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Atrial septal aneurysm
International Journal of Cardiology 69 (1999) 101–103
Atrial septal aneurysm Is it a benign finding? ´ ´ L.F. Valenzuela*, R. Vazquez, M.J. Rodriguez–Hernandez Cardiology Department, Valme University Hospital, Sevilla, Spain Received 4 November 1998; received in revised form 5 January 1999; accepted 5 January 1999
Abstract We report our clinical experience in a single centre with 7 cases of atrial septal aneurysm (ASA) diagnosed by transthoracic echocardiography (TTE) between 1989–1996. They did not present any clinical event compatible with cardiogenic embolism after a five years mean follow-up period. ASA is recognized as a potential source of cardiogenic embolism [2] based on some retrospective and selection biased studies. 1999 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Aneurysm; Echocardiography; Embolism; Stroke
1. Case reports We report our clinical experience in a single centre with 7 cases of atrial septal aneurysm (ASA) diagnosed by transthoracic echocardiography (TTE) between 1989–1996. During this period 18 417 TTE studies were performed in our centre. According to previously reported criteria [1], ASA was defined as a protrusion of the aneurysm of .10 mm beyond the plane of the atrial septum. The prevalence of ASA in our area would be 0.04%, less than previously reported (from 0.1% to 0.5% with TTE) [2,3] . This fact can be explained in part by the more specific criteria used in our centre [2] (Fig. 1). The characteristics of the series are shown in Table 1. No one presented a history of systemic embolism after a five years mean follow-up period. The incidence of supraventricular arrythmia (symp-
*Corresponding author. Tel.: 195-4156476. E-mail address: [email protected] (L.F. Valenzuela)
tomatic or asymptomatic) was 5 / 7571%, higher than the 25–52% reported [1]. We found a rate of cardiac abnormalities commonly associated with ASA very similar to previous reports. Three of our patients (3 / 7543%) had an apparent on colour flow intracardiac left-to-right shunt, two cases of patent foramen ovale and one case of ostium secundum atrial septal defect. By transesophageal echocardiography and using colour doppler or saline contrast the reported incidence of shunt is higher (77–85%) [4]. We also found an association with mitral and tricuspid valve prolapse in 2 / 7528% and 1 / 7514% respectively rather than 20% and 7% reported [1]. The most interesting problem of this anomaly is to define its clinical relevance as a source of embolism and its optimal therapeutic management. Several reports suggest a link between ASA and cardiogenic embolism in patients with otherwise unexplained ischemic stroke [3–5]. According to these series, 20% to 52% of patients with ASA present a history of embolism. A suggested mechanism for embolization might be primary thrombus formation within the
0167-5273 / 99 / $ – see front matter 1999 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 99 )00016-9
L.F. Valenzuela et al. / International Journal of Cardiology 69 (1999) 101 – 103
102
before establishing a causal relation between ASA and embolic episodes. First, a selection bias is present since most patients diagnosed are referred for echocardiography evaluation because of a suspected embolic stroke. Second, there is risk of confusion since several other cardiac abnormalities associated with ASA (Table 1) have at least an undefined potential for embolization. Finally, these studies are retrospective case reports or small series with the exception of a multicenter study which included 195 patients [1]. In summary, up to date the potential for embolization of ASA, although deserving consideration, remains undefined with the published reports [1]. Consequently the best therapeutic approach is uncertain. Randomized control trials are needed to define the risk of systemic emboli as well as the benefits of a specific treatment. The series reported (Table 1) with a follow-up period of almost 5 years (range 2 to 8 years) may contribute in a proper methaanalysis to lessen the alarm respect to the clinical relevance of this entity. It would show a benign abnormality of favourable outcome without specific treatment. Fig. 1. ASA. Various measurements to confirm the diagnosis are shown (small arrows). Major and minor axis (.1.5 cm and .1 cm) respectively. MVP is shown (arrow). LV: left ventricle; LA: left atrium.
aneurysm and paradoxical embolization through an interatrial communication [1,4]. All of these studies have three common limitations that suggest caution
References [1] Mugge A, Daniel W, Angermann C, Spes C, Khandheria B, Kronzon I, et al. Atrial septal aneurysm in adult patients. A multicenter study using transthoracic and transesophageal echocardiography. Circulation 1995;91:2785–92.
Table 1 Atrial septal aneurysm: Summary of findings and follow-up Case no.
Age and sex
RF*
Symptom Examination
Ph.
