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  • PAN-Fibrinoid Necrosis / Adventitia
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    1. 1. Renovascular Disease recognition and management Craig A. Thompson, M.D., MMSc. Cardiac and Vascular Interventional Services Dartmouth Hitchcock Medical Center Lebanon, NH
    2. 2. <ul><li>Old Medical Adage : </li></ul><ul><li>“Even a monkey can do angioplasty.” </li></ul>Caveat : It takes a real doctor to decide: <ul><li>What the diagnostic studies do and don’t say </li></ul><ul><li>What to do afterward </li></ul><ul><li>How to address this problem in the context </li></ul><ul><ul><li>of a living, breathing patient </li></ul></ul>Renovascular Disease: The Clinical Perspective <ul><li>When to </li></ul><ul><li>When not to </li></ul><ul><li>In whom </li></ul>
    3. 3. Progress in Renovascular Disease <ul><li>The disease </li></ul><ul><li>Clinical diagnosis </li></ul><ul><li>Laboratory diagnosis / imaging modalities </li></ul><ul><li>Patient selection: who benefits from intervention? </li></ul><ul><li>Limiting contrast-induced nephropathy </li></ul><ul><li>Atheroembolic protection </li></ul><ul><li>Expanding the pool of eligible patients / interventions </li></ul><ul><li>Limiting restenosis </li></ul>
    4. 4. Progress in Renovascular Disease <ul><li>The Disease </li></ul><ul><li>Clinical diagnosis </li></ul><ul><li>Laboratory diagnosis / imaging modalities </li></ul><ul><li>Patient selection: who benefits from intervention? </li></ul><ul><li>Limiting contrast-induced nephropathy </li></ul><ul><li>Atheroembolic protection </li></ul><ul><li>Expanding the pool of eligible patients / interventions </li></ul><ul><li>Limiting restenosis </li></ul>
    5. 5. Etiology of Renal Artery Stenosis <ul><li>Fibromuscular dysplasia </li></ul><ul><li>Atherosclerosis </li></ul><ul><li>Polyarteritis Nodosa </li></ul><ul><li>Radiation-induced </li></ul><ul><li>Takayasu’s arteritis </li></ul>
    6. 6. Defining the Problem <ul><li>RAS is an important cause of secondary hypertension </li></ul><ul><li>Renovascular disease under-appreciated as cause of CRF </li></ul><ul><li>23% of malignant hypertension is the result of renovascular causes </li></ul><ul><li>Not all patients with RAS are hypertensive as a result </li></ul>
    7. 7. What is “medical therapy” for renovascular disease?
    8. 8. Natural History of Renal Artery Stenosis <ul><li>Serial U/S examination of 170 patients with 295 renal arteries </li></ul><ul><li>Exclusion for congenitally absent / occluded / prior PCI / poor window </li></ul><ul><li>Referred for renal U/S for hypertension or renal insufficiency </li></ul><ul><li>Only included in study if not a candidate for immediate revascularization </li></ul><ul><li>U/S evaluation every 6 months until time of intervention </li></ul><ul><li>Duplex evaluation: Peak Systolic Velocity ( PSV ) in proximal, middle, and distal RA and AO </li></ul><ul><li>Yielding the RAR (Renal-to-Aortic Ratio) </li></ul>Caps et al. Circulation 1998; 98:2866-2872.
    9. 9. Natural History of Renal Artery Stenosis Caps et al. Circulation 1998; 98:2866-2872. Role of lipid lowering and Aggressive risk factor modification?
