Intermittent Bundle Branch Block Research Articles

High incidence of inappropriate alarms due to artifact sensing and misclassification of episodes in patients with wearable cardioverter-defibrillators

Abstract Background The wearable cardioverter-defibrillator (WCD) has become a useful tool used for temporary protection from sudden cardiac death. However, since the WCD uses surface electrodes to detect arrhythmias, it is prone to inappropriate detection. Although shock conversion rates for the WCD are high for detected events, its efficacy in clinical practice tends to be degraded by patient noncompliance. Reasons include wear discomfort and frequent false alarms, that may interrupt sleep and generate anxiety. Data on the incidence of false alarms emitted by the WCD and their predictors are rare. Purpose The aim of our study was to assess both artifact and misclassification burden and wear compliance in patients with a WCD. Methods and Results We conducted a single-centre retrospective observational study analyzing patients with a WCD prescribed at our institution. In total, in 134 patients (mean age 51.7 ± 13.8 ys, 79.1% male) provided with a WCD, arrhythmia recordings were analyzed and categorized as either non-sustained ventricular tachycardia, sustained ventricular tachycardia / fibrillation, and artifact sensing or misclassified episodes. Indication for WCD prescription was both primary and secondary prophylactic. All patients received optimal medical therapy. Baseline evaluation in all patients included transthoracic echocardiography, 12-lead electrocardiogram, and baseline laboratory values. A total of 3019 false WCD alarms were documented in 134 patients (average number of false alarms 22.5 ± 130.4 episodes per patient) over a mean WCD wearing time of 71.5 ± 70.9 days (daily wearing time 20.2 ± 5.9 hs). In total, in 78 patients (58.2%), either artifact sensing (41.8%), misclassified episodes (3.7%) or both (9.7%) occurred. Misclassified episodes included sinus tachycardias, atrial flutter, atrial fibrillation, ventricular extrasystoles, and intermittent bundle branch block. At multivariate analysis, WCD wearing time (HR 1.02; 95% CI 1.01-1.02; P < 0.001) and loop diuretics (HR 0.16; 95% CI 0.06-0.44; P < 0.001) were identified as independent predictors of artifact episode occurrence. In terms of the frequency of artifact episodes, loop diuretics (HR -0.11; 95% CI interval -0.21-0.0001; P = 0.049), angiotensin receptor-neprilysin inhibitors (ARNIs) (HR -0.11; 95% CI -0.22-0.01; P = 0.03), and the R-amplitude (HR -0.17; 95% CI -0.27-0.07; P = 0.01) of the WCD baseline electrocardiogram (ECG) were independent predictors. In addition, WCD wearing time (HR 1.00; 95% CI 1.00-1.01; P = 0.04), atrial fibrillation (HR 4.03; 95% CI 1.15-14.11; P < 0.001), and ARNIs (HR 3.17; 95% CI 1.05-9.52; P < 0.001) were significantly associated with the occurrence of misdetected / misclassified episodes. Conclusions In conclusion, In WCD patients with a ZOLL LifeVest system, false alarms emitted by the device were frequent and most common caused by artefacts.

Unmasking of infra-Hisian conduction abnormality by intravenous isoproterenol during electrophysiology study for syncope.

Recurrent unexplained syncope in the background of bundle branch block (BBB) often requires a pacemaker. But the decision-making for pacemaker is difficult in case of single episode of syncope with intermittent bundle branch block. We encountered one such case with intermittent LBBB, where the results of invasive EP study were even normal, until intravenous isoproterenol unmasked the infra-Hisian disease during decremental atrial pacing.

Electrophysiological ventricular substrate of stroke: a prospective cohort study in the Atherosclerosis Risk in Communities (ARIC) study

ObjectivesThe goal of the study was to determine an association of cardiac ventricular substrate with thrombotic stroke (TS), cardioembolic stroke (ES) and intracerebral haemorrhage (ICH).DesignProspective cohort study.SettingThe Atherosclerosis Risk in...

