HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Cyrus J. Parsa Carmelo A. Milano G. Chad Hughes Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Parsa, C. J. Articles by Hughes, G. C. Search for Related Content PubMed PubMed Citation Articles by Parsa, C. J. Articles by Hughes, G. C. Related Collections Cardiac - other Valve disease

---

Case Reports

A Previously Unreported Complication of Apicoaortic Conduit for Severe Aortic Stenosis

^a Department of Surgery, Division of Thoracic and Cardiovascular Surgery, Duke University Medical Center, Durham, North Carolina
^b Department of Pathology, Duke University Medical Center, Durham, North Carolina
^c Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina

Accepted for publication July 21, 2008.

^_* Address correspondence to Dr Hughes, Thoracic Aortic Surgery Program, Division of Thoracic and Cardiovascular Surgery, Department of Surgery, Box #3051, Duke University Medical Center, Durham, NC 27710 (Email: gchad.hughes{at}duke.edu).

	Abstract

Top Abstract Introduction Comment References

 
Given the aging population, use of an apicoaortic conduit serves as an alternative method to treat severe aortic stenosis, especially in patients with a heavily calcified ascending aorta or prior cardiac surgery. Although an apicoaortic conduit fractionates systemic blood flow, it does so without significant deleterious effects. However, we report a novel complication with thrombosis of the aortic root and subsequent coronary insufficiency that likely resulted from a preponderance of cardiac output though the apicoaortic conduit with stagnation of native antegrade blood flow. Given increasing use of the apicoaortic conduit procedure, surgeons considering this approach should be familiar with this potential complication.

	Introduction

Top Abstract Introduction Comment References

 
As the age and cardiac surgical history of patients increase, alternative therapies must be available to address complicated cardiac anatomy. Originally described in 1910, then clinically implemented by Sarnoff and colleagues [1] in 1955, the application and approach of an apicoaortic (AAC) has varied during the subsequent decades [2]. Currently, an AAC is used to treat aortic stenosis in patients deemed high-risk for conventional sternotomy [3], given heavily calcified "porcelain" ascending aorta or prior cardiac surgery, or both, with patent bypass grafts.

Our patient, an 82-year-old man, has a history of coronary artery bypass grafting and subsequent redo coronary artery bypass grafting and bioprosthetic aortic valve replacement, as well as a history of automatic implantable cardioverter defibrillator placement for ischemic cardiomyopathy. He reported functional status deterioration with progression to New York Heart Association class IV heart failure with associated decrease in ejection fraction from 30% to 15% during a 6-month period. Catheterization confirmed four patent bypass grafts and an aortic valve area of 0.37 cm². A computed tomographic scan showed evidence of circumferential calcification of the ascending aorta and aortic arch with less extensive involvement of the descending aorta.

Given symptomatic, severe bioprosthetic aortic valve stenosis in the setting of a third time redo-sternotomy, patent bypass grafts, and a hostile ascending aorta, the patient was offered an AAC. Intraoperative assessment indicated a cardiac output of 1.7 L/min, mixed venous oxygen saturation of 40%, and an ejection fraction of 15% to 20%. The patient was placed on cardiopulmonary bypass through a left thoracotomy as previously described [3], although arterial cannulation was performed in the distal aortic arch [4]. The conduit consisted of an 18-mm pre-clotted Medtronic Hancock apical left ventricular connector (Medtronic Inc, Minneapolis, MN) sewn to the inflow end of a 21-mm Medtronic Freestyle porcine full root with the outflow end sewn to a 20-mm Hemashield graft (Boston Scientific, Boston, MA).

The patient initially was weaned off cardiopulmonary bypass, but difficulty with mechanical ventilation induced transient hypoxia and a rapid, regular arrhythmia. Synchronized cardioversion failed with subsequent development of a wide complex arrhythmia that rapidly degenerated to ventricular fibrillation. Eventually, unsynchronized cardioversion restored sinus rhythm, although left ventricular function was notably diminished necessitating reinstitution of cardiopulmonary bypass with ultimate placement of a Thoratec CentriMag left ventricular assist device (LVAD) (Thoratec Corp, Pleasanton, CA).

The LVAD cannulation consisted of two 10-mm Abiomed (Abiomed Inc, Danvers, MA) Hemashield (Meadox Medicals Inc, Oakland, CA) cannulas sewn in an end-to-side manner to the AAC proximal to the valve prosthesis and the outflow graft sewn distal to the valve prosthesis, respectively. Hemodynamic stability and separation from cardiopulmonary bypass were achieved with LVAD support. Postoperatively, anticoagulation (heparin drip, 500 units/hour titrated to a partial thromboplastin time of 50 seconds) was initiated after a brief heparin-free window to assist surgical hemostasis.

For the next 48 hours, the patient demonstrated improvement in cardiac indices (ie, improvement in native right ventricular and left ventricular function with estimated ejection fraction of 25% by transesophageal echocardiography) with concomitant reduction of inotropic support. Hence, the LVAD was explanted by simply clipping and dividing the inflow and outflow cannulas at which time the anticoagulation was discontinued.

Recovery was uneventful with progressive weaning of mechanical ventilation and inotropic support. However, 24 hours later, an abrupt diminution in cardiac function necessitated reinstitution of multiple vasopressors and inotropes to maintain marginal hemodynamics. Transesophageal echocardiography demonstrated a large thrombus in the aortic root (Fig 1), with absence of antegrade flow in the aortic root and a significant decrease in ejection fraction. Heparinization was reinitiated (5,000 unit bolus with drip of 1,200 units/hour), but patient comorbidities prohibited further invasive intervention. He progressed to multisystem organ failure and expired. Autopsy confirmed thrombosis of the ascending aorta with thrombotic occlusion of the native left and right coronary ostia, as well as the ostia of all three venous grafts with resultant myocardial infarction.

