BACKGROUND GLORIA-AF (Global Registry on Long-Term Oral Antithrombotic Treatment in Patients with Atrial Fibrillation) is a prospective, global registry program describing antithrombotic treatment patterns in patients with newly diagnosed nonvalvular atrial fibrillation at risk of stroke. Phase 2 began when dabigatran, the first non-vitamin K antagonist oral anticoagulant (NOAC), became available.OBJECTIVES This study sought to describe phase 2 baseline data and compare these with the pre-NOAC era collected during phase 1.METHODS During phase 2, 15,641 consenting patients were enrolled (November 2011 to December 2014); 15,092 were eligible. This pre-specified cross-sectional analysis describes eligible patients' baseline characteristics. Atrial fibrillation disease characteristics, medical outcomes, and concomitant diseases and medications were collected. Data were analyzed using descriptive statistics.RESULTS Of the total patients, 45.5% were female; median age was 71 (interquartile range: 64, 78) years. Patients were from Europe (47.1%), North America (22.5%), Asia (20.3%), Latin America (6.0%), and the Middle East/Africa (4.0%). Most had high stroke risk (CHA(2)DS(2)-VASc [ Congestive heart failure, Hypertension, Age >= 75 years, Diabetes mellitus, previous Stroke, Vascular disease, Age 65 to 74 years, Sex category] score >= 2; 86.1%); 13.9% had moderate risk (CHA2DS2-VASc = 1). Overall, 79.9% received oral anticoagulants, of whom 47.6% received NOAC and 32.3% vitamin K antagonists (VKA); 12.1% received antiplatelet agents; 7.8% received no antithrombotic treatment. For comparison, the proportion of phase 1 patients (of N = 1,063 all eligible) prescribed VKA was 32.8%, acetylsalicylic acid 41.7%, and no therapy 20.2%. In Europe in phase 2, treatment with NOAC was more common than VKA (52.3% and 37.8%, respectively); 6.0% of patients received antiplatelet treatment; and 3.8% received no antithrombotic treatment. In North America, 52.1%, 26.2%, and 14.0% of patients received NOAC, VKA, and antiplatelet drugs, respectively; 7.5% received no antithrombotic treatment. NOAC use was less common in Asia (27.7%), where 27.5% of patients received VKA, 25.0% antiplatelet drugs, and 19.8% no antithrombotic treatment.CONCLUSIONS The baseline data from GLORIA-AF phase 2 demonstrate that in newly diagnosed nonvalvular atrial fibrillation patients, NOAC have been highly adopted into practice, becoming more frequently prescribed than VKA in Europe and North America. Worldwide, however, a large proportion of patients remain undertreated, particularly in Asia and North America. (Global Registry on Long-Term Oral Antithrombotic Treatment in Patients With Atrial Fibrillation [ GLORIA-AF]; NCT01468701) (C) 2017 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.

BACKGROUND Patients with heart failure who receive an implantable cardioverter-defibrillator (ICD) for primary prevention (i.e., prevention of a first life-threatening arrhythmic event) may later receive therapeutic shocks from the ICD. Information about long-term prognosis after ICD therapy in such patients is limited. METHODS Of 829 patients with heart failure who were randomly assigned to ICD therapy, we implanted the ICD in 811. ICD shocks that followed the onset of ventricular tachycardia or ventricular fibrillation were considered to be appropriate. All other ICD shocks were considered to be inappropriate. RESULTS Over a median follow-up period of 45.5 months, 269 patients (33.2%) received at least one ICD shock, with 128 patients receiving only appropriate shocks, 87 receiving only inappropriate shocks, and 54 receiving both types of shock. In a Cox proportional-hazards model adjusted for baseline prognostic factors, an appropriate ICD shock, as compared with no appropriate shock, was associated with a significant increase in the subsequent risk of death from all causes (hazard ratio, 5.68; 95% confidence interval [CI], 3.97 to 8.12; P<0.001). An inappropriate ICD shock, as compared with no inappropriate shock, was also associated with a significant increase in the risk of death (hazard ratio, 1.98; 95% CI, 1.29 to 3.05; P=0.002). For patients who survived longer than 24 hours after an appropriate ICD shock, the risk of death remained elevated (hazard ratio, 2.99; 95% CI, 2.04 to 4.37; P<0.001). The most common cause of death among patients who received any ICD shock was progressive heart failure. CONCLUSIONS Among patients with heart failure in whom an ICD is implanted for primary prevention, those who receive shocks for any arrhythmia have a substantially higher risk of death than similar patients who do not receive such shocks.

