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ABSTRACT: Activation of the CD40 receptor on the proximal tubular epithelium of the kidney results in fibrosis and inflammation in experimental models of kidney injury. Soluble CD40 ligand is released by activated platelets. The role of CD40-soluble CD40 ligand in patients with ischemic renal disease is unknown. Plasma levels of CD40 and soluble CD40 ligand were measured by enzyme-linked immunosorbent assay in a single center cohort of 60 patients with renal artery stenosis recruited from Salford Royal Hospital, Manchester, United Kingdom. A natural log transformation of CD40 and soluble CD40 ligand was performed to normalize the data. Estimated glomerular filtration rate was used as the primary indicator of renal function. By univariate analysis, low baseline levels of circulating CD40 (R(2)=0.06; P<0.05) and baseline creatinine (R(2)=0.08; P=0.022) were associated with loss of kidney function at 1-year follow-up, whereas soluble CD40 ligand was not (R(2)=0.02; P=ns). In a multiple linear regression model, CD40 (P<0.02) and baseline creatinine (P<0.01) continued to be significantly associated with a decline in renal function (model R(2)=0.17; P<0.005). Baseline CD40 levels were somewhat lower in patients who died during follow-up (survivors, 7.3±0.9 pg/mL, n=48 versus nonsurvivors, 6.7±1.0 pg/mL, n=12; P=0.06). The CD40/soluble CD40 ligand signaling cascade may be a novel mechanism contributing to the development and progression of renal injury in patients with atherosclerotic renal artery stenosis.
Hypertension 02/2013; · 6.21 Impact Factor
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ABSTRACT: A 64 year old female underwent percutaneous coronary intervention (PCI) with stent placement through the femoral approach. On femoral angiography after the PCI, the arterial sheath insertion site was found to be in the inferior epigastric artery and not in the common femoral artery. We used an Angioseal vascular closure device for management and there were no access site complications.
Cardiovascular intervention and therapeutics. 08/2012;
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Changxuan Liu,
Yan Bai,
Yiliang Chen,
Yu Wang,
Yoann Sottejeau,
Lijun Liu,
Xiaomei Li,
Jerry B Lingrel,
Deepak Malhotra, Christopher J Cooper,
Joseph I Shapiro,
Zi-jian Xie,
Jiang Tian
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ABSTRACT: Decreases in cardiac Na/K-ATPase have been documented in patients with heart failure. Reduction of Na/K-ATPase α1 also contributes to the deficiency in cardiac contractility in animal models. Our previous studies demonstrate that reduction of cellular Na/K-ATPase causes cell growth inhibition and cell death in renal proximal tubule cells. To test whether reduction of Na/K-ATPase in combination with increased cardiotonic steroids causes cardiac myocyte death and cardiac dysfunction, we examined heart function in Na/K-ATPase α1 heterozygote knock-out mice (α1(+/-)) in comparison to wild type (WT) littermates after infusion of marinobufagenin (MBG). Adult cardiac myocytes were also isolated from both WT and α1(+/-) mice for in vitro experiments. The results demonstrated that MBG infusion increased myocyte apoptosis and induced significant left ventricle dilation in α1(+/-) mice but not in their WT littermates. Mechanistically, it was found that in WT myocytes MBG activated the Src/Akt/mTOR signaling pathway, which further increased phosphorylation of ribosome S6 kinase (S6K) and BAD (Bcl-2-associated death promoter) and protected cells from apoptosis. In α1(+/-) myocytes, the basal level of phospho-BAD is higher compared with WT myocytes, but MBG failed to induce further activation of the mTOR pathway. Reduction of Na/K-ATPase also caused the activation of caspase 9 but not caspase 8 in these cells. Using cultures of neonatal cardiac myocytes, we demonstrated that inhibition of the mTOR pathway by rapamycin also enabled MBG to activate caspase 9 and induce myocyte apoptosis.
