- Email: [email protected]
Significance of atrial fibrillation as a precursor of embolism
elevation (Table II). Similarly, two-thirds of patients at all levels of ST elevation had inducible ventricular tachycardia. This retrospective analysis of patients who had had an anterior wall acute myocardial infarction failed to demonstrate by clinical electrophysiologic testing any distinguishing characteristics of patients with persistence of ST elevation for at least 2 weeks. Patients were equally vulnerable to programmed stimulation irrespective of the presence or magnitude of this finding. The patients studied were highly selected. In 27 of the 36, sudden death or sustained ventricular tachycardia led to the study. Thus, individuals with anterior wall infarction without such rhythm disturbances are underrepresented. Nevertheless, it is unlikely that absence of ST elevation identifies a group with reduced vulnerability to the initiation of ventricular tachycardia during programmed stimulation because in 8 of 13 such individuals that arrhythmia was induced by means of the protocol used. Had all patients undergone testing free of antiarrhythmic drug treatment, some of the 8 who were not inducible while receiving drugs would have been vulnerable to programmed stimulation. Because such patients
Significance
of Atrial
Fibrillation
were equally represented at all levels of ST elevation, it is unlikely that the conclusions of this study would have been altered. Of 6 patients with right bundle branch block, only 1 had ST elevation >l mm. Repolarization abnormalities secondary to the bundle branch block offset what might have been persistent ST elevation. Exclusion of these patients does not, however, unmask a difference. Ventricular tachycardia was induced in 4 of the 6. Thus, clinical electrophysiologic testing does not identify a basis for persistence of ST elevation after healing of a myocardial infarction. Additional hypotheses must be proposed and tested. 1. Mills RM, Young E, Gorlin R, Lesch M. Natural history of ST segment elevation after acute myocardial infarction. Am J Cardiol 1975;35:6lW614. 2. Lindsay J Jr, Dewey RC, Talesnick BS, Nolan NG. Relation of ST-segment elevation after healing of acute myocardial infarction to the presence of left ventricular aneurysm. Am J Cardiol 1984;54:84-86. 3. Arvan S, Varat M. Persistent ST-segment elevation and left ventricular wall abnormalities: a 2-dimensional echocardiographic study. Am J Cardiol 1984;53; 1542-1546. 4. Platia EV, Reid PR. A comparison of programmed electrical stimulation and ambulatory electrocardiographic monitoring in the management of ventricular tachycardia and ventricular fibrillation. JACC 1984;4;493m500.
as a Precursor
of Embolism
Katsuro Shimomura, MD, Tohru Ohe, MD, Satoshi Uehara, MD, Mokuo Matsuhisa, MD, Shiro Kamakura, MD, and lwao Sato, MD his study evaluates to what extent atria1 fibrillaT tion (AF) is associated with embolic events in a variety of conditions. Of 25,202 consecutive patients over 15 years of age referred to the National Cardiovascular Center since August 1, 1977, I ,I 77 (5%, 696 male and 481 female) were found to have AF or atrialjlutter, eitherparoxysma1 or persistent. The following were exclusionary criteria: (I) cardiac operation or implantation of an artificial pacemaker before the first visit to the hospital; (2) a history of embolism in any organ; (3) embolism on current hospital admission; (4) bradycardia-tachycardia syndrome complicated by organic heart disease; (5) coronary artery disease, restrictive or hypertrophic cardiomyopathy, constrictive pericarditis, pulmonary thromboembolism, lung disease, obliterating arteriosclerosis, aortitis, dissecting aneurysm of the aorta and aneurysm of the thoracic or abdominal aorta; and (6) <2 months of follow-up. Of the patients hospitalized for stroke on the initial consultation, 9 had valvular heart disease and 21 had AF occurring alone. Eight of the 9 patients with valvular heart disease (1 with paroxysmal type) and 14 of the 21 with lone AF (4 with paroxysmal type) were diagnosed as having cerebral embolism. For the diagnoFrom the Division of Cardiology, National Cardiovascular 5-7-1, Fujishirodai, Suita-shi, Osaka, Japan 565. Manuscript October 26, 1988; revised manuscript received and accepted 1989.