    10. 10. L. Gabriel Navar and L. Lee Hamm
    11. 11. Mark A. Pohl
    12. 12. L. Gabriel Navar and L. Lee Hamm
    13. 13. Progress in Renovascular Disease <ul><li>The Disease </li></ul><ul><li>Clinical diagnosis </li></ul><ul><li>Laboratory diagnosis / imaging modalities </li></ul><ul><li>Patient selection: who benefits from intervention? </li></ul><ul><li>Limiting contrast-induced nephropathy </li></ul><ul><li>Atheroembolic protection </li></ul><ul><li>Expanding the pool of eligible patients / interventions </li></ul><ul><li>Limiting restenosis </li></ul>
    14. 14. Clinical Clues <ul><li>Onset of diastolic hypertension after age 55 </li></ul><ul><li>Refractory or malignant hypertension </li></ul><ul><li>Development of resistant hypertension in a previously well-controlled patient </li></ul><ul><li>Progressive increase in Creatinine, even if still “normal” </li></ul><ul><li>Presence of atherosclerotic macrovascular disease elsewhere heightens suspicion </li></ul><ul><li>Left heart failure out-of-proportion to LV dysfunction or ischemic burden </li></ul><ul><li>Clinically silent RAS </li></ul>
    15. 15. Progress in Renovascular Disease <ul><li>The Disease </li></ul><ul><li>Clinical diagnosis </li></ul><ul><li>Laboratory diagnosis / imaging modalities </li></ul><ul><li>Patient selection: who benefits from intervention? </li></ul><ul><li>Limiting contrast-induced nephropathy </li></ul><ul><li>Atheroembolic protection </li></ul><ul><li>Expanding the pool of eligible patients / interventions </li></ul><ul><li>Limiting restenosis </li></ul>
    16. 16. <ul><li>Clinical syndrome most important in patient selection </li></ul><ul><li>Various diagnostic modalities: </li></ul><ul><ul><li>Serologic markers </li></ul></ul><ul><ul><li>Duplex ultrasound - in experienced hands can predict with great accuracy the presence or absence of significant RAS </li></ul></ul><ul><ul><li>Captopril renal scan - 10-25% false negative </li></ul></ul><ul><ul><li>MR angiography - rare false negatives / common false positives. Equipment/experience dependent </li></ul></ul><ul><ul><li>Contrast angiography </li></ul></ul>Screening for Renovascular Disease
    17. 17. Duplex U/S for Renovascular Disease <ul><li>Prospective Duplex U/S evaluation and Renal Angiography in 102 pts </li></ul><ul><li>Goal : Validate renal artery U/S as a viable non-invasive modality </li></ul><ul><li>Drawbacks : </li></ul><ul><ul><li>Time and labor intensive </li></ul></ul><ul><ul><li>Technologist dependent </li></ul></ul><ul><ul><li>Not available </li></ul></ul><ul><ul><li>NPO </li></ul></ul><ul><ul><li>Requires a cooperative patient </li></ul></ul>Olin et al. Ann Intern Med. 1995; 122:833-838 . No signal No signal Occlusion > 3.5 < or > 180 cm/sec > 60% < 3.5 > 180 cm/sec < 60% < 3.5 < 180 cm/sec Normal RAR Renal PSV Degree Stenosis
    18. 18. MRA & Contrast Angiography
    19. 19. Screening Aortography RN LN
    20. 20. Progress in Renovascular Disease <ul><li>The Disease </li></ul><ul><li>Clinical diagnosis </li></ul><ul><li>Laboratory diagnosis / imaging modalities </li></ul><ul><li>Patient selection: who benefits from intervention? </li></ul><ul><li>Limiting contrast-induced nephropathy </li></ul><ul><li>Atheroembolic protection </li></ul><ul><li>Expanding the pool of eligible patients / interventions </li></ul><ul><li>Limiting restenosis </li></ul>
    21. 21. What Are the Goals of Treatment for RAS? <ul><li>Control hypertension </li></ul><ul><li>Aid in medical management </li></ul><ul><li>Prevent deterioration in renal function </li></ul><ul><ul><li>Forestall need for dialysis </li></ul></ul><ul><ul><li>Defer death and disability </li></ul></ul>
    22. 22. Hypertension and RAS <ul><li>Among 152 patients with Unilateral or Bilateral RAS undergoing surgical revascularization: </li></ul><ul><li>90% had improvement in BP control </li></ul><ul><li>Only 15% had “cure” of hypertension </li></ul><ul><li>Among 20 published series of PCI for atherosclerotic renal artery disease: </li></ul><ul><li>54% had improvement in hypertension </li></ul><ul><li>9% had “cure” of hypertension </li></ul>Hansen et al. J Vasc Surg 1992;16;319-31.
