房室传导间期(A-V)的自动测量及频谱特征

目的 探讨房室传导间期(A-V)的自动测量,频谱特点及心率对其影响。方法 实验是在去神经的猫上进行,由右颈总动脉插入主动脉根部,测出希氏束(His)电图,通过模板匹配的方法自动检测His电图中心房(A)、希氏(H)波及心室(V)波,并将AA、AV间期数据通过快速傅立叶(FFT)转换,获得其频谱特征。再通过程序控制心房起搏观察了AA间期变化对AV频谱的影响。结果His束中A、H、V波可以自动重复检测,AV频谱与AA频谱均相似,但密度(PSD)较AA小,经标准化后,两者的高频(HF),低频(LF)及高频/低频(HF/LF)相同(P>0.05),通过心房起搏表明AA间期与AV间期呈非线形关系,AV频谱中HF与AA间期的变化率呈负相关(R=-0.97,P<0.01),LF与AA间期的变化率呈正相关关系(R=0.96,P<0.01)。结论心脏His束自动测量揭示了房室传导的频域特征以及心率对AV频谱各成份的相关关系,为研究心脏房室传导障碍性疾病以及心率对心电频谱的影响提供了一个新的方法。     

Evidence for adenosine mediation of atrioventricular block in the ischemic canine myocardium.

Adenosine levels in oxygen-deprived myocardium can rise to 10- 100 microM concentrations known to cause atrioventricular (AV) conduction delay and block. We reported that the AV conduction delay and block caused by hypoxia is markedly attenuated by 10 microM aminophylline, and adenosine competitive antagonist. THe purpose of the present study was to investigate adenosine's role in ischemic AV conduction disturbances. Dogs were anesthetized and instrumented for His bundle and surface electrogram recordings. The total AV conduction time was subdivided in to atrial-His bundle (AH) and His bundle-ventricle intervals. The atrioventricular node artery (AVNA) was cannulated for selective injection of drugs in the AV node region. Adenosine (10 to 100 microgram), as a 2-ml bolus injection, rapidly produced a dose-dependent, transient increase in the AH interval; a 1,000-microgram dose caused second degree AV block. The duration of the increase in AH interval was also dose-dependent. Dipyridamole, and inhibitor of nucleoside transport, potentiated the negative dromotropic effects of adenosine, whereas aminophylline attenuated them. In some dogs, after cannulation of the AVNA, first and second degree AV block occurred spontaneously or were induced by rapid atrial pacing. Injection of the aminophylline (5 mg/kg, i.e.) or theophylline (100-1,000 microgram) into the AVNA rapidly reversed the AV blocks. Upon washout of the drugs the AV blocks recurred. We conclude that endogenously released adenosine may account for a major fraction of the AV conduction delay and block associated with impaired blood supply to the AV node, and the theophylline and aminophylline reverse the AV conduction defect by antagonizing the effects of adenosine.     

Anatomy of the cardiac conduction system

The specialized cardiomyocytes that constitute the conduction system in the human heart, initiate the electric impulse and result in rhythmic and synchronized contraction of the atria and ventricles. Although the atrioventricular (AV) conduction axis was described more than a century ago by Sunao Tawara, the anatomic pathway for propagation of impulse from atria to the ventricles has been a topic of debate for years. Over the past 2 decades, there has been a resurgence of conduction system pacing (CSP) by implanting pacing leads in the His bundle region in lieu of chronic right ventricular pacing that is associated with worse clinical outcomes. The inherent limitations of implanting the leads in the His bundle region has led to the emergence of left bundle branch area pacing in the past 3 years as an alternative strategy for CSP. The clinical experience from performing CSP has helped electrophysiologists gain deeper insight into the anatomy and physiology of cardiac conduction system. This review details the anatomy of the cardiac conduction system, and highlights some of the recently published articles that aid in better understanding of the AV conduction axis and its variations, the knowledge of which is critical for CSP. The remarkable evolution in technology has led to visualization of the cardiac conduction system using noninvasive, nondestructive high‐resolution contrast‐enhanced micro‐computed tomography imaging that may aid in future CSP. We also discuss from anatomical perspective, the differences seen clinically with His bundle pacing and left bundle branch area pacing.     

