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)

Diuretics and beta-blockers have a strong tendency to affect serum lipids adversely, whereas the peripherally acting alpha-blocking agents consistently result in beneficial effects. Most of the other antihypertensive agents (calcium channel blockers, ACE inhibitors, angiotensin II receptor antagonists, and drugs that act centrally) are lipid neutral. The effect of steroid hormones varies with the drug, dose, and route of administration. In general, androgens lower HDL-C and have a variable effect on LDL-C. The effects of progestins vary greatly depending on their androgenicity, and estrogens are beneficial except when hypertriglyceridemia occurs with oral estrogens. Glucocorticoids raise HDL-C and may also increase triglycerides and LDL-C. Retinoids increase triglycerides and LDL-C and also reduce HDL-C. Interferons can cause hypertriglyceridemia. Following organ transplantation, a dyslipidemia often ensues. This is caused in part by the medications used to prevent rejection (glucocorticoids, cyclosporine, and FK-506) and requires close attention and, in some patients, drug therapy to prevent coronary artery disease.
Endocrinol Metab Clin North Am 1998 Sep
PMID:Drugs causing dyslipoproteinemia. 978 60

There is increasing evidence that essential hypertension is associated with a panoply of metabolic abnormalities. Included in these abnormalities are insulin resistance, dyslipidemia, enhanced coagulation, and decreased fibrinolytic activity, microalbuminuria, and platelet abnormalities and endothelial dysfunction. Visceral obesity appears to be the most common and predictive underlying factor for all of these metabolic abnormalities accompanying hypertension as well as increased cardiovascular disease (CVD) risk. As the prevalence of obesity is increasing, there is cause for concern that CVD increases will parallel this risk factor, particularly in especially high-risk populations, such as African-American women. Other important risk factors, such as increased oxidative stress, may require special therapeutic strategies, including the use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin blockers as cornerstones of antihypertensive drug therapy.
Curr Opin Cardiol 1998 Sep
PMID:Diabetic vascular disease and hypertension. 982 85

The aim of this review was to examine the relative contributions of systolic and diastolic blood pressures to the risk of cardiovascular disease on the basis of epidemiologic evidence from the Framingham Heart Study and the change in attitudes toward systolic blood pressure that occurred during the course of the study. Historic texts were evaluated in comparison with data from the Framingham Heart Study, a prospective longitudinal analysis of the relation between blood pressure and occurrence of subsequent cardiovascular morbidity and mortality rates in a fixed cohort. Historically, systolic hypertension has been considered an innocent accompaniment to arterial stiffening, occurring as a compensatory phenomenon in the elderly. Epidemiologic data show that the development of hypertension is neither inevitable nor beneficial. The data also provide evidence that systolic pressure is more important than diastolic pressure as a determinant of cardiovascular sequelae. Mild or moderate elevations of systolic blood pressure, even when unaccompanied by diastolic pressure elevations, are associated with an increased risk of cardiovascular disease. Risk is increased further by the added presence of related metabolic disturbances such as dyslipidemia, glucose intolerance, insulin resistance, cardiac hypertrophy, and obesity. Over-reliance on diastolic blood pressure in assessing the risk of hypertension can be misleading. Systolic pressure constitutes a powerful predictor of cardiovascular disease and a valuable tool when incorporated within multivariate risk formulas for estimating the conditional probability of coronary and stroke events.
Am Heart J 1999 Sep
PMID:Historic perspectives on the relative contributions of diastolic and systolic blood pressure elevation to cardiovascular risk profile. 1046 14

An increasing series of pediatric endocrinopathies and metabolic anomalies has been recognized as related to reduced prenatal growth. We have tested whether the association of precocious pubarche (PP), dyslipidemia, and low serum IGF binding protein-1 in girls is also related to reduced prenatal growth. Fasting serum lipids, lipoproteins, and IGFBP-1 concentrations were measured in 187 girls (83 without PP and 104 with PP; mean age, 11.8 y; range, 5-18 y) with known birthweight and gestational age, the latter being transformed into birthweight SD scores. Birthweight SD scores of girls with PP were lower than those of girls without PP. Within the group of PP girls, those with dyslipidemia and low IGFBP-1 had lower (p < 0.0001) birth-weight SD scores (-2.02+/-0.23; mean +/- SEM) than those with normal lipids, lipoproteins, and IGFBP-1 (-0.37+/-0.15), whereas girls with an intermediate number of abnormalities had intermediate birthweight SD scores (-0.80+/-0.18). In conclusion, dyslipidemia and low serum IGFBP-1 in girls with PP were found to be related to reduced prenatal growth, an observation pointing to the prenatal origin of these metabolic abnormalities.
Pediatr Res 1999 Sep
PMID:Precocious pubarche, dyslipidemia, and low IGF binding protein-1 in girls: relation to reduced prenatal growth. 1047 48

