterized by a marked decrease in left ventricular end-diastolic and stroke volumes but increased ejection rate and cardiac output without significant change in ejection fraction. Heart disease or rapid heart rate during tachycardia appeared to have a deleterious effect on ejection fraction.

Epicardial activation in human left anterior fascicular block.

Four patients with coronary artery disease and chronic marked left axis deviation, defined as a frontal QRS axis more negative than -45 degrees, were studied with epicardial mapping during coronary bypass surgery. All patients had normal right ventricular and inferior left ventricular epicardial breakthrough sites and activation sequence. Normal breakthrough in the basal anterolateral left ventricular epicardium was absent in all four patients. Two patients had breakthrough in the apical region of the anterolateral left ventricle. In the other two this region was activated from wave fronts emerging in the right ventricle and inferior left ventricle. The latest site of left ventricular activation was the basal segment of the anterolateral wall, a site never found to be the latest activated in our previously studied patients without conduction defects. This site was activated during or slightly after the terminal portion of the QRS complex. It is concluded that marked left axis deviation in patients with coronary artery disease reflects delayed activation of the basal anterolateral left ventricle, and is consistent with the presence of block or delay in the anterior "fascicle" of the left bundle branch.

Self-initiated conversion of paroxysmal atrial flutter utilizing a radio-frequency pacemaker.

A patient is described with drug-resistant recurrent paroxysmal atrial flutter. Electrophysiologic studies demonstrated that flutter was inducible with rapid atrial stimulation (stimulation rates of 375 to 400/min) and convertible with rapid atrial stimulation (rates of 400 to 460/min). Because of the latter response, a radio-frequency atrial pacemaker was implanted, which allowed self-initiated conversion of flutter episodes with rapid stimulation.

Prospective comparison of right and left ventricular stimulation for induction of sustained ventricular tachycardia.

Thirty-eight patients who had sustained monomorphic ventricular tachycardia (VT) or sudden cardiac death underwent programmed ventricular stimulation. To assess the relative efficacy of right and left ventricular (RV and LV) stimulation, a tandem protocol with 1 to 4 extrastimuli and burst pacing was used. Each step of the protocol was performed in a rotating sequence at the RV apex, basal RV septum and LV apex. Sustained VT was induced from the RV apex in 26 patients, right ventricle (either site) in 27, and LV apex in 24, and spontaneous VT was reproduced from those sites in 11, 14 and 12 patients, respectively. In the 23 patients who had sustained VT induced from both ventricles, RV stimulation always required fewer or the same number of extrastimuli for induction. At every stage of the protocol, the cumulative yield of sustained VT was consistently greater from the right ventricle than from the left ventricle. After delivering 4 extrastimuli and burst pacing, LV stimulation only increased the yield of sustained VT by 1 patient, and spontaneous VT by 3 patients. Inducibility or noninducibility in the right ventricle generally predicted the same outcome in the left ventricle. Previously undocumented VT or ventricular fibrillation was induced from the right ventricle in 19 patients and from the left ventricle in 13. Thus, LV stimulation was less efficacious than RV stimulation. LV stimulation increased the yield over RV stimulation only minimally and did not reduce the number of extrastimuli required to induce sustained VT.

Effect of bradycardia on dispersion of ventricular refractoriness.

The effect of bradycardia on dispersion of ventricular refractoriness was evaluated. Refractory periods were measured at 3 right ventricular sites in 16 patients with severe bradycardia (average heart rate 39 +/- 5 beats/min) and were compared with those measured in 11 control subjects, (average heart rate 72 +/- 12 beats/min). Patients with bradycardia had significantly longer effective (377 +/- 36 ms) and functional (421 +/- 39 ms) refractory periods (ERP and FRP) than control subjects (ERP 296 +/- 25 ms, FRP 346 +/- 18 ms) (p less than 0.001). However, dispersion of refractoriness was similar in the 2 groups. Dispersion of ERP was 43 +/- 38 ms and FRP was 48 +/- 35 ms in patients with bradycardia. In control subjects dispersion of ERP was 37 +/- 12 ms, and FRP was 36 +/- 20 ms. Pacing of 120 beats/min significantly decreased ERP and FRP in both groups. Pacing shortened dispersion significantly in control subjects. In patients with bradycardia, pacing failed to significantly decrease dispersion. Compared with control subjects with normal heart rates, patients with bradycardia have longer absolute refractory periods but do not have significantly increased dispersion of refractoriness. Single and double, twice threshold ventricular extrastimuli (S2 and S3) failed to induce ventricular tachycardia in any patient during bradycardia. Bradycardia alone does not appear to be a factor in the induction of ventricular tachyarrhythmias.

Effect of increased current, multiple pacing sites and number of extrastimuli on induction of ventricular tachycardia.

