Andrew I. Cohen

Serial electrocardiographic changes in idiopathic dilated cardiomyopathy confirmed at necropsy

Serial electrocardiographic changes in necropsy-proven idiopathic dilated cardiomyopathy are evaluated and a method of predicting heart weight using QRS amplitudes is described. In 34 patients with multiple electrocardiograms (mean 3/patient) progressive prolongation of PR interval (0.18 +/- 0.03 to 0.21 +/- 0.03, p less than 0.001) and QRS duration (0.10 +/- 0.02 to 0.13 +/- 0.03, p less than 0.0001) was noted. Progressive conduction abnormalities were common (82%). QTc interval and QRS- and T-wave axes did not change. In 50 patients with electrocardiograms within 60 days of death, total 12-lead QRS and V1 through V6 QRS amplitude correlated better with heart weight (r = 0.51, p less than 0.0001 and r = 0.55, p less than 0.0001) than the Estes-Romhilt score did. The mean total 12-lead QRS amplitude was 138 mm with a mean of 106 for V1 through V6. In 31 patients cardiac mass index was calculated and showed significant correlation with 12-lead and V1 through V6 QRS amplitudes (r = 0.68, p less than 0.0001 and r = 0.75, p less than 0.0001, respectively). The QRS amplitudes remained constant during the illness. By using total 12-lead QRS or frontal plane QRS amplitude, heart weight can be predicted as early as 2 years before death. Use of body surface area and QRS amplitude criteria increases the accuracy of heart weight prediction. Thus, progressive electrocardiographic changes are common in patients with idiopathic dilated cardiomyopathy and QRS amplitude criteria are more accurate in the prediction of left ventricular hypertrophy than standard criteria.

Importance of left atrial timing in the programming of dual-chamber pacemakers☆

To determine the hemodynamic effect of different programmed atrioventricular (AV) delays and the importance of the actual timing of left atrial (LA) depolarization, 16 patients with dual-chamber pacemakers were studied and all were found to have an optimal programmed AV delay for cardiac function. However, randomly chosen AV delays of 150, 200 or 250 ms actually provided worse stroke volume than VVI pacing in 7 patients. The optimal programmed AV delay was variable between patients and was related to the interatrial conduction delay, measured as the time from right atrial pacing artifact to LA depolarization (mean 144 +/- 82 ms, range 70 to 380.) Patients with short interatrial delays (less than or equal to 90 ms) were served better by shorter programmed AV delays (150 ms), and patients with longer interatrial delays (greater than or equal to 120 ms) were served better by longer programmed AV delays (greater than or equal to 200 ms) (p less than 0.05). Furthermore, as pacing mode changed from dual-chamber sequential pacing (DVI) to atrial synchronous ventricular pacing (VDD), the LA to ventricular sequence increased from 6 +/- 81 ms to 137 +/- 50 ms (p less than 0.001). This change in the LA to ventricular sequence with mode change produced a significant decrease in stroke volume (p less than 0.05). Thus, the optimal programmed AV delay in patients with dual-chamber pacemakers is predicted by the relation of LA and ventricular activation. Because interatrial conduction delays vary widely, optimal programming requires knowledge of the LA to ventricular sequence.(ABSTRACT TRUNCATED AT 250 WORDS)

Myotonic heart disease A clinical follow‐up

We followed 37 patients with myotonic dystrophy for a mean of 6 years. Two developed atrial flutter or fibrillation, 6 developed a new bundle branch block, 1 developed complete heart block requiring a pacemaker, and another with progressive 1st-degree heart block and a widening QRS interval had a sudden death. Most patients had predictable, gradually progressive disease of their cardiac conduction system. We recommend that patients with progressive atrioventricular block or widening QRS interval due to myotonic heart disease have yearly ECGs and be questioned about syncope or presyncope to determine the need for a cardiac pacemaker.

Acute and Long‐Term Outcomes of Catheter Ablation of Atrial Fibrillation Using the Second‐Generation Cryoballoon versus Open‐Irrigated Radiofrequency: A Multicenter Experience

There are limited comparative data on catheter ablation of atrial fibrillation (CAAF) using the second‐generation cryoballoon (CB‐2) versus point‐by‐point radiofrequency (RF). This study examines the acute/long‐term CAAF outcomes using these 2 strategies.

M-mode echocardiograms for determination of optimal left atrial timing in patients with dual chamber pacemakers

To determine if the A wave of the mitral valve echocardiogram can be used as a marker for left atrial (LA) activity and assist in the programming of dual chamber pacemakers, 156 echocardiograms with the mitral A wave present were obtained from 23 patients with dual chamber pacemakers, all of whom had bipolar esophageal recordings of LA depolarization. Twelve of these patients also underwent hemodynamic study with cardiac function determined at 5 different pacemaker settings: ventricular demand pacing and dual chamber sequential pacing at 0 or 25, 150, 200 and 250 ms programming atrioventricular (AV) delay. The time delay from right atrial pacing artifact to onset and peak of mitral A wave was linearly related to the time from atrial pacing artifact to LA depolarization on the esophageal lead (p less than 0.001). As pacing mode changed from dual chamber sequential pacing (DVI) mode to atrial synchronous-ventricular pacing (VDD), the A wave came earlier relative to the ventricular pacing spike, linearly related to the LA to ventricular extension with mode change determined with the esophageal lead (r = 0.94, p less than 0.001). The time from atrial pacing to peak of A wave was shorter in patients whose optimal programmed AV delay was 150 ms compared with those whose optimal AV delay was 200 or 250 ms (p less than 0.02). At the optimal programmed delay for cardiac output, the peak of the A wave was an average of 13 +/- 36 ms after the ventricular pacing spike.(ABSTRACT TRUNCATED AT 250 WORDS)

