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Ann Thorac Surg 1999;68:949-953
© 1999 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Does dilatation of the sinotubular junction cause aortic regurgitation?

Kojiro Furukawa, MDa, Hitoshi Ohteki, MDa, Zhi-Li Cao, MDb, Kazuyoshi Doi, MDb, Yasushi Narita, CEa, Naoki Minato, MDb, Tsuyoshi Itoh, MDb

a Department of Cardiovascular Surgery, Saga Prefectural Hospital, Koseikan, Japan
b Department of Thoracic and Cardiovascular Surgery, Saga Medical School, Saga, Japan

Address reprint requests to Dr Furukawa, Department of Cardiovascular Surgery, Saga Prefectural Hospital, Koseikan, 1-12-9 Mizugae, Saga City 840-8571, Japan
e-mail: ksdpcard{at}bronze.ocn.ne.jp


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. Some patients develop aortic regurgitation (AR) in association with dilatation of the sinotubular junction (STJ), despite having normal aortic valve. However, the relationship between dilatation of the STJ and AR is unclear.

Methods. Canine hearts and aortas were isolated. A suture was placed in each commissure and in the sinus of Valsalva at the STJ. These interrupted sutures were drawn horizontally, and strain on the sutures was varied. The sites of the retracted sutures were changed to various positions, and the opening and closing of the aortic valve was observed endoscopically. A beating heart model was used to observe changes in aortic valve function during mechanical retraction of the commissures or sinuses.

Results. Opening area of the valve increased when strain on all sutures or commissures was increased. When strain was increased on the sinus alone, coaptation of the valve was not affected.

Conclusion. We observed endoscopically that mechanical dilatation of the STJ causes AR. These findings suggest that the principal cause of AR associated with dilatation of the STJ is outward deviation of the commissure.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
The causes of aortic regurgitation (AR) include both abnormalities of the leaflets and the aortic root. This is due to dilatation of the sinotubular junction (STJ), distortion of one or more of the sinuses of Valsalva, annuloaortic ectasia, or a combination of these problems. Some patients have AR with dilatation of the STJ and an anatomically normal aortic valve annulus, leaflet, and sinus of Valsalva. In 1832, Corrigan described this condition [1]. Until now, aortic root replacement with a composite graft has generally been performed for these cases. Recently, some authors have reported remodeling the STJ to correct such AR, which allows preservation of the native valve [2, 3]. However, the relationship between dilatation of the STJ and AR is not proven. Therefore, we created a model of STJ dilatation using canine hearts and evaluated coaptation of the aortic valve at rest and in the beating heart with direct imaging by endoscopy.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
Interrupted horizontal mattress sutures were placed in each commissure and each sinus of Valsalva at the STJ level, and these interrupted sutures were drawn horizontally (Fig 1). This resulted in dilatation of the aorta at the STJ. The table for creating this STJ dilatation model is made of two plastic doughnut-like plates. The upper plate is for drawing sutures horizontally, and the lower plate is for supporting the heart [4].



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  		Fig 1. Experimental model (excerpted from Furukawa et al. [4], with permission).

 
General preparation
All animals were treated in accordance with the Saga Medical School’s guidelines for animal experimentation. Adult mongrel dogs (body weights: 20 to 25 kg) were studied. The dogs were anesthetized with ketamine chloride (10 mg/kg, intramuscular), thiamylal sodium (50 mg, intravenously) and pancuronium bromide (3 mg, intravenously) and the lungs were ventilated through an endotracheal tube with a Harvard type ventilator (Shinano Manufacture, Tokyo, Japan). Subsequently, ketamine chloride (5 to 10 mg/kg ) was added every 20 to 30 minutes. Transverse bilateral thoracotomy entering through the fourth intercostal space was made, and the heart, ascending aorta, aortic arch, descending aorta, and pulmonary veins were exposed. After systemic heparinization (3 mg/kg, intravenously), a cannula for arresting the heart (8 mm inner diameter) was introduced into the innominate artery. After occlusion of the superior vena cava, inferior vena cava, and pulmonary veins, 500 ml of either a high potassium and glucose solution (potassium 20 mEq/L, glucose 50 g/L), for the resting model, or cardioplegic solution (glucose 50 g/L, regular insulin 20 units/L, potassium 20 mEq/L, sodium bicarbonate 2.3 g/L, d-mannitol 4 g/L, and vitriolated magnesium 2 g/L), for the beating heart model, was injected into the coronary arteries through the cannula. Subsequently, the heart and aorta were extracted en bloc. An ice slush was applied for topical cooling in the beating heart model. After aortotomy, an interrupted horizontal mattress suture of 3-0 polyester braided, reinforced with a spaghetti, was placed from inside to outside in an each commissure and each sinus of Valsalva at the STJ level [4]. In addition, a venting tube was placed in left ventricle through the apex to prevent the left ventricle from overdistention during AR, and the excess fluid in the left ventricle was drained by gravity. Next, the heart and thoracic aorta were secured to the table, and the interrupted sutures were drawn horizontally resulting in dilatation of the aorta at the STJ level [4]. The force of the strain on the sutures was adjusted to 20, 25, 50, 70, or 100 points (1 point 3.5 g) by gravity. In addition, three combinations of retracted sutures were tested: all six sutures, the sutures in the three commissures, and three sutures in the sinuses of Valsalva.