Incessant accelerated idioventricular rhythm mimicking preexcitation

ECG of patients with Wolf Parkinson White (WPW) syndrome may simulate other entities such as myocardial infarction, ventricular premature complexes, ventricular bigeminy, accelerated idioventricular rhythm, intermittent bundle branch block or electrical alternans. On the other hand, the opposite can also occur where these other conditions may simulate WPW. We present the case of a young patient referred for WPW ablation showing an incessant accelerated idioventricular rhythm mimicking preexcitation.

Supernormal and alternating conduction in intermittent bundle branch block and intermittent or concealed ventricular preexcitation. Electrophysiological study, mechanisms and clinical considerations

Supernormal and alternating conduction are not rare in clinical arrhythmology, detectable at various levels of the conduction system in different pathophysiological conditions, and often associated, so as to justify the search for a possible link between them. In order to define a possible relationship between supernormal and alternating conduction, the electrophysiological data of two patient groups were analyzed. Group 1 included 9 patients with intermittent bundle branch block in the presence of supernormal conduction through the pathological branch. Group 2 included 16 patients with ventricular preexcitation, intermittent or concealed, in the presence of supernormal conduction through the atrioventricular accessory pathway. In group 1, 8 patients had a phase 3 and 1 patient a phase 3 and phase 4 bundle branch block. In all 9 patients, the area of phase 3 block was interrupted by a window of unexpected conductivity detectable by atrial premature stimulation. In 7/9 cases, by modulating the atrial rate, alternating conduction through the branch was observed, and the cardiac cycle of occurrence of the phenomenon was in the range of supernormal conduction in 6/7 cases. In group 2, 11 patients showed conduction through the accessory pathway only for a narrow range of cardiac cycles, during atrial premature stimulation. One patient had a prolonged accessory pathway refractory period (phase 3 block), but a window of unexpected supernormal conduction within the refractory zone was observed at atrial premature stimulation. Another patient presented a tachycardia and bradycardia-dependent block along the accessory pathway (phase 3 and phase 4 block) and the phase 3 block area was interrupted by a window of supernormal conduction. In the other three cases, supernormal conduction was manifested as unexpected resumption of conductivity through the accessory pathway for atrial cycles more precocious than the actual duration of its effective refractoriness. By modulating the atrial rate, alternating conduction through the accessory pathway was observed in 13/16 cases, and the cardiac cycle at which this phenomenon appeared falling in the range of supernormal conduction in 11/13 cases. It can be hypothesized that supernormal conduction is in relation with the presence of a phase of supernormal excitability experimentally demonstrated in the late phase of repolarization of cardiac cells, and that supernormal and alternating conduction are related phenomena, so that the evidence on ECG of alternating conduction through a pathological branch or an atrioventricular accessory pathway can be considered as a marker of the presence of supernormal conduction through the structure.

Clinical and experimental evidence of supernormal excitability and conduction.

True supernormality of excitability and conduction has been demonstrated in normal Purkinje fibers in in vitro studies. In the clinical setting, supernormality of conduction is manifested better than expected. This phenomenon is much more common than previously thought, particularly in the presence of certain clinical conditions. If a careful scanning of the cardiac cycle is performed on all patients with intermittent bundle branch block and second degree or advanced infranodal AV block, accessory pathways and mulfunctioning pacemakers, it is anticipated that a much larger amount of supernormal excitability and conduction will be unmasked.

