Effect of intravenous procainamide on direct-current cardioversion of atrial fibrillation

H, Goy JJ. Coronary stenting for coronary artery narrowing in a heart transplantrecepient.Transpl Int1996;9:433–436.7. Fischman DL, Leon MB, Baim DS, Schatz RA, Savage MP, Penn I, Detre K,Veltri L, Ricci D, Nobuyoshi M, et al. A randomized comparison of coronarystent placement and balloon angioplasty in the treatment of coronary arterydisease.N Engl J Med1994;331:496–501.8. Serruys PW, Jaegere PD, Keimeneij F, Macaya C, Rutsch W, Heyndrickx G,Emanuelsson H, Marco J, Legrand V, Materne P, et al. A comparison of balloonexpandable stent implantation with balloon angioplasty in patients with coronaryartery disease.N Engl J Med1994;331:489–495.9. Keogh AM, Valentine HA, Hunt SA, Schroeder JS, McIntosh N, Oyer PE,Stinson EB. Impact of proximal or mid vessel discrete coronary artery disease onsurvival after heart transplantation.J Heart Lung Transplant1992;11:892–901.

10. Gao SZ, Schroeder JS, Hunt S, Stinson EB. Retransplantion for severeaccelerated coronary artery disease in heart transplantation recipients.Am JCardiol 1988;62:876–881.11. Hosenpud JD, Novick RJ, Breen TJ, Keck B, Dailey P. The Registry of theInternational Society for the Heart and Lung Transplantation: Twelfth OfficialReport—1995.J Heart Lung Transplant1995;14:805–815.12. Stevenson LW, Warner SL, Steimle AE, Fonarow GC, Hamilton MA,Moraiguchi JD, Kobashigawa JA, Tillisch JH, Drinkwater DC, Laks H. Theimpending crisis awaiting cardiac transplantation: modeling a solution based onselection.Circulation 1994;89:450–457.13. Parry A, Roberts M, Parameshar J, Wallwork J, Schofield P, Large S. Themanagement of post cardiac transplantation coronary artery disease.Eur J Car-diothorac Surg1996;10:528–533.

Effect of Intravenous Procainamide on Direct-CurrentCardioversion of Atrial Fibrillation

Laura O. Jacobs, MD, Thomas C. Andrews, MD, David N. Pederson, MD, andDaniel J. Donovan, MD

D irect-current cardioversion of atrial fibrillation issuccessful in restoring normal sinus rhythm in

approximately 75% to 80% of patients.1 The effect oftype Ia antiarrhythmic agents on the efficacy of car-dioversion has been poorly studied. Data from a small,retrospective observational study suggested that pro-cainamide or quinidine may facilitate cardioversion ofatrial fibrillation,2 although a randomized trial of quin-idine failed to demonstrate a difference in successcompared with placebo.3 We performed a random-ized, placebo-controlled, crossover trial to determinewhether an intravenous loading dose of procainamideincreases the likelihood of successful conversion tosinus rhythm in patients with chronic atrial fibrillation.

• • •We recruited 100 consecutive subjects with atrial

fibrillation of at least 2 weeks’ duration referred to thecardiology service for elective cardioversion. All sub-jects underwent a brief history and physical examina-tion, and the medical record was reviewed for perti-nent clinical, demographic, and echocardiographic in-formation. Patients were randomized to anintravenous infusion of procainamide (15 mg/kg up toa maximum of 1,250 mg) or placebo (normal saline)administered over 60 minutes followed by a continu-ous infusion of blinded medication corresponding to 2mg/ml of procainamide or placebo. Direct-current car-dioversion was attempted with subjects in the fastingstate under conscious sedation using anterior and pos-terior positioned Zoll pads (Zoll Medical Corp., Bur-lington, Massachusetts). A defibrillation sequence of

