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

Hyperlipidaemia and platelet hyperfunction have been considered as high-risk factors for atherogenesis. Simultaneous study of these two parameters was undertaken in 43 patients with atherosclerosis (as evidenced by frank myocardial infarction, MI, in 23 patients and ischemic heart disease, IHD, in 20 patients); and in 36 normal subjects who were matched for age (45 to 60 years). Incidence of either of these parameters being high was 36% in normals, 85% in atherosclerosis. Four subjects with circulating platelet aggregates and hyperlipidaemia showed progression of the lesion by crossing over the category of normal to IHD (two) and from IHD to MI (two). These two risk factors, together or independently, appear to cause and control the progress of atherosclerosis and their simultaneous study can be used for its diagnosis. A concept of subintimal hyperlipidosis is presented since none of the existing theories can explain the existence of atherosclerotic lesions exclusively on the developed vascular musculature.
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PMID:Clinical laboratory assessment of atherosclerosis--role of hyperlipidaemia and hyperactive platelets. 371 96

A project on "Aggregation of Red Cells" has been accepted by NASA in 1977. An automated slit-capillary photo-viscometer has been designed during 1979-1984, and its last version met NASA's space hazards requirements. The 'heart' of instrument is a set of two highly polished glass plates, spaced by a gap of 12.5 micrometers. An original drum-like infusion pump allows utilization of up to eight blood samples. During a sequential process, blood flows through the slit, and then stops to allow formation of aggregates. Micro- and macro-photography is carried out, and 500 photographs are obtained. Blood from normal donors and patients with history of ischaemic heart disease, colon cancer, juvenile-onset diabetes, hyperlipidaemia, etc., is anticoagulated and adjusted to haematocrit of 0.30 using native plasma. Samples are divided, and infused into the 'flight' and 'ground' instruments. Prior to experiment temp. is 5 degrees C; temp. during experiment is 25 degrees C. Experiments took place on 24-25 January 1985, on the middeck of space shuttle 'Discovery'. Subsequent results showed that red blood cells do not change shape under zero gravity; that aggregation of red cells does take place; that aggregates in pathologic blood show morphology of normal rouleaux under zero gravity, while identical blood shows clumps of red cells on the ground. The latter observation suggests that zero gravity might affect cell-to-cell interaction, and perhaps microstructure of the cell membrane. These aspects must remain however tentative till a confirmation by subsequent experiments can be obtained.
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PMID:Execution of "ARC" experiment on space shuttle "Discovery" STS 51-C: some results on aggregation of red blood cells under zero gravity. 377 59

Apolipoprotein E phenotypes were determined on 417 consecutive lipid clinic patients using an isoelectric focussing technique. Of the 15 patients with phenotype E2/2, 13 (3.1%) had type III hyperlipoproteinaemia and 2 obese identical twins had type V. A further 20 patients (4.8%) had similar plasma and lipoprotein lipid levels but were E2 heterozygotes (14 E3/2 and 6 E4/2). They displayed a widened pre-beta-band almost confluent with the beta-band rather than the broad beta-band shown in classical E2/2 type III patients. In view of the similarities between these heterozygotes and the classical homozygous (E2/2) type III patients and their occurrence in the same families we suggest the nomenclature homozygous and heterozygous type III. In a subsequent comparison between 30 E2/2, 22 E3/2 and 8 E4/2 type III individuals the only significant difference in plasma and lipoprotein lipid parameters was a lower VLDL cholesterol to triglyceride ratio of 0.85 in E3/2 patients than that of 1.24 in E2/2 patients (P less than 0.01). Both homozygous and heterozygous patients showed premature ischaemic heart disease and both responded dramatically and similarly to treatment with clofibrate. These observations indicate that apo E phenotyping is worthwhile in all patients with combined hyperlipidaemia and that homozygous and heterozygous type III hyperlipoproteinaemia is not uncommon.
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PMID:Apolipoprotein E phenotypes in hyperlipidaemic patients and their implications for treatment. 386 82

