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The relation between endoleak and aneurysm sac pressure is not completely clear. This review evaluates the effect of endoleaks on aneurysm sac pressure and summarizes the present knowledge regarding aneurysm sac pressure after EVAR.
Methods
A systematic search of literature was carried out using MEDLINE, EMBASE and Web of Science. Studies were included if aneurysm sac pressure measurements as well as systemic pressure measurements were performed during or after EVAR. Mean pressure indices (MPI), ratio mean aneurysm sac pressure to mean systemic pressure), in the absence of endoleaks and in the presence of different type of endoleaks were compared.
Results
Stent-graft deployment does not seem to result in immediate reduction of aneurysm sac in the absence of an endoleak. Aneurysm sac pressure is elevated in the presence of an endoleak. However, the MPIs differ widely between studies both in the absence and presence of an endoleak.
Conclusion
MPI is not specific to the type of endoleak. This implies that the same type of endoleak does not necessarily pose the same MPI and by this the same hazard of aneurysm rupture, because the aneurysm sac pressure is directly related to the aneurysm wall stress.
Clinical experience of the use of self-fixing synthetic prostheses for remote endoprosthetics of the thoracic and the abdominal aorta and iliac arteries through the femoral artery and as intraoperative endoprosthesis for aorta reconstruction.
EVAR aims at prevention of aneurysm rupture with exsanguinations and acute death. Endoleaks are the Achilles heel of EVAR. An endoleak is defined as persistence of blood flow outside the stent-graft, but within the aneurysm sac. Endoleaks occur approximately in 20% of the patients treated by EVAR.
The absence of an endoleak on conventional imaging tools, such as Computer tomography (CT) or angiography, does not exclude the possibility of high pressure in the aneurysm sac and the persistent risk of rupture.
The success of EVAR relies on the extent of isolation of the aneurysm sac from systemic blood flow and systemic pressure. The evaluation of this extent of isolation is difficult. Firstly, it is not known what happens to the aneurysm sac pressure after EVAR without detectable endoleak nor is it known how much pressure is required to cause rupture. Secondly, it is difficult to predict whether and when re-intervention is justified in the presence of endoleaks, solely based on imaging. Graft related endoleaks (Type I and III) are associated with a risk of late rupture and it is assumed but not proven that this is because such endoleaks are associated with significant pressurization of the aneurysm sac.
Little is known about their impact on the aneurysm sac pressure and the risk of aneurysm rupture. The clinical significance of Type V endoleaks, defined as aneurysm growth without detectable endoleaks, also remains uncertain.
Elucidation of the relationship between endoleak and pressure may help clinical decision making. This review evaluates the effect of endoleaks on aneurysm sac pressure and summarizes the present knowledge regarding aneurysm sac pressure after EVAR.
Methods
Search strategy for identification of studies
A systemic search of literature was conducted until December 2006 using PubMed, EMBASE and Web of Science. Our search strategy is given in Table 1 (PubMed), Table 2 (EMBASE) and Table 3 (Web of Science). There was no restriction on language.
Table 1Search strategy used for PubMed
Search
#1
“aortic aneurysm” [MeSH] OR aortic aneurysm* [Text word]
#2
“stents” [MeSH] OR stent* [Text Word]
#3
“blood vessel prosthesis” [MeSH] OR “blood vessel prosthesis implantation” MeSH] OR blood vessel prosthe* [Text Word]
#4
evar [All Fields] OR “endovascular therapy” [All Fields]
#5
#2 OR #3 OR #4
#6
#1 AND #5
#7
endovascular [All Fields] AND (“aneurysm” [MeSH Terms] OR aneursym* [Text Word]) AND (repair* [Text Word] OR treat* [Text Word] OR therap* [Text Word] OR explode therapy [Subheading] OR “therapeutics” [MeSH])
#8
“pressure” [MeSH] OR pressure* [Text Word] OR “manometry” [MeSH] OR manomet* [All fields] OR leak* [All Fields] OR endoleak* [All Fields] OR tension [All fields] OR endotension [All Fields]
Articles of in-vitro, animal and patient-studies were selected by Pubmed, EMBASE and Web of Science, respectively. The abstracts of each article were studied after checking for duplication between the databases. If it appeared that aneurysm sac pressure measurements was concurrently performed with systemic pressure measurements during or after EVAR the full text was studied. Additional articles were sought by checking the reference lists of the relevant articles.