Journal of Biological Chemistry 03/2012; 287(20):16390-8. · 4.77 Impact Factor
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ABSTRACT: Renal artery stenosis (RAS) is an important cause of renal failure; however, the factors associated with loss of kidney function in patients with RAS are poorly described, as are the predictors of an improvement in kidney function after stenting. One hundred patients at seven centers undergoing renal stenting were randomly assigned to an embolic protection device or double-blind use of a platelet glycoprotein IIb/IIIa inhibitor. The glomerular filtration rate (GFR) was measured using the creatinine-derived modified Modification of Diet in Renal Disease (MDRD) equation, cystatin C, and iohexol clearance. In univariate and multivariate models, baseline MDRD and cystatin C GFR were associated with congestive heart failure (CHF) (p = 0.01), lesion length (p = 0.01), and percent stenosis (-0.27, p = 0.01). In multivariate models, MDRD-estimated GFR 1 month after stenting was associated with bilateral stenosis (p < 0.05) and lesion length (p < 0.05), whereas with cystatin C the multivariate model included angiotensin receptor blocker (ARB) (p < 0.05) and minimal luminal diameter (MLD) (p < 0.05). The improvement in GFR from baseline to 1 month, measured as percent change, was related to baseline MDRD (p = 0.009) and cystatin C (p = 0.03) GFR. For MDRD GFR combined treatment with abciximab and Angioguard(®) embolic protection (p = 0.02) remained significant in multivariate analysis as did CHF, which was also significant with cystatin C (p = 0.05). In conclusion, CHF and lesion characteristics (MLD, percent stenosis and lesion length) are determinants of renal function in patients with RAS. In contrast, the acute improvement in renal function after revascularization is most strongly influenced by baseline GFR, and to a lesser degree CHF and combined procedural treatment with abciximab and embolic protection but not lesion characteristics. Clinical Trial Registration - URL:http://www.clinicaltrials.gov. Unique identifier: NCT00234585.
Vascular Medicine 09/2011; 16(5):331-8. · 1.46 Impact Factor
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Steven Haller,
Satjit Adlakha,
Grant Reed,
Pamela Brewster,
David Kennedy,
Mark W Burket,
William Colyer,
Haifeng Yu,
Dong Zhang,
Joseph I Shapiro, Christopher J Cooper
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ABSTRACT: Soluble CD40 ligand (sCD40L) is a marker of platelet activation; whether platelet activation occurs in the setting of renal artery stenosis and stenting is unknown. Additionally, the effect of embolic protection devices and glycoprotein IIb/IIIa inhibitors on platelet activation during renal artery intervention is unknown.
Plasma levels of sCD40L were measured in healthy controls, patients with atherosclerosis without renal stenosis, and patients with renal artery stenosis before, immediately after, and 24 hours after renal artery stenting.
Soluble CD40L levels were higher in renal artery stenosis patients than normal controls (347.5 ± 27.0 versus 65.2 ± 1.4 pg/ml, P < 0.001), but were similar to patients with atherosclerosis without renal artery stenosis. Platelet-rich emboli were captured in 26% (9 of 35) of embolic protection device patients, and in these patients sCD40L was elevated before the procedure. Embolic protection device use was associated with a nonsignificant increase in sCD40L, whereas sCD40L declined with abciximab after the procedure (324.9 ± 42.5 versus 188.7 ± 31.0 pg/ml, P = 0.003) and at 24 hours.
Atherosclerotic renal artery stenosis is associated with platelet activation, but this appears to be related to atherosclerosis, not renal artery stenosis specifically. Embolization of platelet-rich thrombi is common in renal artery stenting and is inhibited with abciximab.
Clinical Journal of the American Society of Nephrology 08/2011; 6(9):2185-91. · 5.23 Impact Factor
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ABSTRACT: Distal embolization is a complication during lower-extremity revascularization procedures that may occur when intervening on acute or subacute lesions. Several studies have demonstrated the safety and feasibility of using embolic protection devices (EPD) and some interventionalists have adapted this technology for use in infrainguinal revascularization procedures. At present, there are no randomized trials to indicate the benefit, safety, and cost-effectiveness of EPD for this application and its use in the United States is considered off-label. However, based on our experience and a review of the published literature, we consider the use of EPD in acute lower-extremity ischemia a reasonable strategy.
Techniques in vascular and interventional radiology 06/2011; 14(2):75-9.