Center, received March 9,
sis of underlying heart diseases, phonocardiogram, Mmode, 2-dimensional and Doppler echocardiography were used. Valvular disease refers to all cases of valvular lesion, whether mitral, aortic, combined, rheumatic or nonrheumatic. We point out that in 98% of cases the mitral valve is compromised. The diagnosis of paroxysmal AF and bradycardia-tachycardia syndrome was made when it was evident from a pertinent letter or electrocardiogram from the referring physician, or when diagnostic electrocardiograms associated with symptoms were obtained within 2 months of initial consultation. AF occurring alone referred to patients with AF or flutter but without evidence of organic heart disease. Therefore, patients with hypertension or hypertensive heart disease (57) or with a history of thyroid disease (15) were included in this category. Bradycardia-tachycardia syndrome as defined here was always idiopathic, characterized by a combination of paroxysmal AF and marked sinus bradycardia, sinoatrial block, intermittent or permanent sinus arrest. Because most of the patients with significant symptoms underwent implantation of an artificial pacemaker soon after initial consultation, cases included here involved either minor symptoms or refusal or reluctance to have an arttjicial pacemaker implanted. Cerebral embolism was diagnosed on the basis of the followingl: (I) sudden onset of clinical symptoms and presence of maximal focal neurologic deficit at time of
THE AMERICAN
JOURNAL
OF CARDIOLOGY
JUNE
1, 1989
1405
BRIEF
REPORTS
TABLE
I
Follow-Up
According
No. of Pts
VHD Persistent
Total
M:F
246
loo:146
Paroxysmal AF Persistent Paroxysmal
8
2:6
151
103:48
97
73~24
WPW + AF
11*
9:2”
Brady-tachy
18
10:8
CHD Persistent
16
7:9
9
7~2
Paroxysmal IDC Persistent
14
Paroxysmal Total
3 572
13:l 3:o
to Underlying
Diseases
Mean Age at Entry fSD (Range)
Mean Follow-Up &SD
Months
(Range)
Patient-Years
No. of Cases with Initial Events
Crude Incidence Rate/ 1,000 Person-Years
53 f 11 (25-78) 48fll (37-68) 63zkll (25-90) 58flO (30-75) 47f 15 (21-70) 57 i 14 (20-78) 56f 11 (36-73) 39f14 (19-58) 52f12 (23-69) 52f4 (48-57)
24f 19 (1-71) 20f17 (3-45) 33f 19 (l-70) 31 f 19 (l-65) 37f 15 (3-58) 36+19 (3-58) 20f18 (3-53) 21 i 16 (3-45) 38i18 (3-68) 433t6 (38-51)
483
21
44
14
0
0
411
4
10
246
5
20
37
0
0
51
2
39
20
0
0
21
0
0
44
2
46
43
0
0
327~245
* Indicates case overlaps with valvular heart disease. AF = atrial fibrillation or flutter (occurring alone); brady-tachy = bradycardia-tachycardia syndrome; CHD = congenital heart disease; IDC = idiopathic dilated cardiomyopathy; = standard deviation; VHD = valvular heart disease; WPW = Wolff-Parkinson-White syndrome.
