reactive intimal proliferation associatedwith the aggre- on to develop such complications in the future. Thus, gation and organization of blood clots occurs within the long-term follow-up, including regular exercisetestsand aneurysm. Specific hemodynamic vessel wall-shearing coronary arteriography, is consideredimportant. stressis present at the inlet and outlet parts of the aneurysm, and this is said to damage endothelial cells and promote stenosis.l 3~14 However, the mechanismby which this stenosisprogressesover a long period of time is still 1. Kawasaki T, Kosaki F, Okawa S, ShigematsuI, Yanagawa H. A new infantile mucocutaneouslympho nodesyndrome(MLNS) prevailing in Japan.Pednxtrics not well understood and requires further study. 1914;54:21 l-216. We have no data concerning the long-term prognosis 2. Kato H, IchinoseE, Yoshioka F, Takeshi T, Matunaga S, Suzuki K, Rikitake Fate of coronary aneurysmsin Kawasaki disease.Serial coronary angiography for children with Kawasaki diseasewho do not haveaneu- N. and long-term follow up study. Am J Cardiol 1982;49:1758-1766. rysms or whose aneurysms have regressed.A normal 3. Kamiya T, Suzuki J. Cardiovascular angiographic findings in Kawasaki disangiogram doesnot necessarilymean complete recovery ease. Jpn J Pediatric Med 1985;17:765-770. Nakano H, Ueda K, Saito A, Nojima K. Repeatedangiogramsin coronary by coronary arteries. Arterial damage may persist and 4. arterial aneurysmsin Kawasaki disease.Am J Cardiol 1985;56:846-851. there is a possibility of the risk of early arteriosclerosisas 5. FlugelmanYM, Hashin Y, BassanMM, Lear R, Gotman SM. Acute myocara sequelaof vasculitis becauseof the characteristic fea- dial infarction 14yearsafter an acute episodeof Kawasaki disease.Am J Cardiol 1983;52:427-428. tures of panarteritis observedin this disease.15 6. Ohyagi Y, Hirose K, Tsujimoto S, Doyama K, WatanabeY, Nakai T. KawasaCoronary artery bypassgraft surgery was performed ki diseasecomplicated by acute myocardial infarction 9 years after onset. Am J 1985;110:670-672. in all patients, and the l- to 4-year postoperativecourses Heart 7. Ishiwata S, Nishiyama S, Nakanishi S, Seki A, WatanabeY, Konishi T, Fuse have been favorable. Arterial grafts, such as from the K. Coronary artery diseaseand internal mammary artery aneurysmsin a young internal thoracic artery or gastroepiploic artery, which woman: possiblesequelaeof Kawasaki disease.Am Hear? J 1990;120:213-217, Fujiwara H, Hamashima Y. Pathology of the heart in Kawasaki disease. can be expectedto retain good patency for a long period 8. Pediatrics 1978;61:1Of-107. of time are currently recommended.However, in casesin 9. Wong CK, Cheng CH, Lau CP, Leung WH. Asymptomatic congenitalcorewhich aneurysms are present throughout the entire nary artery aneurysm in adulthood. Ear Heart J 1989;10:947-949. 10. Landing BM, Larson E. Are infantile periarteritis nodosa with coronary length of the trunk of the coronary arteries, such as in artery involvement and fatal mucocutaneouslymph node syndromethe same? patients 4 and 5, aneurysmsmay also be present in the Comparisonof 20 patientsfrom Hawaii and Japan.Pediatrics 1977;59:651-662, 11. Tanaka N, SekimotoK, Naoe S. Kawasaki disease.Relationshipwith infaninternal thoracic artery, and when this vesselis planed to tile periarteritis nodosa.Arch Pathol Lab Med 1976;100:81-86. be used for grafting, it must be thoroughly evaluated to 12. Fujiwara H, Fujiwara T, Kao TC, Ohshio G, HamashimaY. Pathology of Kawasaki diseasein the healedstage.Relationship betweentypical and atypical exclude presenceof aneurysmspreoperatively. of Kawasaki disease.Acta Pathol Jpn 1986;36:857-867. We believe that Kawasaki diseasegives rise to long- cases 13. Young DF, Tsai FY. Flow characteristicsin modelsof arterial stenoses-steady term complications, such as aneurysmsthat progressto flow. J Biomechnnics 1973;6:395-410. causeangina pectoris or myocardial infarction. A num- 14. Kim BM, Corcoran WH. Experimental measurementsof turbulencespectra to stenosis.J Biomechanics 1974;7:335-342. ber of the infants with Kawasaki diseasecurrently being distal 15. Kato H, Inoue 0, Akagi T. Kawasaki disease,cardiac problem and manageexamined in the department of internal medicine may go ment. Pediatr Rev 1988;9:209-217.