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ABSTRACT: OPINION STATEMENT: Renal artery stenosis (RAS) is a relatively common manifestation of atherosclerosis, although in a small percentage of cases it is due to fibromuscular dysplasia and less frequently may have other etiologies. RAS may be treated by revascularization, using either percutaneous or open surgical techniques. Currently, technical success with percutaneous revascularization utilizing angioplasty and stenting is achieved in 95% or more of cases in which it is attempted. Despite this, at least one third of patients undergoing renal artery stenting do not receive any measurable benefit. Furthermore, randomized trials of stenting for RAS have failed to demonstrate a benefit over medical management alone. Thus, the clinician is faced with a challenge when determining how to manage an individual patient with RAS. In the current era, all patients with RAS should receive "optimal medical therapy." This approach should use medicines to control blood pressure, and specifically utilize agents proven to reduce cardiovascular morbidity and mortality. Other components of "optimal medical therapy" include the use of anti-platelet drugs such as aspirin and statins to minimize progression of atherosclerosis. In addition to these strategies, consideration should be given to revascularization therapy. When deciding to revascularize RAS, the patient should have an appropriate clinical indication, in addition to a significant anatomic stenosis. Importantly, stents should not be placed due to the "oculostenotic reflex." Specifically, patients who continue to have uncontrolled blood pressure or worsening renal function despite an aggressive approach with medical therapy may be particularly good candidates for renal artery stenting. Despite the lack of benefit in randomized trials to date, there is likely still a role for renal artery stenting in RAS; however, careful patient selection is essential to maximize the potential benefit.
Current Treatment Options in Cardiovascular Medicine 01/2011; 13(2):103-13.
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Jiang Tian,
Steven Haller,
Sankaridrug Periyasamy,
Pamela Brewster,
Haifeng Zhang,
Satjit Adlakha,
Olga V Fedorova,
Zi-Jian Xie,
Alexei Y Bagrov,
Joseph I Shapiro, Christopher J Cooper
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ABSTRACT: Cardiotonic steroids, including marinobufagenin, are a group of new steroid hormones found in plasma and urine of patients with congestive heart failure, myocardial infarction, and chronic renal failure. In animal studies, partial nephrectomy induces marinobufagenin elevation, cardiac hypertrophy, and fibrosis. The objective of this study is to test the effect of renal ischemia on marinobufagenin levels in humans with renal artery stenosis (RAS). To test this, plasma marinobufagenin levels were measured in patients with RAS of the Prospective Randomized Study Comparing Renal Artery Stenting With or Without Distal Protection, non-RAS patient controls who were scheduled for coronary angiography, and normal healthy individuals. Marinobufagenin levels were significantly higher in patients with RAS compared with those of the other 2 groups. Multivariate analysis shows that occurrence of RAS is independently related to marinobufagenin levels. In addition, renal artery revascularization by stenting partially reversed marinobufagenin levels in the patients with RAS (0.77±0.06 nmol/L at baseline; 0.66±0.06 nmol/L at 24 hours; and 0.61±0.05 nmol/L at 1 month). In conclusion, we have found that marinobufagenin levels are increased in patients with RAS, whereas reversal of renal ischemia by stenting treatment reduces marinobufagenin levels. These results suggest that RAS-induced renal ischemia may be a major cause of marinobufagenin release.
Hypertension 11/2010; 56(5):914-9. · 6.21 Impact Factor
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ABSTRACT: Inherent risks of stenting include restenosis and thrombosis. Recently, stent fractures have been recognized as a complication that may result in thrombosis, perforation, restenosis, and migration of the stent resulting in morbidity and mortality. Stent fractures were originally seen in the superficial femoral arteries but have since then been reported in almost all vascular sites including the coronary, renal, carotid, iliac, and femoropopliteal arteries. Fractures are the result of the complex interplay between stent manufacturing, the stented segment, pulsatile and nonpulsatile biomechanical forces, and plaque morphology at a particular vascular site. The presentation of a patient with a fracture is highly variable, ranging from asymptomatic in nature, detected on routine screening without any sequelae, to sudden cardiac death related to a thrombosed coronary artery. Despite being recognized as an important complication, consensus on routine surveillance and diagnostic methods to detect fractures continues to be lacking. Fortunately, most cases are relatively benign and can be managed conservatively if detected. In the setting of recurrent symptoms, further intervention is usually sought. In review of the literature most cases are managed with placement of a stent over the fractured area, the stent-in-stent technique, but several other alternatives may be available. As the knowledge of the variables that make stents prone to fracture are identified, better technologies and techniques can be employed to minimize the risk of this complication. This article reviews the available literature on stent fractures and complications using data found on PubMed, MEDLINE, the Manufacturer and User Facility Device Experience (MAUDE) database, and the Cochrane databases.
Journal of Interventional Cardiology 08/2010; 23(4):411-9. · 1.18 Impact Factor
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ABSTRACT: The objective of this study was to identify the predictors of distal embolization (DE) during protected renal artery angioplasty and stenting.
