also lead to plaque rupture or fissure that forms the substrate for thrombus formation. In addition, the morn- ing increase in plasma catecholamines, by further aug- menting the direct effects of the sympathetic nervous system, expands the oxygen demand of the myocardium. All these factors may be the basis for the precipitation of myocardial ischemia in patients with advanced coronary disease.g

Better understanding of the endogenous biologic func- tions and the morning physiologic changes of the clinical manifestations of ischemic heart disease may lead to im- proved control of the precipitating factors and guide toward more effective therapeutic interventions.

1. SPRINT Study Group. Nifedipine in secondary prevention after myccardial infarction. Harefuoh 1989;116:1-6. 2. Muller JE, Ludmer PL, Willich SN, Tofler GH, Aylmer G, Klangos I, Stone PH. Circadian variation in the frequency of sudden cardiac death. Circulation 1987;75:131-138. 3. Muller JE, Stone PH, Turi ZG, Rutherford JD, Czeisler CA, Parker C, Poole WK. Passamani E. Roberts R. Robertson T. Sobel BE. Willerson JT. Braunwald E, and the MILIS’Study Groip. Circadian iariation iA the frequent; of onset of acute myocardial infarction. N Engl J Med 1985;313:1315-1322. 4. Rocco MB, Barry J, Campbell S, Nabel E, Cook EF, Goldman L, Selwyn AP. Circadian variation of transient mvocardial ischemia in oatients with coronarv artery disease. Circulation 1987;75:395-400. 5. Colantonio D, &sale R, Abruzzo BP, Lorenzetti G, Pasqualetti P. Circadian distribution in fatal pulmonary thromboembolism. Am J Cardial 19X%64:403- 404. 6. Tsementzis SA, Gill JS, Hitchcock ER, Gill SK, Beevers DG. Diurnal variation of and activity during the onset of stroke. Neurosurgery 1985;17:901-904. 7. Tofler GH, Brezinski D, Schafer AI, Czeisler CA, Rutherford JD, Willich S, Gleason RE, Williams G, Muller JE. Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death. N Eng/ J Med 1987;316:1514~1518. 8. Millar-Craig MW, Bishop CN, Raftery EB. Circadian variation of blood- pressure. Lmcet 1978;1:795-797. 9. Turton MB, Deegan T. Circadian variations of plasma catecholamine, cortisol

and immunoreactive insulin concentrations in supine subjects. C/in Chim Acta 1974;55:389-397.

APPENDIX SPRINT STUDY GROUP

Henry N. Neufeld, MD (deceased); Jacob Agmon, MD; Solomon Behar, MD; Uri Goldbourt, PhD; Henrietta Reicher- Reiss, MD; Edward Abinader, MD; Jacob Barzilay, MD; Yaa- cov Friedman, MD; Nissim Kauli, MD; Yehezkiel Kishon, MD; Abraham Palant, MD; Benyamin Peled, MD; Leonardo Reisin, MD; Egon Riss, MD (deceased); Zwi Schlesinger, MD; Izhar Zahavi, MD; Monty Zion, MD.

Participating centers, principal investigators and physicians: Assaf Harofeh Hospital, Zerifin: Zwi Schlesinger, MD; Moshe Algom, MD. Barzilai Medical Center, Ashkelon: Leonardo Reisin, MD; Newton Yalom, MD. Beilinson Medical Center, Petach Tikvah: Yaacov Friedman, MD. Carmel Hospi- tal and Medical “Lin” Haifa: Abraham Palant, MD; Ephraim Mayer, MD. Central Emek Hospital, Afula: Jacob Barzilay, MD; Lev Bloch, MD. Hasharon Hospital, Petach Tikvah: Izhar Zahavi, MD; Menachem Katz, MD. Hillel Yaffe Hospital, Hadera: Benyamin Pelled, MD, MSc; Zakki Abu-Mot&h, MD. Kaplan Hospital, Rehovot: Nissim Kauli, MD; Emanuel Liebman, MD. Rambam Medical Center, Haifa: Egon Riss, MD, MSc (deceased); Jamil Hir, MD. Bnei Zion Center, Hai- fa: Edward Abinader, MD; Ehud Goldhammer, MD; Salim Maalouf, MD. Shaare Zedek Medical Center, Jerusalem: Monty Zion, MD; David Rosenmann, MD; Jonathan Balkin, MD. Sheba Medical Center, Tel Hashomer: Henrietta Reicher-Reiss, MD. Wolfson Medical Center, Holon: Yehez- kiel Kishon, MD; Ron Narinsky, MD. Coordinating Center, Sheba Medical Center, Tel Hashomer: Solomon Behar, MD; Uri Goldbourt, PhD; Henrietta Reicher-Reiss, MD; Lori Man- delzweig, MPH.