Neurogenic electrocardiographic changes with intermittent bundle branch block after interventricular hemorrhage

Neurogenic electrocardiographic changes with intermittent bundle branch block after interventricular hemorrhage

Intermittent bundle branch block: a clinical model for the study of electrophysiological phenomena

Disorders of intraventricular conduction (bundle branch block and hemiblock) are usually stable and remain unchanged irrespective of heart rate. Not infrequently, however, their appearance is related to the duration of the cardiac cycle, so that they appear and disappear with changes in heart rate. This may not even represent a pathological phenomenon, since sudden and consistent changes in cardiac cycle can result, even physiologically, in aberrant conduction. However, when a bundle branch block appears intermittently for simple and progressive increments, or even deceleration, of the sinus rate, this is related to a true bundle branch pathology, i.e. tachycardia-dependent (or phase 3) block or bradycardia-dependent (or phase 4) block, respectively. Phase 3 block is believed to express a pathological increase in the duration of the recovery period of the bundle branch. Phase 4 block was best explained on the basis of enhanced phase 4 depolarization of the bundle branch system, with inability of excitation if the cardiac cycle is particularly prolonged. The two types of block, phase 3 and phase 4, often coexist. An intraventricular conduction disturbance that appears during increasing heart rate for a phase 3 block is maintained, if frequency slows down, even for cycles greater than those that brought about its appearance. This is due to retrograde activation of the bundle branch blocked in the antegrade direction, with delay of its action potential inscription. Sometimes, in the presence of phase 3 bundle branch block, very early atrial ectopic beats are paradoxically conducted in the normal way (supernormal conduction). Perhaps, this phenomenon is related to a possible "climb over" of the injured zone of the bundle branch by the blocked impulses that arise beyond the injured area as subliminal impulses, exciting the healthy tissues if catches them during their phase of supernormal excitability. In the presence of intermittent bundle branch block, it is not uncommon to observe long periods of sinus rhythm with regular PP interval, conducted with alternating (2:1) bundle branch block. Intermittent left bundle branch block is a clinical model of cardiac memory: in these cases, negative T waves in the antero-septal leads during normal conduction are often evident. This negativity is an expression of cardiac memory, and not of ischemia as initially interpreted. Intermittent bundle branch block is an excellent model to study in vivo the effects of antiarrhythmic drugs on the pathological bundle branches. Narrowing of the QRS complex in the presence of bundle branch block is not always an expression of intermittent aberrancy: beware of late ectopic beats originating from the ipsilateral ventricle to the blocked branch, that merging with the antegrade beat conducted with bundle branch block, restrict the QRS, simulating intermittent aberrancy.

臨床 一過性・間歇性脚ブロック16例の検討

臨床 一過性・間歇性脚ブロック16例の検討

Combination of cardiac conduction disease and long QT syndrome caused by mutation T1620K in the cardiac sodium channel

The aim of the present study was to elucidate the molecular mechanism underlying the concomitant occurrence of cardiac conduction disease and long QT syndrome (LQT3), two SCN5A channelopathies that are explained by loss-of-function and gain-of-function, respectively, in the cardiac Na+ channel. A Caucasian family with prolonged QT interval, intermittent bundle-branch block, sudden cardiac death, and syncope was investigated. Lidocaine (1 mg/kg i.v.) normalized the prolonged QT interval and rescued bundle-branch block. An SCN5A mutation analysis was performed that revealed a C-to-A mutation at position 4859 (exon 28), predicted to change a highly conserved threonine for a lysine at position 1620. Mutant channels were characterized both in Xenopus oocytes and HEK293 cells. The T1620K mutation remarkably altered the properties of Nav1.5 channels. In particular, the voltage-dependence of the current decay time constants was largely lost. As a consequence, mutant channels inactivated faster than wild-type channels at potentials negative to -30 mV, resulting in less Na+ inward current (loss-of-function), but significantly slower at potentials positive to -30 mV, resulting in an increased Na+ inward current (gain-of-function). Moreover, we found a hyperpolarized shift of steady-state activation and an accelerated recovery from inactivation (gain-of-function). At the same time, channel availability was significantly reduced at the resting membrane potential (loss-of-function). We conclude that lysine at position 1620 leads to both loss-of-function and gain-of-function properties in hNav1.5 channels, which may consequently cause in the same individuals impaired impulse propagation in the conduction system and prolonged QTc intervals, respectively.

Clinical logistics in 24-hour ambulatory electrocardiographic monitoring.