onset; (2) presence of an embolus or reopening of the previously occluded vessel confirmed by cerebral angiography; and (3) presence of hemorrhagic infarct shown by computed tomography. Cerebral infarction was diagnosed when cases were undefinable for cerebral embolism. Transient ischemic attacks were not included. Cerebral angiography was performed at the earliest possible time in 17 of 33 patients admitted after cerebrovascular accident. The diagnosis of embolization involving arteries to other precious organs was based on clinical manifestations. The number ofpatients, age at entry andfollow-up period according to individual underlying conditions are listed in Table I. The age of the 572patients rangedfrom 20 to 90 years (mean 56) and the follow-up period was 1 to 72 months (mean 28). Atria1 flutter was detected singly or in combination with AF in 12 cases (3 with persistent type and 9 with paroxysmal type). Of these 12 patients, 3 had bradycardia-tachycardia syndrome, 1 had congenital heart disease, 1 Wolff-Parkinson-White syndrome and 7 had no organic heart disease. Of 22 patients given anticoagulant drugs, 18 had valvular heart disease. Twenty-four patients with valvular heart disease and 31 with lone AF were given antiplatelet theram. The total number ofpatients with an initial embolism during the follow-up period was 34 (18 male and 16 female); 9% (21 of 246) occurred in patients with valvular heart disease and persistent AF, 3% (4 of 152) in patients with persistent lone AF, 5% (5 of 97) in patients with paroxysmal lone AF, 11% (2 of 18) inpatients with bradycardia- tachycardia syndrome and 14% (2 of 14) in patients with idiopathic dilated cardiomyopathy (Table I). The brain was involved in 79% (27 patients). An ischemic cerebrovascular accident occurred in 33 cases,6 1406
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
63
SD
of which were not diagnostic of cerebral embolism. Embolizations to other organs were observed in 7 patients with valvular heart disease and none in other groups. Single organs involved were left femoral artery in 1, right femoral artery in 1, right brachial artery in 1 and multiple embolic events in 4 patients. Of 35 patients who died during follow-up, 6 died from embolism; 4 (1 with persistent lone AF, 1 with idiopathic dilated cardiomyopathy and 2 with valvular heart disease) from cerebral embolism and 2 (with valvular heart disease) from multiple emboli. Another patient with cardiomyopathy died from cerebral infarction. From the follow-up years of patients, the incidence rate of embolism/l ,000 patient-years was calculated (Table I). The rate was 44 among patients with valvular heart diseases. The rate was 10 among patients with persistent lone AF, which was almost half as frequent compared with paroxysmal AF. The rate was also high in patients with bradycardia-tachycardia syndrome and idiopathic dilated cardiomyopathy: 39 and 46, respectively. Because this study lacks a reference population, the age- and sex-adjusted expected number of embolism was calculated only for cerebral embolism using the incidence of cerebral infarction in Japan2 and the rate of cerebral embolism among cases of cerebral infarction in this institution. The ratios of the observed number to the expected number were 61 (95% confidence interval: 3397), 12 (3-26) and 29 (9-61) for valvular heart disease, persistent and paroxysmal AF occurring alone, respectively. The ratios for bradycardia-tachycardia syndrome and idiopathic cardiomyopathy were 80 (8-229) and 74 (7-212), respectively. We have shown that patients with valvular heart disease who developed embolism all had persistent AF. We
are aware that only a small number of patients with paroxysmal AF were followed, due to the probable short period of the paroxysmal phase. However, patients with lone AF of the paroxysmal type were more prone to embolization than patients with persistent AF. This suggests that in valvular heart disease, embolization may occur differently than it does in lone AF1 The risk of embolism in valvular heart disease is further increased by the enlarged dimension of the left atrium, low cardiac output, turbulent flow or stasis upstream of the diseased or malfunctioning valve. Information on the carotid artery was limited in our study. Cerebral angiography performed on patients with embolism disclosed mild irregularities at carotid bifurcation in 3 of 6 patients with lone AF and arteriosclerotic plaque in the common carotid artery in 1 of 6 with valvular heart disease. Some consider paroxysmal AF to be important for embolization to occur in patients with lone AF.3,4 Although the time relation between paroxysms of the rhythm disorder and embolization is far from clarified in individual patients, 4 of 14 patients who had lone AF when hospitalized for stroke had paroxysmal