DE may contribute to worsening renal function after renal artery stenting. The factors associated with DE, rates of platelet-rich emboli, and treatments that may prevent DE during renal stenting have not been evaluated.
The current study evaluated patients randomized to receive an embolic protection device (EPD) in the RESIST trial. Forty-two patients were identified for inclusion in this study. These patients were further randomized to abciximab (N = 22) or placebo (N = 20). Modification in Diet in Renal Disease glomerular filtration rate (GFR) was used as the primary measure of renal function. Creatinine was measured by a modified Jaffe reaction using the IDMS-traceable assay. The primary endpoint was capture of platelet rich emboli in the angioguard basket.
DE occurred in 15/42 (35%) of the patients and platelet rich DE in 10 (24%) of the patients who received an EPD. Of the angiographic characteristics only lesion length was significantly higher in patients with DE (16 +/- 7 mm vs. 10 +/- 5 mm, P = 0.04). Preprocedural abciximab reduced DE from 42 to 8% (P = 0.02). The rate of platelet rich emboli was 50% with neither abciximab nor a thienopyridine, 36% with thienopyridine only, 15% abciximab only, and 0% in patients who received both a thienopyridine and abciximab. Only Abciximab use was associated with improved renal function at 1-month, thienopyridine was not. Angiographic characteristics including percent stenosis, minimal luminal diameter (MLD), reference diameter, change in MLD, contrast volume, and procedure time were not predictors of DE during renal stenting.
Capture of DE and specifically platelet DE are common during protected renal stenting using a filter-type EPD. Abciximab use, and potentially combined thienopyridine and abciximab use, decreased the rate of platelet rich DE; however, only abciximab improved renal function at 1-month.
Catheterization and Cardiovascular Interventions 01/2010; 76(1):16-23. · 2.29 Impact Factor
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Jiang Tian,
Amjad Shidyak,
Sankaridrug M Periyasamy,
Steven Haller,
Mohamed Taleb,
Nasser El-Okdi,
Jihad Elkareh,
Shalini Gupta,
Sabry Gohara,
Olga V Fedorova, Christopher J Cooper,
Zijian Xie,
Deepak Malhotra,
Alexei Y Bagrov,
Joseph I Shapiro
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ABSTRACT: Spironolactone has been noted to attenuate cardiac fibrosis. We have observed that the cardiotonic steroid marinobufagenin plays an important role in the diastolic dysfunction and cardiac fibrosis seen with experimental renal failure. We performed the following studies to determine whether and how spironolactone might ameliorate these changes. First, we studied rats subjected to partial nephrectomy or administration of exogenous marinobufagenin. We found that spironolactone (20 mg/kg per day) attenuated the diastolic dysfunction as assessed by ventricular pressure-volume loops and essentially eliminated cardiac fibrosis as assessed by trichrome staining and Western blot. Next, we examined the effects of spironolactone and its major metabolite, canrenone (both 100 nM), on marinobufagenin stimulation of rat cardiac fibroblasts. Both spironolactone and canrenone prevented the stimulation of collagen production by 1 nM marinobufagenin but not 100 nM marinobufagenin, as assessed by proline incorporation and procollagen 1 expression, as well as signaling through the sodium-potassium-ATPase, as evidenced by protein kinase C isoform delta translocation and extracellular signal regulated kinase 1/2 activation. Both spironolactone and canrenone also altered ouabain binding to cultured porcine cells in a manner consistent with competitive inhibition. Our data suggest that some of the antifibrotic effects of spironolactone may be attributed to antagonism of marinobufagenin signaling through the sodium-potassium-ATPase.
Hypertension 11/2009; 54(6):1313-20. · 6.21 Impact Factor
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New England Journal of Medicine 11/2009; 361(20):1972-8. · 53.30 Impact Factor
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Christopher J Cooper
Pacing and Clinical Electrophysiology 10/2009; 33(1):107-8. · 1.35 Impact Factor
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Circulation 01/2009; 118(25):2873-8. · 14.74 Impact Factor
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ABSTRACT: The aim of this study was to evaluate whether complete embolic protection is superior to partial embolic protection for preservation of kidney function during renal artery angioplasty and stenting.
Renal artery angioplasty and stenting (RAAS) is a common treatment for atherosclerotic renal artery stenosis. However, RAAS may be complicated by peri-procedural loss of kidney function.