Resting model
Five adult mongrel dogs were studied. Normal saline was perfused to the aorta through the brachiocephalic artery at a pressure of 80 cm H2O. A fiberscope of 6 mm in diameter (Olympus BF type 6C 10, Olympus Corp, Tokyo, Japan) was inserted into the aorta through the left subclavian artery, and the aortic valve was observed endoscopically (Fig 2 ) [4]. The observations were recorded using a home video system (VT 1200, Hitachi Co Ltd, Tokyo, Japan). The opening area of the aortic valve was calculated using a special computer system (Cosmozone 1S system, Nikon Corporation, Tokyo, Japan). The relationship between the opening area of the aortic valve and the force of retraction at each site was determined. A felt strip reinforcing each suture was used for calibration of the area.



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  		Fig 2. A drawing of the resting model. (See text for details.)

 
Beating model
Five adult mongrel dogs were studied. Oxygenated and warmed (37°C) modified Tyrode’s solution was infused via the brachiocephalic artery at a pressure of 80 cm H2O and the left atrium at a pressure of 15 to 20 cm H2O (Fig 3). The electrocardiogram and aortic pressure were monitored simultaneously. The behavior of the aortic valve during retraction of the sutures in the commissures and sinuses of Valsalva was investigated. These observations were recorded by a high-speed video system (NAC, model MHS-200, NAC Inc, Tokyo, Japan, 200 frames/sec).



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  		Fig 3. A representation of the beating model. (P = pump; B.O. = bubble oxygenator.) (See text for details.)

 
Modified Tyrode’s solution contents (mg/L): NaCl 6.0, KCl 0.35, MgCl26H2O 0.1, CaCl22H2O 0.3, NaH2PO42H2O 0.05, NaHCO3 3.0, glucose 2.0; electrolytes (mEq/L): Na 140, K 4.7, Cl 115, Ca 4.5, pH 7.6 to 7.8; osmolarity 300 mOsm/L.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
Resting model
Under conditions where no sutures were being retracted, the aortic valve closed completely and no central opening was observed (Fig 4A). When all six sutures ( Fig 4B) and only three commissures were retracted (Fig 4C), the aortic valve did not close completely, and a central opening was observed. However, when only the sutures in the sinuses of Valsalva were retracted, the coaptation of the aortic valve was not disturbed (Fig 4D). Figure 5 shows that increasing the strain on the sutures results in an increase in opening of the aortic valve. When only the three sutures in the sinuses of Valsalva were retracted, the coaptation of the aortic valve was not disturbed (Fig 5).



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  		Fig 4. Direct images made using the resting model (excerpted from Furukawa et al. [4], with permission). (A) No sutures are retracted. (B) All six sutures are retracted. (C) Sutures in the three commissures are retracted. (D) Sutures in the sinuses of Valsalva are retracted.

 


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  		Fig 5. The relationship between the opening area of the aortic valve and the gravitational force applied to the sutures in the resting model.

 
Beating model
In Figure 6 , the upper and lower panels show a cardiac cycle from the opening of the aortic valve to just before its reopen. When only the sutures in the commissures were retracted, the aortic valve did not close completely, and a central opening of the aortic valve was observed during the diastolic phase of the left ventricle. This condition persisted until reopening of the aortic valve (Fig 6, upper panel). By contrast, when only the sutures in the sinuses of Valsalva were retracted, the aortic valve closed completely and the coaptation of the aortic valve was not disturbed during the diastolic phase of the left ventricle (Fig 6, lower panel). In this model, when only the sutures in the commissures were retracted, the opening area in the just prior to reopen of the aortic valve increased when increasing strain was placed on the sutures. When only those sutures in the sinuses of Valsalva were retracted, the aortic valve closed completely during the diastolic phase of the left ventricle despite increasing the strain on the sutures.



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  		Fig 6. Direct images made using the beating heart model. Upper: Sutures in the three commissures are retracted. Lower: Sutures in the sinuses of Valsalva are retracted.