His bundle lead placement: Is His bundle captured?

A 59-year-old female underwent a dual-chamber pacemaker implantation for intermittent complete heart block. A baseline electrocardiogram showed normal sinus rhythm with first-degree atrioventricular (AV) block and right bundle branch block. A His bundle lead placement was attempted. An intracardiac electrogram from the His bundle lead demonstrated atrial-His, and His-ventricular intervals were 186 and 110 ms, respectively. Pacing was performed from the His bundle lead with a decremental pacing output to assess for the His bundle capture threshold. However, there were no significant QRS morphology changes during the pacing. Is the His bundle captured? The tracing evaluation demonstrated the fascinating physiology of activation wavefront in His Purkinje system that could be applied in the use of conducting system pacing technologies.     

Rate-related left bundle branch block secondary to intra-his block.

A 67-year-old man who had chronic aortic valvular disease with first degree AV block and rate-related left bundle branch block on the surface electrocardiogram was studied by His bundle electrography. During conduction with narrow QRS complexes, the first degree block was AV nodal in origin. With spontaneous heart rate acceleration a QRS pattern of left bundle branch block emerged, and the His electrogram revealed split His potentials. This report adds strong support to the evolving concept that left bundle branch block, in some cases, actually may be secondary to block anatomically localized to the His bundle.     

Jesús Alanís and the First Recording of the His Bundle: The Scientist and the Man

The anatomy and physiology of the specialized conduction system has intrigued investigators since the 19th century and is still not fully understood. Dr. Wilhelm His Jr. is well known because he discovered the A‐V bundle, and Dr. Sunao Tawara is rightly credited with the discovery of the atrioventricular (AV) node, but who was the first to record the electrical activity of the His bundle? This paper reviews the historical background and scientific contributions made by Dr. Jesús Alanís in the middle of the 20th century working at the National Institute of Cardiology in Mexico City. Collaborating with outstanding investigators such as Arturo Rosenblueth, Dr. Alanís recorded for the first time the electrical activity of the His bundle in the isolate canine heart. That the recorded electrogram was indeed the His bundle and not the AV node was confirmed by detailed studies that set the basis for modern clinical electrophysiology. The life and research contributions of this extraordinary man are reviewed in the context of a unique group of investigators who made significant advances in cardiac electrophysiology.     

Electrophysiological evaluation of the sinus node and the cardiac conduction system following the maze procedure for atrial fibrillation

Transient sinus node dysfunction has been demonstrated by noninvasive methods following the maze procedure for atrial fibrillation (AF). However, extensive data from invasive electrophysiological studies have not been previously reported. Thirty-seven patients, mean age 54 +/- 10 years, underwent the maze (III) procedure. Electrophysiological studies with recordings of SNRT, CSNRT, AVN-ERP, point of Wenckebach block, AH, PA, and HV interval, were performed preoperatively and 6 and 15 months postoperatively. Induction of atrial flutter/AF was attempted postoperatively. Based on electrophysiological study evaluation, the maze (III) procedure did not cause permanent damage to the sinus node in any patient with a documented normal sinus node function preoperatively (CSNRT max 541 +/- 210 vs 587 +/- 437 ms, P = 0.26). Postoperative AV node function was normal in all patients with a documented normal AV node function before surgery. One patient had an iatrogenic third degree AV block. There was no difference in PA or HV interval after surgery. Sustained atrial tachyarrhythmias could be induced in 5 patients, of whom 4 developed permanent AF/atrial flutter late after surgery. At late follow-up, (mean 45 months), 27 (73%) patients were in sinus rhythm, 5 (13%) patients had permanent pacing, and 5 patients had recurrent AF requiring His bundle ablation (n = 2) or medical treatment (n = 3). Based on electrophysiological studies, the maze (III) procedure does not cause permanent damage to the sinus or AV nodes or to the right atrial and His-Purkinje conduction systems. Electrophysiological study evaluation may predict the need for postoperative pacemaker. Induction attempts of atrial arrhythmias may predict future recurrences and guide therapeutic efforts.     