50, 100, 200, 360, and 360 J was used. If the initialattempt at cardioversion was unsuccessful, the subjectwas crossed over to the other therapy for anotherattempt at cardioversion the following day. For exam-ple, subjects receiving a placebo infusion on day 1who did not convert to normal sinus rhythm receiveda procainamide infusion on day 2 followed by a sec-ond attempt at cardioversion, and those subjects orig-inally randomized to procainamide had a second at-tempt after placebo infusion. The energy required fora successful cardioversion was recorded along with allcomplications, including sinus pauses.3 seconds,clinically important hypotension, respiratory compro-mise, embolic event, or ventricular dysrhythmia. Con-tinuous variables were compared with the Student’sttest and categorical variables with the chi-square testor Fisher’s exact test when appropriate. The numberof defibrillations and energy used for defibrillationwere compared with the Mann-Whitney U test. Sam-ple size was calculated to allow 80% power to detecta 12% difference in conversion to normal sinusrhythm. A p value,0.05 was considered significant.All statistics were performed using Systat 5.2 forMacintosh. The study was approved by the local in-stitutional review board and all subjects provided writ-ten informed consent.

• • •Clinical characteristics and results are listed in

Table I. There were no significant differences between

From the Department of Cardiology/Division of Medicine, WilfordHall Medical Center, Lackland Air Force Base, the Cardiology Divi-sion/Department of Internal Medicine, University of Texas Southwest-ern Medical Center, Dallas, and Austin Heart PA, Austin, Texas. Dr.Andrews’ address is: Cardiology Division, UT Southwestern MedicalCenter, 5323 Harry Hines Blvd., Dallas, Texas 75235-9047. Manu-script received November 14, 1997; revised manuscript receivedand accepted March 2, 1998.

The views expressed in this article are those of the authors and do notreflect the official policy of the Department of Defense or other depart-ments of the US government.

TABLE I Clinical and Echocardiographic Characteristics andResults of Cardioversion

Procainamide(n 5 50)

Placebo(n 5 50)

Mean age (yrs) 69 6 9 68 6 11Men 34 (68%) 34 (68%)Left atrial size (mm) 46 6 8 47 6 8Valvular heart disease 12 (24%) 16 (32%)Left ventricular ejection fraction ,50% 14 (28%) 15 (30%)Duration of atrial fibrillation (mo) 3.4 6 4.5 3.4 6 2.1Successful cardioversion 41 (82%) 39 (78%)

BRIEF REPORTS 241

the 2 groups in any clinical or echocardiographicvariable. There was no significant difference in suc-cessful conversion to normal sinus rhythm with pro-cainamide therapy (procainamide 82%, placebo 78%,p 5 NS). Subjects randomized to procainamide re-quired significantly fewer shocks and less mean en-ergy compared with placebo-treated subjects (meannumber of shocks: 3.28 compared with 3.78, p50.031; mean energy: 241 vs 290 J, p5 0.028), and 5of 50 procainamide-treated subjects had conversionwith the study drug infusion alone. Of the 9 procain-amide-treated subjects who failed the initial attempt atcardioversion, 1 had spontaneous conversion in theensuing 24 hours, 1 withdrew from the study, and 2 of7 had successful conversion to normal sinus rhythmafter crossing over to placebo (29%). Of the 11 pla-cebo-treated subjects who failed the initial attempt atcardioversion, 1 withdrew from the study and 6 of 10had successful conversion to normal sinus rhythmafter crossing over to procainamide (60%, p5 0.33compared with subjects crossing over to placebo).There were 4 subjects in the procainamide group andnone in the placebo group who experienced hypoten-sion that required the administration of saline anddiscontinuation of study medication (p5 0.12).