Primary hyperbetalipoproteinemia (type II hyperlipoproteinemia) is a common disorder associated with premature vascular disease. It is frequently due to genetic abnormalities, some of which are expressed in childhood. We have examined the manner in which that form of hyperbetalipoproteinemia known as familial hypercholesterolemia may be expressed in 236 children aged 1-19 born of 90 matings in which one parent had hyperbetalipoproteinemia of this variety and one parent did not.Two Gaussian populations were fitted to the distribution of both low density lipoprotein cholesterol (C(LDL)) and plasma cholesterol (C) in these children and a likelihood ratio test strongly favored a two over a one population model for both C(LDL) (X(2) = 18.41, P < 0.0005) and C (X(2) = 7.81, P < 0.025). 45% of the children were in the population identified as affected; their mean C(LDL) was 229. The remaining 55% were in the normal population with a mean C(LDL) of 110 which was indistinguishable from that of an unrelated control population, aged 1-19. On the basis of an assumed frequency of hyperbetalipoproteinemia in the general population of 5%, the Edwards' test indicated that a polygenic model of inheritance was highly unlikely (expected, 22%; observed, 45%). The segregation ratio obtained from the derived intersection between the two population curves (C(LDL), 164 mg/100 ml; C, 235 mg/100 ml) was 45/55 (abnormal/normal). The percentage of abnormal children in the first decade (52%) significantly exceeded that in the second (39%) (P < 0.01). The ratios (II/N) were 50/47 and 55/84 in the offspring of affected female and male parents, respectively (X(2) = 3.819, 0.05 < P < 0.10). Only 10% of hyperbetalipoproteinemic children were considered to have hyperglyceridemia. These children, frequently, but not invariably, had a parent with hyperglyceridemia in addition to hyperbetalipoproteinemia (P < 0.05). None of the affected children who were examined had ischemic heart disease (IHD) and 7% had tendon xanthomas. Half of the parents (mean age, 37.4 yr) who were examined had IHD and three-quarters had xanthomas. The data agree well with the hypothesis that hyperbetalipoproteinemia is inherited as a monogenic trait with early expression in these children. More than one genetic defect within the group is not excluded, but retrospective analyses of the 345 first-degree adult relatives of the affected parents indicated that most of the abnormal parents probably represented familial hypercholesterolemia, rather than combined hyperlipidemia, the other most generally recognized form of familial hyperbetalipoproteinemia.
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PMID:Familial hypercholesterolemia (one form of familial type II hyperlipoproteinemia). A study of its biochemical, genetic and clinical presentation in childhood. 436 6

During 1965-9 22 women aged 41 years or less have been seen with myocardial infarction. Eleven had been taking oral contraceptives. This prevalence of oral contraception (50%) is appreciably greater than that estimated for women of the same age in the general population.Nine of these 11 women had an independent increased risk of developing ischaemic heart disease because of hyperlipidaemia, hypertension, or excessive cigarette smoking. Ten of the 11 not taking an oral contraceptive also had a readily identifiable predisposing factor. None of the 22 showed carbohydrate intolerance. The similarity of the two groups is the striking finding. Details of 15 women of comparable age seen during 1960-4 before oral contraceptives were widely used are also presented, and they had similar characteristics.Oral contraceptives do not appear on their own to increase the risk of developing myocardial infarction, but they may do so in women otherwise prone to ischaemic heart disease. Suggestions are made for the identification of these women.
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PMID:Oral contraceptives and myocardial infarction. 544 7

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.
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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

Platelet aggregability and plasma factor VIII-related antigen (F. VIIIR:AG) level in 16 ischemic heart disease (IHD) patients were increased by isometric exercise and these changes were prevented by administration of a lipid lowering agent, simfibrate, a derivative of clofibrate. Serum total cholesterol (TC) level decreased and the high density lipoprotein-cholesterol (HDL-C)/TC ratio increased with the treatment. Another 7 hyperlipidemics were administered with simfibrate. Platelet malondialdehyde (MDA) production decreased with improvement in lipid profile. In an in vitro study, platelet aggregability and the plasma level of von Willebrand factor (vWF) and F.VIIIR:AG of normal citrated blood were increased by passing it through a glass bead column. Combining above results of the three separate studies, it would be suggested that hyperlipidemia might enhance platelet activation in vivo, which occurred through contact of platelets to atherosclerotic rough vessel surface. The anti-platelet effect of simfibrate might be mediated through its effect on arachidonic pathway in platelets.
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PMID:Influence of lipids metabolism on platelet activation in vivo. 641 24