    23. 23. Chronic Renal Insufficiency and RAS Who Benefits From Revascularization? <ul><li>Trial of 51 patients with Creat>2.0 before revascularization with >75% Bilateral RAS: </li></ul><ul><li>67% had improvement in renal function </li></ul><ul><li>27% had stabilization in renal function </li></ul><ul><li>Only 6% had worsening in renal function </li></ul><ul><li>No demonstrated impact upon mortality </li></ul>Novick et al. J Urol 1983; 129:907-12 .
    24. 24. Experimental Data supporting Stenting for Preservation of Renal Function <ul><li>61 vessels in 31 patients with “global” obstructive atherosclerotic renal disease </li></ul><ul><li>All with chronic renal insufficiency (Creat 1.5 – 4.0) </li></ul><ul><li>Stenting with non-articulated Palmaz stents </li></ul><ul><li>Follow-up Renal U/S, Serum Creat , BP measurements: </li></ul><ul><li>- Improvement in reciprocal slope of serum creatinine </li></ul><ul><li>- Improved BP control (SBP from 170 ±21 Pre-stent vs. 148 ±15mmHg Post-stent; p<0.001) </li></ul><ul><li>- Restenosis (>50%) in only 1 of 61 vessels </li></ul><ul><li>- Stabilization of pole-to-pole renal dimension </li></ul>Watson et al. Circulation. 2000; 102:1671-1677.
    25. 25. Renal Artery Stenting pre post
    26. 26. Global Renal Revascularization
    27. 27. Watson et al. Circulation. 2000; 102:1671-1677.
    28. 28. Watson et al. Circulation. 2000; 102:1671-1677.
    29. 29. Dutch Renal Artery Stenosis Intervention Cooperative Study <ul><li>Results : </li></ul><ul><li>BP same in both groups </li></ul><ul><li>Fewer meds (2.1 vs. 3.2) in the PTA vs. Medical group </li></ul><ul><li>Renal function similar between groups </li></ul><ul><li>Study Design : </li></ul><ul><li>106 hypertensive patients with RAS (>50%) and Creat<2.3 mg/dl </li></ul><ul><li>PTA vs. Medical rx with follow-up of BP/meds/ renal fxn </li></ul><ul><li>at 3&12 mths </li></ul><ul><li>Shortcomings : </li></ul><ul><li>Crossover of patients from medical-to-PTA </li></ul><ul><li>No stents </li></ul><ul><li>Is 50% stenosis physiologically significant? </li></ul><ul><li>Pts with elevated creatinine excluded </li></ul><ul><li>Is the goal of renal artery revascularization improvement in BP control? </li></ul>N Engl J Med 2000; 342:1007-14
    30. 30. Resistive Index Predicts Fate of Renal Function Radermacher et al. NEJM 2001 344: 410-17 Resistive Index PSV - MEDV PSV ( ) =
    31. 31. Factors That Predict Failure Radermacher et al. NEJM 2001; 344: 410-417.
