Pressure-Sensing Guidewire Analysis in RAS
Adapting this coronary-based technology to optimize “functional” renal artery revascularization could have significant clinical implications.
There exists little controversy regarding the clinical benefits of renal artery (RA) PTA/stenting in hemodynamically significant renal artery stenosis (RAS) in several patient subsets, including (1) those with poorly controlled hypertension on multiple antihypertensive medications or those who are intolerant of medications; (2) patients with ischemic nephropathy for preservation of renal function in the patient demonstrating deteriorating renal function and/or renal size; or (3) patients with coronary ischemia, angina, congestive heart failure, or flash pulmonary edema exacerbated by RAS or renovascular hypertension.1-4 Unfortunately, RA PTA/stenting has shown no objective clinical benefit in 30% to 40% of patients.5,6
Therefore, there is significant controversy in several other aspects of RAS treatment, including (1) the definition and identification of a hemodynamically or physiologically (functional) significant RAS; (2) treatment in unilateral or bilateral moderate (50%-70%) RAS; and (3) any treatment recommendation in RA in-stent restenosis (ISR).5-8 Several reports have documented a decline in renal function after PTA/stenting and high ISR rates (12%-29%), further leading to controversy in treating any RAS patient.9-12 This will continue to be true for ad hoc renal interventions performed during “drive-by” cardiac catheterization until outcomes are predictable, improved, and complications minimized.9-13
Meticulous technique and use of distal protection devices to reduce cholesterol and atherosclerotic emboli, and contrast-induced nephrotoxicity, are important issues related to best outcomes, but there is little consensus on the optimal methods of identifying significant RAS and no consensus correlating anatomic RAS to hemodynamic or physiological (functional) revascularization in RAS.
CURRENT RAS ASSESSMENT
Conventional angiography with or without digital subtraction angiography (CADSA) is still considered the “gold standard,” but it is well known that CADSA has significant limitations.14,15 Multidetector CT angiography (MDCTA) may prove to be more sensitive than CADSA in detecting anatomic RAS, but it is not widely available at this time and provides no functional information.16 Discrete ostial lesions and complex, especially oblique, RA ostial origins are common and add to the difficulty in identifying and quantifying RAS. Patients with RA ISR are increasingly returning for evaluation and treatment, and again, there currently exists no consensus treatment or guidelines regarding diagnosis or repeat revascularization.10,17,18
Translesional systolic pressure gradients (TSPG) have recently been advocated by Rundback et al as a standard guideline for reporting RA revascularization in clinical trials, but limitations have been identified with TSPG determinations with 4-F to 6-F end-hole catheters and the threshold values.15,19 There is no consensus as to the exact degree of RAS or minimal TSPG justifying revascularization, and neither CADSA nor TSPG provide physiological RAS information.14,15 Radionuclide scans, renal vein renin assays, captopril renography, and duplex ultrasound resistive index have been advocated as methods to physiologically assess RAS, but all have significant limitations. Additionally, these methods are infrequently used as physiological or functional measures of RAS and therefore are rarely used for decision making in RA revascularization.20-22
THE PressureWire AND FRACTIONAL FLOW RESERVE
It is becoming increasingly incumbent upon clinicians to identify and document objective indications for treatment based on both anatomic and physiologic parameters and have data to support treatment and predict outcomes. With significant controversy still surrounding RA PTA/stenting, no other vascular territory would benefit more from a method or “tool” that would allow functional revascularization decision making than RAS, much like functional assessment for coronary artery disease in the cath lab. The PressureWire is such a tool that allows acquisition of pressure signals on a .014-inch coronary angioplasty guidewire, eliminating false gradients due to large catheters. Use of the PressureWire and physiologic measurements have been found to be beneficial in percutaneous coronary intervention (PCI) in identifying ischemic (functional) lesions, optimizing stent deployment, and in predicting and improving outcomes.23-28 There are limited data describing the use of the PressureWire in peripheral vascular disease and no validated data reporting the utility in determining the fractional flow reserve (FFR) in RAS (FFRren).29-32
Reports by Pijls, Bech, DeBruyne, and Kern have eloquently described the concept of myocardial FFR (FFRmyo) as an accurate, safe, simple, cost-effective, and lesion-specific invasive index of the functional severity of a coronary artery stenosis that is not affected by the microcirculation or hemodynamic variability.24,26-28 Using reasonable clinical assumptions, we have investigated the use of the FFR concept analogously in indexing the functional severity of RAS. The FFR is defined as the maximal blood flow in the presence of a stenosis divided by the theoretical maximum flow without a stenosis; therefore, a normal value (ratio) is 1.0. The FFR does not directly measure blood flow, but it is the transtenotic pressure across a stenosis measured at peak blood flow after administration of an arteriolar vasodilator and indexed for the aortic driving pressure. Several key concepts are that a stenotic lesion obstructs flow only if a pressure gradient develops across the stenosis with maximal hyperemic arteriolar and microvascular dilation. If there is no pressure gradient, the lesion is not the site of a functional obstruction and PTA/stenting cannot physiologically improve blood flow.
