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October 17, 2008
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Matthew A. Corriere, Matthew S. Edwards, Jeffrey D. Pearce, Jeanette S. Andrews*, Randolph L. Geary, Kimberley J. Hansen
Wake Forest University Baptist Medical Center, Winston- Salem, NC
Restenosis following renal artery angioplasty and stenting: incidence and risk factors.
Background:
Atherosclerotic renal artery stenosis (RAS) may cause severe hypertension and/or renal dysfunction and is associated with increased risk for cardiovascular events. Patients with atherosclerotic RAS who have poorly controlled hypertension and/or progressive deterioration of renal function despite appropriate medical management may be treated with renal artery revascularization, although the benefits associated with either treatment remain controversial. Renal artery percutaneous angioplasty and stenting (RA-PTAS) has become the most commonly utilized method of renal artery intervention. Unfortunately, restenosis has been reported in 17-28% of arteries following RA-PTAS and may be associated with recurrence of clinical symptoms despite an initial treatment response. Analyses to date have identified associations between restenosis following RA-PTAS and renal artery diameter, stent diameter, weight/body mass index, and smoking. The purpose of this study was to determine the frequency and predictors of restenosis following primary RA-PTAS in a single-center cohort of adult patients with atherosclerotic RAS.
Methods:
Study population: This investigation was conducted with the approval of the Wake Forest University Health Sciences Institutional Review Board. Consecutive primary RA-PTAS procedures performed for hemodynamically significant atherosclerotic renal artery stenosis were identified from a procedure registry. All treated patients had hypertension with or without renal dysfunction, and indications for RA-PTAS were determined by individual operators. RA-PTAS performed for restenosis or fibromuscular dysplasia were excluded from analysis. All procedures were performed by vascular surgeons at the Wake Forest University School of Medicine between October, 2003 and September, 2007. Standard preparation, procedural management, and follow-up for patients treated with RA-PTAS at our center have been described previously. All stents were balloon-mounted and sized to match the diameter of the distal, normal caliber renal artery as measured by angiography at the time of treatment.
Data collection and management: Clinical data was collected from electronic medical records. Renal duplex ultrasound data, including peak systolic velocity (PSV), resistive index, acceleration time, and renal length, were collected from a prospectively maintained clinical vascular laboratory database. Anatomic information was collected from angiograms performed during RA-PTAS by manual electronic caliper measurement of archived images, and all measurements were performed by the same individual (M.C.). Angiographic percent renal artery stenosis was determined by measuring the smallest luminal diameter at the point of maximal stenosis and comparing it with the lumen of the main renal artery distal to the lesion and any post-stenotic dilatation (if present). Estimated glomerular filtration rate (eGFR) was calculated based on serum creatinine using the abbreviated Modification of Diet in Renal Disease formula. Renal dysfunction was categorized as “severe” for patients with an eGFR <30 mL/min/1.73m2, “moderate” for patients with eGFR 30-60 mL/min/1.73m2, and “none” for patients with eGFR>60 mL/min/1.73m2. Renal artery resistive index was calculated from segmental velocities as [1-(end diastolic velocity [[Unsupported Character - ∕]] peak systolic velocity)].
Assessment of restenosis: Hemodynamically significant recurrent renal artery stenosis was identified using duplex ultrasound. Patients were routinely examined with duplex ultrasound immediately post-treatment and subsequently at one, three and six months. Duplex studies were performed using a 5 MHz curvilinear probe with Doppler color flow capability (Philips C5-1 or C5-2; Philips Healthcare, Andover, MA, USA) using a previously described technique. Restenosis was defined as renal artery peak systolic velocity (PSV) ≥ 180 cm/s in an artery previously documented as free of restenosis. This duplex criterion for restenosis has been previously validated by other groups as well as within a cohort of patients from our own institution (Kappa = 0.6, P=0.05 for agreement with angiographic stenosis >60%). Renal artery PSV ≥ 180 at the time of the first post-intervention duplex ultrasound study was considered residual stenosis and not interpreted as restenosis.