Ours is the first reported randomized trial of pro-cainamide in direct-current cardioversion of atrial fi-brillation. Although the energy required for successfulcardioversion was lower with procainamide than withplacebo therapy, our data suggest that procainamide isof no significant clinical benefit in facilitating theinitial attempt at cardioversion of atrial fibrillation. Inthe small number of subjects in whom the initialattempt was unsuccessful, subsequent treatment withprocainamide was associated with a trend toward agreater likelihood of successful conversion to sinusrhythm, and use of procainamide in this setting war-rants further study.

In conclusion, our data suggest that procain-amide is of no clinical benefit in the initial attemptat cardioversion of atrial fibrillation.

1. Cohen T, Ibrahim B, Denier D, Haji A, Quan W. Active compressioncardioversion for refractory atrial fibrillation.Am J Cardiol1997;80:354–355.2. Szekely P, Wynne N, Pearson D, Batson G, Sideris D. Direct current shock andantidysrhythmic drugs.Br Heart J 1970;34:209–218.3. Hillestad L, Dale J, Stortein O. Quinidine before direct current coutershock: acontrolled study.Br Heart J 1972;34:139–142.

Effect of Enalapril Therapy on Left Ventricular Massand Volumes in Asymptomatic Chronic, Severe Mitral

Regurgitation Secondary to Mitral Valve ProlapseMarc D. Tischler, MD, Michaelanne Rowan, RN, and Martin M. LeWinter, MD

There are theoretical considerations that suggest thatprophylactic vasodilator therapy might not be ben-

eficial in patients with chronic mitral regurgitation(MR).1,2 To understand whether there is a role forprophylactic vasodilators, it is important to first estab-lish what effects these drugs have on left ventricular(LV) mass, volume, and function in asymptomaticpatients. Because there is a paucity of such informa-tion, we conducted a quantitative rest and stress echo-cardiographic study of 12 asymptomatic patients withsevere, chronic MR due to mitral valve prolapse(MVP) with a normal LV ejection fraction at rest, whowere not receiving angiotensin-1 converting enzymeinhibitors (ACE).

• • •We prospectively identified 12 asymptomatic pa-

tients with chronic, severe MR due to MVP and a LVejection fraction at rest of.55% by 2-dimensionalechocardiography. No patient had been previously

treated with an ACE inhibitor or any form of vasodi-lator at any time. Exclusion criteria included mitralstenosis and other valvular heart disease, known cor-onary artery disease, and inadequate echocardio-graphic windows for quantitative 2-dimensional anal-ysis. There were 11 men and 1 woman, age 576 17years (mean6 SD). All patients were in normal sinusrhythm. Two patients were receiving digoxin, and 1was receiving diuretic therapy; therapy was continuedat the time of testing. All studies were performed afterinformed consent was given, as approved by the Com-mittee on Human Research, University of VermontCollege of Medicine. Enalapril was started at a dose of2.5 mg twice daily and titrated to a target dose of 10mg twice daily.

Following an initial training session on the bicycleergometer, patients performed 3 exercise echocardio-grams; 1 while receiving no drugs, one 2 weeks fol-lowing titration to target dose, and a final study 6months after full up-titration. Baseline 2-dimensionalexaminations were performed supine in the left lateraldecubitus position with a phased-array ultrasonoscopedevice (Acuson XP-10, Mountain View, California)using a 2.5-MHz transducer. Images were obtained insequential fashion from the parasternal long-axis,parasternal short-axis, apical 4-chamber, and apical

From the University of Vermont College of Medicine and Fletcher AllenHealth Care, Burlington, Vermont. This study was supported in part bya research grant from the VASOTEC Medical School Grants Commit-tee, Merck Research Laboratories, Rahwah, New Jersey. Dr. Tischler’saddress is: Cardiac Ultrasound Laboratory, Cardiology Unit, McClure1, Fletcher Allen Health Care, 111 Colchester Avenue, Burlington,Vermont 05401. Manuscript received November 3, 1997; revisedmanuscript received and accepted February 23, 1998.

242 THE AMERICAN JOURNAL OF CARDIOLOGYT VOL. 82 JULY 15, 1998