Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated coronary ostial stenosis is a rare condition of unknown etiology previously reported in only 22 patients. Of 2,105 consecutive patients with angiographically defined coronary disease, 27 (1.3%) had 50% or greater stenosis of one or both coronary ostia. Serious complications occurred during angiography in three patients (11%) with one death. Coronary bypass surgery was performed in 25 patients with 1 early death (4.0%) and 1 late death (mean follow-up 28 months). Twenty-two patients (Group 1) had associated multivessel coronary disease, of whom 18 (82%) presented with stable angina of variable duration (43 +/- 53 months) and 10 (46%) were in the New York Heart Association functional class II. The prevalence of risk factors was high, especially among the eight women (3.0 +/- 0.8 per patient), seven of whom had hyperlipidemia. Five patients (Group 2) representing 0.2% of the total had isolated coronary ostial stenosis. All were women (age 41 +/- 6 years). In contrast to patients in Group 1, this group presented with a short history (2.0 +/- 1.7 months) of severe angina and had a low incidence of risk factors (0.8 +/- 0.6 per patient). Histopathologic study in one case showed typical atheroma. Isolated coronary ostial stenosis is a rare lesion occurring predominantly in young or middle-aged women. The clinical and angiographic profile appears unique and, despite the histopathologic findings, suggests a natural history distinct from that usually seen in atherosclerotic coronary disease.
J Am Coll Cardiol 1986 May
PMID:Isolated coronary ostial stenosis in women. 395 82

Family history is an important predictor of coronary risk. However, this relation, in large part, is not explained by the known risk factors such as systemic hypertension or hyperlipidemia. In the present study, plasma lipid, lipoprotein lipid, and plasma low-density lipoprotein (LDL) apoB levels were measured in 66 offspring (myocardial infarction [MI] offspring) of 24 families in which an index parent had premature coronary artery disease and hyperapobetalipoproteinemia. These results were compared to those obtained in 207 control children and young adults. Univariate analysis revealed that plasma LDL apoB and all other lipid and lipoprotein levels except high-density lipoprotein cholesterol were significantly higher in the MI offspring. Multivariate analysis showed plasma LDL apoB and LDL cholesterol best differentiated the MI offspring from control children and young adults. Of the 66 children, 22 had hyperapobetalipoproteinemia, of whom only 7 had clearly abnormal LDL cholesterol or plasma triglyceride levels. Thus, a substantial portion of children born to a parent with premature coronary artery disease and hyperapobetalipoproteinemia have the same disorder of lipoprotein metabolism.
Am J Cardiol 1985 Feb 01
PMID:Familial aggregation and early expression of hyperapobetalipoproteinemia. 396 64

The plasma concentration of beta-thromboglobulin (BTG), a platelet-specific protein released during platelet aggregation, is considered a sensitive marker of in vivo platelet activity. The mean plasma level in 133 asymptomatic individuals was 32.3 +/- 1.1 ng/ml, and there was no difference between those with no risk factors (32.2 +/- 1.2 ng/ml, n = 56), those who smoked (31.8 +/- 1.8 ng/ml, n = 45), those with hyperlipidemia (32.8 +/- 1.7 ng/ml, n = 15), and those exposed to both of these risk factors (34.1 +/- 2.7 ng/ml, n = 17). The mean plasma BTG level in 104 patients with symptomatic ischemic heart disease was significantly elevated (40.9 +/- 1.4 ng/ml, p less than 0.01), but there was considerable overlap with normal levels. Although no difference was found between patients with no risk factors (38.1 +/- 4.0 ng/ml, n = 13) and those with only 1 risk factor (37.0 +/- 1.8 ng/ml, n = 44), patients with 2 or more risk factors ahd a significantly elevated plasma BTG level (45.2 +/- 2.2 ng/nl, n = 47, p less than 0.01). It is concluded that risk factors themselves do not increase platelet activity, but that patients with vascular disease have activated platelets that may contribute to the progression of the disease. Plasma BTG was also measured serially for 10 days in 29 patients after hospitalization with acute ischemic cardiac pain. Although the median plasma level was elevated above normal there were no acute changes in plasma BTG after either acute infarction (n = 22) or acute ischemia (n = 7), except in 2 patients in whom pericardial friction rubs developed. Thus, measurement of systemic plasma BTG did not detect platelet involvement in acute coronary occlusion or acute ischemia.
Am J Cardiol 1982 Dec
PMID:Plasma beta-thromboglobulin as a measure of platelet activity. Effect of risk factors and findings in ischemic heart disease and after acute myocardial infarction. 618 69