Statistical analysis: Data are reported as mean ± standard deviation for continuous variables and count (%) for categorical variables. Baseline comorbid medical conditions, blood pressure, medication use, renal function data, and demographics are reported on a per-patient basis. Comparisons between groups based on restenosis status were performed using two-sample t-tests for continuous variables and Chi-square or Fisher’s exact test for categorical variables. The incidence and temporal distribution of recurrent RAS were analyzed using survival analysis based on treated kidneys, while associations between clinical factors and time to restenosis were examined using Cox proportional hazards regression. Both analyses utilized robust variance estimators to account for correlated observations. Cox proportional hazards regression modeling was performed using stepwise selection (P≤ 0.10 for model entry). Candidate covariates for model selection are listed in Table I. Results were evaluated for significance using α = 0.05.
Results:
Patient sample: Primary RA-PTAS for atherosclerotic RAS was attempted on 112 kidneys during the study period. Of these, eight kidneys were excluded due to residual stenosis on initial post-intervention renal artery duplex, two were excluded due to lack of renal artery duplex follow-up data, and one was excluded due as a technical failure related to inability to access the target renal artery. The remaining 101 kidneys in 91 patients form the basis of this analysis. There were no periprocedural deaths, and distal renal artery balloon occlusion was utilized for embolic protection during 90% of procedures. Mean patient age was 68.8 ± 10.1 years, and all patients had hypertension. Fifty three percent of patients were female and 87% were white. Based on eGFR, moderate or severe renal insufficiency was observed in 72.5% of patients.
Incidence and risk factors of restenosis: Restenosis was identified in 28 renal arteries (28%) in 27 patients at a median post-intervention interval of 5.5 months (inter-quartile range 3.9 - 8.6 months). Proportional hazards regression analysis demonstrated decreased risk for restenosis associated with preoperative statin use (HR 0.35; 95% CI [0.16, 0.74]; P=0.006) and preoperative diastolic blood pressure (DBP) (HR 0.70 per 10mm Hg increase in preoperative DBP; 95% CI [0.49, 0.99]; P=0.049). No other covariates assessed were associated with restenosis-free survival. Predicted restenosis-free survival stratified by statin medication use is displayed graphically in Figure 1.
Clinical manifestations and management of restenosis: Clinical manifestations and management of restenosis are summarized in Table II. 28 recurrent lesions were identified in 27 patients. One patient managed with staged bilateral primary RA-PTAS developed bilateral restenosis, while the remaining restenoses were unilateral. In 17 of 27 patients (63%) with restenosis there were no associated clinical manifestations; in the setting of durable renal function and/or hypertensive responses to RA-PTAS, these patients were managed with continued medical therapy and duplex surveillance. The remaining ten patients (37%) with restenosis identified by duplex ultrasound had associated hypertension and/or decline in eGFR prompting repeat intervention. In these patients, angiography findings confirmed the presence of ≥ 60% diameter-reducing in-stent restenosis in all arteries. Among individuals who underwent repeat intervention for restenosis, procedural management initially consisted of surgical revascularization in one patient and repeat angioplasty in nine; four of the nine repeat angioplasties were performed using cutting balloons. One patient managed with repeat angioplasty developed a second restenosis, and was subsequently treated with aortic endarterectomy plus renal artery bypass. One patient with restenosis was hospitalized for acute hypertensive emergency associated with pulmonary edema and improved clinically with aggressive medical management; following discharge from the hospital, subsequent duplex examination revealed interval progression of the restenosis to occlusion.
Conclusion:
Restenosis following primary RA-PTAS for atherosclerotic RAS is common and may be accompanied by physiologic manifestations. Risk for restenosis is decreased by the use of statins, supporting routine use of these medications in patients undergoing RA-PTAS.
Table I. Candidate covariates for Cox proportional hazards modeling.
Table II. Clinical manifestations and management of restenosis.
*Percentage calculated based on number of patients with clinical manifestations present (N=10)
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Restenosis following Renal Artery Angioplasty and Stenting: Incidence and Risk Factors
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Matthew A. Corriere, Matthew S. Edwards, Jeffrey D. Pearce, Jeanette S. Andrews*, Randolph L. Geary, Kimberley J. Hansen
Wake Forest University Baptist Medical Center, Winston- Salem, NC
Restenosis following renal artery angioplasty and stenting: incidence and risk factors.
