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

The effects of a vasodilating beta-blocker, celiprolol, on insulin sensitivity and cardiovascular risk factors were compared with those of another beta1-selective adrenoceptor blocker, calcium channel blockers, and angiotensin-converting enzyme (ACE) inhibitors. A randomized 21-month crossover trial was carried out with 25 patients with dyslipidemia receiving antihypertensive monotherapy. The study consisted of a 3-month active run-in period and two treatment periods, during which the patients received celiprolol (200-400 mg daily) or the control drug for 12 and 6 months in a crossover manner. A hyperinsulinemic euglycemic clamp and an oral glucose tolerance test (OGTT) were performed every 6 months. According to the clamp tests, the insulin-sensitivity index increased on average by 32% (p < 0.0001) during celiprolol treatment compared with that with the other antihypertensive agents, including ACE inhibitors. In OGTT, area under the incremental glucose curve decreased by 36% (p = 0.002) during celiprolol treatment, whereas insulin secretion diminished on average by 26% (p = 0.006). The mean decrease in fasting serum triglycerides was 11% (NS), whereas the high-density lipoprotein to low-density lipoprotein (HDL/LDL) ratio increased by 15% (p = 0.012). The results suggest that celiprolol improves insulin sensitivity of hypertensive patients with dyslipidemia in long-term therapy.
J Cardiovasc Pharmacol 1998 Jan
PMID:Insulin sensitivity in a long-term crossover trial with celiprolol and other antihypertensive agents. 945 88

The reduction of coronary mortality is not as large as one would expect from the observed blood pressure lowering in trials of antihypertensive medications. This is not surprising; hypertension is a complex disease where the high blood pressure is only one of numerous coronary risk factors. Sympathetic overactivity in hypertension, independent of the blood pressure, may be conducive to premature atherosclerosis by inducing insulin resistance and dyslipidemia. Through its trophic effect on blood vessels, sympathetic overactivity potentiates vasoconstriction. This, in turn, accelerates hypertension and the metabolic syndrome. The hypertrophy of small coronary arterioles decreases the coronary reserve and enhances coronary spasms. Tachycardia, which is due to increased sympathetic tone and a decreased parasympathetic tone, favors arrhythmias and sudden death in congestive heart failure and hypertension. Increased hematocrit is frequently found in male patients with hypertension, and high hematocrit is a predictor of coronary heart disease/thrombosis. The increase of hematocrit is in part due to an alpha adrenergic postcapillary venoconstriction. Enhanced sympathetic drive, insulin resistance and dyslipidemia have been demonstrated also in congestive heart failure, but the clinical importance of these findings is not fully understood.
Scand Cardiovasc J Suppl 1998
PMID:Clinical consequences of the autonomic imbalance in hypertension and congestive heart failure. 954 Jan 30

Our aim was to investigate systemic nitric oxide (NO) production and its potential determinants such as insulin resistance, dyslipidemia, and circulating methylated analogs of L-arginine in uncomplicated essential hypertension (EH). Nineteen newly diagnosed, untreated male subjects with mild pure uncomplicated EH and 11 normotensive controls were studied at rest after an overnight fast. The groups had comparable age, body mass index, creatinine clearance, cholesterol, fasting glucose, and insulin. In hypertensives, the urinary excretion rate of nitrite plus nitrate (Unox), an index of endogenous NO production, was depressed (56+/-17 vs. 77+/-23 micromol/mmol creatinine; p < 0.05), whereas plasma levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthesis, were increased (2.4+/-1.1 vs. 1.1+/-0.7 microM; p < 0.005). Circulating concentrations of symmetric dimethylarginine were similar in both groups (1.4+/-1.3 vs. 1.5+/-1.1 microM; p = NS). The L-arginine-to-ADMA ratio was reduced in hypertension (3.3+/-0.5 vs. 4.5+/-0.8; p < 0.001 for In-transformed data). There was no correlation between Unox and either the magnitude of insulin resistance or dyslipidemia in EH. Thus in male subjects with EH, endogenous systemic NO formation appears depressed, which is unrelated to accompanying insulin resistance or dyslipidemia. Circulating ADMA levels are increased in uncomplicated EH, which may be of potential relevance.
J Cardiovasc Pharmacol 1999 Apr
PMID:Reduced urinary excretion of nitric oxide metabolites and increased plasma levels of asymmetric dimethylarginine in men with essential hypertension. 1021 38

