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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Achieving long-term graft survival and optimal patient health are ultimate clinical goals in renal transplantation. Many factors negatively impact long-term transplant outcomes, including graft rejection, renal dysfunction and increased cardiovascular burden. Additionally, glucose metabolism disturbance, also a cardiovascular risk factor, influences morbidity and mortality. As such, careful consideration of the immunosuppressive strategy and its impact on these factors is critical to optimizing outcomes. Large-scale clinical trials and registry studies conducted over the past decade have demonstrated tacrolimus to be a cornerstone immunosuppressant in renal transplantation. Compared with ciclosporin treatment, tacrolimus has been shown to be associated with decreased acute and chronic rejection, improved renal function over the long term post-transplant, as evidenced by lower serum creatinine concentrations and a slower decline in the glomerular filtration rate, and a superior cardiovascular risk profile, as demonstrated by lower incidences of hyperlipidaemia and hypertension. The incidence of new-onset diabetes in patients receiving tacrolimus is low due to continued refinement of tacrolimus-based regimens and a better understanding of the effects of tacrolimus on metabolic parameters. Together, these findings may translate into improved long-term transplant outcomes with tacrolimus-based immunosuppression. In fact, long-term follow-up results from multicentre trials plus data from registry analyses are already documenting improved survival with this cornerstone immunosuppressant.
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PMID:Improving long-term renal transplant outcomes with tacrolimus: speculation vs evidence. 1557 22

Prevalence of dyslipidaemias in a representative sample of the French population Hypercholesterolaemia is a major factor of risk of coronary atherosclerosis. The prevalence of other types of dyslipidaemia in the general population remains poorly defined. This study was performed to measure the prevalence of various dyslipidaemias in the French population. A representative sample of 3508 men and women between the ages of 35 and 64 years was recruited by the "Multinational MONItoring of trends and determinants in CArdiovascular disease" centres of Lille, Strasbourg and Toulouse. We excluded 162 patients suffering from known cardiovascular disorders, and 409 individuals treated with lipid-lowering drugs. The prevalence of pure hypercholesterolaemia, defined as a total cholesterol concentration >6.2 mmol/l (2.4 g/l) and triglyceride concentration <2.3 mmol/l (2 g/l), was 30% (29-32%). The prevalence of HDL cholesterol concentration <1 mmol/l (0.4 g/l) in men, or <1.3 mmol/l (0.5 g/l) in women, was 12% (11-13%). The prevalence of mixed hyperlipidaemia, defined as a total cholesterol concentration >6.2 mmol/l (2.4 g/l) and triglyceride concentration >2.3 mmol/l (2 g/l) was 5% (4-6%). The prevalence of hypertriglyceridaemia, defined as a total cholesterol concentration <6.2 mmol/l (2.4 g/l) and triglyceride concentration >2.3 mmol/l (2 g/l) was 4% (3-5%). Low HDL cholesterol concentrations were associated with smoking, obesity, and absence of either regular physical exercise or alcohol consumption. This study confirmed the high prevalence of pure hypercholesterolaemia, and revealed an important prevalence of low HDL cholesterol concentration, which represents a major cardiovascular risk factor.
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PMID:[Prevalence of dyslipidaemias in a representative sample of the French population]. 1578 4

Hyperlipidemia is a cardiovascular risk factor. In patients with idiopathic dilated cardiomyopathy (IDC), prognostic roles of endogenous lipoproteins are not fully clarified. It has been known that there is a direct relationship between the levels of cytokines (tumor necrosis factor-alpha [TNF-alpha] and interleukin-6 [IL-6]) and deteriorating functional classes of heart failure and mortality. The present study compared the levels of circulating TNF-alpha, IL-6, lipoproteins, and apolipoproteins in patients with stable IDC (n = 28) with those of patients with unstable IDC (n = 26) and controls (n = 24). Mean serum total cholesterol (TC) was significantly lower in stable IDC patients than controls (p < 0.05). In unstable IDC patients, mean serum TC was also lower than controls but not statistically significant. The IDC patients had significantly higher concentrations of IL-6 and TNF-alpha than the controls (p < 0.01). Serum IL-6 and Apo AI levels were significantly different between stable and unstable IDC patients (p = 0.021 and p = 0.012, respectively). Increased levels of IL-6 were associated with decreased levels of TC (r = -0.266, p = 0.019), LDL-C (r = -0.376, p = 0.001) and apolipoprotein AI (apo AI) (r = -0.495, p < 0.001) in all IDC patients. TNF-alpha was also inversely related to apo AI (r = -0.455, p < 0.001) and LDL-C (r = -0.364, p = 0.001) in all patients. Thus, elevated serum levels of cytokines in patients with IDC are associated with decreased lipoprotein concentrations, which may indicate impaired prognosis.
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PMID:Decreased serum lipoprotein levels as a guide for clinical severity in patients with idiopathic dilated cardiomyopathy. 1594 48

