200 Different Cholesterol Studies
From 1988 to
Life Flow One
The Solution For Heart Disease
by
Karl Loren
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HealthGate Documents
Record 1 from database: MEDLINE
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- Title
- Pathogenesis of cholesterol gallstones.
- Author
- Hofmann AF
- Address
- Department of Medicine, University of California, San Diego, La Jolla 92093.
- Source
- J Clin Gastroenterol, 1988, 10 Suppl 2:, S1-11
- Abstract
- Symptomatic cholesterol gallstone disease occurs because of the combination
of a number of biochemical and physiologic defects: formation of supersaturated
bile, nucleation, crystal retention, stone growth, and gallbladder inflammation.
There are several possible explanations for the high prevalence of
supersaturated bile in the Western adult human as compared to other adult
mammals. First, the human liver is defective in converting cholesterol to bile
acids; the majority of cholesterol is eliminated as cholesterol. Second, the
large flux of cholesterol in vesicular form is not matched by a large flux of
recycling bile acids. Third, humans live sedentary lives and voluntarily reduce
their caloric requirement to prevent obesity. Low caloric intake decreases the
circulation of bile acids (including the flux through the hepatocyte). Fourth,
the human species is a defective bile secretor in terms of biliary volume
(microliter/kg-min) compared to other mammals. This is because human
enterohepatic circulation of bile acids is "sluggish" and because bile
acid-independent flow is also lower than in all other mammals. The accumulation
of deoxycholic acid, a secondary bile acid formed in the colon, appears to cause
secretion of bile that is supersaturated in cholesterol, and may also
contribute. Five additional risk factors explain why cholesterol gallstone
disease is so prevalent. First, the human species has a gallbladder, and the
irregular meal pattern of humans may be responsible for prolonged storage of
bile. Second, bile from cholesterol gallstone patients nucleates cholesterol
more rapidly. Third, defective gallbladder contraction is associated with
cholesterol gallstone disease in the majority of gallstone patients. Fourth, the
healthy gallbladder absorbs cholesterol and desaturates bile--protective
functions that may be lost with chronic cholecystitis. Finally, the presence of
gallstones stimulates mucous secretion, which traps cholesterol crystals.
- Language of Publication
- English
- Unique Identifier
- 89093852
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- MeSH Heading (Major)
- Bile|*; Cholelithiasis|AN/*ET; Cholesterol|*AN
- MeSH Heading
- Animal; Bile Acids and Salts|ME; Energy Intake; Human; Support, Non-U.S.
Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0192-0790
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Bile Acids and Salts); 57-88-5 (Cholesterol)
Record 2 from database: MEDLINE
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- Title
- Structure of genes encoding steroidogenic enzymes.
- Author
- Miller WL
- Address
- Department of Pediatrics, University of California, San Francisco 94143.
- Source
- J Steroid Biochem, 1987, 27:4-6, 759-66
- Abstract
- Synthesis of adrenal steroid hormones from cholesterol entails the actions
of only five enzymes, four of which are specific forms of cytochrome P450. These
cytochrome P450 enzymes have all been isolated and their activities
reconstituted in vitro, showing that each enzyme catalyses multiple steroidal
conversions. Genes or complementary DNAs have been cloned for human P450scc (the
cholesterol side-chain cleavage enzyme), P450c17 (17 alpha-hydroxylase/17,20
lyase) and P450c21 (21-hydroxylase). The sequences for microsomal P450c17 and
P450c21 are much more closely related to one another than either is to the
sequence for mitochondrial P450scc. Each of these P450 enzymes is encoded by a
single human gene; the gene for P450scc lies on chromosome 15, that for P450c17
lies on chromosome 10, and that for P450c21 lies on chromosome 6. The human,
mouse and bovine genomes each have two P450c21 genes. While only one of these is
active in mouse and man, both genes may be active in cattle. A wide variety of
lesions in the human P450c21(B) gene causes congenital adrenal hyperplasia, a
common genetic disorder.
- Language of Publication
- English
- Unique Identifier
- 88092587
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- MeSH Heading (Major)
- Adrenal Cortex Hormones|*BI; Cytochrome P-450|*GE/ME
- MeSH Heading
- Adrenal Glands|ME; Aldehyde-Lyases|GE/ME; Animal; Base Sequence; Cattle;
Cholesterol|ME; Cholesterol Monooxygenase (Side-Chain-Cleaving)|GE/ME;
Comparative Study; DNA|GE; Human; Male; Mice; Multienzyme Complexes|GE/ME;
Progesterone Reductase|GE/ME; Sequence Homology, Nucleic Acid; Steroid
Isomerases|GE/ME; Steroid 17 alpha-Monooxygenase|GE/ME; Steroid
21-Monooxygenase|GE/ME; Testis|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0022-4731
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- EC 1.1.1.145 (Progesterone Reductase); EC 1.14.15.6 (Cholesterol
Monooxygenase (Side-Chain-Cleaving)); EC 1.14.99.10 (Steroid 21-Monooxygenase);
EC 1.14.99.9 (Steroid 17 alpha-Monooxygenase); EC 4.1.2. (Aldehyde-Lyases); EC
4.1.2.30 (17 alpha-Hydroxyprogesterone Aldolase); EC 5.3.3.- (Steroid
Isomerases); 0 (Adrenal Cortex Hormones); 0 (Multienzyme Complexes); 0 (3
beta-hydroxysteroid oxidoreductase-delta(5) 3-ketosteroid isomerase); 57-88-5
(Cholesterol); 9007-49-2 (DNA); 9035-51-2 (Cytochrome P-450)
Record 3 from database: MEDLINE
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- Title
- Probucol, high-density lipoprotein metabolism and reverse cholesterol
transport.