Because flow can be expressed as the ratio of aortic driving pressure to resistance (Rmin), maximal attainable blood flow through the end organ equals the ratio of perfusion pressure (PP) across the end organ (distal RA pressure minus renal venous pressure) and the Rmin. This assumption has been proven true for the heart but remains uninvestigated for the kidney. Using this analogous assumption for the kidney, if there is no RAS, the PP across the RAS/kidney equals Pa – Pv, where Pa = mean aortic pressure and Pv = venous pressure. In RAS, the PP across the kidney has decreased to Pd – Pv, where Pd = hyperemic RA pressure distal to the lesion. Therefore,
FFR = (Pd – Pv) Rmin
(Pa – Pv) Rmin
and, because at maximum RA vasodilation, R is constant and minimal, the Rmin cancel resulting in:
FFR = (Pd – Pv)
(Pa – Pv)
Because Pv is minimal and not increased, the FFR is further simplified:
FFR = Pd
when Pd and Pa are measured simultaneously by a guiding catheter and pressure sensing guidewire after maximum vasodilatation (Figure 1).
THE BENEFITS OF FFRmyo IN PCI:
A POTENTIAL IN RAS
Multiple reports have validated the utilization of FFRmyo, including benefits in identifying functional severity of coronary stenosis, identifying ischemic culprit lesions, facilitating decision making in multivessel coronary artery disease, assessment of intermediate lesions, optimization of PCI stent deployment and outcomes, and in assessing left main disease, ostial lesions, bifurcations, and serial stenosis. Pijls et al demonstrated an FFR <0.75 (the mean pressure distal to the stenotic lesion or <75% of the mean aortic pressure) correlated with functional stenosis and inducible ischemia on exercise testing, thallium scans, and stress echocardiograms.23 Pijls et al also showed that successful PCI in patients with FFR <0.75 relieved symptoms, improved functional class, and reversed ischemia on postprocedural functional stress testing and that PCI in intermediate lesions with FFRmyo >0.75 and worse outcomes than medical therapy alone.23
Hanekamp et al compared quantitative coronary angiography, intravascular ultrasound (IVUS), and FFR to assess optimal PCI stent deployment in 81 patients paired with IVUS and quantitative coronary assessment.25 A concordance was found between FFR/IVUS, IVUS/QCA, and FFR/QCA of 91%, 48%, and 46%, respectively, therefore proposing FFR as a rapid and cheaper alternative to IVUS for optimizing stent deployment and outcomes. Pijls et al analyzed FFR-facilitated, post-PCI outcomes at 6 months and found that FFR was a strong predictor of outcomes, with event rates of 4.9%, 6.2%, 20.3%, and 29.5%, in the post-PCI FFR group >0.85, 0.90 to 0.95, 0.80 to 0.90, and <0.80, respectively (P >.001).26 In a randomized trial, Bech et al determined the appropriateness of PCI in patients with moderate coronary artery disease who did not have documented inducible ischemia and who were referred for PCI. An FFR of < or >0.75 identified those patients who benefited from PCI (<0.75 before and >0.75 after PCI) and proved patients with FFR >0.75 could be safely treated medically.27 Utilizing the proven concepts with the PressureWire in PCI, and considering the recognized limitations with renal PTA/stent, we began a PressureWire safety and feasibility analysis in treating 89 patients with RAS. This analysis in RAS included a comparison between traditional 4-F TSPG, PressureWire-obtained TSPG, FFRren, percent stenosis by MDCTA and CADSA, and an analysis of our clinical decision making in the cath lab based on this anatomic and functional information.
