Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dyslipidemia and progression of cardiovascular calcification (CVC) in patients with end-stage renal disease (ESRD). Cardiovascular calcification (CVC) is commonly encountered both in the general population as well as in patients with end-stage renal disease (ESRD). The etiology of CVC in patients with ESRD is multifactorial. Despite that, current debate remains narrowly focused on the role of calcium loading from calcium-based phosphate binders (CBPB) in the pathogenesis and progression of CVC. Yet, the alleged link between these binders and CVC has not been substantiated in well-designed controlled trials. In contrast, the purported role of sevelamer, a non-calcium-based phosphate binder, in slowing the progression of CVC in dialysis patients has attracted widespread attention. The beneficial effect of sevelamer on progression of calcification was thought to be due to lower calcium loading during its use. However, an alternative and possibly more likely mechanism involves sevelamer-induced lowering of LDL cholesterol. In this context, previous studies in individuals with normal renal function have documented amelioration of coronary artery calcification (CAC) with reduction of LDL-cholesterol by treatment with HMG-CoA reductase inhibitors (statins). Given that CAC is a well-accepted marker of atherosclerosis, and that high plasma cholesterol concentration is one of the main risk factors for atherosclerosis, then it is not unreasonable to suspect that CAC may be halted or even reversed by lowering of LDL cholesterol level with statin therapy. Unfortunately, the effect of lowering the LDL-cholesterol level on CAC has not been studied in patients with ESRD. Therefore, conclusions about this important topic should await the results of well-designed clinical studies that control for all factors potentially implicated in the CVC burden of patients with ESRD. In this review, I will discuss the role of various potential mechanisms involved in the pathogenesis of CVC in patients with ESRD, and emphasize the role of dyslipidemia and its treatment in this important clinical entity.
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PMID:Dyslipidemia and progression of cardiovascular calcification (CVC) in patients with end-stage renal disease (ESRD). 1588 13

Cardiovascular complications are the main cause of mortality and morbidity among patients on dialyses. The aim of the work was to assess the effect of the type of renal replacement therapy on the risk factors and cardiovascular complication in dialyzed patients. The studies were performed retrospectively on 90 hemodialyzed and 49 peritoneally dialyzed patients. Risk factors of cardiovascular diseases as well as serum lipids, complete blood count, serum albumin, fibrinogen, C-reactive protein, calcium, phosphates, PTH, systolic, diastolic, mean blood pressure, left ventricular hypertrophy. Hemodialyzed patients were more anemic, longer on renal replacement therapy, with higher albumin, phosphates, lower fibrinogen, cholesterol, LDL, triglycerides, calcium, systolic and diastolic blood pressure than peritoneally dialyzed patients. Left ventricular hypertrophy more frequently found in hemodialyzed patients than in peritoneally dialyzed patients. In peritoneally dialyzed patients glucose load into the peritoneum, dyslipidemia and hiperfibrinogenemia may further contribute at the cardiovascular complications. In hemodialyzed patients anemia, left ventricular hypertrophy and ischemic heart disease is more frequent than in peritoneally dialyzed patients.
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PMID:[Cardiovascular risk factors in dialyzed patients]. 1596 7

Obesity, insulin resistance, dyslipidemia, and hypertension are components of the pathophysiological state known as metabolic syndrome. Adrenergic vasoconstriction is mediated through increases in cytosolic Ca2+ and the myofilaments' sensitivity to Ca2+. In many pathophysiological states, there is an enhanced role for Rho kinase (ROK)-mediated increases in Ca2+ sensitivity of the contractile apparatus. Thus we hypothesized that there is a greater role for ROK-mediated increases in Ca2+ sensitivity in alpha1-adrenergic vasoconstriction in arteries from obese Zucker (OZ) rats. Therefore, small gracilis muscle arteries from 11- to 12-wk-old and 16- to 18-wk-old lean and OZ rats were isolated, cannulated, and pressurized to 75 mmHg. For some experiments, vessels were loaded with fura 2-AM. Changes in luminal diameter and vessel wall Ca2+ concentration ([Ca2+]) were measured in response to phenylephrine (PE), the thromboxane mimetic U-46619, and KCl. alpha1-Adrenergic vasoconstriction was similar between 11- to 12-wk-old lean and obese animals and greater in older obese animals compared with controls. PE-induced increases in vascular smooth muscle cell [Ca2+] were blunted in OZ animals compared with lean controls in both age groups of animals. KCl and U-46619 elicited similar vasoconstriction and vascular smooth muscle cell [Ca2+] in both groups. ROK inhibition attenuated PE vasoconstriction to a greater degree in arteries from 11- to 12-wk-old OZ rats compared with lean animals; ROK inhibition in arteries from older rats right shifted both concentration-response curves to the same point. Total RhoA and ROKalpha protein expressions were similar between groups. These results suggest an enhanced role for the ROK pathway in alpha1-adrenergic vasoconstriction in metabolic syndrome.
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PMID:Enhanced role for RhoA-associated kinase in adrenergic-mediated vasoconstriction in gracilis arteries from obese Zucker rats. 1614 8