    32. 32. Progress in Renovascular Disease <ul><li>The Disease </li></ul><ul><li>Clinical diagnosis </li></ul><ul><li>Laboratory diagnosis / imaging modalities </li></ul><ul><li>Patient selection: who benefits from intervention? </li></ul><ul><li>Limiting contrast-induced nephropathy </li></ul><ul><li>Atheroembolic protection </li></ul><ul><li>Expanding the pool of eligible patients / interventions </li></ul><ul><li>Limiting restenosis </li></ul>
    33. 33. Options: Contrast minimizing maneuvers Use of low-osmolar, non-iodinated contrast CO2 Angiography Gadolinium contrast Mucomyst (Acetylcysteine) Selective DA-1 agonists HOCM may increase cellular injury when potentiated by hypoxemia c/t LOCM Useful for localization > Anatomic definition -Gadopentatate dimeglumine -Renally cleared by GF -Not nephrotoxic to 0.4mmol/kg -Changing kV may improve image quality AC and hydration reduce Creatinine > hydration alone in CT with CRI (2% vs 21%) May decrease incidence of RCN vs. historical controls (4.7% vs 18.8%)
    34. 34. Progress in Renovascular Disease <ul><li>The Disease </li></ul><ul><li>Clinical diagnosis </li></ul><ul><li>Laboratory diagnosis / imaging modalities </li></ul><ul><li>Patient selection: who benefits from intervention? </li></ul><ul><li>Limiting contrast-induced nephropathy </li></ul><ul><li>Atheroembolic protection </li></ul><ul><li>Expanding the pool of eligible patients / interventions </li></ul><ul><li>Limiting restenosis </li></ul>
    35. 35. Guarding Against Atheroembolism <ul><li>Meticulous “no touch” technique </li></ul><ul><li>Use of low profile, atraumatic catheters </li></ul><ul><li>Limited catheter manipulation </li></ul><ul><li>Primary stenting when feasible </li></ul><ul><li>GP 2b3a Antagonists </li></ul><ul><li>Distal protection devices </li></ul>
    36. 36. Distal Atheroembolic Protection: The Ideal Capture all debris Continued renal perfusion during procedure Limitless reservoir Atraumatic to vessel wall Technically easy to use Low profile Trackable
    37. 37. Pathology of Atheroembolism <ul><li>Plaque / cholesterol </li></ul><ul><li>Endothelial cells </li></ul><ul><li>Platelet-Fibrin Thrombi </li></ul><ul><li>Calcified tissue </li></ul>
    38. 38. Evolution of Distal Protection Devices <ul><li>Initially used in the treatment of patients with coronary bypass graft disease </li></ul><ul><li>These interventions commonly plagued by angiographic “ No Reflow ” phenomenon </li></ul><ul><li>Cardiac enzyme leak </li></ul><ul><li>Clinical myocardial infarction </li></ul><ul><li>Long attributed to RBC lysis and platelet activation with resultant microvascular spasm </li></ul>
    39. 39. Initial Reports: Atheroembolic Protection <ul><li>“ Percusurge Guardwire” </li></ul><ul><li>47% of patients with SVG intervention had gross, macroscopic evidence of red-yellow debris </li></ul><ul><li>An additional 20% of patients had evidence of microscopic debris </li></ul>Carlino et al.Circulation 1999; 99: 3221-3223
    40. 40. SAFER Trial <ul><li>Randomized comparison of SVG lesions treated +/- PercuSurge Guardwire </li></ul><ul><li>Improved outcomes : 42% decrease MACE </li></ul><ul><li>Lower laboratory MI’s </li></ul><ul><li>Safe </li></ul><ul><li>High procedural success </li></ul>Baim et al. Circulation 2002 .
    41. 41. Distal Protection in Renovascular Disease: An Opportunity <ul><li>Most RAS caused by atheromatous disease </li></ul><ul><li>Ostial / proximal segments of disease are common </li></ul><ul><li>Kidney will tolerate longer balloon occlusion time than coronary / cerebral circulation </li></ul><ul><li>Atheroembolism has long been viewed as a major risk / complication of percutaneous intervention of the renal arteries. </li></ul>
    42. 42. FILTER DEVICES OCCLUSION DEVICES Preserve flow Limit Ischemic Time More complete capture Small debris Vascular Injury No antegrade flow Prolonged Ischemic Time Vascular Injury Shoulder Regions + -
    43. 43. FILTER DEVICES Cordis
    44. 44. OCCLUSION DEVICES
    45. 45. Atheroembolization Protection <ul><li>Percusurge Guardwire </li></ul><ul><li>Traverse </li></ul><ul><li>Inflate </li></ul><ul><li>Intervene </li></ul><ul><li>Embolectomize </li></ul>
    46. 46. Early Experience: Distal Protection in Renovascular Intervention <ul><li>28 patients with 32 renal arteries </li></ul><ul><li>29 Lesions ostial location </li></ul><ul><li>100% Technical success with GuardWire </li></ul><ul><li>Visible debris aspirated: 100% cases </li></ul><ul><li>Mean RA occlusion time: 6.55 min (2.29-13.21 min) </li></ul><ul><li>Creatinine post-procedure and at follow-up stable or improved in all cases. </li></ul>Conclusion : Distal protection against atheroembolism is feasible and safe But is it effective? Henry et al.J Endovasc Ther 2001; 8(3): 227-37.