AF compared to 1 of 8 patients with valvular heart disease. Other supportive evidence is that the incidence of embolization is high in patients with bradycardia-tachycardia syndrome.5-7 Embolization could be explained by presumable thrombus formation promoted by stasis in the atria associated with paroxysms of the arrhythmia. According to Fuster et a1,8who studied natural history of idiopathic dilated cardiomyopathy, systemic emboli developed in 33% of patients with AF but in only 14% of patients without it (difference not significant). In this study 2 cases had idiopathic dilated cardiomyopathy complicated by cerebral embolism, and the rate of patient-years was almost as frequent as for bradycardiatachycardia syndrome. Ventricular mural thrombi are frequently present in patients with dilated and hypokinet-
ic left ventricle,9 and systemic embolization is one of the major complications of idiopathic dilated cardiomyopathy. Several retrospective studies reported the beneficial effects of anticoagulant therapy in reducing the risk of thromboembolic events in cases with valvular heart disease associated with AF. Anticipating the same prophylactic effect for embolic events, anticoagulant therapy has been recommended for sick sinus syndrome or idiopathic dilated cardiomyopathy* complicated by AF, although no controlled studies have been performed. As shown herein, the high incidence of embolism associated with lone AF poses a clinically important problem from a therapeutic and prognostic standpoint. However, opinions conflictlOJ1 regarding the necessity of long-term anticoagulant therapy for lone AF, and its indications are determined empirically on an individual basis. Prospective controlled studies are needed. 1. Yamaguchi T, Minematsu K, Choki J, Ikeda M. Clinical and neuroradiological analysis of thrombotic and embolic cerebral infarction. Jpn Circ J 1984;48:50-58. 2. Komachi Y, Tanaka H, Shimamoto T, Handa K, Isomura K, Kojima S, Matsuzaki T, Ozawa H, Takahashi H, Tsunetoshi Y. A collaborative study of stroke incidence in Japan. Stroke 1984;15:28-36. 3. Weintraub G, Sprecage G. Paroxysmal atria1 fibrillation and cerebral embolism with apparently normal heart. N Engl J Med 19S8;259:875-876. 4. Seizer A. Atria1 fibrillation revisited. N Engl J Med 1982;306:1044-1045. 5. Rubenstein JJ, Schulman CL, Yurchak PM, DeSanctis RW. Clinical spectrum of the sick sinus syndrome. Circulation 1972;46513. 6. Fairfax AJ, Lambert CD, Leatham A. Systemic embolism in chronic sinoatrial disorder. N Engl J Med 1976;29S:190m1 92. 7. Bathen J, Span S, Rokseth R. Embolism in sinoatrial disease. Acta Med Stand 1978:203:7-l I 8. Fuster V, Gash BJ, Giulani ER, Tajik AJ, Brandenburg RO, Frye RL. The natural history of idiopathic dilated cardiomyopathy. Am Heart J 2981;47:525531. 9. Gottdiener JS, Gay JA, VanVoahees L, DiBianco R, Fletcher RD. Frequency and embolic potential of left ventricular thrombus in dilated cardiomyopathy: assessment by 2-dimensional echocardiography. Am J Cardiol 1983;52:12811285. 10. Brand FN, Abbott RD, Kennel WB, Wolf PA. Characteristics and prognosis of lone atria1 fibrillation. JAMA 1982;254:3449-3453. 11. Kopecky SL, Gush BJ, Phil CBD, McGoa MD, Whisnant JP, Holmes DR, Ilstrup DM, Frye RL. The natural history of lone atria1 fibrillation: a populationbased study over three decades. N Engl J Med 1987;317:669-674.
THE AMERICAN
JOURNAL
OF CARDIOLOGY
JUNE
1, 1989
1407
Significance
of Atrial
Fibrillation
were equally represented at all levels of ST elevation, it is unlikely that the conclusions of this study would have been altered. Of 6 patients with right bundle branch block, only 1 had ST elevation >l mm. Repolarization abnormalities secondary to the bundle branch block offset what might have been persistent ST elevation. Exclusion of these patients does not, however, unmask a difference. Ventricular tachycardia was induced in 4 of the 6. Thus, clinical electrophysiologic testing does not identify a basis for persistence of ST elevation after healing of a myocardial infarction. Additional hypotheses must be proposed and tested. 1. Mills RM, Young E, Gorlin R, Lesch M. Natural history of ST segment elevation after acute myocardial infarction. Am J Cardiol 1975;35:6lW614. 2. Lindsay J Jr, Dewey RC, Talesnick BS, Nolan NG. Relation of ST-segment elevation after healing of acute myocardial infarction to the presence of left ventricular aneurysm. Am J Cardiol 1984;54:84-86. 3. Arvan S, Varat M. Persistent ST-segment elevation and left ventricular wall abnormalities: a 2-dimensional echocardiographic study. Am J Cardiol 1984;53; 1542-1546. 4. Platia EV, Reid PR. A comparison of programmed electrical stimulation and ambulatory electrocardiographic monitoring in the management of ventricular tachycardia and ventricular fibrillation. JACC 1984;4;493m500.