Data extraction
Particular attention during evaluation of the selected studies was paid to the type of study (in-vitro, animal or patient), the pressure measurement technique, the presence or absences of endoleaks, the time of pressure measurement and the used analysis of pressure measurements. The endoleak classification is given in Table 4.
The interval between pressure measurement and EVAR might be relevant for the interpretation and comparison of measurements. Therefore, we categorized the studies, in which an endoleak was absent, in 4 groups (Group 1: < 1 week after EVAR, Group 2: 1 week to 1 year after EVAR, Group 3: 1 to 2 years after EVAR, Group 4: 2 to 4 years after EVAR). We divided the studies, in which a Type II endoleak was present, in 2 groups (Group 1: 0 to 1 month after EVAR, Group 2: > 1 month after EVAR). Time of pressure measurement is probably less relevant in the presence of a Type I and III leak, because there is a direct connection between the systemic circulation and the aneurysm sac. Consequently, it is not likely that the ratio between aneurysm sac pressure and systemic blood pressure changes over time. Type IV and V endoleak studies were not categorized in moment of pressure measurement, because these endoleaks are investigated only in a small number of studies.
Analysis of data
Peripherally measured systolic and diastolic pressure does not always reflect corresponding pressures in the aorta. The systolic pressure in the brachial artery over-estimates the central aortic systolic pressure.
So the comparison of the ratios between the systolic or pulse aneurysm sac and the systolic or pulse systemic pressure between studies, in which the systemic blood pressure is measured centrally, and studies, in which this pressure is measured peripherally, is biased. However, the mean pressure is virtually identical in central and peripheral arteries.
Therefore, we chose to evaluate the mean pressure index (MPI) to enable meaningful comparisons. The MPI is the ratio between the mean aneurysm sac pressures and the mean systemic blood pressure (MPI). If no single aneurysm sac and systemic pressure were given, we depicted the ratio between the reported mean or median aneurysm sac pressure and the mean or median systemic blood pressure of the experiments.
Data were stored in a database for analyses (Microsoft Excel 2002, Redmond, USA). The mean pressure indices (MPIs) were compared between studies. MPIs were depicted in Box & Whisker plots.
The effect of stent-graft deployment and the occurrence of endoleaks on the pulse pressure in the aneurysm sac were evaluated as well. Because of the difference between centrally and peripherally measured blood pressures, no quantitative analysis of the pulse pressure was performed.
Results
Aneurysm sac pressure without endoleak
Dampening of pulse pressure after stent-graft deployment without endoleak was observed in all studies. Pulse pressure in the aneurysm sac was never totally eliminated.
Intrasac pressure waveforms after endovascular aneurysm repair (EVAR) are a reliable marker of type I endoleaks, but not type II or combined types: an experimental study.
First experience in human beings with a permanently implantable intrasac pressure transducer for monitoring endovascular repair of abdominal aortic aneurysms.
Intra-aneurysm sac pressure measurements after endovascular aneurysm repair: differences between shrinking, unchanged, and expanding aneurysms with and without endoleaks.
Aortic side branch perfusion alone does not account for high intra-sac pressure after endovascular repair (EVAR) in the absence of graft-related endoleak.
Endoleak after endovascular graft repair of experimental aortic aneurysms: does coil embolization with angiographic “seal” lower intraaneurysmal pressure?.
Treatment of type II endoleaks with a novel polyurethane thrombogenic foam: induction of endoleak thrombosis and elimination of intra-aneurysmal pressure in the canine model.
The development of endotension is associated with increased transmission of pressure and serous components in porous expanded polytetrafluoroethylene stent-grafts: characterization using a canine model.
Intrasac pressure waveforms after endovascular aneurysm repair (EVAR) are a reliable marker of type I endoleaks, but not type II or combined types: an experimental study.
First experience in human beings with a permanently implantable intrasac pressure transducer for monitoring endovascular repair of abdominal aortic aneurysms.
Intra-aneurysm sac pressure measurements after endovascular aneurysm repair: differences between shrinking, unchanged, and expanding aneurysms with and without endoleaks.
Aortic side branch perfusion alone does not account for high intra-sac pressure after endovascular repair (EVAR) in the absence of graft-related endoleak.
Endoleak after endovascular graft repair of experimental aortic aneurysms: does coil embolization with angiographic “seal” lower intraaneurysmal pressure?.