    47. 47. Characterization of Debris <ul><li>Characterize debris in carotid intervention </li></ul><ul><li>Can we extrapolate to renal artery intervention? </li></ul><ul><li>Both atheromatous </li></ul><ul><li>Similar patient population </li></ul>Tuber et al.Circulation 2001; 104: 2791-6 .
    48. 48. Characterization of Debris Tuber et al.Circulation 2001; 104: 2791-6 . What type of debris was not captured? Why did complications still occur?
    49. 49. Characterization of Debris Tuber et al.Circulation 2001; 104: 2791-6.
    50. 50. CO2 Aortogram RRA Splenic A LRA
    51. 51. Gadolinium Renal Angiogram R No trans-lesional gradient with 5F catheter
    52. 52. Gadolinium Renal Angiogram IVUS with 87% stenosis c/t reference vessel L 60mmHg gradient with 4F catheter
    53. 53. Gadolinium Renal Angiogram With PercuSurge
    54. 54. RESIST Trial Study Design : Multicenter, randomized trial of renal PTA/Stent +/- Distal atheroembolic protection (Cordis Angioguard XP) +/- Anti-platelet therapy with 2b 3a antagonist (Reopro) Endpoints : 1) Renal function as measured by - Nuclear renal scan with DTPA - GFR estimated by Iohexol clearance - Serum Creatinine 2) Bleeding complications 3) Microscopic assessment of atheromatous debris within the Angioguard XP PI : Christopher J. Cooper, M.D. Medical College of Ohio
    55. 55. Progress in Renovascular Disease <ul><li>The Disease </li></ul><ul><li>Clinical diagnosis </li></ul><ul><li>Laboratory diagnosis / imaging modalities </li></ul><ul><li>Patient selection: who benefits from intervention? </li></ul><ul><li>Limiting contrast-induced nephropathy </li></ul><ul><li>Atheroembolic protection </li></ul><ul><li>Expanding the pool of eligible patients / interventions </li></ul><ul><li>Limiting restenosis </li></ul>
    56. 56. What are the benefits of PCI over Surgical revascularization? <ul><li>Shortened hospital stays </li></ul><ul><li>Reduced post-procedural morbidity / mortality </li></ul><ul><ul><li> (J Vasc Surg 1994; 20: 76-87) </li></ul></ul><ul><ul><li>Early graft failure 5% </li></ul></ul><ul><ul><li>Peri-operative mortality 5.6% </li></ul></ul><ul><ul><li>43% of patients required aortic grafting </li></ul></ul><ul><li>Comparable procedural success and improvement in renal function </li></ul><ul><li>(J Vasc Surg 1993; 18:841-52) </li></ul><ul><ul><li>Procedural success: PTRA 83% vs. Surgery 97% (p=NS) </li></ul></ul><ul><ul><li>Improved or stable renal function: PTRA 83% vs. Surgery 72% (p=NS) </li></ul></ul><ul><li>Broadens pool of patients eligible for revascularization </li></ul>
    57. 57. Benefit of Renal TO Revascularization <ul><li>Surgical revascularization vs. Nephrectomy in 95 patients with 100 Occluded Renal Arteries. </li></ul><ul><li>All patients hypertensive </li></ul><ul><li>88% of patients with renal dysfunction </li></ul><ul><li>Renal function, blood pressure response and survival followed after procedure. </li></ul>Oskin et al. J Vasc Surg 1999. 29 (1):140-149.