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
The mechanism by which the aortic valve opens and closes involves the whole aortic complex, composed of supporting interleaflet tissues, commissures, annulus, sinuses of Valsalva, and ascending aorta [5]. Therefore, despite normal valve leaflets, AR is present when the rest of the aortic complex is abnormal.

One type of AR associated with normal leaflets is that seen in patients with annuloaortic ectasia secondary to Marfan’s syndrome. This type of AR occurs as result of dilation of the aortic root, including the aortic annulus. Another type of AR in which patients have no structural abnormalities of the aortic valve leaflet, annulus, or sinuses of Valsalva, is that associated with aneurysms of the ascending aorta. This phenomenon was reported by Corrigan in 1832 [1]. He suggested that this type of AR was due to dilation of the STJ, but he did not have any imaging technique to prove his theory.

Bellhouse and associates have reported a model which simulated the aortic root in vitro and used this model to investigate the relationship between AR and dilatation of the aortic root [6]. They examined the effects of changing the shape of the sinuses of Valsalva and dilating them because they presumed that this type of AR was caused by a decrease in the fluid-dynamic pressures from the sinus vortices. However, no AR was observed with any of the changes in the sinuses employed. However, when the aortic root was dilated by increasing pressure, AR developed, and this AR could be eliminated by a single ligature placed around the STJ. They presumed that the AR associated with dilatation of the aortic root is caused by insufficient compensatory valvular elongation in response to dilatation of the aortic root. Barret and associates have reported a patient with Marfan’s syndrome in whom the STJ was plicated and the AR was corrected [7]. Frater and associates presumed that AR associated with ascending aortic aneurysms is caused by dilatation of the STJ and reported 5 patients in whom plication of the STJ resulted in reduced AR [2]. Recently, David and associates reported performing ascending aortic replacement with a prosthetic vascular graft based on the same theory as that proposed by Frater [3]. However, there have been no experimental studies proving isolated dilatation of the STJ causes AR, and surgical interventions have been performed based on a hypothesis. To test this hypothesis, we created a canine model of STJ dilatation and evaluated coaptation of the aortic valve with direct endoscopic imaging.

The resting model used in this study simulates the heart during the diastolic phase, when the aortic valve is closed. Using this model, we confirmed a central opening in the aortic valve with direct imaging under conditions of STJ dilation. This central opening recapitulates previous intraoperative endoscopic observations [8, 9]. We believe that the central opening that was observed in this study causes AR. We confirmed these results using the beating heart model. These findings suggest that the principal cause of AR associated with dilatation of the STJ, is outward deviation of the commissures. The normal diameter of the STJ is 15% to 20% smaller than that of the aortic annulus [10, 11]. Whether AR occurs in the setting of dilatation of the STJ is dependent on the length of the aortic valve free margin and the diameter of STJ.

Although STJ dilatation model used in this study allows for the possibility of dilatation of the surgical annulus [5], no such dilatation was observed macroscopically, and its contribution to AR in this model is not likely to be significant. The relationship between changes in the aortic root and coaptation of the aortic valve was not investigated mathematically in this study.

In clinical situations, dilatation of the aortic root may also cause compensatory elongation and thickening of the free margin of the aortic valve [12, 13]. Plication of the STJ alone may not fully correct such cases of AR. In these cases, an additional plasty of the free margin is necessary [14, 15]. However, plication of the STJ alone reduces the AR associated with dilatation of the STJ, and this procedure is indicated in patients without significant elongation of the free margin (for example, cases in which the STJ has dilated rapidly). Currently, replacement of the aortic root, with a composite graft or aortic valve, and the ascending aorta, with prosthetic materials, is performed in patients whose AR is associated with dilatation of the STJ. If surgeons recognize the mechanism of the AR, which can be corrected with plication of the STJ, less complicated invasive surgical treatment will become more standard.

Currently, to realize potential advantages over conventional stented bioprostheses, there has been increasing clinical use of the stentless porcine valve [16, 17]. One of the most important points in avoiding postoperative regurgitation is to assess the diameter of the ascending aorta at the level of the STJ for correct matching of the prosthesis [18, 19]. There is a possibility of postoperative aortic regurgitation after aortic valve replacement with stentless aortic valve, possibly caused by dilatation of the STJ. If the diameter of the ascending aorta at level of the STJ can be larger than the diameter of the stentless valve, central aortic regurgitation may occur postoperatively because of central malcoaptation. Our study validates this phenomenon with direct imaging. When there is the mismatch of these diameters, some techniques which plicate the diameter of the STJ should be needed [18, 19].

In conclusion, we have used aortic endoscopy to validate the hypothesis that dilatation of the STJ causes AR. These findings suggest that the principal cause of AR associated with dilatation of the STJ is outward deviation of the commissure and that dilatation of the sinuses of Valsalva has less influence on AR.