Cardiac resynchronization through selective His bundle pacing in a patient with the so-called InfraHis atrioventricular block

We present a case of infraHis AV block in which selective His bundle pacing with His-ventricular conduction through the conduction system was accomplished. While further investigations are developed, this approach may be an alternative for cardiac resynchronization in cases of difficult coronary sinus access.     

Possible Risks of General Anesthesia in Patients with Intraventricular Conduction Disturbances

In order to assess the risk of complete AV bloek in patients, with intraventricular conduction disturbances who undergo general anesthesia, 20 patients with various conduction defects (7 LBBB, 1 RBBB and 1st degree AV block, 1 incomplete RBBB, 9 RBBB+LAH and 2 RBBB+LPH) were studied by means of His bundle recording and corrected sinus node recovery time (CSNRT) before and after the subministration of thiopental (0.2 g. I.V.), succinylcholine (1 mg/kg I.V.), Eluothane (l%) and Ethrane (1.6%). Nineteen patients displayed signs of dizziness or syncope; both the sinus rate and the CSNRT, did not undergo significant variations. A slight and not significant variation of intranodal conduction during sinus rhythm was observed after Fluothane administration (AH was prolonged by 8%). A less evident negative dromotropic action of thiopental and Ethrane was only revealed by atrial pacing. No significant variations were demonstrated in His-ventricular conduction after administration of the various drugs. The maximum average increase (1.5%) of the H-V interval was observed after administration of succinylcholine. Acute AV block distal to the His bundle appeared in three patients after succinylcholine administration.     

Second-degree atrioventricular block: a reappraisal

In this review, we discuss the various forms and causes of second-degree atrioventricular (AV) block and the reasons they remain poorly understood. Both type I and type II block characterize block of a single sinus P wave. Type I block describes visible, differing, and generally decremental AV conduction. Type II block describes what appears to be an all-or-none conduction without visible changes in the AV conduction time before and after the blocked impulse. Although the diagnosis of type II block is possible with an increasing sinus rate, absence of sinus slowing is an important criterion of type II block because a vagal surge (generally a benign condition) can cause simultaneous sinus slowing and AV nodal block, which can superficially resemble type II block. The diagnosis of type II block cannot be established if the first postblock P wave is followed by a shortened PR interval or is not discernible. A pattern resembling a narrow QRS type II block in association with an obvious type I structure in the same recording (e.g., Holter) effectively rules out type II block because the coexistence of both types of narrow QRS block is exceedingly rare. Concealed His bundle or ventricular extrasystoles confined to the specialized conduction system without myocardial penetration and depolarization can produce electrocardiographic patterns that mimic type I and/or type II block (pseudo-AV block). All correctly defined type II blocks are infranodal. A narrow QRS type I block is almost always AV nodal, whereas a type I block with bundle branch block barring acute myocardial infarction is infranodal in 60% to 70% of cases. A 2:1 AV block cannot be classified in terms of type I or type II block, but it can be nodal or infranodal. Infranodal blocks require pacing regardless of form or symptoms. The widespread use of numerous disparate definitions of type II block appears primarily responsible for many of the problems surrounding second-degree AV block. Adherence to the correct definitions provides a logical and simple framework for clinical evaluation.     

Unusual Mechanism in the Initiation of the Paroxysmal Supraventricular Tachycardia in a Patient with WPW Syndrome

A heretofore unreported unusual mechanism in the initiation of the paroxysmal supraventricular tachycardia (PSVT) in a patient with WPW (Wolff-Parkinson-White) syndrome was observed using His bundle recordings. The patient initially had some degree of AV conduction disturbance at the level of the AV node. A premature atrial impulse initially activated the ventricle exclusively through the accessory pathway and the same impulse re-excited the ventricle via the AV nodal-His axis after finishing the pure pre-excitation with marked prolongation of the AH and the HV intervals. After finishing this double ventricular response it traversed to the atrium to produce the PSVT.     

