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Ann Thorac Surg 1996;62:897-899
© 1996 The Society of Thoracic Surgeons


Case Report

Heart Transplantation Complicated by a Patent Foramen Ovale of the Recipient Atrial Septum

Kwok L. Yun, MD, Hermann Reichenspurner, MD, PhD, Joseph Schmoker, MD, Bob Hu, MD, Edward B. Stinson, MD

Department of Cardiothoracic Surgery and Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California

Accepted for publication April 6, 1996.


    Abstract
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 Abstract
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A patent foramen ovale after heart transplantation is a relatively uncommon occurrence. We report a case of a 58-year-old man with profound hypoxemia after orthotopic cardiac transplantation for end-stage ischemic cardiomyopathy. Transesophageal echocardiography demonstrated the presence of a patent foramen ovale in the recipient atrial cuff. Primary closure was performed with correction of the right-to-left shunt.


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A patent foramen ovale (PFO) of the donor heart complicating cardiac transplantation is a relatively infrequent event [1] despite a substantial prevalence of PFOs in the general population [2]. It can result in severe hypoxemia refractory to increasing concentration of inspired oxygen. Closure of a donor PFO during the time of transplantation is usually performed after visual and probe examination of the donor atrial septum. This report describes the presence of an unrecognized PFO in the residual recipient atrial cuff and emphasizes the importance of careful inspection of the recipient as well as the donor heart for the presence of a PFO.

A 58-year-old man presented with end-stage ischemic cardiomyopathy due to accelerated coronary artery atherosclerotic disease. He underwent three previous coronary artery bypass operations and had prolonged postoperative ventilator dependence after the last two revascularization procedures. Despite maximal medical management, his condition continued to deteriorate with worsening congestive heart failure. He was evaluated at our institution for possible cardiac transplantation.

Physical examination revealed jugular venous distention to 7 cm, a pansystolic murmur, clear lung fields, hepatomegaly, and mild peripheral edema. The electrocardiogram was remarkable for first-degree atrioventricular block, right bundle-branch block, and evidence of a remote inferior wall infarction. Echocardiography showed a diminished shortening fraction of 0.18. Cardiac catheterization demonstrated moderate pulmonary hypertension and low cardiac output (Table 1Go). Pulmonary function testing revealed moderate obstructive ventilatory defect but normal oxygenation on room air (arterial oxygen tension, 81 mm Hg).


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Table 1. . Respiratory and Hemodynamic Data
 
After the patient spent 3 months on the transplant waiting list, a compatible donor heart became available. The donor heart was carefully examined at the time of implantation for the presence of a PFO or atrial septal defect by direct visual inspection and probing. Transplantation was performed using the conventional technique developed by Lower and associates [3], in which systemic and pulmonary venous anastomoses were simplified with atrial cuffs. The procedure was uneventful and the patient was weaned from cardiopulmonary bypass on a low dose of dopamine. The aortic cross-clamp time was 55 minutes and the donor graft ischemic time was 3 hours 5 minutes.

The immediate postoperative period was complicated by profound hypoxemia. On an inspired oxygen fraction of 1.00 and peak end-expiratory pressure of 5 mm Hg, the arterial oxygen tension was 52 mm Hg. Chest roentgenography showed only mild bibasilar atelectasis and minimal pleural effusion. Hemodynamics were consistent with mild right ventricular dysfunction (see Table 1Go). Epinephrine intravenous drip was administered for added inotropic support, and positive end-expiratory pressure was increased to 12 mm Hg in an attempt to improve arterial oxygenation. Despite these measures, the arterial oxygen saturation continued to deteriorate to the range of 75% to 85%. Eight hours postoperatively, the arterial oxygen tension decreased to 44 mm Hg. Transesophageal echocardiography demonstrated an intracardiac right-to-left shunt at the atrial level posterior to the right atrial suture line, suggesting the presence of a PFO in the residual recipient atrial septum (Fig 1Go). The patient was taken back to the operating room, where a large PFO was found superiorly and posteriorly near the interatrial groove. The PFO was repaired primarily using a running polypropylene suture.



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Fig 1.. Two-dimensional transesophageal echocardiogram demonstrating the presence of a significant patent foramen ovale (PFO) in the recipient atrial septal cuff. (LA = left atrium; RA = right atrium.)

 
As shown inTable 1Go, arterial oxygenation markedly improved on postoperative day 1, with an arterial oxygen tension of 80 mm Hg on an inspired oxygen fraction of 0.60. This was paralleled by decreases in central venous pressure and pulmonary arterial pressure. The patient's pulmonary status continued to improve slowly, along with recovery of ventricular performance. He was successfully weaned from the ventilator and was extubated on postoperative day 6 with satisfactory postextubation arterial blood gas. Endomyocardial biopsies on postoperative days 8 and 14 revealed no evidence of cellular rejection. The patient was discharged from the hospital on postoperative day 17 and is currently home progressing well 4 months after transplantation.


