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J Thorac Cardiovasc Surg 1996;112:1129
© 1996 Mosby, Inc.


LETTERS TO THE EDITOR

Atrial natriuretic peptide release after cardiac transplantation

Hans H. Sievers, MD

Klinik fur Herzchirurgie
Medizinische Universität Lübeck
Lübeck, Germany

Reply to the Editor:

In the stage of ventricular overload and especially failure, the secretion of natriuretic peptides (atrial natriuretic peptide, ANP, and brain natriuretic peptide, BNP) is increased with compensatory, beneficial effects like enhanced diuresis, natriuresis, and inhibition of the renin-angiotensin system and the sympathetic nervous system.Go 1 ANP is predominantly released from atrial tissue stimulated by elevated wall stress. Theoretically, the bicaval technique in cardiac transplantation with significantly lower atrial dimensions and pressuresGo 2 and thus wall stress should result in a decrease of the high level of ANP after standard cardiac transplantation. However, we could not measure a significant difference in the ANP levels between the two transplantation techniques, an experience that was confirmed by EL Gamel and associates. Thus other mechanisms probably cause these high ANP levels. Whether one of these mechanisms is related to primary or secondary effects of cyclosporine medication, as stated by EL Gamel's group, remains to be established. We could not find a correlation between the ANP and the cyclosporine trough level (r = -0.1164, p = 0.3828, n = 9). Other possible explantations for increased ANP levels are the denervation of the transplanted heart and a hypersensitivity of ANP-synthesizing cells to circulating catecholamines.Go 3

EL Gamel and coworkers should be congratulated for extending the knowledge of heart transplantation biology inasmuch as they found that the BNP level was significantly higher in the standard transplantation group, reflecting a physiologic response to increased ventricular afterload. This represents a further argument in favor of the bicaval technique in cardiac transplantation. These new findings raise new questions: Are the drastically increased ANP levels after cardiac transplantation still beneficial? Are reinnervation procedures effective to optimize regulation of ANP response? Does BNP level in patients after transplantation provide any prognostic information comparable with patients after myocardial infarction?Go 4 Is intravenous BNP valuable to improve postoperative hemodynamics? Is there any relation between the change of peptide levels and evolving rejection? We look forward with great interest to further progress in research in this context.

References

  1. Saito Y, Nakao K, Nishimura K, Sugawara A, Okumura K, Obata K, et al. Clinical application of atrial natriuretic polypeptide in patients with congestive heart failure: beneficial effects on left ventricular function. Circulation 1987;76:115-2.[Abstract/Free Full Text]
  2. Leyh RG, Jahnke AW, Kraatz EG, Sievers H-H. Cardiovascuclar dynamics and dimensions after bicaval and standard cardiac transplantation. Ann Thorac Surg 1995;59:1495-500.[Abstract/Free Full Text]
  3. Goetz KC, Wang BC, Geer PG, Leadly RJ, Reinhard HW. Atrial stretch increases sodium excretion independent of release of atrial peptide. Am J Physiol 1965;250:R946-50.
  4. Omland T, Aakvaag A, Bonarjee VVS, Caidahl K, Lie TR, Nilsen DWT, et al. Plasma brain natriuretic pepetide as an indicator of left ventricular systolic function and long-term survival after acute myocardial infarction. Circulation 1996;93:1963-70.[Abstract/Free Full Text]




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