In total, 493 ambulatory ECG recordings were studied. Women were preponderant (62.3% vs 37.7%). The average age of women and men patients was 66.9 and 64.7 years, respectively. Of the ECGs studied, 71.4% showed abnormalities and 28.6% appeared completely normal. Urgent abnormalities were noted in 1.4% of the recordings and significant abnormalities were present in 14.6%. Subjective complaints were noted in their logbooks by 18.8% of patients, but correlation of complaints with the electrocardiographic abnormalities was noted in only 1.2% of cases. The attending cardiologist concluded that 23.9% of the tests supported reasons of valid necessity for performance. Two hundred seventy-three recordings were classified as electrocardiographically abnormal (55.4%) but were clinically insignificant. General practitioners requested 59.8% of the tests versus 40.2% by specialists. Preponderant abnormalities included premature atrial and ventricular contractions, supraventricular tachycardia, and atrial fibrillation. Less frequent abnormalities included ventricular tachycardia (4.6%), atrial flutter, atrioventricular block, artificial pacemaker rhythm, nodal rhythm, and intermittent bundle branch block.

Intensive Care Unit ECG Monitoring

Perhaps the most useful means of monitoring the critically ill patient is the electrocardiogram (ECG). A 12lead ECG is useful to rule out cardiac complications in the acutely injured patient, the postoperative patient, and the septic patient [1]. Limb lead II or chest lead V may be continuously monitored for evidence of progressive cardiac disease and complicating dysrhythmias [1]. This section summarizes the usefulness and indications of the ECG in monitoring of the high-risk, critically ill patient and possibilities for future clinical use. Interpretation of the ECG waveform provides the basis for diagnosis and therapy of numerous conditions associated with disorders of the myocardium in the intensive care unit (ICU) [1]. Continuous ECG monitoring is essential for the adult patient with acute myocardial infarction because dysrhythmias are the most common life-threatening complication [1]. Continuous ECG monitoring of the postoperative general surgical patient is not as useful because the incidence of lifethreatening dysrhythmias is lower [1,2]. However, in adults and children with decreased myocardial function, hypovolemia, or hypoxemia, the ECG may show PVCs, PACs, ST segments changes, altered T-waves, and bradycardia [1]. These abnormalities may be produced by inadequate oxygen delivery to the myocardium and therefore serve to alarm the physician of potentially signi~cant pathophysiologic disturbances. One of the main uses for the ECG is the determination of heart rate or pulse. Most ICUs measure heart rate as a calculated time-averaged signal from the bedside ECG monitor. Heart rate is a very nonspeci~c cardiorespiratory variable. However, tachycardia may signal signi~cant and abrupt cardiovascular compromise such as hypovolemia, hypoperfusion, or diminished myocardial contractility in the critically ill patient [3]. The degree of tachycardia is roughly proportional to the severity of the cardiovascular impairment. Tachycardia is also present in association with infection, anxiety, stress, fever, exercise, pain, and anxiety. Bradycardia may occur with inferior myocardial infarction, arteriosclerotic heart disease, or severe systemic hypoxemia [3]. Heart rate may also be used during invasive hemodynamic monitoring with thermodilution pulmonary arterial catheters to calculate stroke volume and other hemodynamic variables. The ECG may be used directly or as an adjunctive test in the diagnosis of numerous diseases and conditions affecting the critically ill patient. Myocardial ischemia may occur in the critically ill patient with shock, even in the absence of primary coronary artery disease [1]. Myocardial ischemia ultimately results in T-wave inversion. Myocardial injury due to ischemia may cause elevation of the ST segment if the ischemia is transmural or ST segment depression if the ischemia is nontransmural and predominantly subendocardial [1]. Progressive ischemia results in myocardial infarction which is often manifested in the ECG by Qwave deepening and distortion, loss of R-wave voltage, and/or an increased R-wave amplitude [1]. However, ECG abnormalities characterizing myocardial ischemia and infarction are nonspeci~c. Serial ECGs should be followed to speci~cally diagnose and localize myocardial ischemia and infarction [1]. Table 1 lists characteristic changes in the ECG associated with other disease states commonly seen in critically ill patients. ECG changes observed in drug overdose or poisoning, and electrolyte and metabolic disturbances are shown in Tables 2 and 3. Abnormal cardiac rhythms may occur during critical illness at any time and are the most common mechanism of death in adults [1]. Automated arrhythmia detection algorithms are commercially available and in use in many ICUs. These algorithms ~lter the incoming ECG signal, detect and classify the QRS complex, identify ectopic events and ventricular rhythms, and generate alarms. For ventricular ectopic beats, the system has a reported sensitivity of up to 90% with a false positive rate of #1%. However, the algorithms may result in false positive alarms if the Tor P-waves are $50% of the R-wave amplitude, and are not useful for detection of aberrantly conducted beats, atrial ~brillation and _utter, and intermittent bundle branch block. In summary, the clinical utility and cost effectiveness of these and other automated forms of ECG monitoring in the ICU, such as automated ST segment monitoring [5] and signal-averaged electrocardiography (detailed in subsequent sections), have yet to be determined. The ECG waveform itself may be an important source of clinical information that has only recently

