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Letters to the Editor |
2nd Department of Cardiac Surgery, Medical University of Silesia, Ziolowa 47, 40-635 Katowice, Poland
Received 18 March 2008; accepted 19 March 2008.
* Corresponding author. Tel.: +48 32 2526093; fax: +48 32 2526093. (Email: mdeja{at}slam.katowice.pl).
Key Words: Internal thoracic artery ADRF CABG Perivascular tissue Nitric oxide Saphenous vein
We thank Dashwood et al. for their interest and comments regarding our manuscript [1]. We used to be enthusiastic regarding ITA skeletonization but with growing awareness of the active role of perivascular tissue we are becoming less and less so [2]. Our study showed that the factor responsible for anticontractile properties of perivascular tissue (PVT) in human internal thoracic artery (ITA) acts independent of NO and PGI2 [3]. It suggests that PVT releases agents, different to these well known relaxing factors that clearly affect vascular reactivity, adventitia/adipocyte derived relaxing factor (ADRF).
We appreciate Dashwood et al.'s findings on the importance of perivascular tissue of saphenous vein [4,5]. Their papers clearly show that preserving perivascular fat results in improved long term patency rates of SV grafts. Dashwood et al. proved that PVT of SV possesses strong NOS activity and argue it might contribute to the improved patency of SV harvested as a pedicle. Still, we do not know if this high NOS activity is found in PVT, nor whether SV PVT releases ADRF. Likewise, it remains to be shown if ADRF, similarly to NO, has the ability to affect patency rates of the vessels.
Meanwhile, we have analyzed the influence of internal thoracic artery's PVT on the function of other vessels such as radial artery and saphenous veins and we failed to find any anticontractile effect. This may suggest that ADRF may be a vessel specific agent. (These data will be presented during the 57th ESCVS International Congress in Barcelona). It is crucial now to establish the nature and precise mechanisms of action of ADRF and check if this is truly a vessel specific factor which may affect clinical outcome of non-skeletonized grafts.
References
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