Treatment of type II endoleaks with a novel polyurethane thrombogenic foam: induction of endoleak thrombosis and elimination of intra-aneurysmal pressure in the canine model.
The development of endotension is associated with increased transmission of pressure and serous components in porous expanded polytetrafluoroethylene stent-grafts: characterization using a canine model.
Patient-studies demonstrate that stent-graft deployment does not usually result in immediate decrease of intrasac pressure. However, Chuter et al. and Gawenda et al. recorded a lower MPI immediately after aneurysm exclusion than other patient-studies (Fig. 1A, red lines).
They deployed aorto-mono-iliac stent-grafts instead of bifurcated. Other patient-studies confirm (Fig. 1A–D, red lines) the suggestion that time is required before pressure reduction in the aneurysm sac takes place. Ellozy et al. performed experiments with wireless pressure sensors to monitor aneurysm sac pressure continuously. They demonstrated that after EVAR the ratio of aneurysm sac pressure to systemic pressure decreased, except in 2 patients, from the time of implantation to 1 month and 3 months, respectively (Fig. 1B, red lines).
First experience in human beings with a permanently implantable intrasac pressure transducer for monitoring endovascular repair of abdominal aortic aneurysms.
Fig. 1MPI without endoleak in patient-studies (red), animal-studies (green) and in-vitro studies (blue). Type of pressure measurement device is given by (??) unknown, (F) fluid filled or (NF) non-fluid filled.
In animal studies, it has also been reported that the intra-aneurysm sac pressure after EVAR without endoleak is not immediately eliminated. Pitton et al. reported a pressure reduction during the period from 6 weeks to 6 months after EVAR (Fig. 1B, green lines).
In in-vitro studies, recorded MPIs are consistently lower than those reported in in-vivo studies. All in-vitro studies, except the study by Chaudhuri et al.,
Intrasac pressure waveforms after endovascular aneurysm repair (EVAR) are a reliable marker of type I endoleaks, but not type II or combined types: an experimental study.
reported a MPI less than 0.55 after successful exclusion of the aneurysm sac (Fig. 1A, blue lines).
Aneurysm sac pressure with type I endoleak
All studies, in which the effect of type I endoleak on the pulse pressure was investigated, demonstrated that aneurysm sac pulse pressure is less reduced in the presence of type I endoleaks than in the absence of type I endoleaks.
Intrasac pressure waveforms after endovascular aneurysm repair (EVAR) are a reliable marker of type I endoleaks, but not type II or combined types: an experimental study.
Aortic side branch perfusion alone does not account for high intra-sac pressure after endovascular repair (EVAR) in the absence of graft-related endoleak.
Aortic side branch perfusion alone does not account for high intra-sac pressure after endovascular repair (EVAR) in the absence of graft-related endoleak.
Fig. 2MPI with type I endoleak in patient-studies (red), animal-studies green) and in-vitro studies (blue). Type of pressure measurement device is given by (??) unknown, (F) fluid filled or (NF) non-fluid filled device.
Criado et al. investigated only the aneurysm sac pressure in animals in the presence of a type I endoleak. The pressure differential between the aneurysm sac pressure and systemic pressure was in 3 dogs <5 mmHg (MPI 1) (Fig. 2, green line).
Intrasac pressure waveforms after endovascular aneurysm repair (EVAR) are a reliable marker of type I endoleaks, but not type II or combined types: an experimental study.
Intrasac pressure waveforms after endovascular aneurysm repair (EVAR) are a reliable marker of type I endoleaks, but not type II or combined types: an experimental study.
First experience in human beings with a permanently implantable intrasac pressure transducer for monitoring endovascular repair of abdominal aortic aneurysms.
Intra-aneurysm sac pressure measurements after endovascular aneurysm repair: differences between shrinking, unchanged, and expanding aneurysms with and without endoleaks.
Aortic side branch perfusion alone does not account for high intra-sac pressure after endovascular repair (EVAR) in the absence of graft-related endoleak.
Treatment of type II endoleaks with a novel polyurethane thrombogenic foam: induction of endoleak thrombosis and elimination of intra-aneurysmal pressure in the canine model.
Relationship between preoperative patency of the inferior mesenteric artery and subsequent occurrence of type II endoleak in patients undergoing endovascular repair of abdominal aortic aneurysms.
Evaluation of the accuracy of a wireless pressure sensor in a canine model of retrograde-collateral (type II) endoleak and correlation with histologic analysis.
