also lead to plaque rupture or fissure that forms the substratefor thrombus formation. In addition, the morning increase in plasma catecholamines,by further augmenting the direct effects of the sympathetic nervous system,expandsthe oxygen demandof the myocardium. All thesefactors may be the basisfor the precipitation of myocardial ischemia in patients with advancedcoronary disease.g Better understandingof the endogenousbiologic functions and the morning physiologic changesof the clinical manifestations of ischemic heart diseasemay lead to improved control of the precipitating factors and guide toward more effective therapeutic interventions.

and immunoreactiveinsulin concentrationsin supine subjects.C/in Chim Acta 1974;55:389-397.

APPENDIX SPRINT STUDY GROUP Henry N. Neufeld, MD (deceased);Jacob Agmon, MD; SolomonBehar, MD; Uri Goldbourt, PhD; Henrietta ReicherReiss,MD; Edward Abinader, MD; JacobBarzilay, MD; Yaacov 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: LeonardoReisin, MD; Newton Yalom, MD. Beilinson Medical Center, PetachTikvah: Yaacov Friedman, MD. Carmel Hospital and Medical “Lin” Haifa: Abraham Palant, MD; Ephraim Mayer, MD. Central Emek Hospital, Afula: Jacob Barzilay, MD; Lev Bloch, MD. Hasharon Hospital, PetachTikvah: 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, Haifa: 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: Yehezkiel Kishon, MD; Ron Narinsky, MD. Coordinating Center, Sheba Medical Center, Tel Hashomer: Solomon Behar, MD; Uri Goldbourt, PhD; Henrietta Reicher-Reiss,MD; Lori Mandelzweig, MPH.

1. SPRINT Study Group. Nifedipine in secondaryprevention 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 suddencardiac death. Circulation 1987;75:131-138. 3. Muller JE, Stone PH, Turi ZG, Rutherford JD, Czeisler CA, Parker C, Poole WK. PassamaniE. Roberts R. RobertsonT. Sobel BE. Willerson JT. Braunwald E, and the MILIS’Study Groip. Circadian iariation iA the frequent; of onsetof 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, PasqualettiP. Circadian distribution in fatal pulmonary thromboembolism.Am J Cardial 19X%64:403404. 6. TsementzisSA, Gill JS, Hitchcock ER, Gill SK, BeeversDG. 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 increasein platelet aggregability and the risk of myocardial infarction and suddencardiac death. N Eng/ J Med 1987;316:1514~1518. 8. Millar-Craig MW, Bishop CN, Raftery EB. Circadian variation of bloodpressure.Lmcet1978;1:795-797. 9. Turton MB, DeeganT. Circadian variations of plasmacatecholamine,cortisol

Decrease of Right and Left Atrial Sizes After Direct-Current 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 n chronic atria1 fibrillation (AF), atria1 enlargementis Irhythmia.rm4 consideredboth a causeand a consequenceof the arIt is not well known whether restoration and long-term maintenance of sinus rhythm indeed causesa reversalof the processof atria1enlargement.5In addition, the influence of the type of underlying heart diseaseon this processhas not beenstudied. Therefore, we assessed whether atria1sizesdecreaseafter electrical cardioversion in patients with chronic AF using 2-dimensionalechocardiography. Between January 1988 and January 1989, 120 patients 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,UniversityHospitalGroningen,Oostersingel59, 9713EZ Groningen,The Netherlands.ManuscriptreceivedJuly 10, 1990;revisedmanuscriptreceivedandaccepted August20, 1990.

months. In 49 of these patients, fully evaluable echocardiographic recordings could be obtained. These 49 patients 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 patient’s history, physical examination, 12-lead electrocardiogram, chest x-ray, 2-dimensional echocardiogram, bicycle exercise test and, if available, coronary angiogram. In all patients, hyperthyroidism was excluded using 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), congenital (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 included in the nonmitral heart disease group. Coronary artery disease was present in 1I patients, hypertensive


1, 1991 93

heart disease in 7 patients, aortic valve disease in 4 patients, corrected hyperthyroidism in 1 patient and mitral valve prolapse without mitral regurgitation in 1 patient. One patient had undergone cardiac surgery because of a myxoma. The other 13 patients formed the group with lone AF. After the cardioversion, antiarrhythmic 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. Transthoracic echocardiographic studies were performed 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 transducer. Two-dimensional recordings were made to evaluate overall left atria1 (LA) and right atria1 (RA) size. Recordings were performed with the patient in the left recumbent 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 performed by 2 cardiologists who were unaware of the patient’s participation in the study. LA long-axis diameter

Decrease of right and left atrial sizes after direct-current electrical cardioversion in chronic atrial fibrillation.

also lead to plaque rupture or fissure that forms the substratefor thrombus formation. In addition, the morning increase in plasma catecholamines,by f...
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