The prevalence of cardiovascular disease (CVD) and atherosclerosis varies among several minority ethnic groups in the United States. Recently, small, dense low density lipoprotein (LDL) particle size has been recognized as a risk factor for CVD. We examined LDL size as a possible explanation for differences in CVD rates in 1571 subjects from the Insulin Resistance Atherosclerosis Study (IRAS), a multiethnic study of insulin resistance and cardiovascular risk factors. LDL size (A) was significantly different by ethnic group (African Americans 262.1+/-0.6, Hispanics 257.6+/-0.6, and non-Hispanic whites 259.2+/-0.4, P<0.001). Ethnic differences in LDL size continued to be statistically significant after adjustment for upper body adiposity, insulin resistance, and glucose tolerance status. However, after further adjustment for other cardiovascular risk factors, especially ethnic differences in triglyceride and high density lipoprotein (HDL) cholesterol levels, the ethnic differences in LDL size were markedly attenuated and in general no longer statistically significant. The relation of triglyceride, HDL cholesterol, insulin resistance, and adiposity to LDL size in each ethnic group was similar. LDL size differs by ethnic group, which is independent of obesity or insulin resistance. These ethnic differences appear to be due to ethnic variations in dyslipidemia (especially differences in triglyceride levels); ethnic differences in LDL size are not consistent with previously reported ethnic dissimilarities in CVD or atherosclerosis.
Arterioscler Thromb Vasc Biol 1999 Sep
PMID:LDL size in African Americans, Hispanics, and non-Hispanic whites : the insulin resistance atherosclerosis study. 1047 67

Large-scale clinical trials have shown that long-term treatment with lipid-lowering therapy results in a significant reduction in the occurrence of heart failure among patients with coronary artery disease without previous evidence of congestive heart failure, suggesting dyslipidemia may have an adverse effect on left ventricular performance. To examine whether dyslipidemia has a detrimental effect on left ventricular systolic function and whether this effect is dependent on the corresponding severity of coronary atherosclerosis, 114 consecutive patients with stable angina and a positive exercise thallium-201 myocardial perfusion single-photon emission computed tomography were studied. All patients underwent measurement of serum lipid profiles, right-sided heart catheterization, left ventriculography, and selective coronary arteriography. Mean serum levels of total cholesterol and triglycerides were 4.5 and 1.4 mmol/l, respectively. In univariate analysis, a significant positive correlation between serum high-density lipoprotein (HDL) cholesterol and left ventricular ejection fraction (LVEF) (r = 0.49, P<0.0001) was found. Patients in the lower tertile of serum HDL cholesterol had a significantly lower mean LVEF than those in the upper tertile (55.9+/-15.2 vs. 72.8+/-6.8%, P<0.0001). Stepwise multiple linear regression analysis revealed that LVEF significantly correlated with HDL cholesterol (P<0.0001), the Gensini score (P = 0.008), and diabetes mellitus (P = 0.08) (r = 0.55, P<0.0001). In subgroup analysis of patients with angiographically normal coronary arteries, serum HDL cholesterol was still significantly associated with LVEF. The present study demonstrated an independent association between low HDL cholesterol and subclinical left ventricular systolic dysfunction in Chinese patients with stable angina whose serum levels of total cholesterol and triglycerides were relatively low. Moreover, this correlation remained significant even in patients with normal coronary angiograms, suggesting HDL cholesterol might influence left ventricular systolic performance through extra-atherosclerotic mechanisms.
Atherosclerosis 1999 Sep
PMID:The effects of dyslipidemia on left ventricular systolic function in patients with stable angina pectoris. 1048 94

It is well known that cardiovascular risk factors and dyslipidemia along with obesity can be identified early in life. Serum lipids and lipoproteins influence skin vessel reactivity in adults. The purpose of this study was to investigate the cutaneous microcirculation and its correlation to dyslipidemia in obese children. Thirty-four obese children and an equal number of age- and sex-matched healthy children were enrolled in this study. Laser Doppler flowmetry and dynamic capillaroscopy were performed to measure total cutaneous blood flow and nutritional blood flow, respectively. A significantly higher cutaneous baseline flow and peak flow after a 1-min arterial occlusion was noticed in obese group as compared to normal control. Results of dynamic capillaroscopy revealed values of resting capillary blood cell velocity that did not differ from controls but a significantly lower peak CBV after a 1-min arterial occlusion in obesity. Plasma lipids examination showed a high triglycerides and low high density lipoprotein cholesterol levels in obesity. Pearson analysis detected no significant correlations between pCBV, baseline flow and peak flow and dyslipidemia in obesity. These results may be explained by the fact that the duration of dyslipidemia in our study population was not long enough to cause vascular damage or the dyslipidemia was not pronounced enough to have an impact on skin vessel activity tests. It is also possible, that the combination of methods used in the present study was not sensitive enough to detect an existing correlations between flow values and high triglycerides/low HDL-cholesterol values in the obese group. Our results suggest that all the responses of the cutaneous microcirculation were mainly due to physiological compensatory rather than pathological reactions in young obese children. The results of cutaneous microcirculatory assessment in obese children provide follow-up parameters for assessing the risk of cardiovascular diseases later in life.
Atherosclerosis 1999 Sep
PMID:Increased cutaneous blood flow but impaired post-ischemic response of nutritional flow in obese children. 1048 2

