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.

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.

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.

Significance of left axis deviation in patients with chronic left bundle branch block.

Forty-nine patients with chronic left bundle branch block and a normal frontal axis were compared with 53 patients with left bundle branch block and left axis deviation. The following clinical variables were more frequent (P less than 0.05) in patients with left axis deviation: greater age, exertional angina, congestive heart failure, cardiomegaly, cardiac functional class II to IV, coronary artery disease and presence of organic heart disease. Absence of organic heart disease (primary conduction disease) was seen only in patients with a normal axis. Patients with left axis deviation had longer (P less than 0.05) mean P-R, A-H and H-V intervals and atrial and atrioventricular (A-V) nodal effective refractory periods. All patients were prospectifely followed up for 30 to 2,271 days with a mean +/- standard error of the mean follo-up period of 538 +/- 72 for the group with a normal axis and 604 +/- 72 days for the group with left axis deviation (difference not significant). A-V block developed in three patients (6 percent) with left axis deviation and in none of those with a normal axis. The cumulative 4 year mortality rate for the entire group approached 75 percent. The patients with left axis deviation had greater cardiovascular mortality (P less than 0.05). In conclusion, among patients with left bundle branch block, those with left axis deviation have a greater incidence of myocardial dysfunction, more advanced conduction desease and greater cardiovascular mortality than those with a normal axis.

Clinical, electrocardiographic and electrophysiologic observations in patients with paroxysmal supraventricular tachycardia.

Seventy-nine patients without ventricular preexcitation but with documented paroxysmal supraventricular tachycardia were analyzed. Electrophysiologic studies suggested atrioventricular (A-V) nodal reentrance in 50 patients, reentrance utilizing a concealed extranodal pathway in 9, sinus or atrial reentrance in 7 and ectopic automatic tachycardia in 3. A definite mechanism of tachycardia could not be defined in 10 patients (including 7 whose tachycardia was not inducible). The three largest groups with inducible tachycardias were compared in regard to age, presence of organic heart disease, rate of tachycardia, functional bundle branch block during tachycardia and relation of the P wave and QRS complex during tachycardia. A-V nodal reentrance was characterized by a narrow QRS complex and a P wave occurring simultaneously with the QRS complex during tachycardia. Reentrance utilizing a concealed extranodal pathway was characterized by young age, absence of organic heart disease, fast heart rate, presence of bundle branch block during tachycardia and a P wave following the QRS complex during tachycardia. Sinoatrial reentrance was characterized by frequent organic heart disease, a narrow QRS complex and a P wave in front of the QRS complex during tachycardia. In conclusion, a mechanism of paroxysmal supraventricular tachycardia could be defined in most patients. Observations of clinical and electrocardiographic features in these patients should allow prediction of the mechanism of the tachycardia.

H-V interval in patients with bifascicular block (right bundle branch block and left anterior hemiblock). Clinical, electrocardiographic and electrophysiologic correlations.

Electrophysiologic studies were performed in 119 adults with chronic bifascicular block manifested by right bundle branch block and left anterior hemiblock. The H-V interval was normal in 86 patients and prolonged in 33. The following clinical variables were more frequent (P less than 0.05) in patients with a prolonged H-V interval: cardiac third sound, mitral systolic murmur, cardiomegaly on chest roentgenogram, congestive heart failure and cardiac functional class III or IV (New York Heart Association criteria). The following differences in the electrocardiographic and electrophysiologic findings were found: Patients with a prolonged H-V interaval had a longer mean P-R interval, QRS duration and A-H interval (P less 0.02). All patients were followed up prospectively in a cardiac conduction disease clinic after initial evaluation. The mean follow-up periods were (mean plus or minus standard error of the mean) 514 plus or minus 49 and 563 plus or minus 34 days for the patients with a prolonged and normal H-V interval, respectively. Progression of conduction disease occurred in three patients (4 percent) with a normal H-V interval and in four (12 percent) with a prolonged interval. The cumulative 3 year mortality rate for the entire group was 25 percent. The patients with a prolonged H-V interval had a higher cumulative 2 year mortality rate than those with a normal H-V interval but the difference was not statistically significant. In summary, a prolonged H-V interval was often associated with serious myocardial dysfunction and a high mortality rate. The risk of progression of conduction disease was slight with either a prolonged or a normal H-V interval during this relatively short follow-up period.

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.

Electrophysiologic effects of atropine on sinus node and atrium in patients with sinus nodal dysfunction.

