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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular (CV) disease in uremic patients is a major concern to the nephrologist because it represents the main cause of morbidity and mortality in chronic renal failure patients, both predialysis and while on dialysis therapy. CV mortality is 3 to 20 times higher in dialysis patients than in the general population at similar age. Of note, a high prevalence of CV comorbidity is already present at start of maintenance dialysis, and is predictive of subsequent mortality on dialysis. CV disease progresses over years prior to the onset of ESRD, because risk factors develop from the early stage of chronic renal insufficiency. However, CV disease may be prevented or attenuated in patients who benefit from early, regular care of CV risk factors. Mechanisms of uremic cardiopathy, the major cause of mortality in uremic patients, are multifactorial and their effects are cumulative. Risk factors for left ventricular hypertrophy are hypertension, anemia, fluid overload and arteriosclosis, all of which are amendable by therapy. Risk factors for accelerated atherosclerosis, responsible for ischemic cardiopathy and myocardial infarction, are both common factors (e.g., hypertension, tobacco smoking and diabetes) and factors more specific for the uremic state (e.g., dyslipidemia, hyperhomocysteinemia and oxidative stress), all of which also are amendable by proper therapy. As a result, mixed hypertensive and ischemic cardiomyopathy develops, ultimately leading to cardiac failure, together with accidents resulting from valvular and arterial calcifications (favored by calcium-phosphate disorders), and from occlusion of coronary, cerebral and peripheral arteries. Cardioprotective therapy thus has become a cornerstone in the management of chronic renal failure patients, in conjunction with renoprotective therapy. Cardioprotective strategy involves optimal treatment of hypertension, anemia, fluid overload, dyslipidemia, hyperhomocysteinemia and calcium-phosphate disorders, and smoking cessation. To achieve a maximal efficacy, such treatment has to be initiated as early as possible in the course of renal failure. Because of its complexity, the integrated combined nephrotective and cardioprotective therapy requires early and sustained guidance by a nephrologist throughout the whole predialysis period.
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PMID:[Cardioprotection: an essential component for predialysis chronic renal failure treatment]. 1272 13

Arteriosclerosis, atherosclerosis and vascular calcification are causally related to the high morbidity and mortality of patients with chronic renal failure. Oxidative stress and carbonyl stress of uremia, dialysis procedure and/or intravenous iron therapy result in AGE (advanced glycation end-product), ALE (advanced lipoxidation end-product) and AOPP (advanced oxidation protein product) formation, favouring together with elevated CRP (C-reactive protein) levels the development of cardiovascular and cerebrovascular complications. Enhanced plasma levels of homocysteine and ADMA (asymmetric dimethylarginine) contribute to this process. In addition, in chronic renal insufficiency hyperphosphatemia and an enhanced calcium x phosphorus ion product are associated with the morbidity and mortality of the patients, particularly in the presence of fetuin deficiency. Phosphorus, AGEs and AOPPs, beside other factors, catalyze the conversion of vascular smooth muscle cells to osteoblast--like cells (particularly in the presence of monocytes/macrophages), resulting in bone matrix protein formation. Other risk factors, such as age, male sex, smoking, hypertension, diabetes, chronic inflammation, insulin resistance or dyslipidemia (enhanced non-HDL-cholesterol) also contribute to the atherosclerotic risk profile of the patient with chronic renal insufficiency. While there is growing understanding of the mechanisms involved in arteriosclerosis, atherosclerosis and vascular calcification in uremia, we are still missing effective therapeutic maneuvers for reduction of excess mortality in uremic patients.
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PMID:[Atherosclerosis and uremia: signifance of non-traditional risk factors]. 1277 74

Patients with chronic renal failure have, as compared with age-matched controls with normal renal function, a markedly higher cardiovascular mortality. The reason is probably accelerated atherosclerosis and left ventricular hypertrophy as a result of accumulation of "classical" cardiovascular risk factors and the presence of some risk factors relatively specific for "uraemia" (e.g. anaemia, hyperhydratation, dyslipidaemia). It is assumed that the reversibility of left ventricular hypertrophy is limited in chronic renal failure due to more marked myocardial fibrosis ("uraemic cardiomyopathy"). Its regression can be achieved by treatment of hypertension with inhibitors of angiotensin converting enzyme with a positive effect on cardiovascular mortality. Regression of left ventricular hypertrophy occurs also in some patients after renal transplantation. Treatment of anaemia reduces the risk of progressive left ventricular dilatation. The cardiovascular risk increases probably already a relatively slight decline of glomerular filtration which need not lead to a significant rise of serum creatinine. The cardiovascular risk obviously increases further with progression of chronic renal insufficiency. Patients with a reduced renal function and chronic renal insufficiency have lower target blood pressure and should have also lower target values e.g. of serum cholesterol. Therapeutic procedures in these patients should not be focused only on a slower progression of chronic renal insufficiency but also on reduction of their high cardiovascular risk.
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PMID:[Cardiovascular complications in patients with chronic renal insufficiency and chronic kidney failure]. 1290 73