Decrease of Right and Left Atrial Sizes After Direct-Current Electrical Cardioversion in Chronic Atrial Fibrillation lsabelle C. Van Gelder, MD, Harry J. Crijns, MD, Wiek H. Van Gilst, PhD, Hans P. M. Hamer, MD, and Kong I. Lie, MD

I n chronic atria1 fibrillation (AF), atria1 enlargement is considered both a cause and a consequence of the ar-

rhythmia.rm4 It is not well known whether restoration and long-term maintenance of sinus rhythm indeed causes a reversal of the process of atria1 enlargement.5 In addition, the influence of the type of underlying heart disease on this process has not been studied. Therefore, we assessed whether atria1 sizes decrease after electrical cardioversion in patients with chronic AF using 2-dimensional echocar- diography.

Between January 1988 and January 1989, 120 pa- tients with chronic AF were cardioverted to sinus rhythm. Sixty patients remained in sinus rhythm for 16

From the Departments of Cardiology, Thoraxcenter, and Clinical Phar- macology, University Hospital Groningen, Oostersingel 59, 9713 EZ Groningen, The Netherlands. Manuscript received July 10, 1990; re- vised manuscript received and accepted August 20, 1990.

months. In 49 of these patients, fully evaluable echocar- diographic recordings could be obtained. These 49 pa- tients were the subject of the present study. Chronic AF was defined as documented AF with a duration of >24 hours without intercurrent sinus rhythm. The type of underlying heart disease was determined from the pa- tient’s history, physical examination, 12-lead electrocar- diogram, chest x-ray, 2-dimensional echocardiogram, bicycle exercise test and, if available, coronary angio- gram. In all patients, hyperthyroidism was excluded us- ing standard tests. “‘Lone” AF was diagnosed only in the absence of any demonstrable underlying heart disease.6 Mitral valve disease was of rheumatic (n = 9), congeni- tal (n = I) or ischemic (n = 1) origin, and IO of the patients in this group had mitral stenosis. Twenty-jive patients with other underlying heart diseases were in- cluded in the nonmitral heart disease group. Coronary artery disease was present in 1 I patients, hypertensive

THE AMERICAN JOURNAL OF CARDIOLOGY JANUARY 1, 1991 93

heart disease in 7 patients, aortic valve disease in 4 patients, corrected hyperthyroidism in 1 patient and mi- tral valve prolapse without mitral regurgitation in 1 pa- tient. One patient had undergone cardiac surgery be- cause of a myxoma. The other 13 patients formed the group with lone AF. After the cardioversion, antiar- rhythmic prophylactic drug treatment was instituted in 42 patients, depending on ongoing antiarrhythmic drug studies. These drugs were continued during follow-up. All other drug therapy was left unchanged. Patients were followed in the outpatient department after 1, 3 ana’ 6 months.

Values are expressed as mean f 1 standard devi- ation. Paired Student’s t test was used to compare data

Transthoracic echocardiographic studies were per- formed on the day of admission and 4 months after the cardioversion. Echocardiograms were recorded with a Toshiba SSH 65A with the use of a 2.5MHz transduc- er. Two-dimensional recordings were made to evaluate overall left atria1 (LA) and right atria1 (RA) size. Re- cordings were performed with the patient in the left re- cumbent position. The LA long-axis diameter was taken as the maximal transverse diameter, with the transducer in the standard long-axis position with a stable view of the aortic and mitral valve as well as of the ventricular septum and posterior left ventricular wall. LA and RA diameters, with the transducer at the apex of the heart, were also measured as maximal diameter at end systole with a stable simultaneous view of both valves. Atria1 area was determined with the following formula: (0.5 X LA diameter in long-axis view) X (0.5 X LA diameter in apical view) X 7~. Echocardiographic studies were per- formed by 2 cardiologists who were unaware of the pa- tient’s participation in the study. LA long-axis diameter <40 mm was defined as normal. The maximum for both the apical LA and RA diameters was set at 55 mm. Using the above-mentioned formula for LA area only, values <1,725 mm2 were considered normal.