An exercise test may be characterized as positive because of the production of either electrocardiographic ST-segment depression or elevation. The relationship of exercise-induced ST-segment deviation to the specific motion abnormalities of the individual segments of the left ventricular wall was investigated. The first 280 subjects to enter the Program of Surgical Control of Hyperlipidemia were studied by treadmill exercise testing and left ventriculography. The results showed that exercise-induced ST-segment elevation could occur without evidence in the resting subject of either dyskinesia or aneurysm of the left ventricle, that the area of left ventricular damage was much greater in subjects with exercise-induced ST-segment elevation than in those with ST-segment depression, and that wall motion abnormalities were concentrated in the inferoposterior area in the group with ST-segment elevation, but were generally scattered throughout the left ventricular wall in the group with ST-segment depression.
Am J Cardiol 1983 Sep 01
PMID:Directional ST-segment deviation in graded exercise tests correlated with motion of the individual segments of the left ventricular wall. 661 66

After nearly 10 years in clinical use, prazosin has been shown in numerous studies worldwide to be an effective antihypertensive agent over the entire range of hypertension (mild, moderate, and severe), when used alone or in multitherapy. In addition to its general effectiveness, prazosin is particularly useful in specific subpopulations of hypertensive patients, such as those with impaired renal function, those on hemodialysis, and those with concomitant heart block, bronchospasm, diabetes mellitus, or disturbed carbohydrate metabolism, hyperlipidemia, or hyperuricemia. The side effects of prazosin are usually mild and transient and seldom require discontinuation of the drug. Sexual dysfunction is uncommon. In clinical experience with 22,000 patients receiving an initial dose of 1 mg of prazosin, syncope was reported in 1 of every 667 patients (0.15%). Withholding diuretics for 1 day before initiating prazosin therapy, utilizing prazosin as first-line therapy, limiting the initial dose to 1 mg, and taking it at bedtime are all helpful in eliminating many of the initial adverse effects. Fluid retention, although rare and not as pronounced as that with other antihypertensive agents, may develop on long-term therapy and may necessitate the addition of a diuretic later on.
Am J Cardiol 1983 Feb 24
PMID:Effectiveness of prazosin as initial antihypertensive therapy. 682 27

A large segment of the population gradually develops insulin resistance, and the related metabolic syndrome is one of the most frequent causes of atherosclerosis. Searching for a practical indicator of insulin resistance, we studied the correlations between fasting serum insulin level, the general manifestations of insulin resistance syndrome, and various aspects of coronary artery disease in 797 men and 322 women. After we classified patients according to the quartiles of serum insulin level, we noted in the top quartile the presence of practically all manifestations of insulin resistance syndrome in persons of both sexes (e.g., increased waist/hip ratio, body mass index, glucose, uric acid, triglycerides, apolipoprotein B and decreased high-density lipoprotein cholesterol levels as well as apolipoprotein A-I/B ratios, and so forth). We also noted a higher prevalence of hypertension, diabetes mellitus, and type IV hyperlipidemia. Significantly more women in the fourth than in the first quartile had angiographically documented significant stenosis of the coronary arteries (p = 0.0016, odds ratio 2.9, 95% confidence interval 1.5 to 5.6) and previous myocardial infarction (p = 0.0297, odds ratio 2.1, 95% confidence interval 1.1 to 4.1). Men in both the first and the fourth quartile had a more disturbed lipid profile and a higher prevalence of significant stenoses of coronary arteries and/or previous myocardial infarction than women; there was a tendency toward a lower prevalence of alcohol consumption (p = 0.0503), a higher prevalence of gout (p = 0.0634), and previous myocardial infarction (p = 0.0791) in men in the fourth than in the first quartile.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1995 Dec 01
PMID:Fasting hyperinsulinism, insulin resistance syndrome, and coronary artery disease in men and women. 748 1

Although combination therapy using 3-hydroxy-3-methylglutaryl coenzyme A (HMG-Co-A) reductase inhibitors and fibrates is efficacious in combined hyperlipidemia, such treatment has been associated with myopathy. For this reason, we studied the effects of fluvastatin and gemfibrozil, alone or in combination, on muscle. A total of 21 patients with combined hyperlipidemia were recruited who were matched for age, body mass index, and baseline levels of total cholesterol, low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), triglycerides, creatine phosphokinase, and myoglobin. Patients were randomized to three groups for 6-week treatment with fluvastatin at 40 mg/day, gemfibrozil at 600 mg twice daily, or a combination of the two drugs. Parameters for muscle damage were rises in levels of serum creatine phosphokinase and myoglobin compared with pre-exercise levels; these were assessed 1 hr and 8 hr after a 45 min lean body mass standardized ergometer test, which was performed before and after treatment in all patients. Biopsies from the quadriceps muscle were taken 48 hr after each test. Fluvastatin lowered total cholesterol and LDL-C by 23% and 35%, respectively (p < 0.01), with no effects on triglycerides and HDL-C. Gemfibrozil lowered triglycerides by 40% (p < 0.01) but did not lower total cholesterol or LDL-C significantly. The combination therapy decreased total cholesterol, LDL-C, and triglycerides by 28%, 29%, and 39%, respectively (p < 0.05). Pre-exercise creatine phosphokinase and myoglobin levels were not affected by treatment in any group.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1995 Jul 13
PMID:Treatment of combined hyperlipidemia with fluvastatin and gemfibrozil, alone or in combination, does not induce muscle damage. 760 87