The .014-inch RADI PressureWire is a high-fidelity, solid-state, electronic .014-inch pressure-sensing, coronary angioplasty guidewire with wire characteristics comparable to a conventional high-torque, floppy angioplasty guidewire (Figure 2). The pressure sensor is located 3 cm proximal from the wire tip, allowing ample room for wire manipulation without requiring repeated wire tip crossing. For our RAS TSPG analysis and PressureWire functional analysis, the PressureWire is introduced through a 4-F catheter, and is calibrated and advanced into the RA. The lesion is crossed positioning the sensor distal to the stenosis. The guiding catheter tip is placed 5 mm to 10 mm into the aorta (away from the renal ostium) and the sensor tip is placed 3 mm to 5 mm distal to the lesion. A resting PressureWire TSPG is first analyzed with the signal RADI analyzer by recording the peak-to-peak systolic pressure difference between the pressure sensor located distal to the lesion and the guiding catheter tip placed well into the aorta. The 4-F guiding catheter is then placed across the lesion and a traditional pull-back, peak-to-peak systolic TSPG is recorded as the catheter is pulled back 5 mm to 10 mm into the aorta (Figure 3).
We used papaverine as our provocative (hyperemic vasodialation) agent because it is known as a potent peripheral arterial vasodilator. To date, there are no published data using papaverine in RAS or intra-arterial RA injection. In our initial experience, we used 30 mg of papaverine because it was a familiar surgical dose used safely in the OR (internal mammary artery preparation during CABG, intra-arterial SFA, or popliteal artery injection during thromboembolectomy). Recently, we have found a 20-mg papaverine injection to be effective, and this is now our routine provocation dose for PressureWire TSPG and FFRren. The RA injection is made as a rapid hand-held 20-mg injection of papaverine in 10 mL of saline. The renal ostia is engaged with the guiding catheter, and we avoid totally crossing the lesion to minimize catheter manipulation at the ostia and lesion. The catheter is immediately pulled back into the aorta for PressureWire TSPG determination because the papaverine response occurs within 5 to 15 seconds. DeBruyne has also found 20 mg of papaverine to be equivalent to adenosine (40 µg/kg per min) for FFRmyo.33 There was no difference in clinical response between 20 mg and 30 mg of papaverine intra-arterial injection. Mixing papaverine and heparin must be avoided to eliminate precipitation.
For FFRren analysis, baseline Pa and Pd measurements are obtained and recorded by the RADI analyzer. RA vasodilatation is performed by an intra-arterial injection of 20 mg of papaverine. Simultaneous phasic and mean aortic and distal RA pressures are monitored and FFRren is calculated as the ratio of Pd/Pa at maximal hyperemic vasodilation. If renal revascularization is performed, a postprocedural Pressurewire TSPG and FFRren is performed (as described previously) and recorded.
Questionnaire and Decision Making
A simple questionnaire was completed in our 89 RAS cases by the treating clinician assessing the influence of this information on immediate procedural decision making comparing the actual procedure performed with the clinician’s best-predicted planned procedure. The clinician was first asked the best prediction of the treatment (stent or no stent) before the PressureWire analysis. The clinician was then asked (A) Did the TSPG or FFRren significantly influence procedure decision making? (yes/no). And, if yes, (B) stenting? (yes/no) or no stenting? (yes/no). Twenty-nine of 89 (32.5%) reported, “yes, this information significantly influenced decision making.” Nineteen of 89 (21.3 %) reported “stented or added a stent,” in cases in which they did not predict a stent would be used. A significant procedural decision-making change was seen most often in patients with a moderate RAS identified on MDCTA or during a previous CADSA in which the RAS was estimated to be 50% to 70%. In these 19 patients, the clinician performed RA PTA/stenting in lesions believed to be significant only after papaverine provocation and a TSPG was found to be >20 mm Hg. In five cases, a >10 mm Hg TSPG found immediately after PTA/stent occurred and resulted in identification of three missed ostia and two underdeployed stents. Each case was corrected immediately and resulted in postprocedural TSPGs <5 mm Hg. IVUS was not routinely performed in this analysis. In 10 of 89 cases (11.2%), a stent was not deployed when resting and postprovocation TSPGs were <20 mm Hg in cases in which the CADSA or MDCTA had predicted >60% to 70% stenosis.