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MITRAL VALVE NON-MITRAL ‘LONE’ ATRIAL DISEASE HEART DISEASE FIBRILLATION

IZI CARDIOVERSION 0 6MONTHS SR

LEFT ATRIAL AREA = MM2/100 *p =0.02

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from the day of cardioversion and after 6 months of sinus rhythm. Unpaired Student’s t test was used to compare echocardiographic data between patients with mitral valve disease, nonmitral heart disease and pa- tients with lone AF. P values <0.05 were considered statistically significant.

Figure 1 shows that patients with mitral valve disease had the largest mean LA area, which was significantly different from that inpatients with lone AF (2592 f 370 vs 2,004 f 592 mm2, p = 0.02). In addition, mean LA area in patients with mitral valve disease was substan- tially larger than it was inpatients with nonmitral heart disease (2,592 f 370 us 2,294 f 391 mm2, p = 0.05). In the latter patient group, LA area tended to be larger than in patients with lone AF, but the difference was not statistically significant (p = 0.08). Six months after restoration of sinus rhythm, LA area had decreased sig- nificantly (8%) to 2,105 f 432 mm2 in patients with nonmitral heart disease (p = 0.02) and to 1,762 f 479 mm2 (1270) in lone AF patients (p = 0.02). LA area did not change in patients with mitral valve disease. For the total group, a 6% reduction of the LA area,from 2,290 f 497 to 2,135 f 583 mm2 @ = 0.03), was found.

At the end of follow-up all patients showed an im- provement in New York Heart Association functional

Figure 2 shows that the apical RA diameter was smallest in the group with lone AF (54 f 7 mm). It was significantly smaller in this group than it was in the group with nonmitral heart disease (59 f 6 mm, p = 0.04). Although patients with underlying mitral valve disease clearly had enlarged right atria (59 f 7 mm), they did not differ significantly from the lone AF pa- tients (p = 0.1). After 6 months of maintained sinus rhythm,patients with mitral valve disease and those with nonmitral heart disease showed a significant decrease in RA dimensions (II%, respectively; 8% size reduction, p = 0.009). This dimension remained unchanged in the group with lone AF.

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94 THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 67

class: a decrease from 2.2 f 0.6 to 1.7 f 0.5 in patients with mitral valve disease @ = 0.02); a decrease from 1.6 f 0.6 to 1.4 f 0.6 in patients with nonmitral heart disease (p = O.OZ); and a decrease in the lone AF group from 1.5 f 0.5 to 1.1 f 0.3 (p = 0.02).

The present study shows that after restoration and long-term maintenance of sinus rhythm, echocardio- graphic LA and RA dimensions may decrease. In the group of patients with lone AF, it appeared that the mean LA area nearly normalized, whereas in the other 2 pa- tient groups the mean RA size returned to normal.

The only parameter not changed after regularization of sinus rhythm was the LA area in patients with mitral valve disease. Almost all patients included in this group had moderate-to-severe mitral valve stenosis with a rheu- matic etiology. This may have precluded reduction in atria1 size, because the hemodynamic consequences of obstruction of the blood flow from the atrium to the ventricle may have outweighed the beneficial effects of the restoration of the atria1 systole after normalization of the rhythm. In addition, the rheumatic disease process may have caused a stiffening of the atria1 wall, thereby hampering morphologic changes.

In patients with lone AF, only the left atrium was enlarged. In contrast, additional RA enlargement had occurred in both of the other patient groups. These latter groups also had the largest mean LA size. These findings suggest that after the onset of AF, altered hemodynamics will affect the left atrium first, whereas the right atrium seems to be relatively protected. Only after the develop- ment of a significant LA enlargement will left-sided he- modynamics affect RA pressure and in particular RA volume, resulting in dilatation.