- Author
- Gwynne JT
- Address
- Division of Endocrinology, University of North Carolina School of Medicine,
Chapel Hill.
- Source
- Am J Cardiol, 1988 Jul 25, 62:3, 48B-51B
- Abstract
- Accumulation of cholesterol within the arterial wall reflects an imbalance
between delivery and efflux. Monocyte-derived macrophages play a major role in
arterial wall cholesterol accumulation. Using tracer methodology in a rabbit
model, several investigators have estimated the rate of cholesterol delivery and
thus the steady-state rate of efflux to be between 0.4 and 2.4
micrograms/cm2/hour. The process responsible for arterial wall cholesterol
efflux, "reverse cholesterol transport," can be conceptualized as a
sequence of events including (1) loss of cell cholesterol, (2) intravascular
cholesterol transport, (3) hepatic cholesterol uptake, and (4) biliary
secretion. Work by many investigators has characterized these individual
processes.
- Language of Publication
- English
- Unique Identifier
- 88279425
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- MeSH Heading (Major)
- Cholesterol|*ME; Lipoproteins, HDL|*ME; Phenols|*PD; Probucol|*PD
- MeSH Heading
- Animal; Arteries|DE/ME; Biological Transport|DE; Diffusion; Human;
Macrophages|DE/ME; Receptors, Cell Surface|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9149
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (HDL receptor); 0 (Lipoproteins, HDL); 0 (Phenols); 0 (Receptors, Cell
Surface); 23288-49-5 (Probucol); 57-88-5 (Cholesterol)
Record 4 from database: MEDLINE
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- Title
- Cholesterol reduction and coronary artery disease. An overview of clinical
trials up to 1986.
- Author
- Tikkanen MJ; Pyörälä K
- Address
- Third Department of Medicine, University of Helsinki, Finland.
- Source
- Drugs, 1988, 36 Suppl 3:, 27-31
- Abstract
- The 'cholesterol hypothesis' has been proven in a wealth of experimental,
clinical, genetic and epidemiological studies. Cholesterol-lowering trials
reviewed here have compared the effects of various treatment modalities on
coronary heart disease reduction. They have shown that prevention of coronary
heart disease depends on the magnitude and duration of cholesterol reduction,
not on the way it was achieved. Collective evidence from all unconfounded trials
indicates that most of the benefit of such intervention is achieved within
relatively few years of starting the intervention. With the possible exception
of adverse effects associated with clofibrate, cholesterol-lowering intervention
has not produced any untoward effects that cause concern.
- Language of Publication
- English
- Unique Identifier
- 89338072
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- MeSH Heading (Major)
- Anticholesteremic Agents|*TU; Cholesterol|*BL; Coronary Disease|*PC
- MeSH Heading
- Clinical Trials; Diet; Human; Support, Non-U.S. Gov't
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0012-6667
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Anticholesteremic Agents); 57-88-5 (Cholesterol)
Record 5 from database: MEDLINE
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- Title
- Regression of atherosclerosis.
- Author
- Arntzenius AC
- Address
-
- Source
- Horm Metab Res Suppl, 1988, 19:, 19-22
- Abstract
- The reverse of progression of atherosclerotic disease is regression of
atherosclerosis: established lesions get smaller. Animal experiments and post
mortem findings have provided investigators with considerable evidence of the
reversibility of atherosclerosis. It was, however, with arteriography in living
man, as used in prospective intervention trials, that proof was given that
atherosclerosis can be made to regress. The Leiden Intervention Trial and the
Cholesterol Lowering Atherosclerosis Study (CLAS) both have shown that with
aggressive lowering of serum cholesterol, be it with diet alone or with diet and
cholesterol-lowering drugs, atherosclerosis growth can be retarded and reversed.
The Leiden Intervention Trial and the CLAS study stress that cholesterol levels
should be lowered in angina pectoris patients and in bypassed patients, whether
their cholesterol levels are high or just slightly elevated.
- Language of Publication
- English
- Unique Identifier
- 89172810
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- MeSH Heading (Major)
- Arteriosclerosis|*TH; Atherosclerosis|BL/PA/*TH; Cholesterol|*BL
- MeSH Heading
- Animal; Body Weight; Disease Models, Animal; Human; Lipoproteins, HDL
Cholesterol|BL; Lipoproteins, LDL Cholesterol|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0018-5043
- Country of Publication
- GERMANY, WEST
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, LDL Cholesterol);
57-88-5 (Cholesterol)
Record 6 from database: MEDLINE
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- Title
- Coronary heart disease in hypertensives: a need to reduce cholesterol.