Background:
Atherosclerotic renal artery stenosis (RAS) may cause severe hypertension and/or renal dysfunction and is associated with increased risk for cardiovascular events. Patients with atherosclerotic RAS who have poorly controlled hypertension and/or progressive deterioration of renal function despite appropriate medical management may be treated with renal artery revascularization, although the benefits associated with either treatment remain controversial. Renal artery percutaneous angioplasty and stenting (RA-PTAS) has become the most commonly utilized method of renal artery intervention. Unfortunately, restenosis has been reported in 17-28% of arteries following RA-PTAS and may be associated with recurrence of clinical symptoms despite an initial treatment response. Analyses to date have identified associations between restenosis following RA-PTAS and renal artery diameter, stent diameter, weight/body mass index, and smoking. The purpose of this study was to determine the frequency and predictors of restenosis following primary RA-PTAS in a single-center cohort of adult patients with atherosclerotic RAS.
Methods:
Study population: This investigation was conducted with the approval of the Wake Forest University Health Sciences Institutional Review Board. Consecutive primary RA-PTAS procedures performed for hemodynamically significant atherosclerotic renal artery stenosis were identified from a procedure registry. All treated patients had hypertension with or without renal dysfunction, and indications for RA-PTAS were determined by individual operators. RA-PTAS performed for restenosis or fibromuscular dysplasia were excluded from analysis. All procedures were performed by vascular surgeons at the Wake Forest University School of Medicine between October, 2003 and September, 2007. Standard preparation, procedural management, and follow-up for patients treated with RA-PTAS at our center have been described previously. All stents were balloon-mounted and sized to match the diameter of the distal, normal caliber renal artery as measured by angiography at the time of treatment.
Data collection and management: Clinical data was collected from electronic medical records. Renal duplex ultrasound data, including peak systolic velocity (PSV), resistive index, acceleration time, and renal length, were collected from a prospectively maintained clinical vascular laboratory database. Anatomic information was collected from angiograms performed during RA-PTAS by manual electronic caliper measurement of archived images, and all measurements were performed by the same individual (M.C.). Angiographic percent renal artery stenosis was determined by measuring the smallest luminal diameter at the point of maximal stenosis and comparing it with the lumen of the main renal artery distal to the lesion and any post-stenotic dilatation (if present). Estimated glomerular filtration rate (eGFR) was calculated based on serum creatinine using the abbreviated Modification of Diet in Renal Disease formula. Renal dysfunction was categorized as “severe” for patients with an eGFR <30 mL/min/1.73m2, “moderate” for patients with eGFR 30-60 mL/min/1.73m2, and “none” for patients with eGFR>60 mL/min/1.73m2. Renal artery resistive index was calculated from segmental velocities as [1-(end diastolic velocity [[Unsupported Character - ∕]] peak systolic velocity)].
Assessment of restenosis: Hemodynamically significant recurrent renal artery stenosis was identified using duplex ultrasound. Patients were routinely examined with duplex ultrasound immediately post-treatment and subsequently at one, three and six months. Duplex studies were performed using a 5 MHz curvilinear probe with Doppler color flow capability (Philips C5-1 or C5-2; Philips Healthcare, Andover, MA, USA) using a previously described technique. Restenosis was defined as renal artery peak systolic velocity (PSV) ≥ 180 cm/s in an artery previously documented as free of restenosis. This duplex criterion for restenosis has been previously validated by other groups as well as within a cohort of patients from our own institution (Kappa = 0.6, P=0.05 for agreement with angiographic stenosis >60%). Renal artery PSV ≥ 180 at the time of the first post-intervention duplex ultrasound study was considered residual stenosis and not interpreted as restenosis.
Statistical analysis: Data are reported as mean ± standard deviation for continuous variables and count (%) for categorical variables. Baseline comorbid medical conditions, blood pressure, medication use, renal function data, and demographics are reported on a per-patient basis. Comparisons between groups based on restenosis status were performed using two-sample t-tests for continuous variables and Chi-square or Fisher’s exact test for categorical variables. The incidence and temporal distribution of recurrent RAS were analyzed using survival analysis based on treated kidneys, while associations between clinical factors and time to restenosis were examined using Cox proportional hazards regression. Both analyses utilized robust variance estimators to account for correlated observations. Cox proportional hazards regression modeling was performed using stepwise selection (P≤ 0.10 for model entry). Candidate covariates for model selection are listed in Table I. Results were evaluated for significance using α = 0.05.