Patients with diabetes mellitus have an increased prevalence of hypertension and associated cardiovascular disease (CVD), including coronary and cerebrovascular disease. The risk of an individual of developing CVD is much greater when both diseases coexist and is further magnified by their frequent association with dyslipidemia, coagulation, platelet, and endothelial abnormalities. Metabolic abnormalities frequently associated with hypertension are insulin resistance, enhanced coagulation, and decreased fibrinolytic activity. Drug treatment of hypertension in diabetic subjects is fraught with potential difficulties, including altered efficacy of medications, possible side effects, worsening of glycemic control, and impairment of lipid metabolism. Because hypertension is a major contributor to morbidity and mortality in diabetes, it should be recognized and treated early and aggressively despite these difficulties. This article reviews the efficacy and side effects of the various classes of antihypertensive agents in patients with diabetes mellitus.
Prog Cardiovasc Dis
PMID:Special considerations in the therapy of diabetic hypertension. 1044 70

There are currently four classes of drugs available to treat dyslipidemia: niacin, bile acid-binding resins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, and fibric acid derivatives. Each acts at a unique point in a complex set of interrelated lipid metabolic pathways. The mechanism of action and adverse effects of these four classes are reviewed briefly. The efficacy of antioxidants and the importance of compliance issues are described.
J Cardiovasc Nurs 2000 Jan
PMID:Pharmacology department: pharmacologic approaches to abnormal blood lipids. 1065 72

Cardiovascular disease remains a frequent cause of morbidity and mortality in industrialized countries, particularly in subjects with hypertension, diabetes mellitus, and dyslipidemia, conditions frequently associated with central obesity. Identification of early morphological and/or functional alterations of the cardiovascular system may help target individuals most likely to benefit from preventive measures. The literature data and our own experience suggest that parameters that are direct expressions of cardiovascular damage, can be identified at an early stage. For example, diastolic dysfunction may precede the clinical expression of several cardiac diseases, left ventricular hypertrophy is one of the first manifestations of cardiac involvement in hypertension, central obesity and diabetes mellitus, and a carotid plaque may point to concomitant coronary artery disease. Other early manifestations of cardiovascular involvement are microalbuminuria and endothelial dysfunction. Insulin resistance and alterations of the renin-angiotensin-aldosterone system play an important physiopathogenic role in the development of cardiovascular damage in obese subjects, and their association with risk and cardiovascular disease has been confirmed in numerous studies. Since all these changes generally precede overt clinical manifestations and are closely related to cardiovascular morbidity, they may help identify individuals at the highest risk of cardiovascular events.
Nutr Metab Cardiovasc Dis 1999 Apr
PMID:Early markers of cardiovascular damage in obese subjects. 1072 13

Atherosclerosis starts in childhood, and is accelerated in some individuals. A cluster of clinical and biochemical factors constitute the risk profile for many of them, perhaps most important being metabolic insulin resistance syndrome. Insulin resistance and its components for children and adolescents, especially obesity and dyslipidemia, are generators of hypertension, glucose intolerance and complications of atherosclerosis in adulthood. Some individuals are genetically predisposed, particularly those with the family history of such disorders. For many subjects, there is 'tracking' of metabolic and lifestyle factors from early age to adulthood. Several new risk factors of atherosclerosis (e.g. level of lipoprotein (a), procoagulant state, hyperhomocysteinemia, low birth weight and adverse in-utero environment, and possibly inflammatory markers) are current and potentially future areas of research concerning children and young individuals. Definition of and research on new and hitherto not investigated factors and formulation of strategies to neutralize the known factors are of paramount importance for primary prevention of atherosclerosis. Simple and effective measures for prevention include increasing awareness of the diseases, maintenance of ideal body weight, regular physical exercise, avoidance of smoking and chewing of tobacco, eating a balanced diet, and early periodic monitoring of blood pressure and metabolic status. These measures, starting from childhood, should be applied to all and in particular to the susceptible offspring, predisposed individuals, and populations.
J Cardiovasc Risk 2000 Jun
PMID:Risk factors for atherosclerosis in young individuals. 1100 92