Effect of bundle branch block on local electrogram morphologic features: Implications for arrhythmia diagnosis by stored electrogram analysis

Analysis of stored local ventricular electrogram recordings is a useful diagnostic tool in the evaluation of patients with implantable cardioverter defibrillators. Visual analysis of local electrogram morphologic features has been demonstrated to be useful in distinguishing ventricular tachycardia from supraventricular rhythm. The effect of bundle branch block (BBB) aberration during supraventricular tachycardia on local electrogram morphologic features is not entirely clear. Erroneous diagnoses resulting from a change in electrogram morphologic features with BBB may occur. To determine whether the development of BBB can produce a change in local electrogram morphologic features and whether this change is dependent on the site of recording, we retrospectively reviewed local electrogram recordings from 23 patients who had intermittent BBB during electrophysiologic evaluation of documented or suspected supraventricular tachycardia. Local electrogram recordings from catheters placed in the right ventricular apex and coronary sinus during supraventricular tachycardia with BBB aberrancy were compared with recordings during narrow complex supraventricular tachycardia or normal sinus rhythm. Bipolar recordings were made with a 5 mm inter-electrode distance with filter settings at 40 to 400 Hz. Three independent blinded observers defined the paired electrograms as the same or distinctly different. During right BBB a change in electrogram morphologic features was demonstrated in 11 (85%) of 13 recordings from the right ventricular apex and in only 1 (8%) of 12 recordings from the coronary sinus. In contrast, during left BBB a change in electrogram morphologic features was seen in 6 (100%) of 6 recordings from the coronary sinus and in only 1 (8%) of 13 recordings from the right ventricular apex. These results demonstrate that when the described recording techniques are used, a change in local ventricular electrogram morphologic features during BBB is predominantly manifest in recording sites ipsilateral to the BBB, whereas recording sites contralateral to the BBB are relatively unaffected. This information may have implications regarding interpretation of stored electrograms when an attempt is made to establish a rhythm diagnosis leading to implantable cardioverter defibrillator therapy.

Contrasting effects of verapamil and procainamide on rate-dependent bundle branch block: Pharmacologic evidence for the role of depressed sodium channel responses