    58. 58. Study Results <ul><li>Blood pressure improved in both groups </li></ul><ul><ul><li>87% with nephrectomy </li></ul></ul><ul><ul><li>92% with revascularization (p=NS) </li></ul></ul><ul><li>Only revascularized patients (49%) demonstrated improved glomerular filtration rate (GFR). </li></ul><ul><li>9 revascularized patients were no longer dialysis-dependant </li></ul><ul><li>The absence of a nephrogram or distal reconstitution of the vessel did not preclude revascularization (done in 48% of these cases) </li></ul><ul><li>Selective renal vein renins or nuclear renal scan may be of benefit in guiding therapy </li></ul><ul><li>Renal biopsy may show hyalinization of glomeruli, tubular atrophy, and loss of cortical thickness, but is not an absolute predictor of renal recovery or failure to recover </li></ul>Oskin et al. J Vasc Surg 1999. 29 (1):140-149.
    59. 59. Renal TO: Technical Difficulties <ul><li>Occluded renal artery without collateral filling of distal vessel – still may be a surgical candidate </li></ul><ul><li>Cautious recanalization to avoid perforation </li></ul><ul><li>Acquisition of both indirect and direct evidence of intravascular position. </li></ul><ul><li>Small balloon predilatation </li></ul><ul><li>Minimize iodinated contrast as most patients have significant baseline CRI </li></ul><ul><li>Stenting a must as there is marked elastic recoil and bulky plaque prolapse </li></ul>
    60. 60. DSA Abdominal Aortogram
    61. 61. Abdominal Aortogram: Late Phase
    62. 62. Selective Left Renal Angiogram Early Phase Late Phase
    63. 63. Selective Right Renal Angiogram ?
    64. 64. Selective Right Lumbar Angiogram
    65. 65. Collateral Circulation of The Kidney A. Suprarenal Complex B. Lumbar Complex C. Ureteric Complex D. Capsular Complex
    66. 66. Selective Lumbar Angiogram: Wire Position 0.018” Glidewire 5F Cobra 5F Cobra / 7F IM Guide
    67. 67. Selective Lumbar Angiogram: Wire Position
    68. 68. Angioplasty and Stenting 6 x 18mm Herculink Stent 6.5mm Post-dilatation
    69. 69. Right Renal Angio: Final
    70. 70. Progress in Renovascular Disease <ul><li>The Disease </li></ul><ul><li>Clinical diagnosis </li></ul><ul><li>Laboratory diagnosis / imaging modalities </li></ul><ul><li>Patient selection: who benefits from intervention? </li></ul><ul><li>Limiting contrast-induced nephropathy </li></ul><ul><li>Atheroembolic protection </li></ul><ul><li>Expanding the pool of eligible patients / interventions </li></ul><ul><li>Limiting restenosis </li></ul>
    71. 71. Summary <ul><li>Renovascular disease is an often-unrecognized contributor to: </li></ul><ul><ul><li>Uncontrolled hypertension </li></ul></ul><ul><ul><li>Volume overload </li></ul></ul><ul><ul><li>Chronic and progressive renal failure </li></ul></ul><ul><li>Existing literature allows data-driven decision making , helping clinicians to properly manage their patients with renovascular disease. However, the optimal treatment of patients with unilateral disease or “clinically silent” disease is ill defined. </li></ul><ul><li>New technologies have expanded the pool of patients eligible for percutaneous intervention, and help to limit procedural risk with renal revascularization. </li></ul><ul><li>Atheroembolic distal protection devices are likely to be a mainstay of therapy in the near future. </li></ul><ul><li>Vascular medicine allows cooperation and collaboration across departmental boundaries. </li></ul>

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