Hypertriglyceridemia is a cardiovascular risk factor in type-2 diabetes. However, this abnormality may be caused by several mechanisms. In familial hypertriglyceridemia, a hyperlipidemia associated with type-2 diabetes, plasma accumulation of non atherogenic particles explains the presence of hypertriglyceridemia. Our objective was to compare the prevalence of coronary insufficiency and carotid artery stenosis in patients with type-2 diabetes with or without familial hypertriglyceridemia. Controls were paired against cases based on age, gender, diabetes duration, treatment and other cardiovascular risk factors. Controls had either a normal lipid profile (n=48) or hyperlipidemia (n=15). The intima-media thickness of the carotid arteries was significantly lower in cases compared to controls (0.55 +/- 0.12 vs 0.63 +/- 0.22 in normolipidemic controls and 0.66 +/- 0.18 mm in hyperlipidemic subjects (p=0.02)). Exercise treadmill testing was abnormal in a similar proportion of cases and controls (4.8 vs 6.2%). Incidence of cardiovascular complications was not different between groups. We therefore conclude that severe hypertriglyceridemia due to familial hypertriglyceridemia is not associated with an increased prevalence of symptomatic atherosclerosis in patients with type-2 diabetes.
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PMID:[Familial hypertriglyceridemia and diabetes mellitus type 2]. 1602 85

Endothelial dysfunction contributes to mechanisms of atherogenesis and its clinical manifestations, including coronary heart disease. Cardiovascular risk factors have been linked directly to a loss of endothelial function, such as endothelium-dependent nitric oxide (NO) release, resulting in abnormal vasodilation in response to various stimuli. There is evidence that multiple risk factors, including hypertension and hyperlipidemia, lead to a synergistic effect on endothelial dysfunction, likely through oxidative stress mechanisms. Damage to the endothelium leads to reduced NO bioavailability and facilitates vessel wall permeability to low-density lipoprotein. Certain agents, including the antihypertensive drug amlodipine and the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) atorvastatin, are known to influence endothelial function and NO bioavailability directly; these properties may contribute to clinical benefits. Recent experimental evidence at the cellular level indicates that these agents stimulate NO release from human endothelial cells in a highly synergistic fashion. The clinical implications of these observations are discussed in this article in the context of cardiovascular risk factor management strategies.
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PMID:A rationale for combination therapy in risk factor management: a mechanistic perspective. 1635 9

Environmental as well as genetic factors are involved in the pathogenesis of myocardial infarction. The disease is a frequent cause of mortality in the middle-aged male population of Estonia. The high prevalence of premature myocardial infarction (PMI) in this country is not fully understood. The association of atherogenic and thrombogenetic risk factors with lifestyle was evaluated in men who had suffered myocardial infarction at 55 years of age (n = 71) and in randomly selected corresponding controls (n = 85). Serum routine lipids, apolipoprotein (apo)A-I, apoB, apoE polymorphism, lipoprotein(a) and fibrinogen levels were determined. Behavioural risk factors, indices of obesity, blood pressure and pedigree data were registered. In 80.6 % of PMI subjects some type of hyperlipidaemia was observed (European Atherosclerosis Society Classification) and lipid-lowering drugs were taken by 13.9 % of patients. In PMI patients the most common positive determinants of atherogenic lipoprotein indices were waist-to-hip ratio and physical inactivity, and in controls, waist-to-hip ratio and apoE phenotype. The odds ratio (OR) of PMI was 8.9-fold greater in the highest tertile of apoB/apoA-I distribution compared with the lowest tertile. The OR of PMI in the highest tertile of fibrinogen distribution versus the lowest tertile was 6.2 (95 % CI 2.46-15.44), and OR of PMI in the highest Lp(a) tertile versus the lowest was 3.1 (95 % CI 1.31-7.40). Thus, atherogenic dyslipidaemia was the most serious cardiovascular risk factor among PMI patients. From two thrombogenesis-related markers, the levels of fibrinogen and Lp(a), the first one was more strongly associated with PMI status.
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PMID:Determinants of risk factors of atherosclerosis in the postinfarction period: the Tallinn MI study. 1671 48