as a Precursor
of Embolism
Katsuro Shimomura, MD, Tohru Ohe, MD, Satoshi Uehara, MD, Mokuo Matsuhisa, MD, Shiro Kamakura, MD, and lwao Sato, MD his study evaluates to what extent atria1 fibrillaT tion (AF) is associated with embolic events in a variety of conditions. Of 25,202 consecutive patients over 15 years of age referred to the National Cardiovascular Center since August 1, 1977, I ,I 77 (5%, 696 male and 481 female) were found to have AF or atrialjlutter, eitherparoxysma1 or persistent. The following were exclusionary criteria: (I) cardiac operation or implantation of an artificial pacemaker before the first visit to the hospital; (2) a history of embolism in any organ; (3) embolism on current hospital admission; (4) bradycardia-tachycardia syndrome complicated by organic heart disease; (5) coronary artery disease, restrictive or hypertrophic cardiomyopathy, constrictive pericarditis, pulmonary thromboembolism, lung disease, obliterating arteriosclerosis, aortitis, dissecting aneurysm of the aorta and aneurysm of the thoracic or abdominal aorta; and (6) <2 months of follow-up. Of the patients hospitalized for stroke on the initial consultation, 9 had valvular heart disease and 21 had AF occurring alone. Eight of the 9 patients with valvular heart disease (1 with paroxysmal type) and 14 of the 21 with lone AF (4 with paroxysmal type) were diagnosed as having cerebral embolism. For the diagnoFrom the Division of Cardiology, National Cardiovascular 5-7-1, Fujishirodai, Suita-shi, Osaka, Japan 565. Manuscript October 26, 1988; revised manuscript received and accepted 1989.
Center, received March 9,
sis of underlying heart diseases, phonocardiogram, Mmode, 2-dimensional and Doppler echocardiography were used. Valvular disease refers to all cases of valvular lesion, whether mitral, aortic, combined, rheumatic or nonrheumatic. We point out that in 98% of cases the mitral valve is compromised. The diagnosis of paroxysmal AF and bradycardia-tachycardia syndrome was made when it was evident from a pertinent letter or electrocardiogram from the referring physician, or when diagnostic electrocardiograms associated with symptoms were obtained within 2 months of initial consultation. AF occurring alone referred to patients with AF or flutter but without evidence of organic heart disease. Therefore, patients with hypertension or hypertensive heart disease (57) or with a history of thyroid disease (15) were included in this category. Bradycardia-tachycardia syndrome as defined here was always idiopathic, characterized by a combination of paroxysmal AF and marked sinus bradycardia, sinoatrial block, intermittent or permanent sinus arrest. Because most of the patients with significant symptoms underwent implantation of an artificial pacemaker soon after initial consultation, cases included here involved either minor symptoms or refusal or reluctance to have an arttjicial pacemaker implanted. Cerebral embolism was diagnosed on the basis of the followingl: (I) sudden onset of clinical symptoms and presence of maximal focal neurologic deficit at time of
THE AMERICAN
JOURNAL
OF CARDIOLOGY
JUNE
1, 1989
1405
BRIEF
REPORTS
TABLE
I
Follow-Up
According
No. of Pts
VHD Persistent
Total
M:F
246
loo:146
Paroxysmal AF Persistent Paroxysmal
8
2:6
151
103:48
97
73~24
WPW + AF
11*
9:2”
Brady-tachy
18
10:8
CHD Persistent
16
7:9
9
7~2
Paroxysmal IDC Persistent
14
Paroxysmal Total
3 572
13:l 3:o
to Underlying
Diseases
Mean Age at Entry fSD (Range)
Mean Follow-Up &SD
Months
(Range)
Patient-Years
No. of Cases with Initial Events
Crude Incidence Rate/ 1,000 Person-Years
53 f 11 (25-78) 48fll (37-68) 63zkll (25-90) 58flO (30-75) 47f 15 (21-70) 57 i 14 (20-78) 56f 11 (36-73) 39f14 (19-58) 52f12 (23-69) 52f4 (48-57)
24f 19 (1-71) 20f17 (3-45) 33f 19 (l-70) 31 f 19 (l-65) 37f 15 (3-58) 36+19 (3-58) 20f18 (3-53) 21 i 16 (3-45) 38i18 (3-68) 433t6 (38-51)
483
21
44
14
0
0
411
4
10
246
5
20
37
0
0
51
2
39
20
0
0
21
0
0
44
2
46
43
0
0
327~245
* Indicates case overlaps with valvular heart disease. AF = atrial fibrillation or flutter (occurring alone); brady-tachy = bradycardia-tachycardia syndrome; CHD = congenital heart disease; IDC = idiopathic dilated cardiomyopathy; = standard deviation; VHD = valvular heart disease; WPW = Wolff-Parkinson-White syndrome.