The current implementation into nephrology clinical practice of guidelines on treatment of cardiovascular (CV) risk factors in chronic kidney disease (CKD) is unknown. We designed a cross-sectional analysis to evaluate the prevalence and treatment of eight modifiable CV risk factors in 1058 predialysis CKD patients (stage 3: n=486; stage 4: n=430, stage 5: n=142) followed for at least 1 year in 26 Italian renal clinics. The median nephrology follow-up was 37 months (range: 12-391 months). From stages 3 to 5, hypertension was the main complication (89, 87, and 87%), whereas smoking, high calcium-phosphate product and malnutrition were uncommon. The prevalence of proteinuria (25, 38, and 58%), anemia (16, 32, and 51%) and left ventricular hypertrophy (51, 55, and 64%) significantly increased, while hypercholesterolemia was less frequent in stage 5 (49%) than in stages 4 and 3 (59%). The vast majority of patients received multidrug antihypertensive therapy including inhibitors of renin-angiotensin system; conversely, diuretic treatment was consistently inadequate for both frequency and dose despite scarce implementation of low salt diet (19%). Statins were not prescribed in most hypercholesterolemics (78%), and epoietin treatment was largely overlooked in anemics (78%). The adjusted risk for having a higher number of uncontrolled risk factors rose in the presence of diabetes (odds ratio 1.29, 95% confidence interval 1.00-1.66), history of CV disease (odds ratio 1.48, 95% confidence interval 1.15-1.90) and CKD stages 4 and 5 (odds ratio 1.75, 95% confidence interval 1.37-2.22 and odds ratio 2.85, 95% confidence interval 2.01-4.04, respectively). In the tertiary care of CKD, treatment of hypertension is largely inadequate, whereas therapy of anemia and dyslipidemia is frequently omitted. The risk of not achieving therapeutic targets is higher in patients with diabetes, CV disease and more advanced CKD.
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PMID:Global approach to cardiovascular risk in chronic kidney disease: reality and opportunities for intervention. 1639 61

Calcium channel blockers and HMG-CoA reductase inhibitors are widely used for the management of hypertension and dyslipidemia, respectively. The use of these agents in the prevention and treatment of cardiovascular disease remains largely based on their actions in lowering blood pressure and lipids. Recent clinical trials, however, indicate that certain members of these two drug classes may slow progression of disease to an extent that cannot be solely attributed to risk factor reduction. The proposed mechanisms for such pleiotropic actions include enhancement of endothelial-dependent nitric oxide bioavailability, anti-inflammatory activity, and inhibition of oxidative stress. To understand the basis for such effects, along with potential synergies, we will review the basic and clinical evidence that indicate a broader opportunity for treatment and protection of cardiovascular events by atheroprotection with these agents beyond risk factor management.
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PMID:A rationale for combined therapy with a calcium channel blocker and a statin: evaluation of basic and clinical evidence. 1650 69

Calcemia is a risk factor for cardiovascular (CV) events in dialyzed patients. The relation between serum calcium and cardiovascular events is continuous and linear. Calcium plays a potent role in the genesis of cardiovascular dysfunction, particularly by promoting vascular calcification. Parathyroid hormone (PTH) also is associated with increased CV risk in both primary and secondary hyperparathyroidism. There is a nonlinear relationship between PTH and CV risk; both high and low PTH concentrations increase CV risk. The CV risk profile (BP, dyslipidemia) is strikingly ameliorated by the administration of calcimimetics. Apart from lowering PTH, whether calcimimetics have intrinsic effects on CV risk profile is unknown.
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PMID:Calcium, calcium regulatory hormones, and calcimimetics: impact on cardiovascular mortality. 1656 53

Vascular calcification increasingly afflicts our aging and dysmetabolic population. Once considered a passive process, it has emerged as an actively regulated form of calcified tissue metabolism, resembling the mineralization of endochondral and membranous bone. Executive cell types familiar to bone biologists, osteoblasts, chondrocytes, and osteoclasts, are seen in calcifying macrovascular specimens. Lipidaceous matrix vesicles, with biochemical and ultrastructural "signatures" of skeletal matrix vesicles, nucleate vascular mineralization in diabetes, dyslipidemia, and uremia. Skeletal morphogens (bone morphogenetic protein-2 (BMP) and BMP4 and Wnts) divert aortic mesoangioblasts, mural pericytes (calcifying vascular cells), or valve myofibroblasts to osteogenic fates. Paracrine signals provided by these molecules mimic the epithelial-mesenchymal interactions that induce skeletal development. Vascular expression of pro-osteogenic morphogens is entrained to physiological stimuli that promote calcification. Inflammation, shear, oxidative stress, hyperphosphatemia, and elastinolysis provide stimuli that: (1) promote vascular BMP2/4 signaling and matrix remodeling; and (2) compromise vascular defenses that limit calcium deposition, inhibit osteo/chondrogenic trans-differentiation, and enhance matrix vesicle clearance. In this review, we discuss the biology of vascular calcification. We highlight how aortic fibrofatty tissue expansion (adventitia, valve interstitium), the adventitial-medial vasa, vascular matrix, and matrix vesicle metabolism contribute to the regulation of aortic calcium deposition, with greatest emphasis placed on diabetic vascular disease.
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PMID:Molecular mechanisms of vascular calcification: lessons learned from the aorta. 1660 Dec 33

