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).

THE development of a clinically applicable, automatic, implantable defibrillator has been described previously.1 This electronic device is designed to monitor cardiac electrical activity, to recogn...

Termination of Malignant Ventricular Arrhythmias with an Implanted Automatic Defibrillator in Human Beings

The mechanism of recurrent sustained ventricular tachycardia (VT) was evaluated in 21 patients. Re-entry as the mechanism for VT was suggested by a) the reproducible initiation (19) and termination (15) of the arrhythmia by programmed stimulation. The rate, ventricle of origin, and stimulation site determined the method of termination. One VPD was usually required with VT rates less than 175/min and/or ventricle of origin ipsilateral to the stimulation site, while two VPDs were usually required for VT with faster rates originating in a contralateral ventricle. The proximal His-Purkinje system (HPS) was not required for initiation or maintenance of VT. Evidence localizing the site of re-entry to a small portion of the ventricles included: a) ventricular capture by ventricular premature depolarizations (VPDs) or pacing (VP) without terminating VT (5), b) sinus capture following VPDs and/or supraventricular fusions without terminating VT (12), and c) atrial pacing normalizing the QRS and H-V intervals without terminating VT (5).

Recurrent sustained ventricular tachycardia. 1. Mechanisms.

Endocardial ventricular mapping of 21 ventricular tachyardias (VT) in 17 patients was performed using electrode catheters. Activation at multiple left and right ventricular sites was utilized to determine the site of origin of the VT. Eleven VT had a left bundle branch block pattern (VT-LBBB) and 10 VT had right bundle branch block pattern (VT-RBBB). In all VT-RBBB the earliest site of activation was in the LV or septum. In VT-LBBB the earliest site was RV (4/11), LV (5/11) and septum (2/11). All ventricular tachycardias with QRS less than 140 msec arose in the septum. In patients with an aneurysm, the site of origin of ventricular tachycardia was always in the aneursm. All VT-LBBB arising from the left ventricle originated in an aneurysm involving the septum. QRS changes during ventricular tachycardia were associated with alterations in the patterm of ventricular activation without alteration of the site of origin. In three patients the site of origin predicted by endocardial ventricular mapping was confirmed intraoperatively by epi- and/or endocardial mapping. We conclude that endocardial ventricular mapping demonstrates the limitations of the surface electrocardiogram in localizing the site of origin of ventricular tachycardia. The method may provide important data upon which the surgical therapy of ventricular tachycardia is based.

Recurrent sustained ventricular tachycardia. 2. Endocardial mapping.

The mechanism of the electrocardiographic pattern termed left atrial enlargement was evaluated in 21 patients. Left atrial size and pressure as well as interatrial conduction were correlated with electrocardiographic left atrial enlargement using echocardiography, mean pulmonary capillary wedge pressure and activation time from the P wave to the coronary sinus. In the group as a whole only prolongation of interatrial conduction time was consistently related to the electrocardiographic pattern of left atrial enlargement; left atrial size or pressure was not predictably abnormal in patients with this pattern. Five patients had neither elevation of pulmonary capillary wedge pressure nor echocardiographic evidence of an enlarged left atrium. When the etiologic type of heart disease was analyzed, an enlarged left atrium correlated with electrocardiographic left atrial enlargement only in patients with rheumatic mitral valve disease (eight of nine patients). Elevated pulmonary capillary wedge pressure correlated with electrocardiographic left atrial enlargement in all four patients with cardiomyopathy. In patients with coronary artery disease the electrocardiographic pattern was unrelated to either left atrial pressure or volume overload. Thus, the electrocardiographic pattern termed left atrial enlargement appears to represent an interatrial conduction defect that can be produced by a variety of factors.

Electrocardiographic left atrial enlargement. Electrophysiologic, echocardiographic and hemodynamic correlates.

Intracardiac electrophysiologic studies as a method for the optimization of drug therapy in chronic ventricular arrhythmia.

The clinical response to therapy with the calcium-blocking agent nifedipine was assessed in 12 patients with variant angina pectoris who were 44 to 67 years old. Five patients had vasospasm of the left anterior descending coronary artery, and seven had spasm of a dominant right coronary artery. Before nifedipine therapy, the frequency of anginal attacks per 24 hour period ranged from 1 to 12, with ventricular tachycardia accompanying ischemic episodes in 7 of 12 patients and high grade atrioventricular block occurring in 2 patients. After therapy with nifedipine, 11 of 12 patients had initial relief of symptoms, and 7 of the 11 had long-term relief. Withdrawal of nifedipine led to recurrence of angina on six occasions in four patients. Provocative testing in the cardiac catheterization laboratory by means of the cold pressor test in one patient and ergonovine maleate in another before and after nifedipine administration showed that this agent can block both alpha adrenergic- and regonovine-induced vasospasm. Nifedipine may have a significant role in the therapy of angina caused by coronary spasm.

John A. Kastor

Papers

Recurrent sustained ventricular tachycardia. 1. Mechanisms.

Recurrent sustained ventricular tachycardia. 2. Endocardial mapping.

Electrocardiographic left atrial enlargement. Electrophysiologic, echocardiographic and hemodynamic correlates.

Intracardiac electrophysiologic studies as a method for the optimization of drug therapy in chronic ventricular arrhythmia.

Nifedipine in the treatment of Prinzmetal's (variant) angina.