OBJECTIVES:This study investigated whether defibrillation threshold (DFT) testing during implantable cardioverter-defibrillator (ICD) implantation predicts clinical outcomes. BACKGROUND:Defibrillation testing is often performed during insertion of ICDs to confirm shock efficacy. There are no prospective data to suggest that this procedure improves outcomes when modern ICDs are implanted for primary prevention of sudden death. METHODS:The analysis included the 811 patients who were randomized to the ICD arm of the SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial) and had the device implanted. The DFT testing protocol in SCD-HeFT was designed to limit shock testing in a primary prevention heart failure population. RESULTS:Baseline DFT data were available for 717 patients (88.4%). All 717 patients had a DFT of < or =30 J, the maximum output of the device in this study. The DFT was < or =20 J in 97.8% of patients. There was no survival difference between patients with a lower DFT (< or =10 J, n = 547) and a higher DFT (>10 J, n = 170) (p = 0.41). First shock efficacy was 83.0% for the first clinical ventricular tachyarrhythmia event; there were no differences in shock efficacies when the cohort was subdivided by baseline DFT. CONCLUSIONS:Low baseline DFTs were obtained in patients with stable, optimally treated heart failure during ICD implantation for primary prevention of sudden death. First shock efficacy for ventricular tachyarrhythmias was high regardless of baseline DFT testing results. Baseline DFT testing did not predict long-term mortality or shock efficacy in this study.

Mortality was reduced by 23% in pts with an EF≤35% and NYHA Class II or III heart failure enrolled in SCD-HeFT and treated with an ICD compared to patients receiving placebo drug and excellent background medical therapy. Of the 829 pts randomized to the ICD arm, 811 pts received an ICD programmed for shock-only therapy. The purpose of this study was to evaluate mortality in pts who received an ICD shock for either an appropriate or inappropriate cause.

The toxic and inotropic effects of a rapid-acting cardiac glycoside, acetylstrophanthidin (ACS), administered as a rapid i.v. bolus was compared in six healthy adult (age 2-3 years) and seven senescent (age 12-14 years) beagles. In the conscious state no age difference was observed in the dosage of ACS at which toxicity, defined as ventricular tachycardia (VT), occurred. Serum levels of ACS at toxicity were 70 ± 15 ng/ml in the senescent and 65 ± 12 ng/ml in the adult (NS). On a separate occasion, the inotropic effect, dP/dt/P50, and the toxic end point were measured in the anesthetized state. As in the awake state, no age difference was seen in the dosage to VT. The control dP/dt/P,, measured with a left ventricular Millar catheter during brief periods of right ventricular pacing at 250 beats/min was not age related. However, the increase in contractility in response to ACS was two times greater in the adult than the senescent (p < 0.001). This difference persisted when A-blockade was effected with practolol. Thus, in senescence, while glycoside toxicity is unaltered, the inotropic efficacy of ACS is significantly diminished. This age difference in inotropy cannot be attributed to an age difference in serum levels of the drug or in sympathetic tone. Additional studies indicated that glycoside inhibition of Na+-K+ ATPase isolated from these dogs was not age related, suggesting that the mechanism for the diminished inotropic response is distal to the inhibition of this receptor enzyme.