There were no PressureWire or papaverine-related complications. Eighty-nine patients had 4-F catheter and PressureWire TSPG analysis with FFRren and were compared to CADSA. Additionally, 48 of 89 patients (56.4%) were compared to MDCTA. CADSA and MDCTA percent stenosis did not strongly correlate to 4-F catheter TSPG (r2 = 0.224) but did correlate strongly with PressureWire TSPG (r2 = 0.610). A FFRren of <0.75 did not strongly correlate with CADSA (r2 = 0.210), MDCTA (r2 = 0.191), or 4-F catheter TSPG (r2 = 0.246), raising the issue that the current FFRmyo concept may be inappropriate in the renal vasculature (FFRren).
To Stent? Or Not to Stent?
The identification and decision to treat moderate-to-intermediate angiographically significant RAS (60%-70% stenosis or ≥50% luminal diameter reduction) is not always straightforward considering the known limitations of CADSA, MDCTA, and TSPG. These intermediate lesions may be functionally significant. No consensus exists as to the minimal TSPG required to treat RAS, and there is a lack of data available to use as a guideline for treatment. Earlier RA PTA/stent trials accepted ≥5 mm Hg transcatheter TSPG to define a suboptimal/failed PTA requiring stenting. A ≥20 mm Hg TSPG has been recently proposed for RAS clinical trials, but this may be an arbitrary number without any physiological basis.19 Considering the lack of a consensus RAS treatment guideline, we currently use >20 mm Hg TSPG, resting or after injection of 20 mg of papaverine, as an indication to primarily treat RAS and <5 mm Hg PressureWire TSPG post-PTA/stent to define our procedural success and rule out missed lesions, dissections, or stent underdeployment.
More than 30% of our cases experienced major clinical decision changes after papaverine provocation, with approximately 20% stented and 10% not stented in cases in which these treatments were not definitely planned. The PressureWire potentially helped identify those patients who have angiographically moderate but functionally significant RAS who would not be offered PTA/stenting who “functionally” need it, and therefore should receive functional benefit from PTA/stenting. Conversely, the PressureWire may have the potential to identify those patients who are not likely to clinically benefit from RA PTA/stenting, therefore not exposing them to the 12% to 29% RA ISR rates and the current 30% to 40% of RAS patients not receiving clinical benefit after RA PTA/stenting. Long-term clinical follow-up will be required to answer these questions.
In our analysis, 12 of 89 (13.5%) had RA ISR, and identifying and treating this ISR patient population is problematic. Traditional CADSA has significant limitations in diagnosing RA ISR, but MDCTA allows improved imaging, and curved coronal imaging and flow probing software have allowed more accurate assessment in RA ISR.16 Treatment for RA ISR is not defined with results of PTA only or restenting reporting approximately 50% restenosis rates.17,18,30,34-36 We now use 4-quadrant excimer laser atheroablation as our treatment of choice in RA ISR patients and we now use the PressureWire to gauge the number of laser catheter passes required to achieve our goal of a TSPG of <5 mm Hg. This technique has decreased our need for aggressive repeat high-pressure PTA and the need for repeat stenting (stent sandwich) (Figure 4). We recently reported this technique in 25 RA ISR patients with a 92% procedural success rate and a 10% 6-month >50% restenosis rate as determined by duplex ultrasound.36
Optimizing Renal Stent Deployment
RA ISR has been reported in 12% to 29% of cases and is dependent on vessel size, minimal luminal diameters (MLD) or acute procedural gain after stent placement, and optimal stent deployment technique.12 Lederman et al reported MLD after RA PTA/stent and vessel size correlated with clinical outcomes and reported RA ISR rates of 36%, 15.8%, and 6.5% for vessels <4.5 mm, 4–6 mm, and >6 mm, respectively.12 Suboptimal stent expansion, missed ostial lesions, and unrecognized distal dissections are all implicated in increased RA restenosis rates and potentially could be identified periprocedurally by TSPG and/or FFRren, allowing for immediate correction and optimized outcomes similar to the reports in PCI by Hanekamp et al and Pijls et al.23,25 This study has confirmed the work of Colyer et al and identified the PressureWire TSPG to be more accurate than 4-F catheter TSPG, therefore highlighting the known limitation of measuring TSPG with guiding catheters.19