In total, 44 patients were randomized to embolic protection devices (EPD) use; 25 complete and 19 partial embolic protection. These patients were further randomized to receive abciximab (n = 23) or placebo (n = 21). [corrected] MDRD glomerular filtration rate (GFR), was used as the primary measure of renal function. Creatinine was measured by a modified Jaffe reaction using the IDMS-traceable assay. The primary endpoint was the percent change in estimated glomerular filtration rate (eGFR) 1 month following stent placement.
There was no difference in percent change eGFR at 1 month between complete or partial protection (-4 +/- 25 vs. +3 +/- 30, P = 0.45). Abciximab was associated with a net improvement in eGFR when compared with placebo (+0.5 +/- 27 vs. -11 +/- 20, P = 0.04). On subgroup analysis, the use of abciximab was associated with significantly improved eGFR in the partial distal embolic protection group (+14 +/- 33 vs. -17 +/- 13 %, P = 0.018) but not in the complete distal embolic protection group (+2.5 +/- 26 vs. -11 +/- 24, P = 0.42), however, there was no interaction between completeness of protection and abciximab on eGFR (P = ns). Capture of embolic material was more likely with complete protection when compared with those receiving partial protection (51% vs. 21%, P < 0.05).
Complete protection was superior to partial protection for the capture of athermanous debris during renal artery stenting. However, this was not associated with improved renal function. Importantly, Abciximab conferred a benefit for renal function that was independent of the degree of embolic protection.
Catheterization and Cardiovascular Interventions 12/2008; 73(6):725-30. · 2.29 Impact Factor
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Christopher J Cooper,
Steven T Haller,
William Colyer,
Michael Steffes,
Mark W Burket,
William J Thomas,
Robert Safian,
Bhagat Reddy,
Pamela Brewster,
Mary Ann Ankenbrandt,
Renu Virmani,
Eric Dippel,
Krishna Rocha-Singh,
Timothy P Murphy,
David J Kennedy,
Joseph I Shapiro,
Ralph D D'Agostino,
Michael J Pencina,
Sadik Khuder
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ABSTRACT: Preservation of renal function is an important objective of renal artery stent procedures. Although atheroembolization can cause renal dysfunction during renal stent procedures, whether adjunctive use of embolic protection devices or glycoprotein IIb/IIIa inhibitors improves renal function is unknown.
One hundred patients undergoing renal artery stenting at 7 centers were randomly assigned to an open-label embolic protection device, Angioguard, or double-blind use of a platelet glycoprotein IIb/IIIa inhibitor, abciximab, in a 2x2 factorial design. The main effects of treatments and their interaction were assessed on percentage change in Modification in Diet in Renal Disease-derived glomerular filtration rate from baseline to 1 month using centrally analyzed creatinine. Filter devices were analyzed for the presence of platelet-rich thrombus. With stenting alone, stenting and embolic protection, and stenting with abciximab alone, glomerular filtration rate declined (P<0.05), but with combination therapy, it did not decline and was superior to the other allocations in the 2x2 design (P<0.01). The main effects of treatment demonstrated no overall improvement in glomerular filtration rate; although abciximab was superior to placebo (0+/-27% versus -10+/-20%; P<0.05), embolic protection was not (-1+/-28% versus -10+/-20%; P=0.08). An interaction was observed between abciximab and embolic protection (P<0.05), favoring combination treatment. Abciximab reduced the occurrence of platelet-rich emboli in the filters from 42% to 7% (P<0.01).
Renal artery stenting alone, stenting with embolic protection, and stenting with abciximab were associated with a decline in glomerular filtration rate. An unanticipated interaction between Angioguard and abciximab was seen, with combination therapy better than no treatment or either treatment alone.
Circulation 05/2008; 117(21):2752-60. · 14.74 Impact Factor
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David J Kennedy,
Jihad Elkareh,
Amjad Shidyak,
Anna P Shapiro,
Sleiman Smaili,
Krishna Mutgi,
Shalini Gupta,
Jiang Tian,
Eric Morgan,
Samer Khouri, Christopher J Cooper,
Sankaridrug M Periyasamy,
Zijian Xie,
Deepak Malhotra,
Olga V Fedorova,
Alexei Y Bagrov,
Joseph I Shapiro
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ABSTRACT: Because of the plethora of genetic manipulations available in the mouse, we performed a partial nephrectomy in the mouse and examined whether the phenotypical features of uremic cardiomyopathy described in humans and rats were also present in the murine model. A 5/6 nephrectomy was performed using a combination of electrocautory to decrease renal mass on the left kidney and right surgical nephrectomy. This procedure produced substantial and persistent hypertension as well as increases in circulating concentrations of marinobufagenin. Invasive physiological measurements of cardiac function demonstrated that the 5/6 nephrectomy resulted in impairment of both active and passive left ventricular relaxation at 4 wk whereas tissue Doppler imaging detected changes in diastolic function after 6 wk. Morphologically, hearts demonstrated enlargement and progressive fibrosis, and biochemical measurements demonstrated downregulation of the sarcoplasmic reticulum calcium ATPase as well as increases in collagen-1, fibronectin, and vimentin expression. Our results suggest that partial nephrectomy in the mouse establishes a model of uremic cardiomyopathy which shares phenotypical features with the rat model as well as patients with chronic renal failure.