Alterations in ventricular loading conditions lead to changes in action potential duration and arrhythmias via contraction-excitation feedback; a decrease in load leads to prolongation of repolarization. To determine whether changes in right ventricular load alter ventricular repolarization in man, the corrected QT interval, a measure of overall ventricular repolarization, was measured in 32 patients before and after valvuloplasty for pulmonary stenosis. Right ventricular systolic pressure decreased (82.5 30.7 to 40.5 ± 9.5 mm Hg, p<.001) and the QTc increased concurrently (409.1 + 24.3 to 440.7 28.0 msec, p<.001) after successful valvuloplasty. The increase in QTc was most marked for those patients with a greater than 30 mm Hg decrease in right ventricular pressure (40.0 ± 22.3 vs 16.3 + 21.3 msec, p.006). In a subset of seven patients in whom monophasic action potentials were recorded, monophasic action potential duration, a measure of local repolarization, was prolonged (230.0 ± 24.3 vs 216.9 ± 21.9, p<.001) after successful valvuloplasty, confirming that the QTc prolongation reflected changes in local ventricular repolarization. In addition, during nine acute right ventricular outflew tract occlusions in a subset of six patients, monophasic action potential duration shortened (206.6 ± 17.6 vs 221.7 + 20.9 msec, p<.01) and early afterdepolarizations developed consistent with contraction-excitation feedback. These data suggest that, in humans, changes in mechanical load are associated with changes in ventricular repolarization consistent with contractionexcitation feedback. Circulation 77, No. 1, 70-77, 1988. BALLOON VALVULOPLASTY has evolved as a therapeutic alternative for patients with stenotic pulmonary valves. 1 2 The present study focuses on the electrocardiographic and electrophysiologic changes that develop in patients undergoing balloon valvuloplasty for congenital pulmonary stenosis. The purpose of this study was to demonstrate that changes in ventricular repolarization consistent with contraction-excitation feedback mechanisms occur in man. In patients undergoing balloon dilatation of stenotic valves, three mechanical states are present: (1) before valvuloplasty, at which time pulmonary stenosis assoFrom the Divisions of Cardiology of the Departments of Medicine and Pediatrics, The Johns Hopkins Hospital, Baltimore. Supported in part by a grant from the National Institutes of Health (ROI-HL:34519-02). Address for correspondence: Joseph H. Levine, M. D., 592 Carnegie, Division of Cardiology, The Johns Hopkins Hospital, 600 North Wolfe St., Baltimore, MD 21205. Received June 16, 1987; revision accepted Oct. 1, 1987. Dr. Levine is the recipient of a Clinician Scientist Research Award of The Johns Hopkins Medical Institutions. 70 ciated with increased right ventricular afterload is present, (2) after valvuloplasty of the stenotic valve, associated with decreased afterload and right ventricular pressure generation, and (3) during balloon occlusion of the right ventricular outflow tract and pulmonary valve, at which time maximal afterload and right ventricular pressure generation are noted and tensions approach those seen under isovolumetric conditions. Contraction-excitation feedback theory predicts that the time course of ventricular repolarization will be influenced by the mechanical loading conditions. Studies in isolated preparations and experimental animals have demonstrated that alterations in mechanical load lead to changes in conduction and refractoriness of ventricular myocardium. I2 addition, changes in monophasic action potentials (MAPs) have been recorded in experimental preparations undergoing acute 5-7, 13 15 occlusion of the aorta. Specifically, increases in mechanical stress have led to shortened action potential durations and shortened effective refractory periods

Purpose: In the Sudden Cardiac Death Heart Failure Trial (SCD-HeFT), the ICD improved survival by 23%. Information regarding rhythm precursors to ventricular tachycardia (VT) or ventricular fibrillation (VF) in a broad based population without prior VT or VF and from a large unbiased ICD database are limited.