Steroid-Tipped Leads Versus Porous Platinum Permanent Pacemaker Leads: A Controlled Study

WISH, M., ET AL.: Steroid‐Tipped Leads Versus Porous Platinum Permanent Pacemaker Leads: A Controlled Study. There is little data directly comparing steroid‐tipped permanent pacemaker leads to otherwise state‐of‐the‐art porous platinum leads. Eighteen patients receiving unipolar generators capable of low voltage outputs were randomized at the time of implant to receive either steroid‐tipped leads or porous platinum leads. All leads were unipolar, tined, passive fixation, and placed in the right ventricular apex or atrial appendage. This study is single center. At implant, threshold pulse width was determined at 3 voltages (2.5, 1.5, and 0.8 V). Follow‐up thresholds were determined at weeks 1, 2, 3, and 4, and at 3 and 6 months. There was no difference in implant thresholds or amplitudes for sensing. By 2 weeks postimplant, lower thresholds were noted for the steroid leads, and this discrepancy grew more significant with time. There was no significant postimplant rise in threshold for steroid‐tipped leads. At 6 months, the average threshold pulse width for ventricular steroid leads at 0.8 V was 0.3 ± 0.1 msec. In contrast, five patients with standard leads did not capture at maximum pulse width at 0.8 V (p < 0.0001). There was no significant difference in the amplitude of the chronic atrial electrogram. This study shows steroid‐tipped leads to offer a significant advantage in reducing thresholds early postimplant and chronically.

Sotalol for refractory sustained ventricular tachycardia and nonfatal cardiac arrest

The efficacy and safety of sotalol were assessed by electrophysiologic testing and ambulatory recordings in 16 patients with recurrent sustained ventricular tachycardia (VT) or nonfatal cardiac arrest who were refractory to an average of 4.8 conventional antiarrhythmic agents. Twenty-four-hour ambulatory recordings were performed before and after sotalol therapy. Fourteen patients underwent baseline electrophysiologic study and sustained VT was inducible in 12. Oral sotalol (320 to 960 mg/day) completely suppressed inducible sustained VT in 7 patients (58%), with modification in 3 (25%). Ventricular premature complexes were suppressed from baseline (mean +/- standard deviation) 431 +/- 616 to 60 +/- 110/hr (p less than 0.03). After a mean follow-up of 19 +/- 7 months, 12 of 14 patients receiving sotalol treatment had successful suppression of ventricular premature complexes (60 +/- 85/hr) and remained clinically free of sustained VT, except 2 who needed additional antiarrhythmic drugs to suppress the recurrent sustained VT. One patient died suddenly after 25 months of sotalol treatment. No severe side effects were noted during sotalol therapy. This study demonstrates that sotalol is a well-tolerated, effective antiarrhythmic agent in patients at high-risk for sudden death. It appears to be beneficial in patients who did not benefit from multiple drug treatment.

Transdiaphragmatic Implantation of the Automatic Implantable Cardioverter Defibrillator

A new surgical approach for implantation of the automatic implantable cardioverter defibrillator without thoracotomy was used in 12 patients, aged 46 to 72 years. Preimplantation arrhythmia was ventricular tachycardia in 7 patients and ventricular fibrillation in 5 patients. The mean ejection fraction was 19%. Six patients were at high risk for general anesthesia for a variety of medical problems, and 2 patients had had a previous cardiac operation. Epidural anesthesia was used in 8 patients without intubation. The surgical approach used a longitudinal epigastric extraperitoneal incision with access to the heart through an incision made in the central tendon of the diaphragm. Two patches and two epicardial sensing leads were placed in all patients. All patients but one could be defibrillated with 20 J or less. There was no operative mortality and minimal morbidity. There were two late deaths due to heart failure. Thus, the transdiaphragmatic approach provides an excellent exposure for automatic implantable cardioverter defibrillator implantation, avoids general anesthesia and thoracotomy, and can be used after a previous cardiac operation.

Relation between ventricular function and antiarrhythmic responses to sotalol

Abstract Sotalol, a unique β-receptor antagonist with additional class III antiarrhythmic action, has remarkable efficacy for suppression of ventricular and supraventricular arrhythmias. 1–6 Unlike other β blockers, sotalol significantly prolongs the myocardial action potential duration. This additional action of sotalol probably accounts for its greater antiarrhythmic efficacy and perhaps its minimal negative or positive inotropic action. Comparison of the effects of sotalol on ventricular premature complex (VPC) suppression in patients with normal and abnormal left ventricular function has not been well studied. We examined the efficacy of sotalol in the treatment of ventricular arrhythmia with respect to left ventricular function.

Reduced acetylation of procainamide by para-aminobenzoic acid

Acetylation is the major route of metabolism of many drugs including the antiarrhythmic agent procainamide. Coadministration of para-aminobenzoic acid was observed to decrease the biotransformation of procainamide to N-acetylprocainamide in a patient with rapid acetylation kinetics. In view of the distinct antiarrhythmic and toxic properties of procainamide and N-acetylprocainamide, the observed drug interference may have great clinical relevance in long-term oral antiarrhythmic therapy and in instances where other drugs converge for acetylation.