- Author
- Heyden S; Schneider KA; Fodor GJ
- Address
- Department of Community and Family Medicine, Duke University Medical Centre,
Durham, NC 27710.
- Source
- Int J Epidemiol, 1988 Dec, 17:4, 784-8
- Abstract
- Ten international long-term hypertension intervention trials between 1980
and 1987 have resulted in significant reduction in the incidence of stroke in
the treatment groups. Yet, eight of these studies have shown disappointing
results in the prevention of coronary heart disease (CHD). Five hypertension
intervention trials revealed high average cholesterol values at baseline. No
cholesterol treatment was provided and the incidence of CHD was high. In four
other trials with stratification into 'low' and 'high' baseline cholesterol
levels, the incidence of CHD was considerably less in the 'low' cholesterol
groups. Only the 10th, the Gothenburg trial, has demonstrated a marked reduction
in CHD by combining antihypertensive medication with cholesterol lowering
treatment. Failure to reduce cholesterol in hypertensives with
hypercholesterolaemia may be one explanation for the limited efficacy of
antihypertensive treatment in the reduction of CHD. We postulate that successful
treatment of hypercholesterolaemia will reduce the incidence of CHD in
well-controlled hypertensive patients to the same extent as it lowers the
incidence of CHD in normotensive people.
- Language of Publication
- English
- Unique Identifier
- 89138785
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Coronary Disease|*CO/PC; Hypercholesterolemia|*CO;
Hypertension|*CO
- MeSH Heading
- Female; Human; Male
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE
- ISSN
- 0300-5771
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 7 from database: MEDLINE
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- Title
- Serum cholesterol level and the risk of colorectal cancer.
- Author
- Törnberg S
- Address
- Department of General Oncology, Karolinska Hospital, Stockholm, Sweden.
- Source
- Biomed Pharmacother, 1988, 42:6, 381-5
- Abstract
- The relation between cancer and serum cholesterol has been studied by many
scientists. In the analyses of cancers of the colon and the rectum, both
negative and positive relations to cholesterol have been described. The
divergent results may, to some extent, be explained by the use of different
statistical methods or non-comparable cohorts. A short review and discussion of
some studies dealing with the question of the relationship between serum
cholesterol and risk of cancer of the colon and the rectum is presented.
- Language of Publication
- English
- Unique Identifier
- 89118428
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Colorectal Neoplasms|*ET
- MeSH Heading
- Colonic Neoplasms|ET; Human; Rectal Neoplasms|ET; Risk Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0753-3322
- Country of Publication
- FRANCE
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 8 from database: MEDLINE
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- Title
- Mechanisms of reversed cholesterol transport.
- Author
- Small DM
- Address
- Department of Medicine, Boston University School of Medicine, Housman
Medical Research Center, Massachusetts.
- Source
- Agents Actions Suppl, 1988, 26:, 135-46
- Abstract
- Reverse cholesterol transport may be defined as the movement of cholesterol
from tissues, organs and cells to the liver (hepatocytes). Once cholesterol
enters the hepatocyte it may be catabolized to bile acids, excreted into bile as
free cholesterol, secreted back into the plasma compartment in lipoproteins or
esterified and stored in the liver. A fraction of the bile acid and cholesterol
excreted into bile is lost in the feces and accounts for the major loss of
cholesterol and its metabolites from the body. If cholesterol was not added to
the body then the mechanisms of reverse transport, bile acid and cholesterol
excretion would deplete the body of sterols. Of course the body can absorb
dietary cholesterol and synthesize cholesterol to keep overall cholesterol
homeostasis. The mechanisms of reverse transport involve 1) the physico-chemical
state of cholesterol and potential for movement within peripheral cells, tissues
and deposits (e.g., atherosclerotic plaques); 2) the net transfer of free
cholesterol from cell, tissues and deposits to acceptors (especially
lipoproteins); 3) the physical state of the acceptors (e.g., the core and
surface of lipoproteins and their capacity to accept cholesterol; 4) the LCAT
reaction; 5) the transfer proteins; 6) the lipase (LPL and HTGL) reactions; and
finally 7) the functional state of the LDL and chylomicron remnant receptors in
the liver. The net transport of cholesterol from peripheral tissues, deposits
and cells to the liver first depends on the rate of influx into the cells plus
the rate of de novo cholesterol synthesis being less than the rate of removal.
The rates of net removal will depend upon the sum of a variety of complex steps
by which cholesterol can move down a gradient to enter acceptors than be
transferred to other lipoproteins which are in turn ultimately taken up by the
liver. A potentially important fraction of cholesterol leaving cells may be
converted into cholesterol ester by LCAT then transferred to larger particles
which can then be taken up by receptor medicated endocytosis in the liver. The
HDL system must have its phospholipids replenished by both the synthesis of
nascent HDL and by the formation of phospholipid-rich surface remnants during
lipolysis of nascent triglyceride-rich lipoproteins which enter the HDL
fraction. Finally, functionally active and vigorous receptor mechanisms are
needed to remove cholesterol-containing particles into the liver.