The cellular electrophysiologic effects of myocardial ablation performed in vitro with argon laser energy were compared with those of high-energy electrical shocks. A border zone of injured but nonnecrotic tissue surrounding the site of energy delivery was present after tissue ablation by both energy modalities. A decrease in resting membrane potential, action potential amplitude, and maximum rate of upstroke velocity was noted in each tissue sample, was greatest nearest the site of energy delivery, and was of graded severity at increasing distances from the crater edge. The extent of injury, as indexed by changes in action potential variables and necrosis, histologically determined, was greater for tissues exposed to high-energy shocks. The relatively focal injury after argon laser photoablation may explain the lower incidence of arrhythmias and hemodyiamnic dysfunction noted with the use of this method of ablation in vivo. Circulation 76, No. 1, 217-225, 1987. TRANSVENOUS CATHETER ablation has evolved as an alternative to surgery in management of clinical tachyarrhythmias. High-energy electrical ablation has been successfully applied to the atrium,' atrioventricular node,2' and accessory pathways7' 8 for control of automatic and reentrant supraventricular tachycardias. More recently, foci of sustained, refractory ventricular tachycardia have been ablated with the use of highenergy electrical shocks.9-'3 Although electrical ablation has been associated with successful control of refractory tachycardias, transient life-threatening proarrhythmic and hemodynamic complications have been reported. 13-16 A potential explanation for these complications has been suggested. Recent work in isolated tissues has demonstrated that, after a catheter-delivered high-energy s'l.ock, a large border zone of injured but nonneFrom the Division of Cardiology, the Johns Hopkins Medical Institutions, Baltimore, and the Department of Animal Biology, the University of Pennsylvania, School of Veterinary Medicine, Philadelphia. Supported in part by grants from the National Institutes of Health (HL 28393, HL 25213, HL 33593, HL 07220-08) and the W. W. Smith Charitable Trust. Drs. Levine and Weisman are recipients of Clinician Scientist Research Awards of the Johns Hopkins Medical Institutions. Address for correspondence: Joseph H. Levine, M.D., 592 Carnegie Building, Division of Cardiology, The Johns Hopkins Hospital, 600 North Wolfe St., Baltimore, MD 21205. Received Jan. 12, 1987; revision accepted March 26, 1987. Vol. 76, No. 1, July 1987 crotic myocardium develops around the ablation site.'7 Depressed action potentials, abnormal conduction and refractoriness, and abnormal membrane phenomena have been demonstrated in this surrounding injured border zone. The use of laser energy has been suggested as an alternative to ablation, since it offers better control of energy delivery.'8 19 Although tissue injury may spread beyond the target site when laser exposure time surpasses the thermal relaxation time of the target tissue, the distribution of spread follows a Gaussian relationship and is expected to be focal. 19 20 Thus, a smaller border zone of injured myocardium should be present after laser photoablation. This in turn may explain the lower incidence of arrhythmic and hemodynamic complications noted in animal studies during laser photoablation.'8 The present series of expenrments was performed to study the consequences of argon laser photoablation in normal canine myocardium. After exposure to laser energy, action potential characteristics, variables sensitive to tissue injury, were recorded at varying distances from the crater to document the extent of cellular injury. The pattern of injury was compared with that after high-energy electrical shocks of sufficient energy to yield craters of comparable size to document

F OR SOME TIME, the implantable cardioverter-defibrillator (ICD) has been recognized as effective but expensive technology. The issue faced by health insurers (ie, Medicare) is how to make best use of scarce resources while making available the protection offered by the defibrillator to the largest group of appropriate patients. Since the majority of patients who receive the ICD have coronary artery disease, treatment is permanent and may not alter the costs that are associated with progression of coronary atherosclerosis, including myocardial infarction or heart failure. Indications for implantation of the ICD have evolved over the last 10 years. The increasing sophistication of both therapy and diagnostic techniques as well as nonthoracotomy approaches have significantly altered the patient population referred for devices. The original recipients of the ICD had survived at least one out-of-hospital episode of cardiac arrest. Presently, consideration is being given to implantation of a device in patients who have not had, but are deemed at high risk for, a first episode of cardiac arrest. From a medical economic viewpoint, the ICD represents an interesting and rapidly evolving technology: clearly effective in many circumstances but with a substantial “up-front” and continuing cost. Nonthoracotomy devices will alter the initial cost, but may further broaden indications, even to prophylactic use. This review will focus on the problems involved in the analysis of ICD costs and benefits, given changing indications and evolving technology.