Anatomic Substrate for Congenital Atrioventricular Block in Middle-Aged Adults

Congenital atrioventricular block is usually a benign disorder not necessitating pacing. In some patients slowing of rate and/or mortality have been noted with aging. However an anatomic substrate has not been established for the progressive slowing of the escape rate. In this study we report an anatomic substrate in two such patients who were dying in congestive heart failure, ages 49 and 42, respectively. Multiple pre-mortem ECG's in both cases revealed wide QRS escape rhythms, and escape rates of approximately 35 and 28 beats/minute, respectively. Conduction system examination by serial section in both cases revealed lack of connection between the atrial septum with the peripheral conduction system with total replacement by fat of the AV nodal approaches and AV node, and advanced sclerosis of the summit of the ventricular septum which was more marked on the right side. In addition, the His bundle showed marked septation in case one and fragmentation in case two. Sclerosis of the summit of the ventricular septum involved the branching bundle and the bundle branches in both cases. In conclusion, both patients had the characteristic lesions of congenital atrioventricular block, namely replacement of the AV node and AV nodal approaches by fat, with lack of connection to the peripheral conduction system, and one also had a fragmented His bundle. In addition premature aging of the summit of the ventricular septum may have reflected the long-standing hemodynamic stresses of chronic bradycardia. This in turn resulted in trifascicular involvement of the conduction system leading to a shifting of the escape rhythm distally eventuating in a slower idioventricular escape rhythm.     

His-Purkinje conduction during retrograde stress.

The pattern of retrograde His-Purkinje conduction was evaluated in 28 patients using ventricular extrastimuli. In each patient progressive prolongations of His-Purkinje conduction (S2H2) which appeared as ventricular extrastimuli were induced at closer coupling intervals (S1S2). There was an inverse linear relationship of S2H2 to S1S2 which was cycle length-dependent: i.e., at any S1S2 interval the resultant S2H2 was less at shorter drive cycle lengths. The degree of S2H2 delay varied widely (from 30 to 340 ms) and was unrelated to the presence of bundle branch block, H-V intervals, or capability of ventriculoatrial conduction. Prolongation of S2H2 was independent of intraventricular (muscle) conduction delay; such delay was usually absent at most, and occasionally all, S1S2 coupling intervals during which S2H2 was lengthening. Furthermore, in two patients both left and right ventricles were activated before the timed depolarization of the His bundle occurred, demonstrating that under the stress of extrastimuli, the impulse conducts through ventricular muscle with less delay than through the His-Purkinje system. We conclude that the His-Purkinje system typically displays slow conduction response to ventricular stress. The site of this conduction delay is probably at the distal "gate".     

His Bundle in Electrocardiographic Semantics of AV Block. Anatomoclinical Considerations

The AV conducting system was examined histologically in 13 selected human hearts (7 control and 6 AV block specimens), focusing attention upon normal His bundle (HB) structure, and upon the histopathologic basis of intrahisian block, with supraventricular QRS configuration. HB revealed a poor morphologic identity, often failing to represent the "undivided stem" of the AV pathway, either due to an early partition into separate longitudinal fascicles, or to varied types and sites of bifurcation, without any definite boundary between nonbranching and branching portions. Split His potentials, the distal component of which has been suggested as arising in the proximal bundle branch system, has been found in a case free of HB histologic abnormality. Supraventricular QRS configuration in escape rhythm was observed in two cases of AV block, not withstanding destruction of the entire His bifurcation, and in experimental bilateral bundle branch block. Pertinent explanations have been suggested. The overall semantic value and usefulness of the current HB nomenclature do not seem to imply, as yet, a precise and constant anatomoclinical correlation.     