- Language of Publication
- English
- Unique Identifier
- 89116028
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document
- MeSH Heading (Major)
- Cholesterol|*ME
- MeSH Heading
- Biological Transport; Human; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0379-0363
- Country of Publication
- SWITZERLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 9 from database: MEDLINE
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- Title
- Effects of acebutolol on the serum lipid profile.
- Author
- Clucas A; Miller N
- Address
- Rhône Poulenc Santé, Antony, France.
- Source
- Drugs, 1988, 36 Suppl 2:, 41-50
- Abstract
- Epidemiological and recent interventional studies have emphasised the
relationship between plasma lipid parameters and the incidence of coronary heart
disease. beta-Blockers, particularly those without intrinsic sympathomimetic
activity (ISA), are generally reported to increase triglyceride levels and
decrease high density lipoprotein (HDL)-cholesterol levels, both changes
theoretically increasing the risk of coronary heart disease. A review of all
published trials concerning the effects of acebutolol (a cardioselective
beta-blocker with mild ISA) on the plasma lipid profile was carried out, with a
particular emphasis on studies reporting a comparison with other beta-blockers.
The results indicate that, on average, acebutolol does not have any adverse
effects on plasma lipids and may even reduce total and low density lipoprotein
(LDL)-cholesterol by 7 and 5%, respectively. In contrast, the other
beta-blockers compared under the same conditions (propranolol, pindolol and
penbutolol) tended to increase triglyceride levels (+19% when compared with
acebutolol) and decrease HDL-cholesterol (-7% when compared with acebutolol) to
an extent that was consistent with previous reports in the literature. In
interpreting these differences in lipid parameters in the light of
epidemiological and interventional study data, the use of acebutolol as opposed
to the other beta-blockers could theoretically lead to a relative reduction in
coronary risk of 20% or more.
- Language of Publication
- English
- Unique Identifier
- 89106964
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- MeSH Heading (Major)
- Acebutolol|AE/*PD; Cholesterol|*BL; Lipoproteins|*BL; Triglycerides|*BL
- MeSH Heading
- Comparative Study; Human; Penbutolol|PD; Pindolol|PD; Propranolol|PD
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0012-6667
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins); 0 (Triglycerides); 13523-86-9 (Pindolol); 36507-48-9
(Penbutolol); 37517-30-9 (Acebutolol); 525-66-6 (Propranolol); 57-88-5
(Cholesterol)
Record 10 from database: MEDLINE
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- Title
- Effects of diuretic drugs on the lipid profile.
- Author
- Ames R
- Address
- St Luke's-Roosevelt Hospital, New York, New York.
- Source
- Drugs, 1988, 36 Suppl 2:, 33-40
- Abstract
- Thiazide-type diuretic drugs modify the lipoprotein profile when used in the
short term treatment of hypertension. Total cholesterol increases by 6 to 7% on
average because of raised concentrations of low density or very low density
lipoprotein cholesterol or both. High density lipoprotein cholesterol does not
change. Spironolactone has a lesser effect on lipids than do thiazides. In
contrast, the methylindoline compound, indapamide, a diuretic with vasodilator
activity, has produced no adverse effects on lipids or lipoproteins. Long term
data on thiazide monotherapy are sparse but suggest a persistence of the lipid
effect for as long as 6 years of treatment. The clinical impact of these lipid
changes is unclear. Although clinical trials have proved the benefit of lowering
cholesterol on the incidence of coronary heart disease, the clinical
significance of these diuretic-induced increases is unknown. A clinical trial
will be required to resolve the issue by comparing antihypertensive drugs with
and without adverse effects on the lipid profile. Because coronary heart disease
is the most common complication of mild hypertension, and as diuretic-based
regimens have not succeeded in curbing it, resolution of this concern is
important.
- Language of Publication
- English
- Unique Identifier
- 89106963
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Diuretics, Thiazide|*PD; Lipoproteins|*BL;
Triglycerides|*BL
- MeSH Heading
- Drug Combinations; Human; Hypertension|BL/DT; Indapamide|PD; Potassium|BL;
Spironolactone|PD
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0012-6667
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Diuretics, Thiazide); 0 (Drug Combinations); 0 (Lipoproteins); 0
(Triglycerides); 26807-65-8 (Indapamide); 52-01-7 (Spironolactone); 57-88-5
(Cholesterol); 7440-09-7 (Potassium)
Record 11 from database: MEDLINE
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- Title
- Adaptive changes in aging and arteriosclerosis--role of cholesterol.
- Author
- Kaunitz H
- Address
- Department of Pathology, Columbia University, New York, NY 10032.