Results:
Patient sample: Primary RA-PTAS for atherosclerotic RAS was attempted on 112 kidneys during the study period. Of these, eight kidneys were excluded due to residual stenosis on initial post-intervention renal artery duplex, two were excluded due to lack of renal artery duplex follow-up data, and one was excluded due as a technical failure related to inability to access the target renal artery. The remaining 101 kidneys in 91 patients form the basis of this analysis. There were no periprocedural deaths, and distal renal artery balloon occlusion was utilized for embolic protection during 90% of procedures. Mean patient age was 68.8 ± 10.1 years, and all patients had hypertension. Fifty three percent of patients were female and 87% were white. Based on eGFR, moderate or severe renal insufficiency was observed in 72.5% of patients.
Incidence and risk factors of restenosis: Restenosis was identified in 28 renal arteries (28%) in 27 patients at a median post-intervention interval of 5.5 months (inter-quartile range 3.9 - 8.6 months). Proportional hazards regression analysis demonstrated decreased risk for restenosis associated with preoperative statin use (HR 0.35; 95% CI [0.16, 0.74]; P=0.006) and preoperative diastolic blood pressure (DBP) (HR 0.70 per 10mm Hg increase in preoperative DBP; 95% CI [0.49, 0.99]; P=0.049). No other covariates assessed were associated with restenosis-free survival. Predicted restenosis-free survival stratified by statin medication use is displayed graphically in Figure 1.
Clinical manifestations and management of restenosis: Clinical manifestations and management of restenosis are summarized in Table II. 28 recurrent lesions were identified in 27 patients. One patient managed with staged bilateral primary RA-PTAS developed bilateral restenosis, while the remaining restenoses were unilateral. In 17 of 27 patients (63%) with restenosis there were no associated clinical manifestations; in the setting of durable renal function and/or hypertensive responses to RA-PTAS, these patients were managed with continued medical therapy and duplex surveillance. The remaining ten patients (37%) with restenosis identified by duplex ultrasound had associated hypertension and/or decline in eGFR prompting repeat intervention. In these patients, angiography findings confirmed the presence of ≥ 60% diameter-reducing in-stent restenosis in all arteries. Among individuals who underwent repeat intervention for restenosis, procedural management initially consisted of surgical revascularization in one patient and repeat angioplasty in nine; four of the nine repeat angioplasties were performed using cutting balloons. One patient managed with repeat angioplasty developed a second restenosis, and was subsequently treated with aortic endarterectomy plus renal artery bypass. One patient with restenosis was hospitalized for acute hypertensive emergency associated with pulmonary edema and improved clinically with aggressive medical management; following discharge from the hospital, subsequent duplex examination revealed interval progression of the restenosis to occlusion.
Conclusion:
Restenosis following primary RA-PTAS for atherosclerotic RAS is common and may be accompanied by physiologic manifestations. Risk for restenosis is decreased by the use of statins, supporting routine use of these medications in patients undergoing RA-PTAS.
Table I. Candidate covariates for Cox proportional hazards modeling.
| Preoperative Factors Age Race Gender Systolic blood pressure Diastolic blood pressure Estimated glomerular filtration rate (eGFR) Number of antihypertensive medications Smoking Medication use aspirin clopidogrel statin Diabetes Ipsilateral renal artery PSV Resistive index Procedural Factors Renal artery diameter Stent diameter Stent :artery diameter ratio Distal protection (complete distal renal artery balloon occlusion) Pre-dilation prior to stent depolyment Unilateral versus staged bilateral RA-PTAS Incomplete revascularization (i.e., unilateral RA-PTAS in the setting of bilateral RAS) |
Table II. Clinical manifestations and management of restenosis.
| N (%) | |
| Clinical Manifestations | |
| Absent | 17 (63) |
| Present | 10 (37) |
| Hypertension* | 6 (60) |
| Renal dysfunction* | 5 (50) |
| Hypertensive emergency* | 3 (30) |
| Management | |
| Medical (without procedural intervention) | 17 |
| Repeat intervention | 10 |
| Repeat angioplasty | 8 |
| Surgical revascularization | 1 |
| Repeat angioplasty followed by surgical revascularization | 1 |
*Percentage calculated based on number of patients with clinical manifestations present (N=10)
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