The 4-F catheter TSPG method is still advocated as a practice guideline and is used in clinical trials.19 Although we were unable to identify a strong correlation between FFRren and TSPG, we found the PressureWire TSPG to highly correlate with CADSA and MDCTA and to be a simple and accurate means to document intraprocedure treatment decisions both before and after stenting. The >30% rate of influence on clinical decision making seen in our 89 patients is the first published data accessing intraprocedure decision making in treating RAS. We now use PressureWire analysis for decision making in treating celiac and superior mesenteric artery disease and we are investigating other utilizations in peripheral vascular disease. Similar to RAS, treating visceral arterial disease is limited by diagnostic imaging accuracy, identification of functional stenosis, and high ISR rates.37
This small single-center study has shown the safety and feasibility of using the PressureWire in accessing RAS but has not provided clinical follow-up or demonstrated clinical efficacy and will require long-term multicenter validation. This study has not unraveled the conundrum between assessing RAS by objective imaging, TSPG, identification of functional RAS, and correlation between RAS, clinical manifestations, and outcomes. This study is, however, a first step in providing insight into optimizing functional renal revascularization. The lack of a correlation between the clinical usefulness of the FFRmyo <0.75 and an analogous FFRren validation in this report should not be surprising because extrapolating experience from PCI and the coronary bed into the renal artery bed is likely not that simple, further underscoring the differences in coronary artery disease and peripheral vascular disease. This study has confirmed that pressure gradients (TSPG) obtained by PressureWire measurements are more accurate in identifying anatomic RAS than gradients obtained by catheter measurements, MDCTA, or CADSA imaging.
The many current limitations in assessing and treating RAS and the proven PCI benefits of FFRmyo are compelling reasons to further pursue PressureWire investigations in peripheral vascular disease and identify the keys to developing a FFRren analogous to FFRmyo. The potential benefits of FFRren in RAS, if analogous to the benefits of FFRmyo in PCI, would have significant clinical implications (Table 1). We now recommend the RADI PressureWire analysis on all RAS cases utilizing a PressureWire TSPG of >20 mm Hg (resting or after papaverine injection) as objective documentation to treat. Our goal is to achieve ≤5 mm Hg PressureWire gradient (resting and postprovocation) after PTA/stenting to define optimal treatment. We now rely heavily on PressureWire TSPG, not catheter gradients or angiography, in our clinical decision making during RAS treatment. It is now time to reproduce the elegant work by Pijls, DeBruyne, Bech, and Kern in PCI and FFRmyo in peripheral arterial disease, and validate an analogous renal model with a goal to provide more optimal functional revascularization in RAS and other peripheral vascular beds, including celiac, mesenteric, and infrainguinal arterial disease.
David E. Allie, MD, is Director of Cardiothoracic and Endovascular Surgery at the Cardiovascular Institute of the South in Lafayette, Louisiana. He has disclosed that he holds no financial interest in any product or manufacturer mentioned herein. Dr. Allie may be reached at (800) 582-2435; David.Allie@cardio.com.
Chris J. Hebert, RT, RCIS, is Director of Cardiovascular Services at the Cardiovascular Institute of the South in Lafayette, Louisiana. He has disclosed that he holds no financial interest in any product or manufacturer mentioned herein. Mr. Hebert may be reached at (800) 582-2435; Chris.Hebert@cardio.com.
Craig M. Walker, MD, is Medical Director and Founder, Cardiovascular Institute of the South in Houma, Louisiana. He has disclosed that he holds no financial interest in any product or manufacturer mentioned herein. Dr. Walker may be reached at (800) 445-9676; Craig.Walker@cardio.com.
1. Bush RL, Najibi S, MacDonald MJ, et al. Endovascular revascularization of renal artery stenosis: technical and clinical results. J Vasc Surg. 2001;33:1041-1049.
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4. Henry M, Amor M, Henry I, et al. Stents in the treatment of renal artery stenosis: long-term follow-up. J Endovasc Surg. 1999;6:42-51.
5. Burket M, Cooper C, Kennedy D, et al. Renal artery angioplasty and stent placement: predictors of a favorable outcome. Am Heart J. 2000;139:64-71.