    Comment
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A PFO causing a significant right-to-left shunt and hypoxemia after cardiac transplantation is a relatively rare complication. This is due to the routine examination of the donor atrial septum by direct inspection and probing. The presence of either a PFO or atrial septal defect is corrected before implantation of the cardiac allograft. Two such cases have been previously reported in the literature [1, 4]. Schulman and associates [1] described a case of a 44-year-old man in whom hypoxemia developed several hours after extubation on the second postoperative day after cardiac transplantation. Transthoracic contrast echocardiography demonstrated right-to-left shunting at the atrial level. It was noted that the foramen ovale of the donor heart was not examined with a probe at the time of implantation. The patient was treated with conservative management with resolution of the refractory hypoxemia. This was in association with the reduction in right atrial pressure due to resolution of right ventricular dysfunction and pulmonary hypertension. In another case of a 27-month-old boy who underwent heart transplantation, O'Laughlin and coworkers [4] identified a residual atrial septal defect by echocardiography in the donor allograft after it had been repaired primarily without a patch at the time of implantation. The residual atrial septal defect was subsequently closed percutaneously with a 28-mm clamshell occluder 3 months later.

Here we report a PFO in the residual recipient atrial septum. The PFO was not obvious during the initial transplantation as it was located superiorly and posteriorly. In this position, it was obscured by the superior vena caval cannula, which was inserted via the right atrium using the conventional method for transplantation [3]. Although the use of intraoperative transesophageal echocardiography might have detected the PFO sooner, it would have required repeat cross-clamping of the aorta. In retrospect, the prolonged postoperative ventilatory support during the patient's last two coronary bypass procedures was probably due, in part, to right-to-left shunting through the PFO. As right ventricular function improved postoperatively, the reduction of right-sided pressures, in combination with persistently elevated left atrial pressure caused by chronic left ventricular dysfunction, resulted in resolution of dynamic shunting via the PFO. However, after cardiac transplantation, left atrial hypertension was no longer present because of normal left ventricular contractile function of the donor heart. This, in turn, exacerbated the degree of right-to-left shunting through the PFO, which produced the observed severe refractory hypoxemia.

For more than a quarter of a century, the technique developed by Lower and associates [3] had been the standard for orthotopic cardiac transplantation. The major advantage of this method is that it avoids the technical difficulties of separate caval and pulmonary venous anastomoses. It has been suggested, however, that loss of normal atrial geometry is responsible for the high prevalence of tricuspid and mitral regurgitation as well as atrial tachyarrhythmias [5, 6]. This has led to the development of alternative techniques of bicaval anastomoses [7] or total orthotopic heart transplantation by bicaval and pulmonary venous anastomoses [8]. With both methods, right atrial anatomy is preserved and the donor right atrium is not in communication with the recipient right atrial cuff. Thus, the complication of right-to-left shunting described in this case could have been avoided if direct caval anastomoses had been used instead. The PFO would have remained closed due to the normally negative intrathoracic pressure. Furthermore, direct caval cannulation would have allowed a more thorough inspection of the recipient atrial septum.

In summary, refractory hypoxemia after orthotopic cardiac transplantation using the conventional biatrial technique may be due to a right-to-left shunt via a PFO in the recipient atrial septum as well as the donor atrial septum. Therefore, it is important that both recipient and donor interatrial septa be evaluated completely by visual and probe examination and a PFO in either be closed at the time of graft implantation.


    Footnotes
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 Footnotes
 Abstract
 Introduction
 Comment
 References
 
Address reprint requests to Dr Yun, Department of Cardiovascular and Thoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, CA 94305-5247.


    References
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 Footnotes
 Abstract
 Introduction
 Comment
 References
 

  1. Schulman LL, Smith CR, Drusin R, Rose EA, Enson Y, Reemtsma K. Patent foramen ovale complicating heart transplantation: a window on posttransplantation hemodynamics. Chest1987;3:569–72.
  2. Hagen PT, Sholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first ten decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc 1984;59:17–20.[Medline]
  3. Lower RR, Stofer RC, Shumway NE. Homovital transplantation of the heart. J Thorac Cardiovasc Surg1961;41:196–202.
  4. O'Laughlin MP, Bricker JT, Mullins CE, Cabalka AK, Gelb BD, Towbin JA. Transcatheter closure of residual atrial septal defect following cardiac transplantation. Cathet Cardiovasc Diagn1993;28:162–3.[Medline]
  5. Angermann CE, Spes CH, Tammew A, et al. Anatomic characteristics and valvular function of the transplanted heart: transthoracic versus transesophageal echocardiographic findings. J Heart Lung Transplant1990;9:331–8.
  6. Kaye DM, Anderson ST, Federman J. Electrocardiographic and echocardiographic features of left atrial size after orthotopic cardiac transplantation. Am J Cardiol1992;70:1096–9.[Medline]
  7. Sievers HH, Weyand M, Kraatz EG, Bernhard A. An alternative technique for orthotopic cardiac transplantation with preservation of the normal anatomy of the right atrium. Thorac Cardiovasc Surg1991;39:70–2.[Medline]
  8. Dreyfus G, Jebara V, Mihaileanu S, Carpentier AF. Total orthotopic heart transplantation: an alternative to the standard technique. Ann Thorac Surg1991;52:1181–4.[Abstract]




This Article
Right arrow Abstract Freely available
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Right arrow Author home page(s):
Kwok L. Yun
Hermann Reichenspurner
Joseph Schmoker
Edward B. Stinson
Right arrow Permission Requests
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Right arrow Articles by Yun, K. L.
Right arrow Articles by Stinson, E. B.
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Right arrow Articles by Yun, K. L.
Right arrow Articles by Stinson, E. B.


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