Left Ventricular Function and After Cardioversion
in Patients with Atrial
Fibrillation
Before
Mahbubul Alam, MD, PhD, and Curt Thorstrand, MD, PhD trial fibrillation (AF) is a clinically important arA rhythmia with important therapeutic and prognostic implications. The disorganizedelectrical and mechanical activity causesloss of active atria1 contraction. This in turn results in insufficient atria1 emptying and impaired ventricular filling. l AF may be convertedto sinusrhythm by meansof direct-current countershock.Hemodynamic studies before and after cardioversion of AF to normal sinus rhythm report conflicting results regarding improvement in hemodynamic function.2-4 Some studies suggestedthat normal atria1 contraction may not occur immediately after successfulcardioversionof AF to sinus rhythm.lT3 The purpose of this study was to evaluate, using echocardiographyand Doppler, the mechanicalactivity of the left atrium and its effect on left ventricular (LV) function after electrocardioversionof AF to sinus rhythm. From the Department of Medicine I, Cardiology Section, Karolinska Institute at South Hospital (SMersjukhuset), 11883 Stockholm, Sweden. Manuscript received July 16, 1991; revised manuscript received and accepted November 4,199l.
694
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 69
The study was begun with 19 patients with electrocardiographic evidence of AF and without history of coronary artery disease or cardiomyopathy. The study was designedfor 1-month follow-up. Seven patients were excluded: 5 owing to reversion to AF before the final echocardiographic examination, and 2 owing to unsuccessful cardioversion. Leftatria1 dimension was not used as an exclusionary criterion. Thus, 12 patients (aged 57 f 9 years) were converted to normal sinus rhythm by means of direct-current cardioversion. Demographic data on the patients are listed in Table I. Digoxin was withdrawn 2 days before cardioversion. Patients were receiving anticoagulation therapy (warfarin sodium) for 12 weeks, with prothrombin time being within the therapeutic range. Inpatients receivingsotalol medication, the drug was continued at the time of cardioversion. Patients were examined before, and 4 hours, 2 weeks and 1 month after cardioversion. All patients underwent complete M-mode and 2-dimensional echocardiography, including pulsed-wave Doppler. An Aloka SSD870 echocardiographic machine with a 2.5 MHz trans-
MARCH 1, 1992
TABLE I Individual Data of Patients with Atrial Fibrillation
No.
Age (yr) & Sex
Duration of AF
Previous AF
1 2
43M 47F
3 mos. 2 weeks
1 1
3 4 5 6 7 8 9
48M 54M 54M 56F 57M 60F 60M
3 mos. 6 mos. 2 mos. lOweeks 8 weeks 6 weeks 10 mos.
1
10 11 12
60M 72M 73M
8 weeks 3 mos. 4 mos.
AF
1 3 1 -
= atrial fibrillation; LAD = Matrial
Cause/ Associated Disease Hypertension Mitral valve prosthesis Unknown Unknown Unknown Unknown Unknown Unknown Mild aortic stenosis Unknown Unknown Diabetes Hypertension
TABLE II Echo-Doppler Parameters and Heart Rate (n = 12)
LAD (mm)
A Wave After 4 Hours
60 58
+ 0
51 43 42 40 44 53 40
0 + + + + 0 +
53 48 53
0 t 0
dimension.
ducer was used. In the presence of AF, the mean of 10 consecutive cardiac cycles was usedfor calculations, and 5 cyclks were used when the patients were in sinus rhythm. The amplitude of the systolic displacement of the atrioventricular valve plane toward the apt& was used as a measure of global LVfunction. This was recorded (Figure I) from the apical 4- and 2-chamber vie& corresponding to the septal, lateral, anterior and posterior walls of the left ventricle, as described elsewhere.5 The mean value of the atrioventricuiar plane displacement from the aforementioned 4 sites was used to assess the global function of the left ventricle. Doppler sample volume size was 3 to $ mm. Wall filters were set at 200 to 600 Hz, and the gain was adjqted to obtain the best spectral recording. The apical I&amber view was used. The sample volume was placed in the left ventricle above the mitral valve, and the b&t recording of the transmitral flow was cartifully searched. Peak velocities of the early (E) and atria1 (A) $lling waves were determined. In the baseline study, the position of the transducer was carefully marked with
I
II
HR (beats/min) Mean + SD Median Range
81 f 14 78 55-105
65 +- 5** 65 55-73
58 k 5** 60 47-61
57 * 7** 59 40-63
LA (mm) Mean f SD Median Range
49 + 7 49.5 40-60
49 2 7 49 40-60
47 2 7 48 37-59
45 2 7* 46 36-58
FS (%) Mean f SD Median Range
28 2 7 31 15-35
35 + 8* 38 1942
39 k 7** 41 28-46
41 t 5** 42 33-47
AV mean (mm) Mean 2 SD Median Range
9.5 k 1.8 10 7-11.5
11.5 -t 1.8” 12 8-13
%A/E Mean + SD Median Range
38 * 6 (n = 7) 38 33-75
Ill
13 2 1.6** 14 9-16 59 + 21 56 35-75
IV
-
14.5? 2** 14.5 lo-18 74 f 18t 73 38-l 12
*p ~0.05, and **p ~0.01 compared with I; tp
Left Ventricular Function and After Cardioversion
in Patients with Atrial
Fibrillation
Before
Mahbubul Alam, MD, PhD, and Curt Thorstrand, MD, PhD trial fibrillation (AF) is a clinically important arA rhythmia with important therapeutic and prognostic implications. The disorganizedelectrical and mechanical activity causesloss of active atria1 contraction. This in turn results in insufficient atria1 emptying and impaired ventricular filling. l AF may be convertedto sinusrhythm by meansof direct-current countershock.Hemodynamic studies before and after cardioversion of AF to normal sinus rhythm report conflicting results regarding improvement in hemodynamic function.2-4 Some studies suggestedthat normal atria1 contraction may not occur immediately after successfulcardioversionof AF to sinus rhythm.lT3 The purpose of this study was to evaluate, using echocardiographyand Doppler, the mechanicalactivity of the left atrium and its effect on left ventricular (LV) function after electrocardioversionof AF to sinus rhythm. From the Department of Medicine I, Cardiology Section, Karolinska Institute at South Hospital (SMersjukhuset), 11883 Stockholm, Sweden. Manuscript received July 16, 1991; revised manuscript received and accepted November 4,199l.