MPIs in the first month after EVAR, in patients with type II endoleaks, vary between 0.5 and 1.0. However, aneurysm sac pressure during this period appears similar to systemic pressure in most patients with type II endoleak (Fig. 3A, red lines).
Intrasac pressure waveforms after endovascular aneurysm repair (EVAR) are a reliable marker of type I endoleaks, but not type II or combined types: an experimental study.
First experience in human beings with a permanently implantable intrasac pressure transducer for monitoring endovascular repair of abdominal aortic aneurysms.
Aortic side branch perfusion alone does not account for high intra-sac pressure after endovascular repair (EVAR) in the absence of graft-related endoleak.
Treatment of type II endoleaks with a novel polyurethane thrombogenic foam: induction of endoleak thrombosis and elimination of intra-aneurysmal pressure in the canine model.
Relationship between preoperative patency of the inferior mesenteric artery and subsequent occurrence of type II endoleak in patients undergoing endovascular repair of abdominal aortic aneurysms.
Fig. 3MPI with type II endoleak in patient-studies (red), animal-studies (green) and in-vitro studies (blue). Type of pressure measurement device is given by (??) unknown, (F) fluid filled or (NF) non-fluid filled device.
First experience in human beings with a permanently implantable intrasac pressure transducer for monitoring endovascular repair of abdominal aortic aneurysms.
Intra-aneurysm sac pressure measurements after endovascular aneurysm repair: differences between shrinking, unchanged, and expanding aneurysms with and without endoleaks.
Treatment of type II endoleaks with a novel polyurethane thrombogenic foam: induction of endoleak thrombosis and elimination of intra-aneurysmal pressure in the canine model.
Treatment of type II endoleaks after endovascular repair of abdominal aortic aneurysms: translumbar puncture and injection of thrombin into the aneurysm sac.
Ellozy et al. measured aneurysm sac pressure immediately after EVAR in a patient with a type II endoleak, at 1 month and at 3 months after EVAR. The MPI decreased from 1.0 to 0.95 and 0.72, respectively.
First experience in human beings with a permanently implantable intrasac pressure transducer for monitoring endovascular repair of abdominal aortic aneurysms.
MPIs, measured by Dias et al. more than 1 month after EVAR (Fig. 3B), are generally lower than those measured in the first month after EVAR (Fig. 3A). These findings imply that aneurysm sac pressure also decreases after a time interval in spite of the presence of a persisting type II endoleak. However, aneurysm sac pressure does not always decrease in the presence of type II endoleak (Fig. 3B).
Treatment of type II endoleaks after endovascular repair of abdominal aortic aneurysms: translumbar puncture and injection of thrombin into the aneurysm sac.
The MPIs in animals in the first month after EVAR ranges from 0.33 to 0.85 (Fig. 3A, green lines) and at more than 1 month after EVAR from 0.42 to 0.94 (Fig. 3B, green lines).
Treatment of type II endoleaks with a novel polyurethane thrombogenic foam: induction of endoleak thrombosis and elimination of intra-aneurysmal pressure in the canine model.
Evaluation of the accuracy of a wireless pressure sensor in a canine model of retrograde-collateral (type II) endoleak and correlation with histologic analysis.
Intrasac pressure waveforms after endovascular aneurysm repair (EVAR) are a reliable marker of type I endoleaks, but not type II or combined types: an experimental study.
Xenos et al. did not demonstrate in their in-vitro model a significant increase in the aneurysm sac pressure in the presence of flow through a type II endoleak (Fig. 3A).
Endoleak after endovascular graft repair of experimental aortic aneurysms: does coil embolization with angiographic “seal” lower intraaneurysmal pressure?.
Endoleak after endovascular graft repair of experimental aortic aneurysms: does coil embolization with angiographic “seal” lower intraaneurysmal pressure?.
Fig. 4MPI with type III endoleak in patient-studies (red), animal-studies (green) and in-vitro studies (blue). Type of pressure measurement device is given by (??) unknown, (F) fluid filled or (NF) non-fluid filled device.
Wintzer et al. investigated aneurysm sac pressure in an in-vitro model. They demonstrated that the MPI depended on the presence of outflow from the aneurysm sac and on the pressure inside this outflow channel. In the absence of outflow through collateral vessels the mean pressure in the aneurysm will increase to mean pressure of the systemic circulation. However, type III endoleak with free outflow without resistance through the open inferior mesenteric artery (IMA) resulted in an aneurysm sac pressure of 0 mmHg. In the presence of the IMA, with a pressure of 100 mmHg, the aneurysm sac pressure appeared to be 96 mmHg.