Radiograph
ECG
Holter
TTE*
Shunt
Follow-up (years)*
Treatment
1 2 3 4
42 36 18 64
HBP* No No HBP
Normal Normal Normal BCRDHH1HSA
SA* SA SA SA
MVP/MVT* No No No
No No L-R(PFO)* L-R(ASD)
8 7 5 5
B-blocker B-blocker No Diuretics
65 woman
Normal
ST-T changes
No
No
No
5
CABG*
6
14 man
HBP, DM*, CAD* No
Normal Normal Normal Systolic murmur Normal
Normal Normal Normal Pletora
5
Palpitations Palpitations Palpitations Exertional dypsnea Angor pectoris No
Normal
Normal
No
No
No
2
No
7
51 woman
HBP
Systolic murmur No
Normal
Normal
SA*
MVP/MR*
L-R (PFO)
2
No
man woman man woman
No
RF: Cardiovascular risk factors; HBP: High blood pressure; DM: Diabetes mellitus; CAD: Coronary artery disease; TTE: Associated abnormalities in transthoracic echocardiography; PFO: Patent foramen ovale; L-R: Left-to-right shunt; ASD: Ostium secundum atrial septal defect; SA: Supraventricular arrythmia; MVP: Mitral valve prolapse; TVP: Tricuspid valve prolapse; MR: Mitral regurgitation; Follow-up: Follow-up without embolic episodes; CABG: Coronary bypass surgery.
L.F. Valenzuela et al. / International Journal of Cardiology 69 (1999) 101 – 103 [2] Redberg RF. Echocardiographic evaluation of the patient with a systemic embolic event. In: Otto Catherin M, editor. The practice of clinical echocardiography. Philadelphia W.B. Saunders Company 1997, 629–648. [3] Hanley PC, Tajik AJ, Hynes JK, Edwards WD, Reeder GS, Hagler DJ, Seward JB. Diagnosis and classification of atrial septal aneurysm by two dimensional echocardiography: report of 80 consecutive cases. J Am Coll Cardiol 1985;6:1370–82.
103
[4] Schneider B, Hanrath P, Vogel P, Meinertz T. Improved morphologic characterization of atrial septal aneurysm by transesophageal echocardiography: relation to cerebrovascular events. J Am Coll Cardiol 1990;16:1000–9. [5] Manning WJ. Role of transesophageal echocardiography in the management of thromboembolic stroke. Am J Cardiol 1997;80(4c):19D–28D.
Atrial septal aneurysm Is it a benign finding? ´ ´ L.F. Valenzuela*, R. Vazquez, M.J. Rodriguez–Hernandez Cardiology Department, Valme University Hospital, Sevilla, Spain Received 4 November 1998; received in revised form 5 January 1999; accepted 5 January 1999
Abstract We report our clinical experience in a single centre with 7 cases of atrial septal aneurysm (ASA) diagnosed by transthoracic echocardiography (TTE) between 1989–1996. They did not present any clinical event compatible with cardiogenic embolism after a five years mean follow-up period. ASA is recognized as a potential source of cardiogenic embolism [2] based on some retrospective and selection biased studies. 1999 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Aneurysm; Echocardiography; Embolism; Stroke
1. Case reports We report our clinical experience in a single centre with 7 cases of atrial septal aneurysm (ASA) diagnosed by transthoracic echocardiography (TTE) between 1989–1996. During this period 18 417 TTE studies were performed in our centre. According to previously reported criteria [1], ASA was defined as a protrusion of the aneurysm of .10 mm beyond the plane of the atrial septum. The prevalence of ASA in our area would be 0.04%, less than previously reported (from 0.1% to 0.5% with TTE) [2,3] . This fact can be explained in part by the more specific criteria used in our centre [2] (Fig. 1). The characteristics of the series are shown in Table 1. No one presented a history of systemic embolism after a five years mean follow-up period. The incidence of supraventricular arrythmia (symp-
*Corresponding author. Tel.: 195-4156476. E-mail address: [email protected] (L.F. Valenzuela)
tomatic or asymptomatic) was 5 / 7571%, higher than the 25–52% reported [1]. We found a rate of cardiac abnormalities commonly associated with ASA very similar to previous reports. Three of our patients (3 / 7543%) had an apparent on colour flow intracardiac left-to-right shunt, two cases of patent foramen ovale and one case of ostium secundum atrial septal defect. By transesophageal echocardiography and using colour doppler or saline contrast the reported incidence of shunt is higher (77–85%) [4]. We also found an association with mitral and tricuspid valve prolapse in 2 / 7528% and 1 / 7514% respectively rather than 20% and 7% reported [1]. The most interesting problem of this anomaly is to define its clinical relevance as a source of embolism and its optimal therapeutic management. Several reports suggest a link between ASA and cardiogenic embolism in patients with otherwise unexplained ischemic stroke [3–5]. According to these series, 20% to 52% of patients with ASA present a history of embolism. A suggested mechanism for embolization might be primary thrombus formation within the
