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  • The Internet Journal of Thoracic and Cardiovascular Surgery
  • Volume 13
  • Number 2

Original Article

A muscular limbic band localized at middle of a large atrial septal defect

U Yetkin, T Güne?, K Ergüne?, B Güven, V Tavl?, A Gürbüz

Keywords

atrial septal defect, large defect, limbic band, muscular band

Citation

U Yetkin, T Güne?, K Ergüne?, B Güven, V Tavl?, A Gürbüz. A muscular limbic band localized at middle of a large atrial septal defect. The Internet Journal of Thoracic and Cardiovascular Surgery. 2008 Volume 13 Number 2.

Abstract

Atrial septal defect is a common congenital heart defect.In this study we describe a case of a muscular limbic band localized at middle of a large atrial septal defect.

 

Introduction

Secundum atrial septal defect (ASD) is a common congenital heart disease and accounts for approximately 6% to 10% of all congenital cardiac defects[1]. The most frequent ASD was the OO type (FS) with 64.78%, followed by common atrium, true FS, FP, superior and inferior sinus venosus, types each one with 2.81% and one coronary sinus venosus type (1.40%)[3]. Understanding the cardiac anatomy in the malformation of atrioventricular septal defect is an absolute prerequisite for successful surgery, and should be facilitated by recognizing the fundamental nature of the morphology[4]. Abnormal apoptosis and retarded developmental growth are proposed as pathogenic mechanisms[3].

Case Presentation

Our case was a 8-years-old woman. She was admitted to our Pediatric Cardiology Outpatient Clinic with complaints of exertional dyspnea and increasing fatigue. The transthoracic echocardiography (TTE) which was performed in admittance, showed a dropout image in interatrial septum compatible with large ASD and dilatation of right-sided structures of the heart (diameter of right ventricle: 31.6 millimeters). Cardiac catheterization showed atrial septal defect. Cardiac catheterization pointed out no additional pathology. Qp/Qs was calculated 1.57. Pulmonary/systemic vascular resistance was 0.4 (Figure 1).

Figure 1
Figure 1

She was operated under endotracheal general anesthesia and in supine position.Following a median sternotomy,pericardium was opened longitudinally. After heparinization, extra-corporeal circulation is established between the venae cavae and the ascending aorta. A cross clamp was placed on aorta and by antegrade intermittant isothermic blood cardioplegia from aortic root,cardiac arrest was established.Hypothermia was moderate (32ºc).A vent was placed via the right superior pulmonary vein. Standart right atriotomy was made. ASD was evaluated regarding its localization, size, other related cardiac structures and possible associated abnormalities.We explorated a muscular limbic band localized at middle of this large atrial septal defect (Figures 2&3).

Figure 2
Figure 2

Figure 3
Figure 3

We resected this band primarily. After this step ASD was made an uniform defect with exicision of this band. We performed an e-PTFE patch closure of atrial septal defect. Right atriotomy was closed in a standard fashion. Postoperative rhythm was sinusal. She didn’t required inotropic support during weaning from cardiopulmonary bypass and early postoperative period. The post-operative course was uneventful with successful anatomical correction.Postoperatively an echocardiographic investigation was revealed no residual shunt for the repaired ASD. She was followed at our outpatient clinic without additional problem.

Discussion

Heart morphogenesis comprises 2 major consecutive steps, chamber formation followed by septation. Septation is the remodeling of the heart from a single-channel peristaltic pump to a dual-channel, synchronously contracting device with 1-way valves. In the human heart, septation occurs between 4 and 7 weeks of development. Cardiac looping and chamber formation bring the contributing structures into position to engage in septation[5].

The recent identification of a second mesodermal region as a source of cardiomyocytes has challenged the views on the formation of the heart[6]. This second source of cardiomyocytes is localized centrally on the embryonic disc relative to the remainder of the classic cardiac crescent, a region also called the pharyngeal mesoderm. During evolution, the heart developed initially only with the components required for a systemic circulation, namely a sinus venosus, a common atrium, a 'left' ventricle and an arterial cone, the latter being the myocardial outflow tract as seen in the heart of primitive fishes. These components developed in their entirety from the classic cardiac crescent[6].