Furthermore, Mehta et al. demonstrated that the aneurysm sac pressure is equivalent to that of the systemic circulation if a type III endoleak and lumbar outflow are present. In the presence of type III endoleak without lumbar branch outflow, the aneurysm sac pressure was higher than that of the systemic circulation.
Three studies, one animal (Fig. 5, green line) and two in-vitro studies (Fig. 5, blue lines), are performed to investigate the effect of stent-graft porosity on the aneurysm sac pressure. Although a type IV endoleak was present, the pulse pressure in the aneurysm sac was reduced in all studies.
These studies demonstrate that graft porosity causes systemic pressure in the aneurysm sac (MPI>0.9) (Fig. 5).
Fig. 5MPI with type IV endoleak in patient-studies (red), animal-studies (green) and in-vitro studies (blue). Type of pressure measurement device is given by (F) fluid filled or (NF) non-fluid filled device.
Intra-aneurysm sac pressure measurements after endovascular aneurysm repair: differences between shrinking, unchanged, and expanding aneurysms with and without endoleaks.
Fig. 6MPI with type V endoleak in patient-studies (red), animal-studies (green) and in-vitro studies (blue). Type of pressure measurement device is given by (F) fluid filled or (NF) non-fluid filled device.
Dias et al. measured MPIs in patients with shrinking, stable and expanding aneurysms after EVAR without detectable endoleak. Although the number of patients was too small for definitive conclusion, they associated a MPI above approximately 0.35 with a subsequent AAA expansion.
Intra-aneurysm sac pressure measurements after endovascular aneurysm repair: differences between shrinking, unchanged, and expanding aneurysms with and without endoleaks.
This review demonstrates that the MPI after EVAR without detectable endoleak differ widely between studies. This can be understood since the aneurysm sac pressure is mulitfactorial. The presence of efferent side branches, the size of endoleak, the type of graft, the mechanical properties of the aneurysm wall and the aneurysm volume have been investigated as determinants of aneurysm sac pressure.
Stent-graft deployment, in absence of an endoleak, does not result in immediate reduction of intra-sac pressure of many patients (Fig. 1A).
Since aneurysm sac pressure is a direct determinant of aneurysm wall stress, the risk of aneurysm rupture is not immediately reduced after successful EVAR. Pressure reduction in the aneurysm sac takes some time varying from 1 week to two years in most cases whereas sometimes pressure reduction never takes place (Fig. 1A–D). Theoretically, the aneurysm sac pressure decreases only if there is an outflow or resorption since the aneurysm sac is filled with incompressible material. The rate of pressure reduction depends on the outflow resistance in the efferent vessels and the rate of resorption which is influenced by biochemical factors. Hence it is understandable that time is needed before pressure reduction will take place.
The MPIs in in-vitro studies are lower. This might be explained by misdiagnosing endoleaks in in-vivo studies. However, differences between the in-vitro experimental set-up and the in-vivo situation also contribute to the low MPI in in-vitro studies. In-vitro models are only appropriate to evaluate aneurysm sac pressure after successful EVAR if the stent-graft is deployed in a running artificial circulation. During some in-vitro studies the aneurysm sac was separately filled after deployment of a stent-graft.
Intrasac pressure waveforms after endovascular aneurysm repair (EVAR) are a reliable marker of type I endoleaks, but not type II or combined types: an experimental study.
Of course, the aneurysm sac pressure in this set-up depends on the amount of liquid injected in the aneurysm sac and misrepresents the in-vivo aneurysm sac pressure after successful stent-graft deployment.
Pulse pressure is reduced after EVAR. Persistence of systemic pulse pressure in the aneurysm sac and aneurysm pulsatility have been considered as an important guide to evaluate the success of EVAR.
Aortic side branch perfusion alone does not account for high intra-sac pressure after endovascular repair (EVAR) in the absence of graft-related endoleak.
However, Mehta et al. demonstrated that the aneurysm pulsatility did not correlate with the absolute aneurysm sac pressures, but appeared to be dependent on the presence or absence of side-branch outflow. Therefore, they concluded that aneurysm pulsatility is an unreliable guide to predict aneurysm sac pressurization.