American journal of physiology. Renal physiology 03/2008; 294(2):F450-4. · 3.68 Impact Factor
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Circulation 02/2007; 115(2):263-9; discussion 270. · 14.74 Impact Factor
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ABSTRACT: Although treatment of renal artery stenosis (RAS) with stents has been shown to improve blood pressure (BP) and renal function in some patients, little is known about the effect on health-related quality of life. A composite quality of life survey was administered in a cross-sectional cohort fashion to 149 patients presenting with angiographically and hemodynamically confirmed RAS either before (baseline, n = 37) or after (follow-up, n = 112) stent revascularization. BP, renal function, and antihypertensive medication use were also assessed. Systolic BP was lower in the revascularized patients (166 +/- 23 vs. 153 +/- 26, p < .01). The Short Form-36 Physical Component Summary (PCS) scores were higher (better) in revascularized patients (37 +/- 9 vs. 31 +/- 9, p < .01), whereas Mental Component Summary scores were equivalent (49 +/- 13 vs. 51 +/- 11, p = ns). Sleep dysfunction scores were lower (better) in the revascularized patients (32 +/- 26 vs. 48 +/- 32, p < .001), whereas self-reported appetite was higher (better; 62% +/- 29% vs. 73% +/- 27%,p < .05). After matching for age and gender, Short Form-36 PCS remained higher in the revascularized cohort (37 +/- 8 vs. 32 +/- 8, p < .05). Importantly, in multivariate analysis, revascularization was the most significant determinant of a higher PCS score (r2 = .07, beta = 5.21, p < .01). The current data suggest that renal artery stenting may improve health-related quality of life in patients with renovascular disease.
Biological Research for Nursing 11/2006; 8(2):129-37. · 1.28 Impact Factor
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Christopher J Cooper,
Timothy P Murphy,
Alan Matsumoto,
Michael Steffes,
David J Cohen,
Michael Jaff,
Richard Kuntz,
Kenneth Jamerson,
Diane Reid,
Kenneth Rosenfield,
John Rundback,
Ralph D'Agostino,
William Henrich,
Lance Dworkin
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ABSTRACT: Atherosclerotic renal artery stenosis is a problem with no consensus on diagnosis or therapy. The consequences of renal ischemia are neuroendocrine activation, hypertension, and renal insufficiency that can potentially result in acceleration of atherosclerosis, further renal dysfunction, myocardial infarction, heart failure, stroke, and death. Whether revascularization improves clinical outcomes when compared with optimum medical therapy is unknown.
CORAL is a randomized clinical trial contrasting optimum medical therapy alone to stenting with optimum medical therapy on a composite cardiovascular and renal end point: cardiovascular or renal death, myocardial infarction, hospitalization for congestive heart failure, stroke, doubling of serum creatinine, and need for renal replacement therapy. The secondary end points evaluate the effectiveness of revascularization in important subgroups of patients and with respect to all-cause mortality, kidney function, renal artery patency, microvascular renal function, and blood pressure control. We will also correlate stenosis severity with longitudinal renal function and determine the value of stenting from the perspectives of quality of life and cost-effectiveness. The primary entry criteria are (1) an atherosclerotic renal stenosis of > or = 60% with a 20 mm Hg systolic pressure gradient or > or = 80% with no gradient necessary and (2) systolic hypertension of > or = 155 mm Hg on > or = 2 antihypertensive medications. Randomization will occur in 1080 subjects. The study has 90% power to detect a 28% reduction in primary end point hazard rate.
CORAL represents a unique opportunity to determine the incremental value of stent revascularization, in addition to optimal medical therapy, for the treatment of atherosclerotic renal artery stenosis.
American heart journal 08/2006; 152(1):59-66. · 4.65 Impact Factor
