https://www.heartrhythmjournal.com/article/S1547-5271(08)00462-1/pdf

ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): Developed in Collaboration With the American Association for Thoracic Surgery and Society of Thoracic Surgeons

ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities

Developed in Collaboration With the American Association for Thoracic Surgery and Society of Thoracic Surgeons 

Andrew E. Epstein, MD, FACC, FAHA, FHRS, Chair ; John P. DiMarco, MD, PhD, FACC, FHRS; Kenneth A. Ellenbogen. MD, FACC, FAHA, FHRS; N.A. Mark Estes III, MD, FACC, FAHA, FHRS; Roger A.

2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society.

https://cdr.lib.unc.edu/downloads/zc77ss357

ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices--summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines).

Small, high-frequency electrocardiographic signals were recorded from the body surface in 39 patients with and 27 patients without ventricular tachycardia (VT). All patients were in normal sinus rhythm, had a previous myocardial infarction, were not taking antiarrhythmic drugs, and did not have bundle branch block. Bipolar X, Y, Z leads were signal averaged and processed by a bidirectional digital filter that allowed low-amplitude signals to be detected in the terminal QRS complex and ST segment. The high-pass filter frequency was 25 Hz. Patients with VT had a lower amplitude of high-frequency signal in the late QRS complex. In the last 40 msec of the filtered QRS complex, the patients with VT had 14.9 +/- 14.4 microV of high-frequency signal; patients without VT had 73.8 +/- 47.7 microV (p less than 0.0001). Ninety-two percent of the patients with VT had less than 25 microV of high-frequency voltage; only 7% of patients without VT had less than 25 microV (p less than 0.0001). Patients with VT had a longer QRS duration than those without VT, 139 +/- 26 vs 95 +/- 10 msec (p less than 0.0001). The QRS duration was longer than 120 msec in 72% of the patients with VT but in none of the patients without VT (p less than 0.0001). In all patients there was no separate and discrete high-frequency signal in the ST segment. Advanced signal processing of the ECG accurately identified the patients in the study with VT after myocardial infarction.

Use of signals in the terminal QRS complex to identify patients with ventricular tachycardia after myocardial infarction.

Twenty-one of 496 (4%) patients with chronic bifascicular block, studied and followed prospectively, had block distal to the His bundle (BDH) induced by atrial pacing during initial electrophysiologic studies. In six, BDH was noted during pacing-induced atrioventricular (AV) nodal Wenckebach periods (at paced rates of 150--190 beats/min), with BDH in the short HH cycles after the AV nodal blocked P (lond cycle). The AH interval was normal in all six patients and HV was normal in four. None of the six patients has developed AV block during a mean follow-up of 5.33 +/- 0.48 years. In 15 patients, pacing-induced BDH was noted during intact AV nodal conduction (paced rate of 80--200 beats/min). The AH interval was prolonged in one, and HV was prolonged in 10 of the 15 patients. During a mean follow-up of 3.4 +/- 0.59 years, seven of these patients developed AV block, one had treadmill-provoked AV block, and two died suddenly (major morbid event in 10 of 15 patients). In conclusion, BDH induced by atrial pacing is an infrequent finding in patients with bifascicular block, and can be a functional as well as a pathologic response. The latter is associated with a high risk of major morbid events (AV block and sudden death).

Significance of block distal to the His bundle induced by atrial pacing in patients with chronic bifascicular block.

Seventeen consecutive patients with chronic recurrent ventricular tachycardia (VT) were studied in an attempt to delineate the reproducibility and mechanism of this arrhythmia. Six patients had nonsustained and 11 had sustained VT. The following electrophysiological techniques were utilized in an attempt to reproduce VT: 1) rapid atrial and ventricular pacing (17 pts); 2) atrial extrastimulus technique (17 pts); 3) ventricular extrastimulus technique (17 pts); 4) V1V2V3 stimulation technique (5 pts); 5) ventricular pacing from two or more sites (5 pts). Ventricular tachycardia was induced in six of 11 (54%) patients with sustained VT. However, in four there was only a single induction and only in the remaining two patients could VT be repetitively induced. In the latter two patients ventricular tachycardia was induced with both atrial and ventricular stimulation. Ventricular tachycardia could not be induced in any patient with nonsustained VT, although three had spontaneous episodes of ventricular tachycardia during study. In conclusion, in the present series of patients with chronic recurrent VT, this rhythm could not be reproducibly induced in the majority of patients in the cardiac catheterization laboratory utilizing catheter stimulation techniques.