The type of endoleak does not directly correlated to the aneurysm sac pressure, because great differences exist between studies in which identical type of endoleaks are investigated. We will discuss the results of various types of endoleaks separately.
Type I and III endoleak
Type I and III endoleaks are considered as the most dangerous, even if sealing appears to have occurred.
The level of MPIs in Fig. 2, Fig. 4 are probably high enough to contribute to aneurysm sac rupture. These endoleaks are often associated with “systemic” pressure in the aneurysm sac. However, even in the presence of these endoleaks, not every study demonstrates MPIs of 1.0 (Fig. 2, Fig. 4). Differences between studies are probably caused by the presence or absence of outflow from the aneurysm sac. The levels of the MPI are less in the presence of an outflow channel (Fig. 4).
Theoretically, the pressure in the outflow channel influences the aneurysm sac pressure since it determines the outflow resistance. Low outflow resistance enhances its ability to depressurize the aneurysm sac (also in the presence of an endoleak).
Type IV
If the stent-graft is permeable for blood (type IV endoleak), the MPI will be around 1.0 (Fig. 5).
The mechanism of type V endoleaks is still unclear. Endotension may represent a very low flow endoleak that is not visualized with conventional imaging. Risberg et al. described a theory that degradation of aneurysm sac thrombus with formation of proteins and protein particles may cause osmotic pressure.
The management of massive ultrafiltration distending the aneurysm sac after abdominal aortic aneurysm repair with a polytetrafluoroethylene aortobiiliac graft.
Although the pathogenesis of endotension (AAA growth without detectable endoleak) remains unclear, it is hypothesized that an elevated aneurysm sac pressure is a contributory factor.
Intra-aneurysm sac pressure measurements after endovascular aneurysm repair: differences between shrinking, unchanged, and expanding aneurysms with and without endoleaks.
However, elevated aneurysm sac pressure itself is probably not the only explanation for endotension since an increase in sac volume cannot occur without accumulation of more luminal content.
In the presence of a type II endoleak, all patient studies demonstrated a significant pressurization of the aneurysm sac in the first month after EVAR with type II endoleaks (Fig. 3A). However, in view of the fact that the aneurysm sac is not depressurized immediately after EVAR in absence of any endoleak (Fig. 1A), it is not absolutely certain that “systemic” aneurysm sac pressure is caused by the presence of a type II endoleak.
Side-branches can act as afferent (feeding) and efferent (outflow) vessels depending on the pressure gradient between aneurysm sac and side branch.
Aortic side branch perfusion alone does not account for high intra-sac pressure after endovascular repair (EVAR) in the absence of graft-related endoleak.
The pressure did not rise to the levels recorded within the aneurysm after endograft deployment. They suggest that retro-grade perfusion via patent side-branches cannot be the only explanation for maintenance of pressure within the aneurysm sac.
Since the mean aneurysm sac pressure immediately after successful EVAR is similar to the systemic mean pressure (Fig. 1A), the aneurysm sac pressure level is higher than the pressure level in the side branches.
Aortic side branch perfusion alone does not account for high intra-sac pressure after endovascular repair (EVAR) in the absence of graft-related endoleak.
This means that the non-thrombosed side branches of the aneurysm will be efferent vessels immediately after EVAR. The level of aneurysm sac pressure will decrease to the pressure level in the patent side branches.
This pressure reduction probably takes time, as can be derived from literature findings that the MPIs of aneurysms with a type II endoleak more than 1 month after EVAR
First experience in human beings with a permanently implantable intrasac pressure transducer for monitoring endovascular repair of abdominal aortic aneurysms.
Intra-aneurysm sac pressure measurements after endovascular aneurysm repair: differences between shrinking, unchanged, and expanding aneurysms with and without endoleaks.
are generally lower than MPIs measured at an earlier date (Fig. 3A). This is supported by data of the animal studies by Pitton et al., in which is demonstrated that the MPI decreases during the period from 6 weeks to 6 months (Fig. 3B).
Considering these findings, the situation may be comparable immediately after EVAR without endoleak and with type II endoleak; a time interval in both situations is needed before the depressurization of the aneurysm sac takes place. The extent of pressure reduction will be less in the presence of a type II endoleak, because in this situation the aneurysm sac pressure will not decrease beneath the pressure level in the side branch.
Hence, the risk of type II endoleaks depends on the side branch pressure level. Furthermore, pressure level in side branches differs individually from patient to patient which results in different MPIs.