Insulin resistance is a common metabolic abnormality that is associated with an increased risk of both atherosclerosis and type 2 diabetes. The phenotype of insulin resistance includes a dyslipidemia characterized by an elevation of very low-density lipoprotein triglyceride, a reduction in high-density lipoprotein cholesterol, and the presence of small, triglyceride-enriched low-density lipoproteins. The underlying metabolic abnormality driving this dylipidemia is an increased assembly and secretion of very low-density lipoprotein particles, leading to an increased plasma level of triglyceride. Hypertriglyceridemia, in turn, results in a reduction in the high-density lipoprotein level and the generation of small, dense low-density lipoproteins; these events are mediated by cholesteryl ester transfer protein. In addition, hypertension, obesity, and a prothrombotic state are also integral components of the insulin resistance syndrome. In this review, we will provide a pathophysiologic basis, based on studies on humans and in tissue culture, for the dyslipidemia of insulin resistance. We will also review the effects of insulin resistance on the coagulation and fibrinolytic pathways. It is hoped that this review will allow health professionals better to evaluate and treat their patients with insulin resistance, thereby reducing the very much increased risk of atherosclerotic cardiovascular disease carried by these individuals.
J Cardiovasc Risk 2000 Oct
PMID:The insulin resistance syndrome: impact on lipoprotein metabolism and atherothrombosis. 1114 62

The manifestations of syndrome X increase the risk of coronary heart disease (CHD) as much, if not more so, than elevated low-density lipoprotein (LDL) cholesterol concentrations. The fundamental abnormality leading to the manifestations that comprise syndrome X is resistance to insulin regulation of muscle glucose uptake and adipose tissue lipolysis. To prevent decompensation of glucose tolerance, patients with syndrome X secrete large amounts of insulin. Treatment should be aimed at 1) increasing insulin sensitivity, 2) attenuating day-long hyperinsulinemia, and 3) pharmacologic treatment of the specific manifestations of syndrome X if lifestyle interventions are not entirely successful. The two major lifestyle modulators of insulin action are body weight and physical fitness--the heavier and the more sedentary a patient is, the greater the degree of insulin resistance and compensatory hyperinsulinemia. In overweight, insulin-resistant patients, the magnitude of insulin resistance is attenuated with weight loss (10 to 15 pounds). Aerobic exercise (30 minutes a session, three to four times a week) is equally effective, irrespective of the presence of obesity. In the absence of associated weight loss, the usually recommended low-fat, high-carbohydrate diet makes the manifestations of syndrome X worse. This is because the more carbohydrates present in the insulin-resistant patient's diet, the greater the insulinogenic stimulus to the pancreas, and hence day-long plasma insulin levels are higher. Replacing saturated fat with monounsaturated and polyunsaturated fat instead of carbohydrates provides the same favorable effect on LDL cholesterol concentrations without the insulin-stimulating effect of low-fat, high-carbohydrate diets. This intervention does not affect insulin resistance, but maintains day-long insulin levels as low as possible. Although lifestyle changes can be very effective in attenuating the manifestations of syndrome X, it may be necessary to initiate pharmacologic treatment aimed at controlling dyslipidemia and hypertension. The major obstacle to reducing the risk of CHD in patients with syndrome X is becoming aware of its manifestations. After this is accomplished, the relatively simple approaches outlined herein are an effective treatment strategy.
Curr Treat Options Cardiovasc Med 2001 Aug
PMID:Syndrome X. 1144 62

The major goal in treatment of patients with dyslipidemia is to decrease the short- and long-term incidence of cardiovascular events, including myocardial infarction, unstable angina, stroke, and death. A second goal in patients with severe hypertriglyceridemia is to decrease the risk of acute pancreatitis. Improvement of the lipid profile can be achieved through a combination of aggressive lifestyle modification and effective drug therapy. Treatment should be tailored to the individual patient, based on the specific lipid abnormalities, the presence or absence of pre-existing coronary artery or other atherosclerotic vascular disease, and an assessment of overall cardiovascular risk.
Curr Treat Options Cardiovasc Med 2001 Aug
PMID:Dyslipidemia. 1144 64


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>