- Source
- Mech Ageing Dev, 1988 Jul, 44:1, 35-43
- Abstract
- The "lipid theory" assumes that cholesterol has a causal part in
the development of arteriosclerosis; however, in view of the fact that
cholesterol has always accompanied life processes, the "lipid theory"
contradicts the evolutionary principle of "teleonomy" which predicts
that long lasting metabolic effects must have beneficial consequences. Support
for the theory was claimed from the correlation between high serum cholesterol
and arteriosclerotic complications, from observations in cholesterol fed animals
and from cardiac lesions in familial hypercholesterolemia. However, correlations
do not prove causality; whether the animal experiments and the observations in
familial hypercholesterolemia are pertinent is questionable. Therefore, the
possibility was considered that the cholesterol changes are an adaptive
mechanism. This is supported by the "normal" cholesterol content of
the early lesion, by the stabilization of the DNA helix by cholesterol in
appropriate concentration, by the beneficial effects of cholesterol-rich
granulomata; by recent reliable "intervention" trials with low
cholesterol diets and by the observation that persons dying from ischemic heart
disease (having high serum cholesterol) live at least as long as those dying
from other causes. Furthermore, studies with serum cholesterol lowering drugs
are difficult to interpret and often misleading. The symptomatology of the serum
cholesterol changes in arteriosclerosis suggests that they belong to the
adaptive aging phenomenon. This would be in line with evolutionary thinking.
- Language of Publication
- English
- Unique Identifier
- 89082082
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- MeSH Heading (Major)
- Aging|*; Arteriosclerosis|ET/*PP; Cholesterol|*PH
- MeSH Heading
- Human; Lipids|PH
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0047-6374
- Country of Publication
- SWITZERLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 12 from database: MEDLINE
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- Title
- Discovery, biochemistry and biology of lovastatin.
- Author
- Alberts AW
- Address
- Merck Sharp & Dohme Research Laboratories, Department of Biochemical
Regulation, Rahway, New Jersey 07065.
- Source
- Am J Cardiol, 1988 Nov 11, 62:15, 10J-15J
- Abstract
- Cholesterol is a 27-carbon steroid that is an essential component of the
cell membrane, the immediate precursor of steroid hormones, the substrate for
the formation of bile acids, and is required for the assembly of very low
density lipoprotein in the liver. Because as much as two-thirds of total body
cholesterol in patients is of endogenous origin, an effective means to control
cholesterogenesis may occur by inhibition of its biosynthesis. Cholesterol is
biosynthesized in a series of more than 25 separate enzymatic reactions that
initially involve the formation of 3-hydroxy-3-methylglutaryl coenzyme A (HMG
CoA). Early attempts to pharmacologically block cholesterol synthesis focused
only on steps later in the biosynthetic pathway and resulted in compounds with
unacceptable toxicity. Recent research had identified that HMG CoA reductase is
a key rate-limiting enzyme in this pathway and is responsible for the conversion
of HMG CoA to mevalonate. Additional research with fungal metabolites identified
a series of compounds with potent inhibiting properties for this target enzyme,
from which lovastatin was selected for clinical development. A reduction in
cholesterol synthesis by lovastatin has been subsequently confirmed in cell
culture, animal studies and in humans. A resultant decrease in circulating total
and low-density lipoprotein (LDL) cholesterol has also been demonstrated in
animals and humans. Because hepatic LDL receptors are the major mechanism of LDL
clearance from the circulation, further animal research has confirmed that these
declines in cholesterol are accompanied by an increase in hepatic LDL receptor
activity. Lovastatin effectively diminishes endogenous cholesterol synthesis
providing useful therapeutic properties for patients with hypercholesterolemia.
- Language of Publication
- English
- Unique Identifier
- 89047165
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- MeSH Heading (Major)
- Hydroxymethylglutaryl CoA Reductases|*AI; Hypercholesterolemia|*DT;
Lovastatin|*/PD/TU
- MeSH Heading
- Animal; Chemistry; Cholesterol|BI; Human; Liver|ME; Receptors, LDL|DE
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9149
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- EC 1.1.1.88 (Hydroxymethylglutaryl CoA Reductases); 0 (Receptors, LDL);
57-88-5 (Cholesterol); 75330-75-5 (Lovastatin)
Record 13 from database: MEDLINE
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- Title
- Cholesterol emboli after cardiac catheterization. Eight cases and a review
of the literature.
- Author
- Colt HG; Begg RJ; Saporito JJ; Cooper WM; Shapiro AP
- Address
- Department of Medicine, Shadyside Hospital, Pittsburgh, Pennsylvania 15232.
- Source
- Medicine (Baltimore), 1988 Nov, 67:6, 389-400
- Abstract
- Cholesterol embolization is a puzzling event that may be increasingly
iatrogenic in origin. Diagnosis is difficult and requires a high index of
suspicion, an appropriate clinical picture, and usually, confirmation by biopsy.
Certain laboratory abnormalities may be helpful; the elevated sedimentation rate
and relative eosinophilia found in our patients concurs with other cases
reported in the literature. Prognosis is related to the extent of systemic
involvement, but renal disease is particularly threatening and gangrene and
infection can be lethal. Multiple therapeutic regimens have been generally
unsuccessful in altering the course of the disease process. The most significant
impact on the disease can be made by its prevention. Cholesterol emboli occur
spontaneously, but also after invasive aortic procedures such as diagnostic
angiography or cardiovascular surgery. In addition, cardiac catheterization and
percutaneous transluminal coronary angioplasty have the potential for arterial
trauma and consequent cholesterol embolization. Although the apparent increasing
numbers of cholesterol emboli may be a reflection of the increased use of
arterial invasive procedures, they are being performed on an older, more
severely ill population, with other risk factors for the development of embolic
phenomena, i.e., age, smoking history, diabetes mellitus, hypertension, and
peripheral vascular disease. Our observed cases and review of the literature do
not furnish information concerning the comparative incidences of embolization as
related to the suggested etiologies. Careful documentation of the clinical
situation preceding the event, the type of procedure, the site of arterial
entry, and the duration, difficulty, and extent of the intravascular invasion
(i.e., above or below the left subclavian artery) are necessary for this
purpose. Such data should help to develop guidelines for patient and procedure
selection in order to minimize the possibility of cholesterol embolization.