Traditional risk factors do not adequately explain the high prevalence of cardiovascular disease in patients with chronic renal insufficiency. Currently, there is a lot of evidence that hypomagnesaemia may play a significant role in the pathogenesis of cardiovascular diseases in general population. The aim of this study was to test the hypothesis that magnesium status in haemodialysis patients is related to the degree of atheromatosis of carotid arteries, as assessed by B-mode ultrasound. Intima-media thickness of both common carotids was assessed by B-mode ultrasound in 93 stable chronic haemodialysis patients and in 182 age- and sex-matched healthy controls. Intracellular magnesium as well as serum magnesium levels were obtained in the haemodialysis patients. Intracellular magnesium was estimated by determination of this ion in isolated peripheral lymphocytes. Haemodialysis patients had also a significantly higher mean common carotid intima-media thickness than controls (0.87+/-0.16 vs 0.76+/-0.13 mm, p < 0.001). Multivariate analysis revealed that in haemodialysis patients both serum magnesium and intracellular magnesium were negatively associated with common carotid intima-media thickness (p = 0.001 and p = 0.003 respectively). Significant associations between the age of the haemodialysis patients, the existence of diabetes mellitus as well as the serum calcium x serum phosphate product with common carotid intima-media thickness of haemodialysis patients were also observed. A strong negative association of both extracellular and intracellular magnesium with common carotid intima-media thickness exists in haemodialysis patients. The above finding suggests that magnesium may play an important protective role in the development and/or acceleration of arterial atherosclerosis in patients with chronic renal insufficiency.
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PMID:Intra- and extracellular magnesium levels and atheromatosis in haemodialysis patients. 1531 42

Dyslipidemia is a common feature of various renal diseases. This perturbed lipid metabolism results in accelerated atherosclerosis and increased cardiovascular morbidity and mortality. Treatment of dyslipidemia, in addition to normalization of blood pressure and reduction of proteinuria, could provide additional means to retard the progression of chronic renal insufficiency. Possible therapeutic approaches include mainly dietary and life-style modifications, selective use of some technical components of dialysis systems, and the judicious prescriptions of lipid-lowering drugs. Even with relatively normal lipid and lipoprotein profiles statin therapy seems to prevent atherogenesis acceleration. A wide range of therapeutic interventions, targeting the lipid abnormalities that may develop in chronic renal patients and end-stage renal disease (ESRD) are currently available, though still without convincing evidence based on long-term prospective studies which clearly demonstrate a significant reduction in cardiovascular morbidity and mortality of ESRD patients. However, extensive investigations, concerning the best long-term therapeutic strategy for this high-risk population of patients, are still missing.
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PMID:Treatment of dyslipidemia in chronic kidney disease. 1556 Jun 75

Vascular calcifications are the consequence of several pathological conditions such as atherosclerosis, diabetes, hypercholesterolemia and chronic renal insufficiency. They are associated with risks of amputation, ischemic heart disease, stroke and increased mortality. A growing body of evidence indicates that vascular smooth muscle cells (VSMCs) undergo chondrogenic commitment eventually leading to vascular calcification, by mechanisms similar to those governing ossification in the cartilage growth plate. Our knowledge of the formation of cartilage growth plate can therefore help us to understand why and how arteries calcify and, consequently, develop new therapeutic strategies. Reciprocally, thorough consideration of the events leading to ectopic chondrocyte differentiation appears crucial to further increase our understanding of growth plate formation. In this context, we will review the effects of known or suspected factors that promote chondrogenic differentiation in growth plate and arteries.
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PMID:Cartilage formation in growth plate and arteries: from physiology to pathology. 1595 94

Ischemic nephropathy is recognized as a distinct cause of renal insufficiency and it is defined as a significant reduction in glomerular filtration rate in patients with hemodynamically significant renovascular occlusive disease. We argue the epidemiologic and clinical manifestations of atherosclerotic renovascular disease, and we evaluate the pronostic agents. Published studies of the outcome of revascularization for renal-artery stenosis have been excellent, offering a durable patency and functional improvement but they have had numerous limitations. The atherosclerosis is a systemic disease and it provides the general prognosis of patients. We conclude that ischemic renal disease is a nephropathy of smoker men, with proteinuria excretion similar to nephropathy with unilateral stenosis. The age of patients is the clinical feature that decide the treatment: surgery, angioplasty/stent or medical management. Comparative analysis of percutaneous transluminal angioplasty and operation for renal revascularization and medically treated patients have proved that the advanced chronic renal insufficiency is associated with an unfavourable response of treatment of the ischemic nephropathy. But, in this nephropathy the revascularization can be the better therapy for selected patients. The revascularization with angioplasty/stent for patients with unilateral renal stenosis and chronic renal insufficiency has a doubtful effectiveness, as the chronic renal failure is result of nephroangiosclerosis.
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PMID:[Ischemic renal disease: revascularization or conservative treatment?]. 1605 7