We accept that direct comparison of studies is hampered by different methods of reporting, different measurements of systemic pressure (peripheral or central), different time of measurement and different measuring techniques, but comparison of the material is needed to determine the value of aneurysm sac pressure monitoring during follow-up after EVAR. We took these factors into account to compare the results of different studies in the best possible way.
As mentioned, this review demonstrates that the MPI after EVAR differs between studies in which same type of endoleaks are investigated. Hence the risk of aneurysm rupture and therefore the need for re-intervention could differ per patient. This explains why identical types of endoleaks, as detected by imaging techniques, probably do not have identical clinical relevance. Therefore, continuous aneurysm sac pressure monitoring by wireless pressure sensors could be a valuable tool to estimate the risk of aneurysm rupture.
Unfortunately, aneurysm sac pressure monitoring is probably not that straightforward, because pressure measurements are often performed in a thrombosed aneurysm sac. Differences in pressure readings under identical pressure conditions could occur caused by the thrombus.
Future research is needed to develop accurate methods of aneurysm sac pressure measurements and to evaluate the pitfalls of aneurysm sac pressure monitoring. Furthermore, patient studies with continuous aneurysm sac pressure monitoring are needed to determine the threshold of MPI when re-intervention is necessary to prevent aneurysm rupture.
In conclusion, MPIs differ widely in the presence as well as in absence of an endoleak. MPIs are not specific to the type of endoleak, because the determinants of aneurysm sac pressure are multi-factorial. This implies that the same type of endoleaks, detected by imaging, probably does not cause an identical risk of aneurysm rupture. Wireless aneurysm sac pressure monitoring could be valuable tool during follow-up after EVAR. However, further research is necessary to investigate the pitfalls of aneurysm sac pressure measurements before the clinical relevance of aneurysm sac pressure monitoring can be evaluated.
Acknowledgment
We thank Mrs. Brand-de Heer, Walaeus Library Leiden University Medical Center, for her assistance in developing a systematic search strategy for identification of studies.
References
Parodi J.C.
Palmaz J.C.
Barone H.D.
Transfemoral intraluminal graft implantation for abdominal aortic aneurysms.
Clinical experience of the use of self-fixing synthetic prostheses for remote endoprosthetics of the thoracic and the abdominal aorta and iliac arteries through the femoral artery and as intraoperative endoprosthesis for aorta reconstruction.
Intrasac pressure waveforms after endovascular aneurysm repair (EVAR) are a reliable marker of type I endoleaks, but not type II or combined types: an experimental study.
First experience in human beings with a permanently implantable intrasac pressure transducer for monitoring endovascular repair of abdominal aortic aneurysms.
Intra-aneurysm sac pressure measurements after endovascular aneurysm repair: differences between shrinking, unchanged, and expanding aneurysms with and without endoleaks.
Aortic side branch perfusion alone does not account for high intra-sac pressure after endovascular repair (EVAR) in the absence of graft-related endoleak.
Endoleak after endovascular graft repair of experimental aortic aneurysms: does coil embolization with angiographic “seal” lower intraaneurysmal pressure?.
Treatment of type II endoleaks with a novel polyurethane thrombogenic foam: induction of endoleak thrombosis and elimination of intra-aneurysmal pressure in the canine model.
The development of endotension is associated with increased transmission of pressure and serous components in porous expanded polytetrafluoroethylene stent-grafts: characterization using a canine model.
Relationship between preoperative patency of the inferior mesenteric artery and subsequent occurrence of type II endoleak in patients undergoing endovascular repair of abdominal aortic aneurysms.
Evaluation of the accuracy of a wireless pressure sensor in a canine model of retrograde-collateral (type II) endoleak and correlation with histologic analysis.
Treatment of type II endoleaks after endovascular repair of abdominal aortic aneurysms: translumbar puncture and injection of thrombin into the aneurysm sac.
The management of massive ultrafiltration distending the aneurysm sac after abdominal aortic aneurysm repair with a polytetrafluoroethylene aortobiiliac graft.
EVAR aims at excluding the aneurysm sac from blood flow and systemic pressure. It is surprising the relatively little knowledge gathered on intra-aneurysm sac pressure after EVAR, especially taking into account that EVAR has been introduced 16 years ago. The review done by Hinnen and coworkers on this important subject is therefore greatly appreciated.
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