   Acknowledgments
 
We are grateful to Mr Shinichi Yasutake for his technical assistance.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

  1. Corrigan D.J. Permanent patency of the mouth of the aorta. Edinburgh Med Surg 1832;37:111.
  2. Frater R.W. Aortic valve insufficiency due to aortic dilatation. Circulation 1986;74(suppl 1):136-142.
  3. David T.E., Feindel C.M., Bos J. Repair of the aortic valve in patients with aortic insufficiency and aortic root aneurysm. J Thorac Cardiovasc Surg 1995;109:345-352.[Abstract/Free Full Text]
  4. Furukawa K., Ohteki H., Doi K., et al. Does dilatation of sinotubular junction cause aortic regurgitation? The use of the experimental model and preliminary result. J Cardiol 1998;31(Suppl 1):67-71.
  5. Sutton J.P., Ho S.Y., Anderson R.H. The forgotten interleaflet triangles. Ann Thorac Surg 1995;59:419-427.[Abstract/Free Full Text]
  6. Bellhouse B.J., Bellhouse F., Abbot J.A., Talbot L. Mechanism of valvular incompetence in aortic sinus dilatation. Cardiovasc Res 1973;7:490-494.[Medline]
  7. Barrett J.S., Helwig J., Kay C.F., Johnson J. Cine-aortographic evaluation of aortic insufficiency. Unsuspected idiopathic aneurysmal dilatation of the aortic root as a possible indication of the Marfan syndrome. Ann Intern Med 1964;61:1071-1083.[Medline]
  8. Itoh T., Ohtsubo S., Furukawa K., Norita H. Aortic root endoscopy in valve sparing operations. J Thorac Cardiovasc Surg 1997;114:141-142.[Free Full Text]
  9. Furukawa K., Higuchi S., Ueno T., Suda H., Natsuaki M., Itoh T. An aortic valve-sparing operation (David’s operation) for a patient with annulo-aortic ectasia (AAE) and aortic regurgitation (AR) —evaluation by intraoperative endoscopy. J Jpn Assn Thorac Surg 1996;44:826-829.
  10. Reid K. The anatomy of the sinus of Valsalva. Thorax 1970;25:79-85.[Abstract/Free Full Text]
  11. Kunzelman K.S., Grande K.J., David T.E., Cochran R.P., Verrier E.D. Aortic root and valve relationships. J Thorac Cardiovasc Surg 1994;107:162-170.[Abstract/Free Full Text]
  12. Silver M.A., Roberts W.C. Detailed anatomy of the normally functioning aortic valve in hearts of normal and increased weight. Am J Cardiol 1985;55:454-461.[Medline]
  13. David T.E. Aortic root aneurysms. Ann Thorac Surg 1997;64:1564-1568.[Abstract/Free Full Text]
  14. Carpentier A. Cardiac valve surgery—the "French correction". J Thorac Cardiovasc Surg 1983;86:323-337.[Medline]
  15. Noji S., Kitamura N., Yamaguchi A., et al. Intermediate to late results of aortic or mitral valvuloplasty by rasping procedure. J Jpn Assn Thorac Surg 1995;43:797-803.
  16. Sintek C.F., Fletcher A.D., Khonsari S. Stentless porcine aortic root. J Thorac Cardiovasc Surg 1995;109:871-876.[Abstract]
  17. Mohr F.W., Walther T., Baryalei M., et al. The Toronto SPV bioprosthesis. Ann Thorac Surg 1995;60:171-175.[Abstract/Free Full Text]
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  19. Siebenmann R.P. Implantation of the Toronto SPV stentless porcine bioprosthesis in dilated ascending aorta. Ann Thorac Surg 1997;64:1197-1200.[Abstract/Free Full Text]
Accepted for publication March 25, 1999.


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T. E. David, S. Armstrong, J. Ivanov, C. M. Feindel, A. Omran, and G. Webb
Results of aortic valve-sparing operations
J. Thorac. Cardiovasc. Surg., July 1, 2001; 122(1): 39 - 46.
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 Journal of Diagnostic Medical SonographyHome page
S. M. Bierig and A. D. Waggoner
Aortic Insufficiency: Etiology, Pathophysiology, Natural History, and the Role of Echocardiography
Journal of Diagnostic Medical Sonography, March 1, 2001; 17(2): 59 - 71.
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 J. Thorac. Cardiovasc. Surg.Home page
T. E. David, A. Omran, J. Ivanov, S. Armstrong, M. P.L. de Sa, B. Sonnenberg, and G. Webb
DILATION OF THE PULMONARY AUTOGRAFT AFTER THE ROSS PROCEDURE
J. Thorac. Cardiovasc. Surg., February 1, 2000; 119(2): 210 - 220.
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