Electrophysiological studies in patients with chronic recurrent ventricular tachycardia.

Syncope was prospectively evaluated in 186 patients with chronic bifascicular block. Syncope occurred in 21 of 124 patients with right bundle-branch block and left anterior hemiblock, 3 of 24 patients with right bundle-branch block and left posterior hemiblock, and 6 of 38 patients with left bundle-branch block. Each case was evaluated by using prolonged electrocardiographic monitoring, His bundle recordings, and other indicated studies. Probable and possible causes of syncope included intermittent heart block in five patients, sinus exit block in one patient, orthostatic hypotension in two patients, seizure disorders in three patients, ventricular arrhythmia in nine patients, and acute blood loss in one patient. No cause could be identified in nine patients. Comparison of patients with and without syncope did not show significant differences. Syncope was recurrent in only five patients (four with heart block and one with seizure disorder). The incidence of late sudden death in patients with and without syncope was identical. Syncope in patients with bifascicular block reflected various cardiac and noncardiac causes and tended not to recur. Permanent pacing seemed indicated in only those patients with documented serious bradyarrhythmia.

Syncope in patients with chronic bifascicular block. Significance, causative mechanisms, and clinical implications.

This report details our experience with documented chronic second-degree atrioventricular (AV) nodal block (proximal to His [H]) in 56 patients. Forty-six men (82%) and 10 women (18%), ages 18-87 years, were studied. Nineteen of the patients (34%) had no organic heart disease (including seven trained athletes) and 37 (66%) had organic heart disease. ECGs in all patients demonstrated episodes of type I second-degree block; five patients also had periods of 2:1 block. Prospective follow-up patients with no organic heart disease (157-2280 days, mean 1395 +/- 636 days) revealed one patient with clear indication for permanent pacing because of bradyarrhythmic symptoms (permanently placed on day 220 of follow-up). Two patients died nonsuddenly. In patients with organic heart disease (prospective follow-up of 60-2950 days, mean 1347 +/- 825 days), pacemakers were implanted in 10 patients, primarily for treatment of congestive heart failure in eight and syncope in two. Sixteen patients died -- three suddenly, seven with congestive heart failure, two of an acute myocardial infarction and four of causes unrelated to cardiac disease. In summary, chronic second-degree AV nodal block has a relatively benign course in patients without organic heart disease. In patients with organic heart disease, prognosis is poor and related to the severity of underlying heart disease.

Natural history of chronic second-degree atrioventricular nodal block.

A 41-year-old man had chronic, recurrent, drug-resistant paroxysmal right atrial tachycardia. Electrophysiologic studies revealed features suggesting atrial reentrance, including induction and termination of tachycardia with rapid atrial pacing and atrial extrastimuli. Endocardial catheter mapping localized the origin of tachycardia to the right atrial appendage. Intraoperative epicardial mapping refined the localization to the posterolateral rim of the appendage. The appendage was excised and the tachycardia was permanently cured. Microelectrode studies on the excised tissue revealed an inducible rhythm localized to a small area of the atrial endocardium, characterized by rapid pacing induction, rhythmicity generated from a suprathreshold afterdepolarization, low maximum diastolic potential, low overshoot potential and a smooth transition from phase 4 to phase 0, suggesting triggered automaticity. This is the first observation in man of probable triggerable atrial automaticity, which may be a direct counterpart of the clinical arrhythmia. The successful surgical outcome indicates that a focal atrial tachycardia can be excised in selected patients.

C Wyndham

Papers

Significance of block distal to the His bundle induced by atrial pacing in patients with chronic bifascicular block.

Electrophysiological studies in patients with chronic recurrent ventricular tachycardia.

Syncope in patients with chronic bifascicular block. Significance, causative mechanisms, and clinical implications.

Natural history of chronic second-degree atrioventricular nodal block.

Successful surgical excision of focal paroxysmal atrial tachycardia. Observations in vivo and in vitro.