Electrophysiologic studies were conducted in 21 patients with sinus nodal dysfunction before and after intravenous administration of 1 to 2 mg of atropine. The mean sinus cycle length (+/- standard error of the mean) was 1,171 +/- 35 msec before and 806 +/- 29 msec after administration of atropine (P less than 0.001). Mean sinus nodal recovery time determined at a aced rate of 130/min and maximal recovery time were, respectively, 1,426 +/- 75 and 1,690 +/- 100 msec before and 1,169 +/- 90 and 1,311 +/- 111 msec after atropine (P less than 0.001 and less than 0.001). Mean calculated sinoatrial conduction time, measured in 16 patients, was 113 +/- 8 msec before and 105 +/- 9.7 msec after atropine (difference not significant). Mean atrial effective refractory period, measured at an equivalent driven cycle length, was 262 +/- 11.1 msec before and 256 +/- 10.3 msec after atropine (not significant). Mean atrial functional refractory period was 302 +/- 12.5 msec before and 295 +/- 11.3 msec after atropine (not significant). The shortening of sinus cycle length and sinus recovery time with atropine was similar to that noted in patients without sinus nodal dysfunction. In contrast, atropine had insignificant effects on sinoatrial conduction and atrial refractoriness in this group whereas it shortens both in normal subjects. This finding may reflect altered perinodal and atrial electrophysiologic properties in patients with sinus node disease.

Electrophysiologic effects of atropine on human sinus node and atrium.

Electrophysiologic studies were conducted in 17 patients without apparent sinus node disease before and after intravenous administration of 1 to 2 mg of atropine. Mean values in milliseconds (+/- standard error of the mean) before and after administration of atropine were as follows: sinus cycle length 846 +/- 26.4 versus 647 +/- 20.0 (P less than 0.001); sinus nodal recovery time 1,029 +/- 37 versus 774 +/- 36 (P less than 0.001); mean calculated sinoatrial (S-A) conduction time 103 +/- 5.7 versus 58 +/- 3.9 (P less than 0.001); mean P-A interval 34 +/- 1.5 msec versus 31 +/- 1.5 (P less than 0.05); mean atrial effective and functional refractory periods during sinus rhythm 285 +/- 11.3 versus 238 +/- 7.9 and 331 +/0 11.6 versus 280 +/- 8.6, respectively (P less than 0.001 for both); mean atrial effective and functional refractory periods measured at equivalent driven cycle length 239 +/- 7.7 versus 213 +/- 7.4 and 277 +/- 11.4 versus 245 +/- 9.5, respectively (P less than 0.001 for both). In conclusion, atropine shortened sinus cycle length, sinus nodal recovery time and calculated S-A conduction time. The shortening of atrial refractory periods with atropine implies that vagotonia prolongs atrial refractoriness in man.

Chronic right bundle branch block and left posterior hemiblock. Clinical, electrophysiologic and prognostic observations.

Twenty-one patients with long-term right bundle branch block and left posterior himiblock were studied electrophysiologically and then followed up prospectively. The group consisted of 19 men and 2 woman aged 61 +/- 2.7 years (mean +/- standard error of the mean). The majority of patients had either hypertensive cardiovascular disease (48 percent) or primary conduction disease (33 percent). Initial electrophysiologic studies revealed A-H intervals of 58 to 152 msec (mean 98 +/- 7.7) and H-V intervals of 40 to 80 msec (mean 52 +/- 2.1). Six patients (29 percent) had prolonged H-V intervals. The follow-up period ranged from 91 to 1,231 days (mean 671 +/-68). Three of 21 patients (14 percent) needed a permanent pacemaker after development of the following symptomatic conduction disease: sinoatrial block on day 3 of follow-up; second degree atrioventricular (A-V) block, site undetermined, on day 118; and second degree A-V block proximal to the His bundle on day 398. One patient died suddenly (on day 571), and two others died of noncardiac causes. In conclusion, combined right bundle branch block and left posterior hemiblock was associated with less trifascicular disease than reported previously. The clinical course of most of the patients was benign and the incidence of sudden death was relatively small. Symptomatic conduction disease occurred but could be definitely related to trifascicular disease in only one patient. These short-term data suggest that prophylactic pacemaker insertion is not routinely indicated in patients with chronic right bundle branch block and left posterior hemiblock.

Alternating Wenckebach periodicity: A common electrophysiologic response.