Infraatrial supraventricular tachycardias: mechanisms, diagnosis, and management

Tachycardias are traditionally classified as either ventricular tachycardia (VT) or supraventricular tachycardia (SVT). VT can be defined as a tachycardia which requires only ventricular structures for perpetuation. SVT is defined in terms of exclusion of VT and hence is any tachycardia which requires participation of at least one supraventricular structure for perpetuation. Certain SVTs require only participation of the atrioventricular node (AVN) and the His bundle (HB) but not the atrial myocardium or any of the great thoracic veins for perpetuation and hence can be described as "infraatrial." The three main mechanisms of infraatrial SVTs are: (1) intranodal atrioventricular reentrant tachycardia; (2) junctional ectopic tachycardia; and (3) nodoventricular reentrant tachycardia. The clinical significance of infraatrial SVTs is that they are compatible with any A:V ratio and even atrioventricular (AV) dissociation. Infraatrial SVTs are often suspected when a narrow complex tachycardia presents with apparent AV dissociation and a counterintuitive A:V ratio of < 1:1. However, if the same tachycardia is conducted with aberrant conduction or preexcitation, a broad complex tachycardia with an A:V ratio of < 1:1 will arise and that can be easily mistaken for VT. The possible patterns of electrical association and dissociation between different cardiac structures are examined, and how individual types of infraatrial SVT can be diagnosed and managed are reviewed.     

Effect of Isoetharine on Cardiac Conduction in Man

The effects of isoetharine on the His bundle electrogram were studied in 10 patients with heart disease. Recordings were made at varied heart rates using atrial pacing. Isoetharine significantly reduced the AH interval with atrial pacing, but it had no effect on the HV interval. Second degree heart block occurred at higher pacing rates after isoetharine treatment as compared to the control state. The heart rate and blood pressure showed no significant change after isoetharine. The functional and effective refractory period were measured with the use of the extra-stimulus technique. The functional refractory period of the AV node, as well as the effective refractory period of the atrium, significantly decreased after isoetharine. Thus, isoetharine can improve conduction through the atrioventricular node. The drug does have a cardiac effect as measured by its action on the human conduction system.     

Mapping Guided Laser Catheter Ablation of the Atrioventricular Conduction in Dogs

Safety and efficacy of mapping guided laser catheter ablation of the AV junction was tested in a canine model. A total of 43 laser pulses (continuous wave, Nd:YAG, 1,064 nm, 30 W, irradiated spot diameter 2.0–2.5 mm) were delivered in 15 dogs (2–5 per dog) via a novel laser catheter system. Pulses were selectively aimed at: (1) the AV node: (2) the His bundle; and (3) the bundle branches. Laser pulses of 9.7 ± 1.1 seconds (n = 31) produced reversible conduction disturbances in the targeted segment of the AV conduction system, while pulses of 28.6 ± 7.9 seconds (n = 9) resulted in chronic block. The dogs survived the procedure without complications. Follow-up was 6.5–10.5 months. Histopathologically, lesions showed clear-cut oval-shaped areas of fibrosis of 0.5–18.0 mm in diameter and 0.5–3.5 mm (transmural) in depth, depending on the irradiation time. Pervenous mapping guided laser catheter irradiation of the AV junction can produce AV block consistently and selectively in the targeted segment of the right ventricular conduction system in dogs. The method is safe and can be performed in a controllable manner by using the catheter system presented.     

Histopathologic Changes in the Heart Including the Conduction System after Catheter Ablation

The pathology of the heart, including that of the conduction system, after various catheter techniques used to ablate the various parts of the conduction system and the myocardium, were examined histologically by serial sections. The experiments were conducted on canines. The conduction system studies included the approaches to the AV node, the AV node, the AV bundle and bundle branches, as well as, the central fibrous body, the tricuspid, mitral and aortic valves. The methods of ablation were DC shock, laser and radio frequency energy. Production of the complete AV block clinically was associated with fibrosis with or without cartilage formation of the approaches to the AV node, the AV node, the bundle and the beginning of the bundle branches in most cases. On the other hand, creation of first degree AV block was associated with fibrotic changes in the approaches to the AV node and the AV node, and second degree block with more changes to the AV node. Coronary sinus ablation resulted in necrosis and fibrosis of the coronary sinus wall with occasional thrombosis of the coronary sinus. The adjacent atrial and/ or the ventricular myocardium also showed fibrosis. Likewise, ventricular septal ablation was associated with focal areas of fibrosis of the myocardium. The conduction system was intact in both of the above experiments. In one human where complete AV block was created to manage intractable atrial fibrillation, the AV node, the bundle, and the bundle branches were fibrosed. In addition, there was a fibrosed atrio-Hisian connection and the patient died suddenly six weeks after the ablative procedure. The surrounding structures close to the vicinity of the conduction system, such as the aortic, tricuspid, mitral valve, the central fibrous body, and the summit ventricular septum are involved to a varing degree. In summary, (1) Whatever the method of ablation may be, the end result was fibrosis with or without cartilage formation of the ablative area. (2) Congenital anomalies of the conduction system such as an atrio-Hisian connection may remain elusive for ablative methods, and arrhythmias may presist and may cause sudden death in some cases.     