The physiological oscillation of cytosolic [Ca2+] that underlies each heart beat is generated by the sarcoplasmic reticulum (SR) in response to an actin potential (AP) and occurs relatively synchronously within and among cells. When the myocardial cell and SR Ca2+ loading become sufficiently high, the SR can also generate spontaneous, i.e., not triggered by sarcolemmal depolarization, Ca2+ oscillations (S-CaOs). The purpose of this review is to describe properties of S-CaOs in individual cells, myocardial tissue, and the intact heart, and to examine the evidence that may link S-CaOs to the initiation or maintenance of ventricular fibrillation (VF). The SR Ca2-release that generates S-CaOs occurs locally within cells and spreads within the cell via Ca2+ induced Ca2+ release. The localized increase in cytosolic [Ca2+] due to S-CaOs may equal that induced by an AP and causes oscillatory sarcolemmal depolarizations of cells in which it occurs. These oscillatory depolarizations are due to Ca2+ activation of the Na/Ca exchanger and of nonspecific cation channels. Asynchronous occurrence of diastolic S-CaOs among cells within the myocardium causes inhomogeneity of diastolic SR Ca2+ loading; this leads to inhomogeneity of the systolic cytosolic [Ca2+] transient levels in response to a subsequent AP, which leads to heterogeneity of AP repolarization, due to heterogeneous Ca2+ modulation of the Na/Ca exchanger, nonspecific cation channels, and of the L-type Ca2+ channel. In a tissue in which asynchronous S-CaOs am occurring in diastole, the subsequent AP temporarily synchronizes SR Ca2+ loading and release within and among cells. Varying extents of synchronized S-CaOs then begin to occur during the subsequent diastole. The partial synchronization of this diastolic S-CaOs cells within myocardial tissue produces aftercontractions and diastolic depolarizations. When S-CaOs are sufficiently synchronized, the resultant depolarizations summate and can be sufficient to trigger a spontaneous AP. S-CaOs occurrence within some cells during a long AP plateau also modulates the removal of voltage inactivation of L-type Ca2+ channels and increases the likelihood for "early after depolarizations" to occur in myocardial tissue. S-CaOs have an apparent modulatory role in the initiation of VF in the Ca2+ overload model and in the reflow period following ischemia. Likewise, in non-a priori Ca2+ overloaded hearts, S-CaOs modulate die threshold for VF induction (induced typically by alternating current) but may not be essential for VF induction. The role of S-CaOs in maintenance of VF in these VF models is less clear: to date there is no evidence that inhibition of S-CaOs can abolish VF once it has been established. The precise definition of the role of S-CaOs in the initiation and mechanisms of VF merits further study.

Sudden cardiac death is the leading cause of cardiac mortality in patients with heart disease. Approximately 400000 such deaths occur in the United States alone each year [1], It has been established that the vast majority of sudden cardiac deaths are due to ventricular tachyarrhythmias, with only approximately 20% of such cases due to identifiable etiology such as acute myocardial infarction [2, 3]. Tragically, when out-of-hospital cardiac arrest occurs, only one of five individuals will survive to hospital discharge. Those patients at high risk for sudden cardiac death are survivors of out-of-hospital cardiac arrest without identifiable causes and patients with recurrent ventricular tachycardia with underlying heart disease, particularly those with remote myocardial infarction with associated poor left ventricular function and those with cardiomyopathy. In such patients, the automatic implantable cardioverter defibrillator (AICD) has been the landmark breakthrough in therapy [4].