Vitamin E, cholesterol and triglycerides were measured in blood sera of 167 patients (40-59 years old) with angina pectoris. An increase in concentration of vitamin E was observed only in patients with hyperlipidemia, whereas the vitamin content was similar to the control values in patients with hypertension, in smokers and in the persons free of risk factor. Distinct correlation was found only between vitamin E and the triglycerides contents (r = 0.42). These data corresponded to the results of a previous examination of 224 men and 435 women without ischemic heart disease: in men the content of vitamin E correlated with triglycerides (r = 0.50) and in women--with cholesterol (r = 0.34). The ratio of vitamin E/triglycerides appears to be a more adequate index of the vitamin content in men.
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PMID:[Vitamin E and serum lipids in ischemic heart disease]. 647 33

We analyzed the heterogeneity of apo E in very low density lipoprotein from 58 hyperlipidemic subjects with or without atherosclerosis, 69 patients with ischemic heart disease, and 100 apparently healthy individuals. Apo E gene frequencies in the group of healthy individuals were comparable with those in German and American populations. The distribution of six common apo E phenotypes in the groups of hyperlipidemia and ischemic heart disease was similar to that in the healthy group. In addition to the three major isoforms of apolipoprotein E (apo E-4, E-3, and E-2) and the new one (apo E-5) which was recently found in this laboratory, we have discovered an additional series of components, which showed themselves as at least three bands on an isoelectric focusing gel in the region of E-VII through E-V, in four patients with hyperlipidemia and atherosclerosis. The new series of apo E components, named apo E-Suita, was identical with the ordinary apo E in its interaction with heparin-Sepharose gel and with anti-apo E antibody. The most basic component of apo E-Suita (E-VII) was the unsialylated form and other components (E-VI and E-V), the sialylated forms. Family studies revealed that apo E-Suita was determined by inheritance of a new apo E allele located at the same locus as the hitherto known apo E components. Apo E-5 and apo E-Suita isoproteins had isoelectric points more basic than apo E-3, the parent type, by two and four units of charge, respectively. While the apo E-Suita isoprotein had the same molecular weight as ordinary major apo E isoproteins, the molecular weight of the apo E-5 isoprotein was approximately 1,500-2,000 lower than the other apo E isoproteins by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The incidence of abnormal apo E components, including apo E-5 and apo E-Suita, was high among patients with hyperlipidemia and ischemic heart disease (7:127), while we could not find such components among 100 healthy individuals. Moreover, five of seven patients with the abnormal apo E had overt atherosclerotic disease. The findings suggest that these kinds of apolipoprotein mutation are closely related to the development of atherosclerosis.
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PMID:New mutants of apolipoprotein E associated with atherosclerotic diseases but not to type III hyperlipoproteinemia. 648 Aug 26

From March 1960 through January 1968, 71 patients underwent operations for renovascular hypertension at our center. There were three operative deaths in 94 procedures. Primary nephrectomy was performed in 26 patients. Attempted revascularization of 62 kidneys was successful in 46 (74%). In 13 (87%) of the 15 cases considered operative failures, the patients underwent either secondary nephrectomy (11) or repeat revascularization (two). Based on the results of the final operation, initial blood pressure response (1 to 6 months postoperatively) in the surviving patients indicated 44% cured (30 patients), 40% improved (27), and 16% unchanged (11). The sequential clinical, functional, and anatomic follow-up evaluations to time of death or to date are available in 66 of the 68 patients (97%) who survived operation and form the basis of this report. Fifteen- to 20-year arteriographic follow-up in 16 patients revealed one late neointimal anastomotic stenosis and an additional three aortic suture line false aneurysms in Dacron aortorenal grafts. During this 15- to 23-year follow-up, 71% of atherosclerotic (AS) patients and 23% of fibromuscular dysplasia (FMD) patients died. Cardiovascular (CV) morbid events occurred in 77% of AS patients and in 19% of FMD patients. The cumulative incidence of death and CV morbid events during follow-up is examined by Kaplan-Meier life tables and Cox's proportional hazards regression analysis in these respective groups to identify preoperative markers predictive of longer event-free survival in relation to blood pressure benefit by operation (for example, focal vs. diffuse AS, presence of cerebrovascular disease, ischemic heart disease, left ventricular hypertrophy seen by electrocardiography, azotemia, smoking, diabetes, and hyperlipidemia).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Operative management of renovascular hypertension. Results after a follow-up of fifteen to twenty-three years. 648 67


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