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      Determinants of Mortality in Patients with Chronic Kidney Disease Undergoing Percutaneous Coronary Intervention

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          Background: Renal impairment is a known predictor of mortality in both the general population and in patients with cardiac disease. The aim of this study was to evaluate factors that determine mortality in patients with chronic kidney disease (CKD) who have undergone percutaneous coronary intervention (PCI). Methods: In this study we included 293 consecutive patients with CKD who underwent PCI between 1st January 2007 and 30th September 2012. The primary outcome that we studied was all-cause mortality in a follow-up period of 12-69 months (mean 38.8 ± 21.7). Results: Age (p < 0.001), PCI indication (p = 0.035), CKD stage (p < 0.001) and left ventricular ejection fraction (p < 0.001) were significantly related to mortality. CKD stage 5 [hazard ratio (HR) = 6.39, 95% CI: 1.51-27.12) and severely impaired left ventricular function (HR = 4.04, 95% CI: 2.15-7.59) were the strongest predictors of mortality. Other factors tested (gender, hypertension, diabetes, hyperlipidaemia, established peripheral vascular disease/stroke, coronary arteries intervened, number of vessels treated, number of stents implanted and length of lesion treated) did not show any correlation with mortality. Conclusions: The mortality of patients with CKD undergoing PCI increases with age, worsening CKD stage and deteriorating left ventricular systolic function, and it is also higher in patients with acute coronary syndromes compared to those with stable coronary artery disease.

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          Most cited references 24

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          Guidelines on myocardial revascularization.

           W Wijns,  P Kolh,  N Danchin (2010)
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            Strong association between malnutrition, inflammation, and atherosclerosis in chronic renal failure.

            Atherosclerotic cardiovascular disease and malnutrition are widely recognized as leading causes of the increased morbidity and mortality observed in uremic patients. C-reactive protein (CRP), an acute-phase protein, is a predictor of cardiovascular mortality in nonrenal patient populations. In chronic renal failure (CRF), the prevalence of an acute-phase response has been associated with an increased mortality. One hundred and nine predialysis patients (age 52 +/- 1 years) with terminal CRF (glomerular filtration rate 7 +/- 1 ml/min) were studied. By using noninvasive B-mode ultrasonography, the cross-sectional carotid intima-media area was calculated, and the presence or absence of carotid plaques was determined. Nutritional status was assessed by subjective global assessment (SGA), dual-energy x-ray absorptiometry (DXA), serum albumin, serum creatinine, serum urea, and 24-hour urine urea excretion. The presence of an inflammatory reaction was assessed by CRP, fibrinogen (N = 46), and tumor necrosis factor-alpha (TNF-alpha; N = 87). Lipid parameters, including Lp(a) and apo(a)-isoforms, as well as markers of oxidative stress (autoantibodies against oxidized low-density lipoprotein and vitamin E), were also determined. Compared with healthy controls, CRF patients had an increased mean carotid intima-media area (18.3 +/- 0.6 vs. 13.2 +/- 0.7 mm2, P or = 10 mg/liter). Malnourished patients had higher CRP levels (23 +/- 3 vs. 13 +/- 2 mg/liter, P < 0.01), elevated calculated intima-media area (20.2 +/- 0.8 vs. 16.9 +/- 0.7 mm2, P < 0.01) and a higher prevalence of carotid plaques (90 vs. 60%, P < 0.0001) compared with well-nourished patients. During stepwise multivariate analysis adjusting for age and gender, vitamin E (P < 0.05) and CRP (P < 0.05) remained associated with an increased intima-media area. The presence of carotid plaques was significantly associated with age (P < 0.001), log oxidized low-density lipoprotein (oxLDL; P < 0.01), and small apo(a) isoform size (P < 0.05) in a multivariate logistic regression model. These results indicate that the rapidly developing atherosclerosis in advanced CRF appears to be caused by a synergism of different mechanisms, such as malnutrition, inflammation, oxidative stress, and genetic components. Apart from classic risk factors, low vitamin E levels and elevated CRP levels are associated with an increased intima-media area, whereas small molecular weight apo(a) isoforms and increased levels of oxLDL are associated with the presence of carotid plaques.
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              Renal insufficiency as a predictor of cardiovascular outcomes and the impact of ramipril: the HOPE randomized trial.

              The cardiovascular risk associated with early renal insufficiency is unknown. Clinicians are often reluctant to use angiotensin-converting enzyme inhibitors in patients with renal insufficiency. To determine whether mild renal insufficiency increases cardiovascular risk and whether ramipril decreases that risk. Post hoc analysis. The Heart Outcomes and Prevention Evaluation (HOPE) study, a randomized, double-blind, multinational trial involving 267 study centers. 980 patients with mild renal insufficiency (serum creatinine concentration >/= 124 micromol/L [>/=1.4 mg/dL]) and 8307 patients with normal renal function (serum creatinine concentration 0.2 for the difference). In patients who had preexisting vascular disease or diabetes combined with an additional cardiovascular risk factor, mild renal insufficiency significantly increased the risk for subsequent cardiovascular events. Ramipril reduced cardiovascular risk without increasing adverse effects.

                Author and article information

                Cardiorenal Medicine
                Cardiorenal Med
                S. Karger AG (Basel, Switzerland karger@ 123456karger.com http://www.karger.com )
                May 2016
                19 February 2016
                : 6
                : 3
                : 169-179
                aDepartment of Cardiology and bRenal Department, Royal Free Hospital, and cDepartment of Primary Care and Public Health Sciences, King's College London, London, UK
                CRM2016006003169 PMC4886034 Cardiorenal Med 2016;6:169-179
                © 2016 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 2, References: 28, Pages: 11
                Original Paper


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