The mechanisms responsible for intermittent bundle branch block are still under debate. The role of the time-dependent behavior of the slow calcium channel has recently been emphasized. To test this hypothesis and ascertain the possible involvement of the fast sodium channel, the effects of the slow calcium channel blocker verapamil and the fast sodium channel blocker procainamide were compared in 10 patients with intermittent bundle branch block. All 10 patients showed bundle branch block during spontaneous sinus rhythm. Maneuvers to slow cardiac rate (that is, carotid sinus massage, Valsalva maneuver) were performed to identify normal conduction as well as phase 4 bundle branch block.Thus, the ranges of diastolic intervals (RR) resulting in phase 3 (tachycardia-dependent) bundle branch block, phase 4 (bradycardia-dependent) bundle branch block and normal conduction were measured in two control studies performed before intravenous administration of verapamil (control 1) and procainamide (control 2) and at the peak effect of both drugs. In the control studies, all 10 patients showed phase 3 bundle branch block, whereas phase 4 bundle branch block occurred in only 4 patients. The ranges of phase 3 bundle branch block, phase 4 bundle branch block and normal conduction were very similar in control studies 1 and 2. The phase 3 bundle branch block range was slightly shortened by verapamil (983 ±83.5 ms in control 1; 930 ±69.4 ms at the peak effect of verapamil), whereas phase 4 bundle branch block remained unchanged. In contrast, conduction was systematically worsened by procainamide. The phase 3 bundle branch block range was prolonged 80 to 1,770 ms in five of the six patients with apparently isolated phase 3 bundle branch block, and rate-independent bundle branch block occurred in all four patients with both phase 3 and phase 4 bundle branch block as well as in one patient showing an isolated phase 3 bundle branch block.The absence of any depressing action of verapamil and the marked effects induced by procainamide strongly support the view that clinical intermittent bundle branch block is related to depressed fast responses and not to slow calcium-mediated responses. Hence, these conduction disturbances probably occur in tissues operating at a subnormal but still relatively high level of membrane potential.

Rate-dependent changes in excitability of depressed cardiac Purkinje fibers as a mechanism of intermittent bundle branch block.

When the heart rate is accelerated, rate-dependent intraventricular block may occur. This block has been attributed to abnormal action potential prolongation in a diseased conducting pathway. Less often, intraventricular block develops during slowing of the heart rate and has been explained in terms of phase 4 depolarization in potentially automatic cells within the diseased fascicle. We tested these hypotheses in isolated bundles of Purkinje fibers placed in a three-chambered tissue bath. In one group of experiments, conditions of localized injury and depressed excitability were mimicked by superfusing the central segment with sucrose solution. Action potentials were initiated in the proximal segment while the slope of phase 4 of cells in the distal end was controlled by intracellular ramps of current of either polarity. In these preparations, phase 4 depolarization facilitated rather than retarded propagation across the depressed segment, even at takeoff potentials as low as -45 mV. In a second group, depressed excitability was induced by exposing the three fiber segments to Tyrode's solution that contained high concentrations of KCl and CaCl2 or isoproterenol (0.1 microgram/ml). Under these conditions, Purkinje fibers did not undergo phase 4 depolarization and did not generate abnormally prolonged action potentials. These preparations showed a biphasic time dependence of conduction during premature stimulation or in response to changes in the basic cycle length. Conduction impairment and block were manifest at either side of an optimal interval or cycle length. Our results suggest that phase 4 depolarization and abnormally prolonged action potentials are not necessary conditions for intermittent block. Both tachycardia and bradycardia-dependent intraventricular conduction abnormalities may be associated with time-dependent variations in the excitability of depolarized conducting fibers as well as in the amplitude of the slow responses generated by these fibers. These alterations can be explained in terms of regulation of slow inward current by the intracellular calcium concentration.

The effect of intermittent bundle branch block on the coupling interval of ventricular premature depolarizations.

The mechanism of origin of ventricular premature depolarizations (VPDs) is explained by automaticity or reentry. We studied three patients with intermittent left bundle branch block (LBBB) and unifocal VPDs of right bundle branch block (RBBB) morphology (assumed left ventricular origin). We examined the effect of different types of intraventricular conduction on the coupling intervals of the VPDs. Specifically, we proposed that the coupling intervals of VPDs would be longer during LBBB conduction of sinus beats (ipsilateral to the ventricle of origin of VPDs) compared with the coupling intervals during normal intraventricular conduction. We found that the coupling intervals during LBBB were significantly longer than those during normal conduction in all three cases (patient 1, 596 +/- 7 vs 484 +/- 5 msec; patient 2, 639 +/- 9 vs 534 +/- 11 msec; patient 3, 444 +/- 4 vs 382 +/- 9 msec) (p less than 0.005). We also examined the length of the preceding RR intervals and counted sinus beats intervening between successive VPDs (S values). One case demonstrated S values suggestive of concealed bigeminy; the other cases had S values suggesting concealed bigeminy and its variants. We have demonstrated that some VPDs are dependent on an initiating sinus beat. This dependence on a preceding beat is consistent with both a reentrant mechanism or triggered automaticity.