onset; (2) presence of an embolus or reopening of the previously occluded vessel confirmed by cerebral angiography; and (3) presence of hemorrhagic infarct shown by computed tomography. Cerebral infarction was diagnosed when cases were undefinable for cerebral embolism. Transient ischemic attacks were not included. Cerebral angiography was performed at the earliest possible time in 17 of 33 patients admitted after cerebrovascular accident. The diagnosis of embolization involving arteries to other precious organs was based on clinical manifestations. The number ofpatients, age at entry andfollow-up period according to individual underlying conditions are listed in Table I. The age of the 572patients rangedfrom 20 to 90 years (mean 56) and the follow-up period was 1 to 72 months (mean 28). Atria1 flutter was detected singly or in combination with AF in 12 cases (3 with persistent type and 9 with paroxysmal type). Of these 12 patients, 3 had bradycardia-tachycardia syndrome, 1 had congenital heart disease, 1 Wolff-Parkinson-White syndrome and 7 had no organic heart disease. Of 22 patients given anticoagulant drugs, 18 had valvular heart disease. Twenty-four patients with valvular heart disease and 31 with lone AF were given antiplatelet theram. The total number ofpatients with an initial embolism during the follow-up period was 34 (18 male and 16 female); 9% (21 of 246) occurred in patients with valvular heart disease and persistent AF, 3% (4 of 152) in patients with persistent lone AF, 5% (5 of 97) in patients with paroxysmal lone AF, 11% (2 of 18) inpatients with bradycardia- tachycardia syndrome and 14% (2 of 14) in patients with idiopathic dilated cardiomyopathy (Table I). The brain was involved in 79% (27 patients). An ischemic cerebrovascular accident occurred in 33 cases,6 1406
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
63
SD
of which were not diagnostic of cerebral embolism. Embolizations to other organs were observed in 7 patients with valvular heart disease and none in other groups. Single organs involved were left femoral artery in 1, right femoral artery in 1, right brachial artery in 1 and multiple embolic events in 4 patients. Of 35 patients who died during follow-up, 6 died from embolism; 4 (1 with persistent lone AF, 1 with idiopathic dilated cardiomyopathy and 2 with valvular heart disease) from cerebral embolism and 2 (with valvular heart disease) from multiple emboli. Another patient with cardiomyopathy died from cerebral infarction. From the follow-up years of patients, the incidence rate of embolism/l ,000 patient-years was calculated (Table I). The rate was 44 among patients with valvular heart diseases. The rate was 10 among patients with persistent lone AF, which was almost half as frequent compared with paroxysmal AF. The rate was also high in patients with bradycardia-tachycardia syndrome and idiopathic dilated cardiomyopathy: 39 and 46, respectively. Because this study lacks a reference population, the age- and sex-adjusted expected number of embolism was calculated only for cerebral embolism using the incidence of cerebral infarction in Japan2 and the rate of cerebral embolism among cases of cerebral infarction in this institution. The ratios of the observed number to the expected number were 61 (95% confidence interval: 3397), 12 (3-26) and 29 (9-61) for valvular heart disease, persistent and paroxysmal AF occurring alone, respectively. The ratios for bradycardia-tachycardia syndrome and idiopathic cardiomyopathy were 80 (8-229) and 74 (7-212), respectively. We have shown that patients with valvular heart disease who developed embolism all had persistent AF. We