6. Harden P, MacLeod M, Rodger R, et al. Effect of renal-artery stenting on progression of renovascular renal failure. Lancet. 1997;349:1133-1139.
7. Dorros G, Jaff M, Mathiak L, et al. A four-year follow-up of Palmaz-Schatz stent revascularization as treatment for atherosclerotic renal artery stenosis. Circulation. 1998;98:642-647.
8. Pickering TG, Devereaux RB, James GD, et al. Recurrent pulmonary edema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or surgical revascularization. Lancet. 1998;9:551-552.
9. Perkovic V, Thomson KR, Mitchell PJ, et al. Treatment of renovascular disease with percutaneous stent insertion: long-term outcomes. Australas Radiol. 2001;45:438-443.
10. Shammas NW, Kapalis MJ, Dippel EJ, et al. Clinical and angiographic predictors of restenosis following renal artery stenting. J Invasive Cardiol. 2004;16:10-13.
11. Dorros G, Jaff M, Jain A, et al. Follow-up of primary Palmaz-Schatz stent placement for atherosclerotic renal artery stenosis. Am J Cardiol. 1995;75:1051-1055.
12. Lederman RJ, Mendelsohn FO, Santos R, et al. Primary renal artery stenting: characteristics and outcomes after 363 procedures. Am Heart J. 2001;142:314-323.
13. White CJ. Renal artery disease: facts and myths. Endovasc Today. 2003;2:52-58.
14. Roach-Singh K. Aortorenal artery translesion pressure gradients in renovascular hypertension: in search of clinical significance. Cathet Cardiovasc Intervent. 2003;59:378-379.
15. Colyer WR, Cooper CJ, Thomas WJ, et al. Utility of a 0.014” pressure-sensing guidewire to assess renal artery translesional systolic pressure gradients. Cathet Cardiovasc Intervent. 2003;59:372-377.
16. Allie DE, Hebert CJ, Walker CM, et al. Multidetector computed tomography angiography. Endovasc Today. 2004;3(3):1-8.
17. Mali BL, Van De Ven PJ, et al. Repeated intervention for in-stent restenosis of the renal arteries. J Vasc Intervent Radiol. 2002;13:1219-1224.
18. Munneke GJ, Engelke C, Belli AM, et al. Cutting balloon angioplasty for resistant renal artery in-stent restenosis. J Vasc Intervent Radiol. 2002; 13: 327-331.
19. Rundback J, Sacks D, Kent K, et al. Guidelines for the reporting of renal artery revascularization in clinical trials. J Vasc Intervent Radiol. 2002;13:959-974.
20. Radermacher J, Chavan A, Haller H, et al. Use of a Doppler ultrasonography to predict the outcome of therapy for renal-artery stenosis. N Engl J Med. 2001;344:410-417.
21. Leung D, Hoffman U, Debatin J, et al. Magnetic resonance imaging versus duplex sonography for diagnosing renovascular disease. Hypertension. 1999;33:726-731.
22. Bongers V, Bakker J, De Klerk J, et al. Assessment of renal artery stenosis: comparison of captopril renography and gadolinium-enhanced breath-hold MR angiography. Clin Radiol. 2000;55:346-352.
23. Pijls NHJ, De Bruyne B, Koolen JJ, et al. Measurement of fractional flow reserve to assess the functional severity of coronary artery stenosis. N Engl J Med. 1996;334:1703-1708.
24. De Bruyne B, Piljs N, Wijns W, et al. Fractional flow reserve in patients with prior myocardial infarction. Circulation. 2001;Dec:157-162.
25. Hanekamp CE, Koolen JJ, Bonnier H, et al. Comparison of quantitative coronary angiography, intravascular ultrasound, and coronary pressure measurement to assess optimum stent deployment. Circulation. 1999;99:1015-1021.
26. Piljs NHJ, Klauss V, De Bruyne B, et al. Coronary pressure measurement after stenting predicts adverse events at follow-up: a multicenter registry. Circulation. 2002;105:2950-2954.
27. Bech G, De Bruyne B, Wijns W, et al. Fractional flow reserve to determine the appropriateness of angioplasty in moderate coronary stenosis: a randomized trial. Circulation. 2001;103:2928-2934.