0167-5273 / 99 / $ – see front matter 1999 Elsevier Science Ireland Ltd. All rights reserved. PII: S0167-5273( 99 )00016-9
L.F. Valenzuela et al. / International Journal of Cardiology 69 (1999) 101 – 103
102
before establishing a causal relation between ASA and embolic episodes. First, a selection bias is present since most patients diagnosed are referred for echocardiography evaluation because of a suspected embolic stroke. Second, there is risk of confusion since several other cardiac abnormalities associated with ASA (Table 1) have at least an undefined potential for embolization. Finally, these studies are retrospective case reports or small series with the exception of a multicenter study which included 195 patients [1]. In summary, up to date the potential for embolization of ASA, although deserving consideration, remains undefined with the published reports [1]. Consequently the best therapeutic approach is uncertain. Randomized control trials are needed to define the risk of systemic emboli as well as the benefits of a specific treatment. The series reported (Table 1) with a follow-up period of almost 5 years (range 2 to 8 years) may contribute in a proper methaanalysis to lessen the alarm respect to the clinical relevance of this entity. It would show a benign abnormality of favourable outcome without specific treatment. Fig. 1. ASA. Various measurements to confirm the diagnosis are shown (small arrows). Major and minor axis (.1.5 cm and .1 cm) respectively. MVP is shown (arrow). LV: left ventricle; LA: left atrium.
aneurysm and paradoxical embolization through an interatrial communication [1,4]. All of these studies have three common limitations that suggest caution
References [1] Mugge A, Daniel W, Angermann C, Spes C, Khandheria B, Kronzon I, et al. Atrial septal aneurysm in adult patients. A multicenter study using transthoracic and transesophageal echocardiography. Circulation 1995;91:2785–92.
Table 1 Atrial septal aneurysm: Summary of findings and follow-up Case no.
Age and sex
RF*
Symptom Examination
Ph.
Radiograph
ECG
Holter
TTE*
Shunt
Follow-up (years)*
Treatment
1 2 3 4
42 36 18 64
HBP* No No HBP
Normal Normal Normal BCRDHH1HSA
SA* SA SA SA
MVP/MVT* No No No
No No L-R(PFO)* L-R(ASD)
8 7 5 5
B-blocker B-blocker No Diuretics
65 woman
Normal
ST-T changes
No
No
No
5
CABG*
6
14 man
HBP, DM*, CAD* No
Normal Normal Normal Systolic murmur Normal
Normal Normal Normal Pletora
5
Palpitations Palpitations Palpitations Exertional dypsnea Angor pectoris No
Normal
Normal
No
No
No
2
No
7
51 woman
HBP
Systolic murmur No
Normal
Normal
SA*
MVP/MR*
L-R (PFO)
2
No
man woman man woman
No
RF: Cardiovascular risk factors; HBP: High blood pressure; DM: Diabetes mellitus; CAD: Coronary artery disease; TTE: Associated abnormalities in transthoracic echocardiography; PFO: Patent foramen ovale; L-R: Left-to-right shunt; ASD: Ostium secundum atrial septal defect; SA: Supraventricular arrythmia; MVP: Mitral valve prolapse; TVP: Tricuspid valve prolapse; MR: Mitral regurgitation; Follow-up: Follow-up without embolic episodes; CABG: Coronary bypass surgery.
L.F. Valenzuela et al. / International Journal of Cardiology 69 (1999) 101 – 103 [2] Redberg RF. Echocardiographic evaluation of the patient with a systemic embolic event. In: Otto Catherin M, editor. The practice of clinical echocardiography. Philadelphia W.B. Saunders Company 1997, 629–648. [3] Hanley PC, Tajik AJ, Hynes JK, Edwards WD, Reeder GS, Hagler DJ, Seward JB. Diagnosis and classification of atrial septal aneurysm by two dimensional echocardiography: report of 80 consecutive cases. J Am Coll Cardiol 1985;6:1370–82.
103
[4] Schneider B, Hanrath P, Vogel P, Meinertz T. Improved morphologic characterization of atrial septal aneurysm by transesophageal echocardiography: relation to cerebrovascular events. J Am Coll Cardiol 1990;16:1000–9. [5] Manning WJ. Role of transesophageal echocardiography in the management of thromboembolic stroke. Am J Cardiol 1997;80(4c):19D–28D.