694
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 69
The study was begun with 19 patients with electrocardiographic evidence of AF and without history of coronary artery disease or cardiomyopathy. The study was designedfor 1-month follow-up. Seven patients were excluded: 5 owing to reversion to AF before the final echocardiographic examination, and 2 owing to unsuccessful cardioversion. Leftatria1 dimension was not used as an exclusionary criterion. Thus, 12 patients (aged 57 f 9 years) were converted to normal sinus rhythm by means of direct-current cardioversion. Demographic data on the patients are listed in Table I. Digoxin was withdrawn 2 days before cardioversion. Patients were receiving anticoagulation therapy (warfarin sodium) for 12 weeks, with prothrombin time being within the therapeutic range. Inpatients receivingsotalol medication, the drug was continued at the time of cardioversion. Patients were examined before, and 4 hours, 2 weeks and 1 month after cardioversion. All patients underwent complete M-mode and 2-dimensional echocardiography, including pulsed-wave Doppler. An Aloka SSD870 echocardiographic machine with a 2.5 MHz trans-
MARCH 1, 1992
TABLE I Individual Data of Patients with Atrial Fibrillation
No.
Age (yr) & Sex
Duration of AF
Previous AF
1 2
43M 47F
3 mos. 2 weeks
1 1
3 4 5 6 7 8 9
48M 54M 54M 56F 57M 60F 60M
3 mos. 6 mos. 2 mos. lOweeks 8 weeks 6 weeks 10 mos.
1
10 11 12
60M 72M 73M
8 weeks 3 mos. 4 mos.
AF
1 3 1 -
= atrial fibrillation; LAD = Matrial
Cause/ Associated Disease Hypertension Mitral valve prosthesis Unknown Unknown Unknown Unknown Unknown Unknown Mild aortic stenosis Unknown Unknown Diabetes Hypertension
TABLE II Echo-Doppler Parameters and Heart Rate (n = 12)
LAD (mm)
A Wave After 4 Hours
60 58
+ 0
51 43 42 40 44 53 40
0 + + + + 0 +
53 48 53
0 t 0
dimension.
ducer was used. In the presence of AF, the mean of 10 consecutive cardiac cycles was usedfor calculations, and 5 cyclks were used when the patients were in sinus rhythm. The amplitude of the systolic displacement of the atrioventricular valve plane toward the apt& was used as a measure of global LVfunction. This was recorded (Figure I) from the apical 4- and 2-chamber vie& corresponding to the septal, lateral, anterior and posterior walls of the left ventricle, as described elsewhere.5 The mean value of the atrioventricuiar plane displacement from the aforementioned 4 sites was used to assess the global function of the left ventricle. Doppler sample volume size was 3 to $ mm. Wall filters were set at 200 to 600 Hz, and the gain was adjqted to obtain the best spectral recording. The apical I&amber view was used. The sample volume was placed in the left ventricle above the mitral valve, and the b&t recording of the transmitral flow was cartifully searched. Peak velocities of the early (E) and atria1 (A) $lling waves were determined. In the baseline study, the position of the transducer was carefully marked with
I
II
HR (beats/min) Mean + SD Median Range
81 f 14 78 55-105
65 +- 5** 65 55-73
58 k 5** 60 47-61
57 * 7** 59 40-63
LA (mm) Mean f SD Median Range
49 + 7 49.5 40-60
49 2 7 49 40-60
47 2 7 48 37-59
45 2 7* 46 36-58
FS (%) Mean f SD Median Range
28 2 7 31 15-35
35 + 8* 38 1942
39 k 7** 41 28-46
41 t 5** 42 33-47
AV mean (mm) Mean 2 SD Median Range
9.5 k 1.8 10 7-11.5
11.5 -t 1.8” 12 8-13
%A/E Mean + SD Median Range
38 * 6 (n = 7) 38 33-75
Ill
13 2 1.6** 14 9-16 59 + 21 56 35-75
IV
-
14.5? 2** 14.5 lo-18 74 f 18t 73 38-l 12
*p ~0.05, and **p ~0.01 compared with I; tp