28. Kern MJ, Donohue TJ, Aguirre FV, et al. Clinical outcome of deferring angioplasty in patients with normal translesional pressure-flow velocity measurements. J Am Coll Cardiol. 1995;25:178-187.
29. van der Hulst VP, van Baalen J, Kool LS, et al. Renal artery stenosis: endovascular flow wire study for validation of Doppler ultrasound. Radiology. 1996;200:165-168.
30. Nahman NS, Maniqm P, Hernandez RA, et al. Renal artery pressure gradients in patients with angiographic evidence of atherosclerotic renal artery stenosis. Am J Kidney Dis. 1994;24:695-699.
31. Privat C, Ravel A, Chirossel P, et al. Endovascular Doppler guide wire in renal arteries: correlation with angiography in 20 patients. Invest Radiol. 1999;34:530-535.
32. Gross CM, Kramer J, Weingartner O, et al. Determination of renal arterial stenosis severity: comparison of pressure gradient and vessel diameter. Radiology. 2001;220:751-756.
33. De Bruyne B, Pijls NHJ, Wijns W, et al. Intracoronary and intravenous (central vs. peripheral) administration of ATP and adenosine to induce maximal coronary vasodilatation [abstract]. Circulation. 1999;100(Suppl I):I-376.
34. Bax LM, Mali WP, Beek FJ, et al. Repeated intervention for in-stent restenosis of renal arteries. J Vasc Intervent Radiol. 2002;13:1219-1224.
35. Blum U, Krumme B, Flugel P, et al. Treatment of ostial renal-artery stenosis with vascular endoprostheses after unsuccessful balloon angioplasty. N Engl J Med. 1997;336:459-465.
36. Walker CM, Hebert CJ, Lirtzman MD, et al. Renal artery in-stent restenosis: early results with excimer laser atheroablation. Poster 17th International Congress on Endovascular Interventions, Scottsdale, Arizona, February 8-12, 2004. J Endovasc Ther. 2004; 11: I1-I47; I43.
37. Matsumo AH, Angle JF, Spinosa DJ, et al. Percutaneous transluminal angioplasty and stenting in chronic mesenteric ischemia: results and long term follow-up. J Am Coll Surg. 2002;194:Suppl 1:522-531.s considered feasible in the majority of cases,1-11 with a low procedural complication rate.14 Most reports on endovascular stent revascularization of renal artery stenosis resulted in improved blood pressure control.16-19 Survival after successful stenting for severe ostial renal artery stenosis depends on baseline serum creatinine and left ventricle function. Efforts must be made to avoid the development of advanced ischemic nephropathy and congestive heart failure.20
Discrepant results on the effect of stent angioplasty of renal artery stenosis on renal function have been published.16-19 Transient renal dysfunction after renal artery angiography or PTRA/stenting occurs in approximately 15% of patients, but persistent renal failure is uncommon. Pre-existing renal impairment and amount of contrast agent are independent risk factors. Endovascular treatment of renal artery stenosis is not associated with a higher risk of renal deterioration compared to selective renal angiography.6
An acceptable renal in-stent restenosis rate is roughly 13% to 17%. Target vessel diameter is considered to be the only independent predictor for restenosis in the multivariate analysis: the smaller the diameter the higher the restenosis rate.20,21
A definite consensus on renal artery stenting still has not been reached because of a lack of level 1 scientific evidence regarding improvement of renal function after renal artery stenting. The results of ongoing studies may identify subgroups of patients with renal artery stenosis who gain a clear benefit from revascularization. In the meantime, it seems reasonable to attempt revascularization in severe hypertension resistant to medical therapy, rapidly progressive renal failure with no obvious cause other than renal artery stenosis, and recurrent flash pulmonary edema.8
New low-profile devices (dedicated guiding catheters, .014-inch wires, premounted stents with a very low crossing profiles) are more frequently accepted as standard technical equipment for dealing with renal artery stenting, with or without predilatation. Outcome results seem encouraging.1,9-11
Our initial experience with renal direct stenting shows a positive trend in terms of procedural success, complication rate, and in-hospital outcome, as well as 9-month clinical and echo-Doppler follow-up.