are aware that only a small number of patients with paroxysmal AF were followed, due to the probable short period of the paroxysmal phase. However, patients with lone AF of the paroxysmal type were more prone to embolization than patients with persistent AF. This suggests that in valvular heart disease, embolization may occur differently than it does in lone AF1 The risk of embolism in valvular heart disease is further increased by the enlarged dimension of the left atrium, low cardiac output, turbulent flow or stasis upstream of the diseased or malfunctioning valve. Information on the carotid artery was limited in our study. Cerebral angiography performed on patients with embolism disclosed mild irregularities at carotid bifurcation in 3 of 6 patients with lone AF and arteriosclerotic plaque in the common carotid artery in 1 of 6 with valvular heart disease. Some consider paroxysmal AF to be important for embolization to occur in patients with lone AF.3,4 Although the time relation between paroxysms of the rhythm disorder and embolization is far from clarified in individual patients, 4 of 14 patients who had lone AF when hospitalized for stroke had paroxysmal AF compared to 1 of 8 patients with valvular heart disease. Other supportive evidence is that the incidence of embolization is high in patients with bradycardia-tachycardia syndrome.5-7 Embolization could be explained by presumable thrombus formation promoted by stasis in the atria associated with paroxysms of the arrhythmia. According to Fuster et a1,8who studied natural history of idiopathic dilated cardiomyopathy, systemic emboli developed in 33% of patients with AF but in only 14% of patients without it (difference not significant). In this study 2 cases had idiopathic dilated cardiomyopathy complicated by cerebral embolism, and the rate of patient-years was almost as frequent as for bradycardiatachycardia syndrome. Ventricular mural thrombi are frequently present in patients with dilated and hypokinet-
ic left ventricle,9 and systemic embolization is one of the major complications of idiopathic dilated cardiomyopathy. Several retrospective studies reported the beneficial effects of anticoagulant therapy in reducing the risk of thromboembolic events in cases with valvular heart disease associated with AF. Anticipating the same prophylactic effect for embolic events, anticoagulant therapy has been recommended for sick sinus syndrome or idiopathic dilated cardiomyopathy* complicated by AF, although no controlled studies have been performed. As shown herein, the high incidence of embolism associated with lone AF poses a clinically important problem from a therapeutic and prognostic standpoint. However, opinions conflictlOJ1 regarding the necessity of long-term anticoagulant therapy for lone AF, and its indications are determined empirically on an individual basis. Prospective controlled studies are needed. 1. Yamaguchi T, Minematsu K, Choki J, Ikeda M. Clinical and neuroradiological analysis of thrombotic and embolic cerebral infarction. Jpn Circ J 1984;48:50-58. 2. Komachi Y, Tanaka H, Shimamoto T, Handa K, Isomura K, Kojima S, Matsuzaki T, Ozawa H, Takahashi H, Tsunetoshi Y. A collaborative study of stroke incidence in Japan. Stroke 1984;15:28-36. 3. Weintraub G, Sprecage G. Paroxysmal atria1 fibrillation and cerebral embolism with apparently normal heart. N Engl J Med 19S8;259:875-876. 4. Seizer A. Atria1 fibrillation revisited. N Engl J Med 1982;306:1044-1045. 5. Rubenstein JJ, Schulman CL, Yurchak PM, DeSanctis RW. Clinical spectrum of the sick sinus syndrome. Circulation 1972;46513. 6. Fairfax AJ, Lambert CD, Leatham A. Systemic embolism in chronic sinoatrial disorder. N Engl J Med 1976;29S:190m1 92. 7. Bathen J, Span S, Rokseth R. Embolism in sinoatrial disease. Acta Med Stand 1978:203:7-l I 8. Fuster V, Gash BJ, Giulani ER, Tajik AJ, Brandenburg RO, Frye RL. The natural history of idiopathic dilated cardiomyopathy. Am Heart J 2981;47:525531. 9. Gottdiener JS, Gay JA, VanVoahees L, DiBianco R, Fletcher RD. Frequency and embolic potential of left ventricular thrombus in dilated cardiomyopathy: assessment by 2-dimensional echocardiography. Am J Cardiol 1983;52:12811285. 10. Brand FN, Abbott RD, Kennel WB, Wolf PA. Characteristics and prognosis of lone atria1 fibrillation. JAMA 1982;254:3449-3453. 11. Kopecky SL, Gush BJ, Phil CBD, McGoa MD, Whisnant JP, Holmes DR, Ilstrup DM, Frye RL. The natural history of lone atria1 fibrillation: a populationbased study over three decades. N Engl J Med 1987;317:669-674.
THE AMERICAN
JOURNAL
OF CARDIOLOGY
JUNE
1, 1989
1407