- Language of Publication
- English
- Unique Identifier
- 89039240
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- MeSH Heading (Major)
- Cholesterol|*; Embolism|*ET; Heart Catheterization|*AE
- MeSH Heading
- Aged; Case Report; Female; Human; Male; Middle Age
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE
- ISSN
- 0025-7974
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 14 from database: MEDLINE
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- Title
- Multiple cholesterol emboli syndrome complicating angiographic techniques.
- Author
- Palmer FJ; Warren BA
- Address
- Department of Radiology, Prince Henry Hospital, Sydney, Australia.
- Source
- Clin Radiol, 1988 Sep, 39:5, 519-22
- Abstract
- Three cases of widespread microembolisation of cholesterol crystals
following angiography are described. The multiple cholesterol emboli syndrome
has been well described as a spontaneous phenomenon and it is surprising that
its occurrence during angiography appears rare. Only 19 cases could be found in
the literature and these are reviewed. Dissemination of particulate cholesterol
material produces irreversible organ ischaemia when a threshold 'dose' is
reached. Males and patients with clinical evidence of widespread atherosclerosis
are at increased risk. Prognosis is poor and available therapy unsatisfactory.
- Language of Publication
- English
- Unique Identifier
- 89029526
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- MeSH Heading (Major)
- Angiography|*AE; Cholesterol|*; Embolism|*ET
- MeSH Heading
- Aged; Case Report; Human; Male; Middle Age; Syndrome
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW OF REPORTED CASES
- ISSN
- 0009-9260
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 15 from database: MEDLINE
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- Title
- European Consensus on Primary Prevention of Coronary Heart Disease.
- Author
- Assmann G
- Address
- Central Laboratory Institute for Clinical Chemistry, Westfalische Wilhelms
Universitat Münster, West Germany.
- Source
- Can J Cardiol, 1988 Jul, 4 Suppl A:, 21A-23A
- Abstract
- The European Consensus on Primary Prevention of Coronary Heart Disease has
recommended that providing care for individuals at particular risk for coronary
artery disease (CAD) requires case finding through medical examinations in
primary care, hospital and employment health examination settings. Decisions
concerning management of elevated lipid levels should be based on overall
cardiovascular risk. The goal of reducing cholesterol levels through risk
reduction can ultimately be accomplished only with the implementation of health
education efforts directed toward all age groups and actions by government and
supranational agencies, including adequate food labelling to identify fat
content, selective taxation to encourage healthful habits and wider availability
of exercise facilities. Only measures directed at the overall population can
eventually reach the large proportion of individuals at mildly to moderately
increased risk for CAD. The European Policy Statement on the Prevention of
Coronary Heart Disease recognizes that the question of lipid elevation as a risk
factor for CAD involves assessment, not only of cholesterol level alone, but
also of triglycerides and the HDL cholesterol lipid fraction. Five specific
categories of dyslipidemia have been identified, with individualized screening
and treatment strategies advised for each. It is the consensus of the study
group panel members that these procedures are both practical and feasible. They
begin the necessary long term process to reduce the unacceptably high levels of
morbidity and mortality due to CAD throughout the European community.
- Language of Publication
- English
- Unique Identifier
- 89027866
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- MeSH Heading (Major)
- Coronary Disease|*PC
- MeSH Heading
- Cholesterol|BL; Europe; Human; Hyperlipidemia|PC; Lipoproteins, HDL
Cholesterol|BL; Risk Factors
- Publication Type
- CONSENSUS DEVELOPMENT CONFERENCE; JOURNAL ARTICLE; REVIEW; REVIEW LITERATURE
- ISSN
- 0828-282X
- Country of Publication
- CANADA
- CAS Registry/EC Number
- 0 (Lipoproteins, HDL Cholesterol); 57-88-5 (Cholesterol)
Record 16 from database: MEDLINE
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- Title
- Coronary prevention and regression studies updated.
- Author
- Little JA
- Address
- Department of Medicine, St Michael's Hospital, Toronto, Ontario.
- Source
- Can J Cardiol, 1988 Jul, 4 Suppl A:, 11A-15A
- Abstract
- There have been a multitude of clinical, animal and epidemiology studies
which prove that high serum cholesterol and low density lipoprotein (LDL)
cholesterol concentrations are specific causes of coronary artery disease (CAD).
