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Ann Thorac Surg 2008;85:58-59. doi:10.1016/j.athoracsur.2007.08.005
© 2008 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Invited commentary

Stephen Large, MA, MS

The Surgical Unit, Papworth Hospital, Papworth Everard, Cambridgeshire CB3 8RE, United Kingdom

(Email: stephen.large{at}papworth.nhs.uk).

Postoperative atrial fibrillation (POAF) after heart surgery is a demanding problem. It is responsible for increased bed days and thus increased costs, and may be responsible for the life-threatening issues of low output syndrome, stroke, and bowel infarction. The incidence of POAF depends on its definition. Certainly, it is very common, at about 60%, if defined as any episode of irregular, narrow complex tachycardia after heart surgery as identified by continuous monitoring during the defined period of review.

Cohn and colleagues [1] seek to describe the incidence of POAF in 500 consecutive heart transplant recipients as recognized in their retrospective review of patient records. Their review period was the first 30 days after transplantation. Clearly, by choice of study method, their described incidence of POAF is a shortfall of the true incidence. Nonetheless we can accept that POAF is probably lower than expected compared with the rate after nontransplant surgery. Why might this be so?

1 Could it be that the transplanted heart is resistant to POAF due to excision of pulmonary veins (effective pulmonary vein isolation)? We must remember that POAF is very different from the AF seen in distantly operated on or unoperated on hearts. We do not know the mechanism of POAF, but it appears to be more common in structurally abnormal hearts, those with a heavy load of coronary artery atheroma, and in the older patient. To compound all of this, a narrow complex irregular tachycardia is common after the Cox-Maze procedure (probably an irregularly transmitted atrial flutter), suggesting pulmonary vein isolation to be of little or no importance in POAF or flutter.
2 Could it be that the donor heart is a young, structurally normal heart? Donor hearts tend to be chronologically young, but they are structurally abnormal as a result of injury that occurs around the time of brain death [2]. We also recognize AF as a hallmark of acute rejection. This the authors have addressed. Those without rejection showed a low incidence of AF seemingly independent of implantation method. Donor hearts were inserted in two different ways in this study. Cohn and colleagues suggest that there might be a trend towards even less POAF in those with bicaval compared to those with biatrial cuffs. Numbers were small, and in any event, we do not know whether AF arose within the recipient or donor atria of these constructs nor do we know if the recipient was or was not in AF before the transplant procedure!
3 Could it be that all of this is due to denervation of the transplanted heart? Certainly, denervation is an effective way to control established AF and has been offered in the past as a way to control intrusive AF. So, "yes" it could be, but we do not know the impact of denervation on POAF.
4 Could it be related to the drugs required with transplantation? We traditionally give chronotropic drugs in various forms to heart recipients. These would be expected to promote POAF. We also give immunosuppression. This is steroid-based, and an interesting literature is emerging on the use of steroids in the cardioversion of POAF, so much so that we use this approach to control POAF in our nontransplant practice [3].

So, are we further forward in our understanding of the mechanism(s) of POAF after Cohn and colleagues’ contribution? Perhaps a little bit. Their contribution will, hopefully, encourage further work in this area. Ideally, this work will adopt a prospective approach to this subject with a design to tease out answers to the four questions posed here.


    References
 Top
 References
 

  1. Cohn WE, Gregoric ID, Radovancevic B, Wolf RK, Frazier OH. Atrial fibrillation after cardiac transplantation: experience in 498 consecutive cases Ann Thorac Surg 2008;85:56-59.[Abstract/Free Full Text]
  2. Stoica SC, Satchithananda DK, White PA, et al. Brain death leads to abnormal contractile properties of the human donor right ventricle J Thorac Cardiovasc Surg 2006;132:116-123.[Abstract/Free Full Text]
  3. Oh J, Chung J, Kang S. Use of corticosteroids to prevent atrial fibrillation after cardiac surgery JAMA 2007;18:283298.

Related Article

Atrial Fibrillation After Cardiac Transplantation: Experience in 498 Consecutive Cases
William E. Cohn, Igor D. Gregoric, Branislav Radovancevic, Randall K. Wolf, and O.H. Frazier
Ann. Thorac. Surg. 2008 85: 56-58. [Abstract] [Full Text] [PDF]




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