Left ventricular hypertrophy (LVH) is an early manifestation of cardiovascular target organ damage in patients with arterial hypertension. It is not only a target organ response to increased after-load, but is also the most potent cardiovascular risk factor. LVH is multifactorial sign which has several causative factors in addition to blood pressure. Asymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of NO synthase. ADMA plasma levels have been shown to be elevated in diseases related to endothelial dysfunction such as hypertension, hyperlipidemia, diabetes mellitus. Because cardiac remodeling is associated with endothelial NO pathway, some recent studies investigated whether the plasma ADMA was related to LVH and found that there is a link between ADMA and left ventricular mass and geometry. ADMA was two times higher in patients with concentric LVH than in those normal controls. In many experimental systems, accumulation of ADMA is accompanied by reduced dimethylarginine dimethylaminohydrolase (DDAH) activity. Plasma ADMA is cleared in small part by urinary excretion, but the bulk of ADMA is degraded by DDAH. Therefore, we proposed that change in DDAH activity could disturb the metabolism of ADMA and result in hypertensive LVH through the ADMA/NO pathway.
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PMID:Dimethylarginine dimethylaminohydrolase (DDAH)--a critical regulator of hypertensive left ventricular hypertrophy? 1798 7

Diabetes mellitus (DM) is an important cardiovascular risk factor and is associated with abnormalities in endothelial and vascular smooth muscle cell function, evoked by chronic hyperglycemia and hyperlipidemia. Chronic insulin deficiency or resistance is marked by decreases in the intensity of glucose transport, glucose phosphorylation, and glucose oxidation, plus decreases in ATP levels in cardiac myocytes. It is important to search for new agents that promote glucose consumption in the heart and partially inhibit extensive fatty acid beta-oxidation observed in diabetic, ischemia. When the oxygen supply for myocardium is decreased, the heart accumulates potentially toxic intermediates of fatty acid beta-oxidation, that is, long-chain acylcarnitine and long-chain acyl-CoA metabolites. Exogenous glucose and heart glycogen become an important compensatory source of energy. Therefore we studied the effect of the antidiabetic 1,4-dihydropyridine compound cerebrocrast at concentrations from 10(-10) M to 10(-7) M on isolated rat hearts using the method of Langendorff, on physiological parameters and energy metabolism. Cerebrocrast at concentrations from 10(-10) M to 10(-7) M has a negative inotropic effect on the rat heart. It inhibits L-type Ca(2+)channels thereby diminishing the cellular Ca(2+) supply, reducing contractile activity, and oxygen consumption, that normally favors enhanced glucose uptake, metabolism, and production of high-energy phosphates (ATP content) in myocardium. Cerebrocrast decreases heart rate and left ventricular (LV) systolic pressure; at concentrations of 10(-10) M and 10(-9) M it evokes short-term vasodilatation of coronary arteries. Increase of ATP content in the myocytes induced by cerebrocrast has a ubiquitous role. It can preserve the integrity of the cell plasma membranes, maintain normal cellular function, and inhibit release of lactate dehydrogenase (LDH) from cells that is associated with diabetes and heart ischemia. Administration of cerebrocrast together with insulin shows that both compounds only slightly enhance glucose uptake in myocardium, but significantly normalize the rate of contraction and relaxation ( +/- dp/dt). The effect of insulin on coronary flow is more pronounced by administration of insulin together with cerebrocrast at a concentration of 10(-7) M. Cerebrocrast may promote a shift of glucose consumption from aerobic to anerobic conditions (through the negative inotropic properties), and may be very significant in prevention of cardiac ischemic episodes.
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PMID:Acute effect of antidiabetic 1,4-dihydropyridine compound cerebrocrast on cardiac function and glucose metabolism in the isolated, perfused normal rat heart. 1799 Feb 88

The metabolic syndrome represents a cluster of cardiovascular risk factors that occur together more commonly than expected from the prevalence of their individual rates. Insulin resistance is widely believed to be the common denominator causing, in susceptible individuals, the development of various cardiovascular risk factor components of the syndrome (e.g., hyperlipidemia, hypertension, and hyperglycemia). The major cause of this insulin resistance appears to be obesity, especially the accumulation of visceral fat. This obesity is due to the combination of excessive caloric intake and inadequate physical activity rather than alterations in energy utilization. In individuals whose beta cells cannot increase their insulin secretion adequately to compensate for insulin resistance, hyperglycemia occurs.
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PMID:Glycemic control in the metabolic syndrome and implications in preventing cardiovascular disease. 1837 Jul 49

Worldwide, along with the increasing prevalence of obesity, the number of people with prediabetes is increasing. The diagnostic criteria for prediabetes include impaired fasting glucose, impaired glucose tolerance, and metabolic syndrome. The presence of two or more of these three criteria renders a person at high risk for future diabetes. The treatment goal of prediabetes is to prevent future development of type 2 diabetes and diabetes-related cardiovascular complications. The treatment approach is twofold: glycemic control and control of cardiovascular risk factors, mainly hypertension and hyperlipidemia. Intensive lifestyle modification is the mainstay of treatment in low-risk patients. When lifestyle modification fails and in high-risk patients, medications such as metformin and/or acarbose are recommended. For high-risk patients and those who progress despite intensive lifestyle modification, thiazolidinediones are also recommended. The goals for cardiovascular risk factor control are similar to those for patients with diabetes.
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PMID:What is the best treatment for prediabetes? 1979 2


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