Although the variations in experimental design make comparisons difficult, the
aggregate results of many human prevention trials since 1960 lead to the
definite conclusion that a 10% lowering of serum cholesterol reduces the risk of
CAD by one-sixth. Recently, other factors for CAD risk have been identified that
will be useful in guiding treatment, namely serum high density lipoprotein (HDL)
cholesterol, apolipoproteins B and AI, HDL triglycerides and phosphatidylcholine
to free cholesterol ratio. Studies have shown that aggressive drug and diet
therapy slows progression and causes regression of atheromas. Primary prevention
of CAD is obviously preferable to secondary prevention. Also, the evidence to
date indicates that prevention of CAD through lifestyle changes should begin in
childhood.
- Language of Publication
- English
- Unique Identifier
- 89027864
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document
- MeSH Heading (Major)
- Cholesterol|*BL; Coronary Disease|*PC
- MeSH Heading
- Clinical Trials; Coronary Arteriosclerosis|PC; Human; North America; Risk
Factors
- Publication Type
- CLINICAL TRIAL; JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE
- ISSN
- 0828-282X
- Country of Publication
- CANADA
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 17 from database: MEDLINE
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- Title
- Atherosclerosis and apoprotein E. An enigmatic relationship.
- Author
- Getz GS; Mazzone T; Soltys P; Bates SR
- Address
- Department of Pathology, University of Chicago, IL 60637.
- Source
- Arch Pathol Lab Med, 1988 Oct, 112:10, 1048-55
- Abstract
- In this article, we consider the role of apoprotein E in lipoprotein
metabolism and especially in the metabolism of potentially atherogenic
lipoproteins. Particular consideration has been given to three features of
apoprotein E involvement in lipid cell interactions. Evidence implicating free
cholesterol as a mediator of apoprotein E biosynthesis in cholesterol-loaded
macrophages is presented. Experiments pointing to apoprotein E as the ligand
promoting the interaction of beta-very-low-density lipoprotein (beta-VLDL) with
macrophages are summarized. Finally, we describe the influence of fat and
cholesterol fed to rhesus monkeys and baboons on the generation of hepatogenous
(from isolated liver perfusates) VLDL enriched in cholesterol ester and
apoprotein E. These hepatic VLDLs, none of which exhibits beta-electrophoretic
mobility, promote cholesterol esterification in macrophages in proportion to
their apoprotein E content. The complex role of apoprotein E in the genesis and
reversal of atherosclerosis is briefly discussed.
- Language of Publication
- English
- Unique Identifier
- 89025045
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- MeSH Heading (Major)
- Apolipoproteins E|BI/ME/*PH; Arteriosclerosis|*ET; Atherosclerosis|*ET
- MeSH Heading
- Animal; Cholesterol|BL/ME; Esterification; Human; Lipoproteins, VLDL|ME;
Macrophages|ME; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0003-9985
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoproteins E); 0 (Lipoproteins, VLDL); 57-88-5 (Cholesterol)
Record 18 from database: MEDLINE
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- Title
- Assessing and managing hyperlipidemia.
- Author
- Crouch MA
- Address
- Department of Family Medicine and Comprehensive Care, Louisiana State
University Medical Center, School of Medicine, Shreveport.
- Source
- J Am Board Fam Pract, 1988 Jul-Sep, 1:3, 175-88
- Abstract
- Because more than one-half of adult Americans have total blood cholesterol
levels that often contribute to atherosclerotic blockage of their coronary
arteries, routine random screening of all adults and high-risk children for
hypercholesterolemia is recommended. Reduced intake of saturated fat and
cholesterol can lower total and low-density lipoprotein (LDL) cholesterol by
10-20 percent, while several medications lower total and LDL cholesterol by
15-40 percent. A highly effective cholesterol-lowering medication, lovastatin,
has been recently marketed. The efficacy and long-term safety of ingesting large
amounts of omega-3 fatty acids in fish oil supplements are unproven.
Hypercholesterolemia is a family problem transmitted between generations by
various combinations of genetic factors and learned behaviors. The family
physician can be most effective by working with entire families to detect and
treat hypercholesterolemia early in life to prevent serious consequences of
prolonged cholesterol elevation.
- Language of Publication
- English
- Unique Identifier
- 89022187
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- MeSH Heading (Major)
- Hyperlipidemia|BL/DH/DT/*PC
- MeSH Heading
- Antilipemic Agents|TU; Cholesterol|BL; Dietary Fats, Unsaturated|TU; Human;
Life Style; Mass Screening; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0893-8652
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Antilipemic Agents); 0 (Dietary Fats, Unsaturated); 0 (Triglycerides);
57-88-5 (Cholesterol)
Record 19 from database: MEDLINE
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- Title
- Bilateral cholesterol granuloma of the skull base: case report and review of
the literature.
- Author
- Gamache FW Jr; McLure T; Deck M; Linstrom C
- Address
- Department of Neurosurgery, Cornell University Medical College, The New York
Hospital, New York.
