Relationship between severity of renal impairment and 2-year outcomes after sirolimus-eluting stent implantation

Ota, Terukazu; Umeda, Hisashi; Yokota, Shigeki; Miyata, S.; Takamura, Atsushi; Sugino, Shigeo; Hayashi, Kazutaka; Ishiki, Ryoji; Takeichi, Yasushi; Iwase, Mitsunori; Inagaki, Hiroki; Murohara, Toyoaki

doi:10.1016/j.ahj.2009.04.013

Cited by 42 publications

(30 citation statements)

References 28 publications

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“…Clinical events caused by in-stent restenosis and downstream revascularization could contribute to the increased mortality hazard with DES in the long term. 43 The signal pertaining to adverse clinical outcomes with BMS seems to be quite consistent as well, despite the observational nature of the data; BMS would seem to be a less preferable clinical choice unless extenuating circumstances exist, such as major bleeding diathesis or upcoming high-risk surgery.…”

Section: Putting It All Together: Pragmatic Tradeoffs In the Choice Omentioning

confidence: 79%

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Coronary Revascularization in Patients with CKD Stage 5D: Pragmatic Considerations

Shroff

Herzog

2016

JASN

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Coronary revascularization decisions for patients with CKD stage 5D present a dilemma for clinicians because of high baseline risks of mortality and future cardiovascular events. This population differs from the general population regarding characteristics of coronary plaque composition and behavior, accuracy of noninvasive testing, and response to surgical and percutaneous revascularization, such that findings from the general population cannot be automatically extrapolated. However, this high-risk population has been excluded from all randomized trials evaluating outcomes of revascularization. Observational studies have attempted to address long-term outcomes after surgical versus percutaneous revascularization strategies, but inherent selection bias may limit accuracy. Compared with percutaneous strategies, surgical revascularization seems to have long-term survival benefit on the basis of observational data but associates with substantially higher short-term mortality rates. Percutaneous revascularization with drug-eluting and bare metal stents associates with a high risk of in-stent restenosis and need for future revascularization, perhaps contributing to the higher long-term mortality hazard. Off-pump coronary bypass surgery and the newest generation of drugeluting stent platforms offer no definitive benefits. In this review, we address the nuances, complexities, and tradeoffs that clinicians face in determining the optimal method of coronary revascularization for this high-risk population.

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Section: Putting It All Together: Pragmatic Tradeoffs In the Choice Omentioning

confidence: 79%

“…42 Hemodialysis was an independent predictor of major adverse cardiovascular outcomes at 2 years after DES among patients with CKD 5D versus patients without CKD driven by higher mortality (12% versus 0.6%) and target vessel revascularization (24% versus 9%) rates. 43 …”

Section: Des Versus Bms: Mortality and In-stent Restenosismentioning

confidence: 99%

Coronary Revascularization in Patients with CKD Stage 5D: Pragmatic Considerations

Shroff

Herzog

2016

JASN

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“…Concerning coronary artery disease in patients with CKD, restenosis is the major clinical limitation of percutaneous coronary angioplasty. The restenosis rate is higher in dialysis than in nondialysis patients [56] . Regarding arteriovenous fistula, stenosis due to intimal hyperplasia is the most common cause of long-term thrombosis [53] .…”

Section: Impaired Vascular Repair and Neointimal Hyperplasiamentioning

confidence: 99%

Does Uremia Cause Vascular Dysfunction

Brunet

Gondouin

Duval-Sabatier

et al. 2011

Kidney Blood Press Res

131

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Vascular dysfunction induced by uremia has 4 main aspects. (1) Atherosclerosis is increased. Intima-media thickness is increased, and animal studies have established that uremia accelerates atherosclerosis. Uremic toxins are involved in several steps of atherosclerosis. Leukocyte activation is stimulated by guanidines, advanced glycation end products (AGE), p-cresyl sulfate, platelet diadenosine polyphosphates, and indoxyl sulfate. Endothelial adhesion molecules are stimulated by indoxyl sulfate. Migration and proliferation of vascular smooth muscle cells (VSMC) are stimulated by local inflammation which could be triggered by indoxyl sulfate and AGE. Uremia is associated with an increase in von Willebrand factor, thrombomodulin, plasminogen activator inhibitor 1, and matrix metalloproteinases. These factors contribute to thrombosis and plaque destabilization. There is also a decrease in nitric oxide (NO) availability, due to asymmetric dimethylarginine (ADMA), AGE, and oxidative stress. Moreover, circulating endothelial microparticles (EMP) are increased in uremia, and inhibit the NO pathway. EMP are induced in vitro by indoxyl sulfate and p-cresyl sulfate. (2) Arterial stiffness occurs due to the loss of compliance of the vascular wall which induces an increase in pulse pressure leading to left ventricular hypertrophy and a decrease in coronary perfusion. Implicated uremic toxins are ADMA, AGE, and oxidative stress. (3) Vascular calcifications are increased in uremia. Their formation involves a transdifferentiation process of VSMC into osteoblast-like cells. Implicated uremic toxins are mainly inorganic phosphate, as well as reactive oxygen species, tumor necrosis factor and leptin. (4) Abnormalities of vascular repair and neointimal hyperplasia are due to VSMC proliferation and lead to severe reduction of vascular lumen. Restenosis after coronary angioplasty is higher in dialysis than in nondialysis patients. Arteriovenous fistula stenosis is the most common cause of thrombosis. Uremic toxins such as indoxyl sulfate and some guanidine compounds inhibit endothelial proliferation and wound repair. Endothelial progenitor cells which contribute to vessel repair are decreased and impaired in uremia, related to high serum levels of β₂-microglobulin and indole-3 acetic acid. Overall, there is a link between kidney function and cardiovascular risk, as emphasized by recent meta-analyses. Moreover, an association has been reported between cardiovascular mortality and uremic toxins such as indoxyl sulfate, p-cresol and p-cresyl sulfate.

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“…Since the effect seems to result from a late thrombosis rather than stenosis that occurs usually after the patients have finished their course of anticoagulation, some have suggested that this problem may be improved. Similarly, sirolimus appears particularly ineffective in patients with renal failure who have vascular disease [84] . In fact, it is unclear whether any stent placement improves patency [85] .…”

Section: Nonpharmacological Interventionmentioning

confidence: 99%

Novel Insights into the Pathobiology of the Vascular Access – Do They Translate into Improved Care?

Diskin

2010

Blood Purif

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While recent developments have allowed greater insight into the vascular pathobiology and intimal hyperplasia, very few of these advances have led to improved clinical care of hemodialysis vascular accesses. Indeed the most common procedure for the treatment of access stenosis and thrombosis is the same model for the creation and study of intimal hyperplasia. The evolution of our understanding of vascular thrombosis is reviewed with a current concept that includes a dynamic interplay of the biophysics, chemistry and biology of the blood vessel with the blood and its constituents. Implications for possible future interventions based on these novel concepts are offered, and the significance of improving our understanding of the pathobiology is emphasized.

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Relationship between severity of renal impairment and 2-year outcomes after sirolimus-eluting stent implantation

Cited by 42 publications

References 28 publications

Coronary Revascularization in Patients with CKD Stage 5D: Pragmatic Considerations

Coronary Revascularization in Patients with CKD Stage 5D: Pragmatic Considerations

Does Uremia Cause Vascular Dysfunction

Novel Insights into the Pathobiology of the Vascular Access – Do They Translate into Improved Care?

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