Usefulness of the ajmaline test in patients with latent bundle branch block

Twelve patients were studied with intermittent bundle branch block whose conduction disturbance disappeared completely and could no longer be recorded even after provoked changes in heart rate. Premature atrial stimulation and atrial pacing at rapid rates were performed in nine patients; in none of these nine were these procedures able to evoke the complete bundle branch block pattern that all patients exhibited before the spontaneous normalization of conduction. In marked contrast, the administration of ajmaline (1 mg/kg body weight, intravenously in 90 seconds) caused the bundle branch block pattern to reappear in 10 (83.3 percent) of the 12 patients 30 to 120 seconds after the end of the injection, and in 11 patients (91.6 percent) when additional atrial stimulation was performed in 1 of the 2 “failures.” This pharmacologie test was much more rapid and simple than electrophysiologic testing and it was noninvasive. Results of this study suggest that some form of subclinical fascicular injury was present (or had persisted) at a time when intraventricular conduction was persistently normal even though no significant physiologic alteration could be demonstrated by the atrial stimulation techniques. The ajmaline test may become a valuable tool for uncovering cases of latent bundle branch block and furthering our knowledge of the early natural history of intraventricular block.

Effects of isoproterenol on abnormal intraventricular conduction.

An isoproterenol infusion (1.0-4.0 microgram/min) was administered to 15 patients with intermittent bundle branch block (BBB) and two patients with apparently fixed BBB. Three main effects were documented: (1) In all patients with phase 3, or tachycardia-dependent, BBB, isoproterenol caused a pronounced shortening of refractoriness in the affected fascicle. (2) In patients showing phase 4, or bradycardia-dependent, BBB, isoproterenol prolonged the phase 4 block range, probably because of enhanced diastolic depolarization. In one patient (four studies) in whom phase 4 block was not present, isoproterenol caused the appearance of a phase 4 block range. (3) In the two patients with fixed BBB, isoproterenol restored conduction, probably as a result of a hyperpolarizing effect. This study shows that isoproterenol tends to restore or improve conduction related to tachycardia-dependent block, but may impair conduction related to bradycardia-dependent block.

臨床 空間心室 gradient の恒常性の臨床的検討

臨床 空間心室 gradient の恒常性の臨床的検討

Recent Insights into Paroxysmal Supraventricular Tachycardia– An Integrated Approach to Diagnosis and Therapy

Paroxysmal supraventricular tachycardia may result from re-entrance in the AV node, the normal A-V pathway with an accessory AV connection, in the sino-atrial node, in the atria, or else reflect ectopic impulse formation in a spontaneously automatic supraventricular focus. Electrocardiographic criteria which are helpful in differentiating these mechanisms involve an analysis of cycle length, changes in cycle length with intermittent bundle branch block, P wave morphology and the relationship of P wave to QRS complex, P-R interval, the presence of A-V block during tachycardia and the influence of autonomic tone on the tachycardia. Electrophysiologic studies further elucidate mechanism by demonstrating the mode of induction and termination of the tachycardia, the characteristics of antegrade and retrograde A-V conduction curves and refractory periods, atrial activation sequence of echo beats and the influence of premature beats introduced during tachycardia. These features are summarised in Table 1. Therapy can be accurately planned according to the results of experimental administration of antiarrhythmic agents and of pacing sequences upon induction and termination of tachycardia in the catheterisation laboratory.