OBJECTIVE To determine whether anti-Ro/SS-A antibodies selectively bind to neonatal cardiac cells and alter membrane repolarization. METHODS An in vitro electrophysiologic and immunocytochemical experimental model contrasting neonatal and rabbit cardiac tissue was employed. RESULTS Sera and IgG-enriched fractions from anti-Ro/SS-A antibody-positive mothers of infants with neonatal lupus erythematosus and congenital heart block bind to neonatal, rather than adult, rabbit cardiac tissue and alter the transmembrane action potential (i.e., inhibit repolarization). The additional presence of anti-La/SS-B antibodies was not additive or synergistic for these immunocytochemical and electrophysiologic features. Sera containing other antibody specificities (i.e., anti-native DNA, cardiolipin, Sm, and nuclear RNP) failed to stain the neonatal cardiac tissue or produced alterations in membrane repolarization. CONCLUSION Anti-Ro/SS-A antibodies may play a pathophysiologic role in the development of congenital heart block in neonatal lupus.

We analyzed our 10‐year cumulative experience of 40 consecutive patients with idiopathic dilated Cardiomyopathy and associated ventricular tachyarrhythmias, treated with implantable Cardioverter defibrillators. Dilated Cardiomyopathy was defined as left ventricular ejection fraction (EF) ≤50% with no defineable etiology. Patient characteristics included: 24 male, mean age 52 years, mean EF = 33%, New York Heart Association Class I–III, presenting syndrome—cardiac arrest (n = 28), syncope/near syncope (n = 12). At 2.5 years mean follow‐up, there were 16 deaths: one operative, three sudden, two incessant ventricular tachycardia/ventricular fibrillation (VT/VF), six heart failure, and four noncardiac. The actuarial mortality at 1 and 4 years was 0% and 14% for sudden death, 11% and 34% for cardiac death. The projected mortality was 52% and 78% for same time intervals (P < 0.01). No useful baseline variable predicted who would or would not receive an ICD shock in follow‐up. ICD therapy appears effective in reducing sudden death mortality in this high risk population.