This review describes the clinical profile and rationale for the development of a single-pill formulation of the calcium channel blocker amlodipine besylate, a blood pressure-lowering agent with pleiotropic effects, and atorvastatin calcium, a statin with lipid-lowering as well as pleiotropic anti-atherosclerotic properties. Amlodipine and atorvastatin have been demonstrated in numerous clinical trials to be highly effective in lowering blood pressure and low-density lipoprotein cholesterol (LDL-C). Furthermore, both amlodipine and atorvastatin have been demonstrated to reduce cardiovascular events in a broad range of patients. The amlodipine/atorvastatin single pill has been shown to improve patients' achievement of national guideline-recommended blood pressure and lipid target levels and exhibits a safety profile consistent with its parent compounds. The combination pill is available in formulations appropriate for administration across therapeutic dose ranges targeted to a wide variety of hypertensive patients with additional risk factors and differing degrees of cardiovascular risk, or with manifest cardiovascular disease. Single-pill amlodipine/atorvastatin has the potential to improve the management of hypertensive patients with additional cardiovascular risk factors, especially dyslipidemia, by reducing pill burden and prescription costs. This potential has important implications because hypertensive patients with additional risk factors represent a large proportion of those at risk for cardiovascular events.
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PMID:A single-pill combination of amlodipine besylate and atorvastatin calcium. 1662 58

Insulin resistance and the consequent metabolic disorders are associated with a state of platelet hyperactivity. Oxidative stress is responsible for the persistent platelet activation. We sought to study the inhibitory effect of cardiotonic pills, an oral herbal component, on platelet function in a dog model with insulin resistance induced by high-fat feeding. We fed 18 dogs with a high-fat diet and six dogs with normal chow as control for 6 months. Then, six dogs were fed with a high-fat diet and received additional aspirin (250 mg/day), and another six dogs received additional cardiotonic pills (1,000 mg/day) for 4 months. Time-course changes in metabolic parameters and platelet function were detected. After high-fat feeding for 6 months, 18 dogs developed a series of metabolic disorders including obesity, dyslipidemia, oxidative stress and insulin resistance. In addition, a platelet hyperactivity state, characterized by increased agonist (arachidonic acid, ADP and collagen) induced platelet aggregation, platelet expression of adhesion molecules (P-selectin and GP IIb/IIIa), and platelet intracellular calcium concentration, was indicated. Cardiotonic pills showed a significant antioxidative activity by presenting an increase in plasma superoxide dismutase and decrease in erythrocyte glutathione, as well as a lipid-lowering effect (decrease in both plasma cholesterol and triglyceride). Either aspirin or cardiotonic pills could significantly reverse the platelet hypersensitivity and hyperfunction. Compared with aspirin, cardiotonic pills showed a more exaggerated inhibitory effect on platelet function (a significantly decreased collagen-stimulated platelet aggregation, and expression of adhesion molecules). In conclusion, cardiotonic pills inhibited platelet hyperfunction in dogs with insulin resistance. This inhibitory effect may mainly be explained by antioxidative activity and metabolic control.
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PMID:Inhibitory effects of cardiotonic pills on platelet function in dogs fed a high-fat diet. 1665 67

Cardiovascular disease (CVD), including atherosclerosis, hypertension, myocardial infarction, and cerebrovascular accidents, constitutes an important cause of morbidity and mortality in adults with chronic kidney disease (CKD). However, evidence has been accumulating over the past several years that children and young adults with CKD also experience significant cardiovascular complications. Studies in the United States and Europe have shown that CVD is a leading cause of death in young adults diagnosed with CKD in childhood. Risk factors include hypertension, dyslipidemia, anemia, and abnormal calcium-phosphorus metabolism, all of which are present in many children with CKD. Although improved control of uremia and treatment of traditional and nontraditional cardiovascular risk factors have proved to be beneficial in adults with CKD, no such data exist for children. The NIH is currently conducting a large-scale, prospective observational study of children with CKD that should help to elucidate the role of CVD in the progression of CKD in children and what interventions might reduce the risk of cardiovascular complications in these young patients.
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PMID:Cardiovascular disease in children with chronic renal failure. 1669 98


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