The aim of the present study was to use intravascular ultrasonography (IVUS) to assess plaque morphology and morphometry in patients with varying degrees of chronic renal insufficiency, including end-stage renal disease (ESRD) on dialysis replacement. Cardiovascular disease is the main cause of death for patients with chronic renal insufficiency, particularly in patients with ESRD. The impact of several degrees of renal insufficiency (including ESRD) on coronary plaque characteristics has not been determined. A total of 142 patients who underwent IVUS imaging of a de novo native coronary artery stenosis before percutaneous intervention were matched for age, gender, and diabetes and were grouped according to calculated creatinine clearance (CrCl): CrCl >70 ml/min (n = 39); CrCl 50 to 69 ml/min (n = 41); CrCl <50 ml/min, (n = 37), and ESRD (n = 25). Standard clinical, angiographic, and IVUS parameters were measured. The ESRD group had more African-American (p = 0.002) and hypertensive (p = 0.002) patients. No significant difference was found in any of the IVUS measurements among patients with CrCl >70, 50 to 69, and <50 ml/min: reference and lesion site arterial, lumen, and plaque areas and volumes, and arterial calcium (p = NS for all comparisons). Conversely, patients with ESRD had larger reference segment arterial and lumen areas and volumes; larger lesion site arterial, lumen, and plaque areas; and larger arcs of calcium (p <0.05 for all post hoc comparisons between patients with ESRD and patients with CrCl >70, 50 to 69, and <50 ml/min). Thus, chronic renal insufficiency in the absence of dialysis is not associated with increased reference segment or lesion site plaque burden and calcium. However, the transition to the need for dialysis is associated with progressive calcific atherosclerosis (larger lesion plaque area and calcium).
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PMID:Impact of renal function on coronary plaque morphology and morphometry in patients with chronic renal insufficiency as determined by intravascular ultrasound volumetric analysis. 1618 11

Chronic renal insufficiency leads to many cardiovascular complications and provide worst prognosis, especially when patients need hemodialysis. The atherosclerosis of chronic hemodialysis patients is qualified as "accelerated" by some authors, because of a very fast and large progression. To improve prognosis, it seems to be very important to detect and treat the frequent and serious underlying cardiovascular disease. Because of the high rate of diabetes mellitus, silent ischemia is a very frequent clinical situation. In the other hand, coronary artery disease in chronic hemodialysis patients is frequently complex, with a large coronary extension and high rate of coronary calcifications. Consequently, this disease needs a specific therapeutic approach. Even though, percutaneous coronary interventions (PCI) are more complex in this population, it provides good results, and improves patient's prognosis. However, the rate of complications of the vascular approach and the rate of restenosis is high. New devices, such as Drug Eluting Stents (DES) can critically decrease restenosis rate, and closure devices for trans-femoral approach, provides very encouraging results in this high risk population. Despite, good results of PCI with DES use, the mortality is still high in this population. To improve our efficiency, we have to progress in our therapeutic strategies and optimize medical approach to treat the important biological perturbations.
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PMID:[Coronary artery disease and coronary angioplasty in chronic hemodialysis patients]. 1734 33

Among patients with chronic renal failure 10-20 times higher cardiovascular mortality than in the control group is observed. It increases further among dialyzed patients. The occurrence of the traditional risk factors only partially explains this phenomenon. Increasing evidence suggests that disturbances in the complex system of cytokine network, matrix metalloproteinases and oxidative stress may cause acceleration of the course of atherosclerosis. The activation of immunological response (partially as a result of infections) leads to exceeded expresion of proinflammatory cytokines, dysregulation of matrix metalloproteinases and their inhibitors system and increased synthesis of neopterine. These processes induce in turn oxidative stress and separately result in atherosclerosis progression. New possibilities of therapeutic interventions seem to appear, e.g. involving cytokine network. They may bring us closer to the aim, which is improvement of prognosis in chronic renal insufficiency.
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PMID:[Cytokines, metalloproteinases, neopterin and cardiovascular mortality among patients with chronic renal failure]. 1747 92


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