The accelerated atherosclerosis in diseases associated with elevated remnant lipoprotein levels has directed interest toward the response of this lipoprotein species to lipid-lowering treatment. The effect of fluvastatin--a synthetic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor--was compared with that of placebo on parameters of remnant metabolism in 57 patients with moderate hypercholesterolemia, but not heterozygous familial hypercholesterolemia, type III hyperlipidemia, or endogenous hypertriglyceridemia. Fluvastatin therapy resulted in decreases versus baseline in plasma total cholesterol, low density lipoprotein cholesterol (LDL-C) and LDL apolipoprotein (apo) B levels of 18%, 20%, and 18%, respectively (p < 0.01). Plasma parameters related to remnant metabolism were also significantly decreased: intermediate density lipoprotein by 43% and apo E by 22% (p < 0.01). The percent decrease in plasma intermediate density lipoprotein cholesterol level was twice that of LDL-C and 50% greater than the decrease seen in very low density lipoprotein cholesterol (VLDL-C), which was decreased by 28%. Total triglycerides were reduced by 11% and VLDL apo B by 24%, whereas high density lipoprotein cholesterol (HDL-C) rose significantly by 8%, HDL2-C by 24%, and HDL3-C by 3%. There were no increases in apo A-I levels compared with placebo nor any significant change in plasma lipoprotein(a) levels. The composition of LDL and VLDL particles did not appear to be altered by therapy, as assessed by the LDL-C:LDL-B, VLDL-C:VLDL-B, or triglyceride:VLDL-B ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1995 Jul 13
PMID:Effect of fluvastatin on intermediate density lipoprotein (remnants) and other lipoprotein levels in hypercholesterolemia. 760 88

High-risk patients with dyslipidemias resistant to diet and single-agent pharmacotherapy may require combination therapy to achieve target levels of low density lipoprotein, triglycerides, and high density lipoprotein. Combinations of fibrates and 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors are effective, but because of safety concerns related to myopathy and rhabdomyolysis, it is important to consider the possibility of pharmacokinetic interactions when such combinations are used. In this study, the area under the curve, maximum plasma concentration, and time to maximum concentration for fluvastatin and gemfibrozil are compared, when used alone and in combination, in patients with hyperlipidemia and either coronary or carotid atherosclerosis, or a family history of coronary artery disease. A total of 17 patients were studied in a random sequence, open-label, crossover study of fluvastatin at 20 mg twice daily, gemfibrozil at 600 mg twice daily, and the combination of the 2 drugs. No significant difference was observed in area under the curve, maximum plasma concentration, and time to maximum concentration when comparing the combination with each drug alone. These pharmacokinetic data add support to the clinical observations that the combination of fluvastatin and gemfibrozil is both effective and safe.
Am J Cardiol 1995 Jul 13
PMID:Pharmacokinetics of the combination of fluvastatin and gemfibrozil. 760 6

This study was designed to evaluate the therapeutic effectiveness of 3 different pharmacologic lipid-lowering regimens in the treatment of patients with clustered lipid risk factors. Sixty-five patients with low high-density lipoprotein (HDL) levels and hypertriglyceridemia were randomized to 1 of 3 treatment arms: pravastatin/niacin, pravastatin/magnesium, or pravastatin/placebo. After 18 weeks, patients in the pravastatin/niacin group had a -41% change in the total cholesterol/HDL ratio compared with -13% in the pravastatin/magnesium arm and -16% in the pravastatin/placebo group. The HDL2 and HDL3 subfractions, as well as the apolipoprotein A-I levels, were increased significantly only in the pravastatin/niacin arm. The levels of small dense low-density lipoprotein (LDL) cholesterol (LDL3) were decreased to a greater extent in the pravastatin/niacin arm (-43%) than in either the pravastatin/magnesium (-13%) or the pravastatin/placebo (-20%) arm. Only the pravastatin/niacin regimen significantly diminished postprandial lipemia (-32% change in the remnant particle triglyceride concentration and decreased very-low-density lipoprotein remnant levels). Thus, in this group of patients with clustered risk factors, the combination of pravastatin and niacin resulted in significant improvements in HDL and triglyceride levels, total cholesterol to HDL ratio, small dense LDL levels, and postprandial lipemia. Pravastatin alone or in combination with magnesium resulted in less significant changes that were largely limited to LDL cholesterol reduction.
Am J Cardiol 1995 Sep 01
PMID:Effects of pravastatin with niacin or magnesium on lipid levels and postprandial lipemia. 765 48


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