View larger version (68K): [in this window] [in a new window]   Fig 1. Mid-esophageal aortic valve, long-axis view showing the aortic root, which is completely filled with spontaneous echocardiographic contrast suggestive of thrombus formation. (AR = aortic root; LA = left atrium; LV = left ventricle.)

	Comment

Top Abstract Introduction Comment References

The complication reported has not been previously described, although an incidental and clinically insignificant aortic arch thrombus visualized on surveillance computed tomography has been published [6]. Our case substantiates the potential for aortic thrombus after AAC in a more profound and unfortunately catastrophic presentation.

Although concern exists regarding partitioning stroke volume [6, 7], blood flow has been shown to distribute evenly throughout the systemic and coronary circulations despite diversion [5]. Similar flow disruption is described in the LVAD literature. In the LVAD population, a reduction in native aortic valve ejection with secondary stagnation of blood flow in the ascending aorta has resulted in massive myocardial infarction from coronary artery occlusion in some patients [8]. This flow characteristic is dependent on the variable of outflow cannula placement in the ascending aorta versus the descending aorta [8].

Although it is not a focus of this article, this appears to be the first report of LVAD placement through cannulation of the AAC. The inflow and outflow cannulas were placed without compromising additional myocardium or the AAC using two end-to side grafts that were simply clipped and oversewn at explantation. Short-term LVAD can be a useful adjunct in AAC patients.

The LVAD literature, as well as the case report by Takeda and colleagues [6], hints at increased thrombogenicity of the ascending aorta with flow stagnation, thus raising the issue of long-term anticoagulation after an AAC, even in patients who receive biologic valves. Lockowandt [7] uses 3 months of warfarin routinely. Although one could argue that LVAD placement potentiated flow distribution in our patient, his clinical deterioration did not manifest until device explantation and discontinuation of heparinization, suggesting that the aortic root thrombus was secondary to flow diversion from the AAC.

	References

Top Abstract Introduction Comment References

 

1. Sarnoff SJ, Donovan TJ, Case RB. The surgical relief of aortic stenosis by means of apical aortic valvular anastomoses Circulation 1955;11:564-574.[Abstract/Free Full Text]
2. Cooley DA, Lopez RM, Absi TS. Apicoaortic conduit for left ventricular outflow tract obstruction Ann Thorac Surg 2000;69:1511-1514.[Abstract/Free Full Text]
3. Gammie JS, Brown JW, Brown JM, et al. Aortic valve bypass for the high-risk patient with aortic stenosis Ann Thorac Surg 2006;81:1610-1611.[Free Full Text]
4. Gillinov AM, Lytle BW, Hoang V, et al. The atherosclerotic aorta at aortic valve replacement: surgical strategies and results J Thorac Cardiovasc Surg 2000;120:957-963.[Abstract/Free Full Text]
5. Nihill MR, Cooley DA, Norman JC, et al. Hemodynamic observations in patients with left ventricle to aorta conduit Am J Cardiol 1980;45:573-582.[Medline]
6. Takeda K, Matsumiya G, Takano H, et al. Unusual thrombus formation in the aorta after apicoaortic conduit for severe aortic stenosis J Thorac Cardiovasc Surg 2006;132:155-156.[Free Full Text]
7. Lockowandt U. Apicoaortic valve conduit: Potential for progress? J Thorac Cardiovasc Surg 2006;132:796-801.[Abstract/Free Full Text]
8. Kar B, Delgado 3rd RM, Frazier OH, et al. The effect of LVAD aortic outflow-graft placement on hemodynamics and flow: implantation technique and computer flow modeling Tex Heart Inst J 2005;32:294-298.[Medline]

This article has been cited by other articles:

				A. L. Estrera Invited Commentary Ann. Thorac. Surg., January 1, 2012; 93(1): 293 - 293. [Full Text] [PDF]

				C. E. Stauffer, J. Jeudy, M. Ghoreishi, C. Vliek, C. Young, B. Griffith, and J. S. Gammie Magnetic Resonance Investigation of Blood Flow After Aortic Valve Bypass (Apicoaortic Conduit) Ann. Thorac. Surg., October 1, 2011; 92(4): 1332 - 1338. [Abstract] [Full Text] [PDF]

				Y. Takahashi, Y. Tsutsumi, O. Monta, and H. Ohashi Thrombus formation due to flow competition after apico-aortic conduit Eur J Cardiothorac Surg, April 1, 2010; 37(4): 978 - 979. [Abstract] [Full Text] [PDF]

				J. S. Gammie and J. W. Brown Rarity of Aortic Thrombus After Aortic Valve Bypass (Apicoaortic Conduit) Surgery Ann. Thorac. Surg., January 1, 2010; 89(1): 341 - 342. [Full Text] [PDF]

				C. J. Parsa and G. C. Hughes Reply Ann. Thorac. Surg., January 1, 2010; 89(1): 342 - 342. [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Cyrus J. Parsa Carmelo A. Milano G. Chad Hughes Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Parsa, C. J. Articles by Hughes, G. C. Search for Related Content PubMed PubMed Citation Articles by Parsa, C. J. Articles by Hughes, G. C. Related Collections Cardiac - other Valve disease