Our data are even more encouraging if compared to the results on renal stenting related to a “standard technique subset” homogeneous in terms of inclusion criteria, exclusion criteria, and materials and methods, and in which the stent delivery was always preceded by balloon lesion predilatation.
Even if no significant statistical difference can be demonstrated between the two study groups, the comparison pointed out some remarkable findings. Similar data have been reported by other groups,1,4-7 but only a few experiences specifically report data on indication, technical management, and outcome results of direct renal stenting. The likely explanation of the good results we report in the subset of renal direct stenting probably lies in patient selection and procedure management.
The technical key points of direct renal stenting are (1) patient selection, (2) atraumatic engagement of dedicated guiding catheter of the renal artery ostium, (3) precise positioning of the low-profile premounted stent, (4) speed and minimum use of devices across the lesion, and (5) reduced need of contrast media.
Despite the encouraging data we report, we do not think renal direct stenting can be applied to all lesions and anatomies. In our study, we only admitted patients and renal lesions to direct renal stenting that complied with the specific inclusion and exclusion criteria.
Any time we determined that direct renal stenting was the strategy of choice, we put into practice an individual treatment strategy based on matching the specific lesion morphology and complexity to the technical features of renal stenting dedicated devices. Echo-Doppler and/or angiographic evidence of diffuse parietal calcifications at the renal lesion site were considered a contraindication to renal direct stenting. In such cases, it could be dangerous to directly implant a balloon-expandable endoprosthesis because the lesion could not be dilated at the balloon delivery burst pressure. If the delivery balloon blows up before achieving the optimal stent expansion, it may be difficult or dangerous to remove the balloon, and the probability of stent migration and loss is not negligible. In cases of very diffuse lesion calcifications, we always try to remodel the calcified plaque before stent implantation with progressive inflations of standard noncompliant balloons or, better, by performing cutting balloon angioplasty.
Long preocclusive lesions (string sign lesion), as well as the appearance of fresh thrombus at the renal lesion site, have to be considered another contraindication to renal direct stenting. In these cases, even if the target lesion can be easily crossed by a .014-inch hydrophilic wire, stent insertion without predilatation could detach soft material and provoke distal embolization.
In our experience, direct renal artery stenting, when performed in a selected population by using dedicated premounted, low-profile, and flexible stents, proved to be as safe and effective as renal stenting conducted by previous lesion dilatation. Direct renal stenting can significantly reduce the need for adjunctive balloon angioplasty after stenting. By using this strategy, we significantly reduced the occurrence of renal artery dissection and the need of adjunctive stents.
Alberto Cremonesi, MD, is from the Interventional Cardio-Angiology Unit, Villa Maria Cecilia Hospital, Cotignola, Italy. He has disclosed that he is a paid consultant for Boston Scientific Corporation. Dr. Cremonesi may be reached at +39 0545 37202; firstname.lastname@example.org.
Fausto Castriota, MD, is from the Interventional Cardio-Angiology Unit, Villa Maria Cecilia Hospital, Cotignola, Italy. He has disclosed that he is a paid consultant for Boston Scientific Corporation. Dr. Castriota may be reached at +39 0545 37202; email@example.com..
Raffaella Manetti, MD, is from the Interventional Cardio-Angiology Unit, Villa Maria Cecilia Hospital, Cotignola, Italy. He has disclosed that he holds no financial interest in any product or manufacturer mentioned herein. Dr. Manetti may be reached at +39 0545 37202; firstname.lastname@example.org.
Armando Liso, MD, is from the Interventional Cardio-Angiology Unit, Villa Maria Cecilia Hospital, Cotignola, Italy. He has disclosed that he holds no financial interest in any product or manufacturer mentioned herein. Dr. Liso may be reached at +39 0545 37202; email@example.com.
Enrico Ricci, MD, is from the Interventional Cardio-Angiology Unit, Villa Maria Cecilia Hospital, Cotignola, Italy. He has disclosed that he holds no financial interest in any product or manufacturer mentioned herein. Dr. Ricci may be reached at +39 0545 37202; firstname.lastname@example.org.
Kareem Oshoala, MD, is from the Interventional Cardio-Angiology Unit, Villa Maria Cecilia Hospital, Cotignola, Italy. He has disclosed that he holds no financial interest in any product or manufacturer mentioned herein. Dr. Oshoala may be reached at +39 0545 37202; email@example.com.
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