1. Henry WL, Morganroth J, Pearlman AS, Clark CE, Redwood DR, Itscoitz SB, Epstein SE. Relation between echocardiographically determined left atrial size and atrial fibrillation. Circulation 1976,53:273-279. 2. Keren G, Etzion T, Sherez J, Zelcer AA, Megidish R, Miller HI, Laniado S. Atria1 fibrillation and atrial enlargement in patients with mitral stenosis. Am HeartJ 1987;114:1146-1155. 3. Ewy GA, Ulfers L, Hager D, Rosenfeld AR, Roeske WR, Goldman S. Re- sponse of atrial fibrillation to therapy: role of etiology and left atrial diameter. J Eiectrocordiol 1980:13:119~124. 4. Petersen P, Kastrup J, Brinch K, Godtfredsen J, Boysen G. Relation between left atrial size and duration of atrial fibrillation. Am J Cardiol 1987;60:382-384. 5. Manning WJ, Come PC. Pulsed Doppler evaluation of atrial mechanical function after electrical cardioversion of atrial fibrillation. J Am Coil Cardiol 1989;13:617-623. 6. Evans W, Swarm P. Lone auricular fibrillation. Er Hearr J 1954;16:189-194.

Cardiac Rhythm Precipitating Automatic Implantable Cardioverter- Defibrillator Discharge in Outpatients as Detected from Transtelephonic Electrocardiographic Recordings Jonathan S. Steinberg, MD, and John S. Sugalski, BS

1 he automatic implantable cardioverter-defibrillator (AICD) has become a mainstay in the nonpharma-

cologic management of sustained ventricular tachyar- rhythmias.’ One of the most significant management problems for the AICD population is that of AICD dis- charge for cardiac rhythms other than sustained ventricu- lar tachyarrhythmias, the rhythms that the AICD ~was designed to sense and terminate.2~5 This type of AICD discharge has been termed “inappropriate,” “spurious,” or “false positive,” can be due to a variety of cardiac rhythms, and, if recurrent, may be associated with delete- rious medical or psychological consequences.’ Although the problem clearly exists, the occurrence of inappropri- ate AICD discharges is difficult to define in clinical prac- tice because the current AICD system has no internal memory or telemetry functions to document the rhythms that precipitated the AICD discharge. There is little pub- lished information that documents the cause of AICD discharges in an outpatient population. The objective of this study was to survey the records of all AICD outpa-

From the Division of Cardiology, Department of Medicine, Columbia University College of Physicians & Surgeons, 630 West 168th Street, New York, New York 10032; and Medtronic Cardiocare, Inc., Forest Hills, New York. Manuscript received July 3, 1990; revised manuscript received August 3 1, 1990, and accepted September 3.

Dr. Steinberg is an Investigator of the American Heart Association, New York City Affiliate, New York, New York.

tients enrolled in a transtelephonic electrocardiogram monitoring service, and to review the records for (1) the cardiac rhythms responsible for the AICD discharges, and (2) the patients’ symptoms preceding the AICD dis- charge.

Thirty-six patients who had been enrolled in the AICD follow-up service of Medtronic Cardiocare (For- est Hills, New York) were studied. These patients were enrolled at the discretion of their primary physician, probably after II unexplained AICD discharges, and all had Ventak AICD (Cardiac Pacemakers, Incorporat- ed, St. Paul, Minnesota) units. The patients in this pro- gram were studied with transtelephonic electrocardio- graphic (ECG) monitors that had looping memory capa- bility to record data simultaneously from 2 ECG leads. When the patient activated the device to record a symp- tomatic episode, the previous 30 seconds of electrocar- diogram were frozen in memory and an additional 45 second electrocardiogram was recorded from each of the channels. For each transtelephonic recording, thefollow- ing were examined: the presence and number of AICD discharges, the cardiac rhythm and rate preceding AICD discharges, the patients’ symptoms preceding AICD dis- charges and the cardiac rhythm following AICD dis- charges.

Sixteen patients did not experience an AICD dis- charge (n = 12) or did not successfully record the dis-

THE AMERICAN JOURNAL OF CARDIOLOGY JANUARY 1, 1991 95