Reproduction of spontaneously occurring ventricular tachycardia (VT) and induction of previously undocumented VT were studied prospectively in 98 patients: 48 with documented sustained VT or ventricular fibrillation, 25 with nonsustained or exercise-induced VT, and 25 with no documented VT. Patients received 1 to 4 ventricular extrastimuli and ventricular burst pacing at 2 right ventricular (RV) sites, first at twice late diastolic threshold, and then at 10 mA using a prospective, tandem study design. Spontaneously occurring VT was reproduced in 37 of 48 patients (77%) at twice late diastolic threshold and in 1 other patient (2%) at 10 mA. VT was reproduced at both RV sites in 17 of 48 patients (35%) and at 1 site in 20 of 48 patients (42%) at twice late diastolic threshold. A previously undocumented VT was induced in 7 of 25 patients (28%) with no documented VT at twice diastolic threshold and 14 of 25 patients (56%) at 10 mA. A previously undocumented VT was induced in 33 of 73 patients (45%) with a history of sustained or nonsustained VT at twice late diastolic threshold and in 47 of 73 patients (64%) at 10 mA. In patients with documented sustained VT, the use of up to 4 ventricular extrastimuli at multiple RV sites increases the sensitivity of the test. In patients without documented VT, the induction of previously undocumented VT with more than 3 ventricular extrastimuli limits the specificity of the test. Increased current provides only a slight advantage over 4 ventricular extrastimuli at twice late diastolic threshold in terms of reproduction of spontaneously occurring VT, but leads to a marked increase in induction of previously undocumented VT.

Electrophysiologic evaluation of pirmenol for sustained ventricular tachycardia secondary to coronary artery disease.

The efficacy and electrophysiologic effects of pirmenol were evaluated in 21 patients with a history of sustained ventricular tachycardia (VT) and coronary artery disease. Intravenous pirmenol (0.7- to 1.1-mg/kg bolus, followed by a 35- to 40-micrograms/kg/min infusion) significantly prolonged the PR, QRS, QT and corrected QT intervals, HV interval and right ventricular effective refractory period, and shortened the sinus cycle length and atrioventricular nodal block cycle length. All 21 patients had inducible VT (20 sustained, 1 nonsustained) during programmed stimulation in the control state. After intravenous pirmenol, 5 patients (24%) no longer had inducible VT. In those in whom VT was still inducible, the VT cycle length was prolonged significantly. The 5 patients who responded to intravenous pirmenol were given oral pirmenol (200 to 250 mg every 8 hours) for 1 to 3 days and retested with programmed stimulation. In 4 of these 5, VT could not be induced with oral pirmenol administration; in 1 patient sustained VT was induced and pirmenol therapy was discontinued. Oral pirmenol suppressed recurrent VT during a follow-up of 315 +/- 133 days in 4 patients. However, pirmenol therapy was discontinued in 2 patients because of possible deleterious effects (worsened heart failure in 1 patient and elevated liver function test results in 1). Thus, pirmenol, a type IA antiarrhythmic drug, had an overall efficacy of approximately 19% in patients with sustained VT secondary to coronary artery disease.

Electrophysiology of Ethmozine (moricizine HCl) for ventricular tachycardia.

Moricizine HCl, an antiarrhythmic phenothiazine drug, was investigated for its efficacy against ventricular tachycardia (VT) in a group of 60 patients from 8 institutions using electrophysiologic testing before and after oral administration. Moricizine HCl significantly prolonged PR, QRS, AH and HV intervals and cycle length for atrioventricular nodal block, but had minimal or no effect on repolarization or cardiac refractory periods. Induction of sustained VT (in 33 patients) and nonsustained VT (in 14 patients) occurred at baseline. During moricizine HCl therapy, sustained VT was induced in 31 patients and nonsustained VT in 7 patients. In individual patients, suppression of VT induction was obtained in 18% of patients with sustained VT and in 27% of patients with nonsustained VT. Cycle length of induced VT was significantly prolonged by moricizine HCl therapy. During prospective follow-up of 37 patients, electrophysiologic study predicted recurrence of nonrecurrence of VT with a sensitivity value of 82% and specificity of 65%.

Significance of A-H interval in patients with chronic bundle branch block. Clinical, electrophysiologic and follow-up observations.

His bundle electrograms were recorded in 308 adults with chronic bundle branch block. The A-H interval was normal in 249 patients and prolonged in 59. Comparison of patients with normal and prolonged A-H intervals revealed a greater incidence of demonstrable organic heart disease in the latter (P less than 0.01). Dyspnea, cardiomegaly and congestive heart failure were more frequent in patients with A-H prolongation. These patients also had longer P-R intervals and atrioventricular (A-V) nodal effective refractory periods, lower paced rates producing second degree A-V block proximal to the His bundle and a greater frequency of H-V prolongation. All patients were prospectively followed up in a conduction disease clinic with mean follow-up periods (+/- standard error of the mean) of 523 +/- 23 and 588 +/- 47 days in the patients with normal and prolonged A-H intervals, respectively. Seven (3 percent) of the patients with a normal A-H interval had A-V block with probable or definite site of block proximal to the His bundle in three and distal to the His bundle in four. In five of the six patients with a prolonged A-H interval who experienced A-V block (10 percent), the probable or definite site of block was proximal to the His bundle. Mortality (both sudden and nonsudden) was not significantly different in the patients with normal and prolonged A-H intervals. In summary, A-H prolongation was associated with increased incidence of organic heart disease and myocardial dysfunction. The risk of development of A-V nodal block was greater in patients with a prolonged A-H interval but appeared to be of minimal clinical significance.