Long-Term Prognostic Significance and Electrophysiological Evolution of Intraventricular Conduction Disturbances Complicating Acute Myocardial Infarction

Fifty-nine patients with post-infarctional, isolated intraventricular conduction disturbances (IVCD) who survived the acute stage of myocardial infarction were followed up after hospital discharge for a mean period of 11.4 ± 4.8 months. Fourteen patients (24%) had HV interval prolongation (>55 ms) during AMI (group A), and 45 patients had normal HV intervais (76%. group B). His bundle recordings were repeated during follow-up in 48 survivors after a mean period of 7.2 ± 0.7 months. Infranodal conduction delay in the acute stage of infarction was correlated with a higher incidence of heart failure during AMI (78% of patients in group A vs 22% in group B, p < 0.01), and with higher rate of cardiac mortality during follow-up (50% in group A vs 13% in group B. p < 0.01). Survivors of group A showed a higher functional NYHA class, a higher incidence of CHF, and a higher prevalence of complex ventricular arrhythmias at Holter monitoring. No statistically significant difference in late sudden death was evident between the two groups of patients, and the global incidence of late AV block was 2%. At repeat His bundle recording no significant change (>5 ms) in HV interval could be demonstrated in comparison to the acute phase recording, neither in patients with prolonged nor in patients with normal HV time. We conclude that HV prolongation in patients with isolated, post-infarctional IVCD is correlated with a worse prognosis, both during acute infarction and during the follow-up period, which presumably reflects wider anatomic damage in comporison to patients with normal HV time. The low incidence of late AV block and the electrophysiological demonstration of the stability of infranodal conduction several months after AMI indicate that these patients do not require permanent prophylactic pacing after acute myocardial infarction.     

Transvascular Argon Laser Ablation of Atrioventricular Conduction in Dogs: Feasibility and Morphological Results

The purpose of this study was to ablate atrioventricular (AV) conduction in dogs with an argon laser using a transvascular approach. Six dogs were anesthetized and underwent a right thoracotomy and atriotomy. A bipolar #7 French lumen catheter containing a 400 u silica fiber was used to map the region of the AV junction. When a stable His deflection was obtained, the silica fiber was extruded from the end of the catheter and argon laser radiation was delivered for up to 20 s at 3.0-4.5 watts. In five of six dogs, complete heart block was successfully created after 3 to 15 lasings. A continuous His bundle electrogram in one dog showed gradual prolongation of the HV interval before the development of complete infrahisian block. The mean R-R intervals in the five dogs with complete heart block increased from 435 +/- 56 ms to 1216 +/- 197 ms (P less than 0.001), and the QRS duration increased from 78 +/- 26 ms to 91 +/- 19 ms (P = ns). Gross inspection showed multiple 1-2 mm2 craters in the atria just above the tricuspid valve ring. Complications included one instance each of aortic root perforation and creation of a small ventricular septal defect. These lesions were so small that there was no hemodynamic compromise in either animal in which they occurred and the lesions themselves were only detected on careful postmortem examination. Histology revealed two patterns of injury involved in conduction ablation. One was direct vaporization of tissue resulting in a wedge shaped incision and the other was formation of a hematoma and thermal necrosis at the lasing site with little evidence of tissue vaporization. Although catheter modifications are necessary to avoid perforation, this study demonstrates that ablation of conduction can be successfully accomplished using an argon laser.