Alternating Wenckebach periods are defined as episodes of 2:1 atrioventricular (A-V) block in which conducted P-R intervals progressively prolong, terminating in two or three blocked P waves. In this study, His bundle recordings were obtained in 13 patients with pacing-induced alternating Wenckebach periods. Three patterns were noted: Pattern 1 (one patient with a narrow QRS complex) was characterized by 2:1 block distal to the H deflection (block in the His bundle) and Wenckebach periods proximal to the H deflection, terminating with two blocked P waves. Pattern 2 (four patients) was characterized by alternating Wenckebach periods proximal to the His bundle, terminating with three blocked P waves. Pattern 3 (eight patients) was characterized by alternating Wenckebach periods proximal to the His bundle, terminating with two blocked P waves. Alternating Wenckebach periods are best explained by postulating two levels of block. When alternating Wenckebach periods are terminated by three blocked P waves (pattern 2), the condition may be explained by postulating 2:1 block (proximal level) and type I block (distal level). When alternating Wenckebach periods are terminated by two blocked P waves (patterns 1 and 3), the condition may be explained by postulating type I block (proximal level) and 2:1 block (distal level). Pattern 1 reflects block at two levels, the A-V node and His bundle. Patterns 2 and 3 most likely reflect horizontal dissociation within the A-V node.

The clinical spectrum of chronic His bundle block.

This report details our total experience with documented chronic His bundle block in 24 patients. Ten patients had second-degree block (eight with 2:1 block and two with type-1 block), and 14 patients had complete heart block. There were 16 women (67 percent) and eight men (33 percent) with ages ranging from 17 to 87 years. Diagnoses were as follows: hypertensive cardiovascular disease, nine patients (38 percent); arteriosclerotic heart disease, six patients (25 percent); aortic valvular disease, three patients (13 percent); primary conduction disease, two patients (8 percent); primary myocardial disease, two patients (8 percent); congenital heart block, one patient (4 percent); and traumatic heart block, one patient (4 percent). Pacing was instituted in 20 patients because of the following; congestive heart failure, seven patients; syncope, seven patients; fatigue, four patients; and recurrent dizziness, two patients. Permanent pacing was indicated within ten days of initial diagnosis in 13 patients, from 20 to 80 days in four patients, and later than 100 days in three patients. An additional two asymptomatic patients were treated with prophylactic pacing.

Failure of surgery in preexcitation. Correlation with pathologic findings.

A 37-year-old man with mitral stenosis and recurrent drug-resistant paroxysmal atrial fibrillation, paroxysmal supraventricular tachycardia, and preexcitation, underwent two surgical attempts to ablate an anomalous pathway (AP). Electrophysiologic study demonstrated a left posterior AP with a short antegrade refractory period. Epicardial mapping at the time of mitral valve replacement (left lateral thoracotomy) suggested a posterior right AP. Mitral valve replacement and incision of the left atrial wall failed to cure preexcitation. Epicardial mapping at a second operation (median sternotomy) demonstrated a subepicardial left posterior AP. Right atrial and atrial septal incisions failed to cure preexcitation. Serial section of the atrioventricular rings and conduction system demonstrated an intact left posterior anomalous atrioventricular muscle bundle with surgical incision placed above the plane of the mitral anulus.

Effect of anomalous pathway location on rate of canine experimental A-V reentrant tachycardia.

The effect of anomalous pathway (AP) location and conduction time on the cycle length (CL) and sustainability of paroxysmal A-V reentrant tachycardia was studied in 15 dogs, using an anomalous pathway simulator (APS). The APS was a programmable digital electronic circuit with ability for unidirectional conduction, ventricular sensing, adjustable delay, and atrial stimulation. Contiguous pairs of ventricular sensing electrodes were placed along the A-V ring in each dog at the following sites: anterior, posterior, and lateral right (AR, PR, and LR) and anterior, posterior, and lateral left (AL, PL, and LL) and septal (S). There were significant differences in the CL of tachycardias among the tested sites (P less than 0.01). The CL of tachycardias from the LL site was significantly longer and from the PR site significantly shorter than that from the other sites (P less than 0.05). These differences in CL of tachycardias in relation to the AP location were explicable in terms of corresponding variation in conduction times of the various components of the tachycardia circuit (e.g., intra-atrial, A-V nodal, intraventricular conduction times). The differences in magnitude of the CL of tachycardias, although significant, were small. It was also found that all sites allowed maintenance of tachycardias up to an AP conduction time of 10 ms. In 27% of experiments, atrial refractoriness prevented sustained tachycardias at pathway delays of 1 ms. The relationship between AP conduction time and CL of tachycardias was exponential.