Eur J Cardiothorac Surg 2006;29:863-864
© 2006 Elsevier Science NL
Reply to Mishra
Thierry Caus
*
Department of Cardiac Surgery, University Hospital SUD, Avenue Salouël-Laënnec, 80000 Amiens, France
Received 25 January 2006;
accepted 26 January 2006.
* Tel.: +33 43 22 455925; fax: +33 32 2455331. (Email: caus.thierry{at}chu-amiens.fr).
Key Words: MRS • Coronary circulation • Transplantation
I thank Dr Mishra for expressing his interest in our original article [1] through his letter to the editor [2]. The structure of this letter is articulated around three points of argument. The first point is a request for additional precisions about epidemiologic data concerning both donors and recipients. Cardiac allograft vasculopathy (CAV) is mainly the consequence of post-transplant endothelial injury mediated by immunologic reactions and lacks definitive relationships with many of the usual risk factors for coronary artery disease. We therefore presented only data which were relevant for the occurrence of CAV during follow-up and, in particular, we chose not to publish the age of recipients at the time of transplant for the following reasons: (i) incidence of CAV is not related to the age of recipient but to the age of donors [3]; and (ii) since ANOVA found a near significance (p
= 0.06) existing between the age of our three groups that was attributed only to a younger age in volunteers (no difference being observed after post hoc comparison of groups A and B), the result might have been confusing for readers. Concerning the distribution of other unpublished risk factors within the population of donors, incomplete data precluded us to present them in the manuscript. In no way would they have affect the main result of the study which was the determination of specificity and sensitivity of 31P-MR chemical shift imaging for the diagnosis of CAV when compared to conventional coronary angiography. The second point or argument developed by Dr Mishra is related to the observed discrepancy between the expected and observed prevalence of CAV in our population with respect to the time elapsed from transplant (we indeed used the prevalence which is a picture of the population at a certain time and not the incidence which is a different matter). He suggests that this discrepancy could be the result of our policy for detecting CAV with routine coronary angiograms. In our paper, we have already commented on this point (end of paragraph 2 in Discussion) and have today nothing to add but to stress that it has never been our practice (like for any centre I know) to rely on symptoms to indicate transplanted patients for coronary angiograms. In particular, each of the patients presented here were submitted to systematic coronary angiograms on an annual basis. Therefore, the observed prevalence of CAV in our series is accurate. The last point of argument relates to the definition of CAV used in this study and to the implications this might induce concerning appropriate treatment. Indeed, as specified we focussed on high grade lesions according to the Gao et al.'s classification [4] which are believed to be the most characteristic lesions of CAV and which are actually the main target of new immunosuppressive protocols [5]. In our experience, proximal, focal lesions accessible to angioplasty occur early after transplantation and are mainly a consequence of pre-existing classical atherosclerosis and of post-transplant hypercholesterolemia.
References
- Caus T, Kober F, Marin P, Mouly-Bandini A, Quilici J, Métras D, Cozzone PJ, Bernard M. Non-invasive diagnostic of cardiac allograft vasculopathy by (31)P magnetic resonance chemical shift imaging. Eur J Cardiothorac Surg 2006 Jan;29(1):45-49.[Abstract/Free Full Text]
- Mishra PK. Reliable non-invasive diagnosis of coronary allograft vasculopathy: is it still a widhfull thinking. Eur J Cardiothorac Surg 2006;29:862-863.[Free Full Text]
- Gao HZ, Hunt SA, Alderman EL, Liang D, Yeung AC, Schroeder JS. Relation of donor age and preexisting coronary artery disease on angiography and intracoronary ultrasound to later development of accelerated allograft coronary artery disease. J Am Coll Cardiol 1997;3(29):623-629.
- Gao SZ, Alderman EL, Schroeder JS, Silverman JF, Hunt SA. Accelerated coronary vascular disease in the heart transplant patient: coronary arteriographic findings. J Am Coll Cardiol 1988;12:334-340.[Abstract]
- El-Sayed O, Magorien RD, Orsini A, Ferketich AK, Leier CV. Advancing immunosuppression therapy to counter the progression of cardiac allograft vasculopathy. J Card Fail 2005;11(2):137-141.[Medline]