Recent studies have suggested that hypercholesterolemia is associated with endothelial dysfunction. In patients with type 2 diabetes mellitus, dyslipidemia is mainly characterized by hypertriglyceridemia, low high density lipoprotein, and a preponderance of small dense low density lipoprotein (LDL) particles. We have examined the relationships among LDL subfractions, the susceptibility of LDL to oxidation in vitro, and endothelial function in type 2 diabetes mellitus. LDL subfractions were measured by density gradient ultracentrifugation. The susceptibility of LDL to oxidation was determined by measuring the kinetics of conjugated dienes formation during copper-mediated oxidation of LDL. Endothelium-dependent and independent vasodilation of the brachial artery were assessed by high resolution vascular ultrasound. Diabetic patients had a higher concentration of small dense LDL-III than matched controls (P < 0.01). The lag phase of conjugated dienes formation was shorter in the diabetic patients (P < 0.05), and the rate of LDL oxidation was faster (P < 0.05). Both endothelium-dependent (P < 0.01) and independent dilation of the brachial artery (P < 0.01) were impaired in the diabetic patients. On multivariate analysis, the rate of oxidation and LDL-III concentration accounted for 12% and 6%, respectively, of the variation in endothelium-dependent vasodilation (adjusted r2 = 0.18; P < 0.05), whereas LDL-III concentration and the maximum amount of conjugated dienes formed accounted for 27% and 5%, respectively, of the variation in endothelium-independent vasodilation (adjusted r2 = 0.32; P < 0.01) in the diabetic patients. In conclusion, endothelial and smooth muscle cell dysfunction in type 2 diabetes were related to abnormalities in LDL subfractions and in LDL oxidation.
J Clin Endocrinol Metab 1999 Sep
PMID:Influence of low density lipoprotein (LDL) subfraction profile and LDL oxidation on endothelium-dependent and independent vasodilation in patients with type 2 diabetes. 1048 89

Modern cardiac rehabilitation is a comprehensive program of secondary prevention for patients with heart disease. Moreover, it is an important context in which to broach issues of impaired sexual function. Sexual problems plague a large portion of our cardiac patient population. Unspoken+ concerns about impotence, now more correctly called erectile dysfunction (ED), are common, as are concerns about the safety of engaging in sexual activity, especially after major cardiac events or therapeutic interventions. A large proportion of patients do not return to normal sexual activity after a cardiac event. Many factors, including normal age-related changes in sexual response, medication-induced dysfunction, and vascular changes associated with risk factors (e.g., diabetes and dyslipidemia), as well as the emotional impact of symptomatic heart disease, may influence sexual function in these patients. These factors, occurring alone or in combination, probably explain the discouraging prevalence of sexual dysfunction in patients with manifest cardiac disease. Because so few patients have specific cardiac reasons for limiting sexual activity, a clear opportunity exists for cardiologists and their staff to help enhance the emotional well-being and overall quality of life of their cardiac patients.
Am J Cardiol 1999 Sep 09
PMID:Sexual activity and the cardiovascular patient: guidelines. 1050 70

In the United States, coronary heart disease (CHD) is the leading cause of death in women. The incidence of CHD rises dramatically in women following menopause, which can be partially attributed to a more atherogenic lipoprotein profile. For years, observational and epidemiological data have suggested that estrogen and progesterone therapy reduced CHD end points. However, the first prospective trial that evaluated hormone replacement therapy (HRT) for secondary CHD prevention demonstrated no positive cardiovascular benefit of HRT compared with placebo. In interventional studies, the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA)reductase inhibitors significantly reduced CHD outcomes in postmenopausal women, and these agents have emerged as the drugs of choice for primary and secondary CHD prevention. The selective estrogen receptor modulators (SERMs) may have a role in CHD prevention, but long-term clinical trials evaluating end points are needed. An evidence-based approach is necessary when deciding the appropriate pharmacotherapy of dyslipidemia in postmenopausal women.
J Womens Health Gend Based Med 1999 Sep
PMID:Pharmacotherapy of dyslipidemia in postmenopausal women: weighing the evidence. 1053 93


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