Journal of Interventional CardiologyVolume 4, Issue 3 p. 211-220 Implantable Cardioverter Defibrillators in Cardiovascular Practice: Report of the Policy Conference of the North American Society of Pacing and Electrophysiology MICHAEL H. LEHMANN, Corresponding Author MICHAEL H. LEHMANN The NASPE Policy Conference CommitteeMichael H. Lehmann, M.D., Division of Cardiology, Harper Hospital, 3990 John R, Detroit, MI 48201.Search for more papers by this authorSANJEEV SAKSENA Editors, SANJEEV SAKSENA Editors The NASPE Policy Conference CommitteeSearch for more papers by this authorMICHAEL H. LEHMANN, MICHAEL H. LEHMANN The NASPE Policy Conference CommitteeSearch for more papers by this authorSANJEEV SAKSENA, SANJEEV SAKSENA The NASPE Policy Conference CommitteeSearch for more papers by this authorMASOOD AKHTAR, MASOOD AKHTAR The NASPE Policy Conference CommitteeSearch for more papers by this authorJ. THOMAS BIGGER JR., J. THOMAS BIGGER JR. The NASPE Policy Conference CommitteeSearch for more papers by this authorA. JOHN CAMM, A. JOHN CAMM The NASPE Policy Conference CommitteeSearch for more papers by this authorELIZABETH J. DARLING, ELIZABETH J. DARLING The NASPE Policy Conference CommitteeSearch for more papers by this authorLEONARD DREIFUS, LEONARD DREIFUS The NASPE Policy Conference CommitteeSearch for more papers by this authorMARGARET FAUST, MARGARET FAUST The NASPE Policy Conference CommitteeSearch for more papers by this authorJOHN D. FISHER, JOHN D. FISHER The NASPE Policy Conference CommitteeSearch for more papers by this authorSEYMOUR FURMAN, SEYMOUR FURMAN The NASPE Policy Conference CommitteeSearch for more papers by this authorNORA F. GOLDSCHLAGER, NORA F. GOLDSCHLAGER The NASPE Policy Conference CommitteeSearch for more papers by this authorJERRY C. GRIFFIN, JERRY C. GRIFFIN The NASPE Policy Conference CommitteeSearch for more papers by this authorTHOMAS GUARNIERI, THOMAS GUARNIERI The NASPE Policy Conference CommitteeSearch for more papers by this authorGERARD M. GUIRAUDON, GERARD M. GUIRAUDON The NASPE Policy Conference CommitteeSearch for more papers by this authorJ. WARREN HARTHORNE, J. WARREN HARTHORNE The NASPE Policy Conference CommitteeSearch for more papers by this authorJEREMY N. RUSKIN, JEREMY N. RUSKIN The NASPE Policy Conference CommitteeSearch for more papers by this authorRICHARD M. LUCERI, RICHARD M. LUCERI The NASPE Policy Conference CommitteeSearch for more papers by this authorJAMES D. MALONEY, JAMES D. MALONEY The NASPE Policy Conference CommitteeSearch for more papers by this authorFRANCIS E. MARCHLINSKI, FRANCIS E. MARCHLINSKI The NASPE Policy Conference CommitteeSearch for more papers by this authorROBERT J. MYERBURG, ROBERT J. MYERBURG The NASPE Policy Conference CommitteeSearch for more papers by this authorLOIS SCHURIG, LOIS SCHURIG The NASPE Policy Conference CommitteeSearch for more papers by this authorGERALD C. TIMMIS, GERALD C. TIMMIS The NASPE Policy Conference CommitteeSearch for more papers by this authorALBERT L. WALDO, ALBERT L. WALDO The NASPE Policy Conference CommitteeSearch for more papers by this authorSALIM YUSUF, SALIM YUSUF The NASPE Policy Conference CommitteeSearch for more papers by this authorDOUGLAS P. ZIPES, DOUGLAS P. ZIPES The NASPE Policy Conference CommitteeSearch for more papers by this author MICHAEL H. LEHMANN, Corresponding Author MICHAEL H. LEHMANN The NASPE Policy Conference CommitteeMichael H. Lehmann, M.D., Division of Cardiology, Harper Hospital, 3990 John R, Detroit, MI 48201.Search for more papers by this authorSANJEEV SAKSENA Editors, SANJEEV SAKSENA Editors The NASPE Policy Conference CommitteeSearch for more papers by this authorMICHAEL H. LEHMANN, MICHAEL H. LEHMANN The NASPE Policy Conference CommitteeSearch for more papers by this authorSANJEEV SAKSENA, SANJEEV SAKSENA The NASPE Policy Conference CommitteeSearch for more papers by this authorMASOOD AKHTAR, MASOOD AKHTAR The NASPE Policy Conference CommitteeSearch for more papers by this authorJ. THOMAS BIGGER JR., J. THOMAS BIGGER JR. The NASPE Policy Conference CommitteeSearch for more papers by this authorA. JOHN CAMM, A. JOHN CAMM The NASPE Policy Conference CommitteeSearch for more papers by this authorELIZABETH J. DARLING, ELIZABETH J. DARLING The NASPE Policy Conference CommitteeSearch for more papers by this authorLEONARD DREIFUS, LEONARD DREIFUS The NASPE Policy Conference CommitteeSearch for more papers by this authorMARGARET FAUST, MARGARET FAUST The NASPE Policy Conference CommitteeSearch for more papers by this authorJOHN D. FISHER, JOHN D. FISHER The NASPE Policy Conference CommitteeSearch for more papers by this authorSEYMOUR FURMAN, SEYMOUR FURMAN The NASPE Policy Conference CommitteeSearch for more papers by this authorNORA F. GOLDSCHLAGER, NORA F. GOLDSCHLAGER The NASPE Policy Conference CommitteeSearch for more papers by this authorJERRY C. GRIFFIN, JERRY C. GRIFFIN The NASPE Policy Conference CommitteeSearch for more papers by this authorTHOMAS GUARNIERI, THOMAS GUARNIERI The NASPE Policy Conference CommitteeSearch for more papers by this authorGERARD M. GUIRAUDON, GERARD M. GUIRAUDON The NASPE Policy Conference CommitteeSearch for more papers by this authorJ. WARREN HARTHORNE, J. WARREN HARTHORNE The NASPE Policy Conference CommitteeSearch for more papers by this authorJEREMY N. RUSKIN, JEREMY N. RUSKIN The NASPE Policy Conference CommitteeSearch for more papers by this authorRICHARD M. LUCERI, RICHARD M. LUCERI The NASPE Policy Conference CommitteeSearch for more papers by this authorJAMES D. MALONEY, JAMES D. MALONEY The NASPE Policy Conference CommitteeSearch for more papers by this authorFRANCIS E. MARCHLINSKI, FRANCIS E. MARCHLINSKI The NASPE Policy Conference CommitteeSearch for more papers by this authorROBERT J. MYERBURG, ROBERT J. MYERBURG The NASPE Policy Conference CommitteeSearch for more papers by this authorLOIS SCHURIG, LOIS SCHURIG The NASPE Policy Conference CommitteeSearch for more papers by this authorGERALD C. TIMMIS, GERALD C. TIMMIS The NASPE Policy Conference CommitteeSearch for more papers by this authorALBERT L. WALDO, ALBERT L. WALDO The NASPE Policy Conference CommitteeSearch for more papers by this authorSALIM YUSUF, SALIM YUSUF The NASPE Policy Conference CommitteeSearch for more papers by this authorDOUGLAS P. ZIPES, DOUGLAS P. ZIPES The NASPE Policy Conference CommitteeSearch for more papers by this author First published: September 1991 https://doi.org/10.1111/j.1540-8183.1991.tb00795.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume4, Issue3September 1991Pages 211-220 RelatedInformation

