Abstract

I read with interest the article by Dias et al1Dias N.V. Ivanev K. Resch T.A. Maina M. Sonesson B. Endoleaks after endovascular aneurysm repair lead to nonuniform intra-aneurysm sac pressure.J Vasc Surg. 2007; 46: 197-203Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar describing the measurement on intra-aneurysm sac pressure in patients with endoleaks post-endovascular aneurysm repair (EVAR) and congratulate the authors for their pioneering work in the area of sac pressure measurement. However, I believe it necessary to challenge certain statements in the manuscript that apply to alternative technologic approaches to long-term surveillance of EVAR patients. In their article, the authors state that “the results of this study show that the endoleak nidus (channel) has consistently higher pressure than the intra-sac thrombus”. Their observations that the pressure within the sac is nonuniform and that the pressure by the endoleak nidus is higher than it would be within the thrombus are consistent with previous clinical and experimental studies examining distribution of pressure resulting from an endoleak.2Xenos E.S. Stevens S.L. Freeman M.B. Pacanowski J.P. Cassada D.C. Goldman M.H. Distribution of sac pressure in an experimental aneurysm model after endovascular repair: the effect of endoleak types I and II.J Endovasc Ther. 2003; 10: 516-523Crossref PubMed Scopus (15) Google Scholar, 3Timaran C.H. Ohki T. Veith F.J. Lipsitz E.C. Gargiulo 3rd, N.J. Rhee S.J. et al.Influence of type II endoleak volume on aneurysm wall pressure and distribution in an experimental model.J Vasc Surg. 2005; 41: 657-663Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar It is important to point out that attenuation of the pressure waveform as it moves away from the source is a different physical phenomena than what has been described as “compartmentalization”, which suggests that there exist areas within the sac that are isolated from the source of increased pressure. I believe the authors are blurring this distinction and using this position to incorrectly conclude that “this varying distribution of sac pressure in patients with endoleaks, although consistently higher in expanding AAAs, may question the reliability of systems based on pressure measurements in a single spot, such as with implantable pressure sensors”. I have been closely involved with the development of implantable pressure sensors, which are being actively studied in multiple areas of the body.4Ohki T. Ouriel K. Silveira P.G. Katzen B. White R. Criado F. et al.Initial results of wireless pressure sensing for endovascular aneurysm repair: the APEX Trial--Acute Pressure Measurement to Confirm Aneurysm Sac EXclusion.J Vasc Surg. 2007; 45: 236-242Abstract Full Text Full Text PDF PubMed Scopus (100) Google Scholar, 5Castro P.F. Concepcion R. Bourge R.C. Martinez A. Alcaino M. Deck C. et al.A wireless pressure sensor for monitoring pulmonary artery pressure in advanced heart failure: initial experience.J Heart Lung Transplant. 2007; 26: 85-88Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar Although the long-term data is still being assembled, I strongly believe that Dias et al1Dias N.V. Ivanev K. Resch T.A. Maina M. Sonesson B. Endoleaks after endovascular aneurysm repair lead to nonuniform intra-aneurysm sac pressure.J Vasc Surg. 2007; 46: 197-203Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar and Carpenter JP (Commentary, J Vasc Surg 2007;46:203) are failing to note that the fundamental difference between the work presented in this manuscript and the use of permanently implanted sensors is that the measurements performed by the physicians in Malmo represent a single moment, whereas the implantable sensors allow multiple pressure readings to be taken over time, thus providing a history of the sac’s pressure environment. The significance of this point is that since, as Dias points out, sac pressure is elevated even in the thrombus in the presence of an endoleak, serial measurements of the sac, irrespective of the exact position of the sensor within the sac, should allow the physician to prospectively see changes in pressure that signal the stent graft may be in the process of failing. This same conclusion could not be reached retrospectively with a single measurement. I believe that the use of implantable pressure measurement systems will become an important tool in management of the post-EVAR patient. Clinical trials to prove the long-term efficacy of implantable pressure sensors are currently being designed and I actively look forward to future reports detailing the chronic use of these devices. ReplyJournal of Vascular SurgeryVol. 47Issue 4PreviewWe thank Dr Ohki for his valuable comments on our article1 and appraise his unique contribution on the introduction of implantable pressure sensors. Our study is the first report on late pressure measurements in the endoleak nidus (flow channel) and the thrombus with the same technique and confirms a difference in pressure gradient between these two locations. The previously reported association of aneurysm shrinkage with intra-sac depressurization in the absence of endoleaks2 seems also to be present with endoleaks. 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