In the study of Wessels et al., the development of the atrial chambers in the human heart was investigated immunohistochemically using a set of previously described antibodies. This study demonstrates a poorly appreciated role of the dorsal mesocardium in cardiac development. From the earliest stage investigated onward, the mesenchyme of the dorsal mesocardium protrudes into the dorsal wall of the primary atrial segment. This dorsal mesenchymal protrusion is continuous with a mesenchymal cap on the leading edge of the primary atrial septum. Closure of the primary atrial foramen by the primary atrial septum occurs as a consequence of the fusion of these mesenchymal structures[7].

The morphologically and topographically knowledge of atrial septal defect is useful to interpret the imaging studies of this cardiopathy and is basic for the surgeon and the interventionist cardiologist[3]. Echocardiography was the most frequently used investigative modality in all defect sizes and types[8]. The transthoracic approach was successful in capturing sufficient data to create 3-D images, which can provide an accurate assessment of secundum ASD[9].Before repair,we suggest that use cardiac catheterization to fully evaluate a secundum ASD if it is large.

The timing of repair was mainly dependent on patient age and symptomatology in different defects, with the presence of associated anomalies contributing to that in primum and sinus venosus ASD[8]. Atrial septal defects may close spontaneously during the first few years of life[210]. Most centers advocate elective closure of moderate-to-large ASDs between 4 and 6 years of age[211]. Surgical closure of ASD has a low perioperative mortality and morbidity[2].

References

1. Dickinson DF,Arnold R,Wilkinson JL. Congenital heart disease among 160,480 live-born children in Liverpool 1960 to 1969 Implications for surgical treatment, Br Heart J 1981;46 :55-62.
2. Diab KA, Cao QL, Bacha EA, Hijazi ZM. Device closure of atrial septal defects with the Amplatzer septal occluder: safety and outcome in infants. J Thorac Cardiovasc Surg. 2007;134(4):960-6.
3. Castellanos LM, Nivon MK, Zavaleta NE, Sánchez HC. Atrial septal defect. A morphopathological and embryological study. Arch Cardiol Mex 2006 ;76(4):355-65.
4. Adachi I, Uemura H, McCarthy KP, Ho SY. Surgical anatomy of atrioventricular septal defect.Asian Cardiovasc Thorac Ann 2008 ;16(6):497-502.
5. Lamers WH, Moorman AF. Cardiac septation: a late contribution of the embryonic primary myocardium to heart morphogenesis. Circ Res 2002 26;91(2):93-103.
6. Moorman AF, Christoffels VM, Anderson RH, van den Hoff MJ. The heart-forming fields: one or multiple? Philos Trans R Soc Lond B Biol Sci 2007 29;362(1484):1257-65.
7. Wessels A, Anderson RH, Markwald RR, Webb S, Brown NA, Viragh S, Moorman AF, Lamers WH. Atrial development in the human heart: an immunohistochemical study with emphasis on the role of mesenchymal tissues. Anat Rec 2000 ;259(3):288-300.
8. Kharouf R, Luxenberg DM, Khalid O, Abdulla R. Atrial septal defect: spectrum of care. Pediatr Cardiol 2008 ;29(2):271-80. Epub 2007 Oct 23.
9. Lu JH, Hsu TL, Hwang B, Weng ZC. Visualization of Secundum Atrial Septal Defect Using Transthoracic Three-Dimensional Echocardiography in Children: Implications for Transcatheter Closure. Echocardiography 1998;15(7):651-660.
10. Helgason H, Jonsdottir G. Spontaneous closure of atrial septal defects. Pediatr Cardiol 1999;20: 195-9.
11. Black MD, Freedom RM. Minimally invasive repair of atrial septal defects. Ann Thorac Surg 1998;65: 765-7.

Author Information

Ufuk Yetkin
Clinic Deputy Chief in Cardiovascular Surgery, Department of Cardiovascular Surgery, İzmir Atatürk Training and Research Hospital

Tevfik Güne?
Resident in Cardiovascular Surgery, Department of Cardiovascular Surgery, İzmir Atatürk Training and Research Hospital

Kaz?m Ergüne?
Specialist in Cardiovascular Surgery, Department of Cardiovascular Surgery, İzmir Atatürk Training and Research Hospital

Bar?? Güven
Fellow Resident, Pediatric Cardiology Department, Dr.Behçet Uz Children’s Hospital

Vedide Tavl?
Clinic Chief, Pediatric Cardiology Department, Dr.Behçet Uz Children’s Hospital

Ali Gürbüz
Clinic Chief in Cardiovascular Surgery, Department of Cardiovascular Surgery, İzmir Atatürk Training and Research Hospital

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