Antiarrhythmic drugs may alter the energy for Cardioversion of ventricular arrhythmias. This study compares the energy necessary for cardioverting chronic atrial fibrillation in 57 patients taking type Ia, Ic, or type III antiarrhythmic drugs. Patients taking Ia (n = 22) or III (n = 14) drugs had a median energy for Cardioversion of 100 joules, while the patients taking Ic (n = 17) drugs had a median energy of 200 joules (P = 0.03). There were no differences in the frequency of unsuccessful Cardioversion, There were no serious adverse events in any of the three groups, although three patients in the Ic group had > 3 second pauses after the shock. The data suggest that the use of Ic antiarrhythmic drugs results in a higher energy for cardioversion of atrial fibrillation. However with higher energies, conversion is as successful as for type Ia and type III.

Amiodarone, an antiarrhythmic drug approved for use in patients who survive cardiac arrest, has been associated with infiltration of or inflammatory changes in various tissues. To date thyroid dysfunction has been the only endocrine disturbance noted. In an initial group of seven amiodarone-treated men undergoing evaluation for sexual dysfunction, an elevation in serum gonadotropin concentration was detected, suggesting testicular dysfunction.Because of this finding, gonadal function was prospectively evaluated in 44 men (18 who had been treated with amiodarone for > 1 year and 26 survivors of cardiac arrest who had been treated with antiarrhythmic drugs other than amiodarone). Amiodarone-treated men had higher serum follicle-stimulating hormone (41.8 +/- 22.8 vs. 14.4 +/- 10.4 mIU/ml, p < 0.001) and luteinizing hormone (34.8 +/- 26.4 vs. 10.1 +/- 5.2 mIU/ml, p < 0.001) concentrations compared with control subjects. Although serum total and free testosterone levels were comparable between the two patient groups, these levels were inversely correlated (r = -0.53, p < 0.05; r = -0.62, p < 0.01, respectively) with cumulative amiodarone dose.Hyperresponsiveness to the administration of gonadotropin-releasing hormone was noted in the 10 amiodarone-treated men evaluated by this diagnostic test. Sexual dysfunction was common in both groups (70% of control subjects and 82% of amiodarone-treated subjects), although atrophic testes were more commonly observed in amiodarone-treated men (p < 0.05).Because of the elevated serum gonadotropin level, it is concluded that testicular dysfunction may result from prolonged amiodarone treatment.