- Source
- Neurosurgery, 1988 Jun, 22:6 Pt 1, 1098-101
- Abstract
- A unique case of bilateral cholesterol granuloma of the skull base and its
treatment is presented. Cholesteatoma, a pathological entity often confused with
cholesterol granuloma, is differentiated from cholesterol granuloma. Cholesterol
granuloma is not rare. This tumor seems to derive from an inflammatory process
at the skull base that results in bony erosion surrounding a cyst wall of
inflammatory tissue. Neurological abnormalities reflect the location of the
tumor in relation to the brain stem. Radiographically, the cyst wall enhances
with the administration of i.v. contrast agent, and the center of the lesion is
isodense with brain on computed tomography, unlike cholesteatoma. Magnetic
resonance imaging characteristics are currently being defined. At operation,
cholesterol granuloma consists primarily of a viscous fluid within a capsule of
inflammatory tissue. Treatment requires establishing a pathway for drainage of
the granuloma. The advantages of transsphenoidal, transclival drainage of such
lesions are outlined.
- Language of Publication
- English
- Unique Identifier
- 88334862
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document
- MeSH Heading (Major)
- Bone Diseases|*DI/ME/SU; Cholesterol|*AN; Granuloma|*DI/ME/SU; Magnetic
Resonance Imaging|*; Skull|*RA/SU
- MeSH Heading
- Adult; Case Report; Female; Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW OF REPORTED CASES
- ISSN
- 0148-396X
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 20 from database: MEDLINE
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- Title
- Physiological and pharmacological regulation of small intestinal cholesterol
synthesis.
- Author
- Strandberg TE; Tilvis RS
- Address
- Second Department of Medicine, University of Helsinki, Finland.
- Source
- Gen Pharmacol, 1988, 19:3, 321-9
- Abstract
- 1. The small intestine is an important site of cholesterol synthesis in the
body and at least in experimental animals, it also contributes to the
circulating plasma pool of cholesterol. 2. Studies on synthesis regulation have
been partly contradictory but it is now concluded that the cellular cholesterol
balance is the basic regulatory factor of intestinal cholesterol synthesis.
However, the balance is affected differently in various specialized cells and
parts of the small intestine. 3. Most data on synthesis regulation are derived
from experimental animals but the few human studies suggest that similar
regulatory factors function in man, too.
- Language of Publication
- English
- Unique Identifier
- 88329608
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- MeSH Heading (Major)
- Cholesterol|*BI/BL; Intestinal Mucosa|DE/*ME; Intestine, Small|DE/*ME
- MeSH Heading
- Animal; Antilipemic Agents|PD; Bile Acids and Salts|ME; Cell Cycle;
Circadian Rhythm; Diet; Fasting; Hormones|PH; Human; Lipoproteins|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0306-3623
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Antilipemic Agents); 0 (Bile Acids and Salts); 0 (Hormones); 0
(Lipoproteins); 57-88-5 (Cholesterol)
Record 21 from database: MEDLINE
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- Title
- Labeling of participants in high blood pressure screening programs.
Implications for blood cholesterol screenings.
- Author
- Lefebvre RC; Hursey KG; Carleton RA
- Address
- Division of Health Education, Memorial Hospital of Rhode Island, Pawtucket
02860.
- Source
- Arch Intern Med, 1988 Sep, 148:9, 1993-7
- Abstract
- Screening programs have expanded to identify the many persons who are
unaware of their high blood cholesterol level and thus are at an increased risk
for coronary heart disease. These programs bring both potential benefits and
potential risks to the participant. One potential risk is that of iatrogenic
effects of learning one's risk status, often referred to as the "labeling
phenomenon." Research that has addressed the labeling phenomenon in blood
pressure screening programs has important implications for blood cholesterol
screenings. Detrimental effects on screening participants are possible, but they
can be attenuated by careful attention to characteristics of the debriefing and
counseling that should be included in screening protocols.
- Language of Publication
- English
- Unique Identifier
- 88325754
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document
- MeSH Heading (Major)
- Blood Pressure Determination|*; Cholesterol|*BL; Hypertension|CO/EP/*PX;
Mass Screening|*; Sick Role|*
- MeSH Heading
- Absenteeism; Counseling; Evaluation Studies; Human;
Hypercholesterolemia|BL/CO/EP/PX; Life Style; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0003-9926
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 57-88-5 (Cholesterol)
Record 22 from database: MEDLINE
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- Title
- Cholesterol gallstone disease: the current status of nonsurgical therapy.
- Author
- Bilhartz LE
- Address
- Department of Medicine, University of Texas Southwestern Medical Center,
Dallas 75235-9030.
- Source
- Am J Med Sci, 1988 Jul, 296:1, 45-56
- Abstract
- Gallstone disease is a common disease that appears to be related to a
Western diet. The underlying pathogenesis is a subtle alteration in the liver
such that excessive cholesterol is extracted from the liver cell by bile acids
undergoing an enterohepatic recirculation. Gallstone disease progresses through
well-defined stages, beginning with a bile supersaturated with cholesterol and
proceeding to crystal formation, stone growth, and finally symptoms caused by
impaction of a stone in either the cystic duct or the common bile duct. The
natural history is that most stones never cause symptoms. Stones that cause
symptoms have been present for an average of 12 years. The treatment of truly
asymptomatic stones should be observation. Ultrasonography of the right upper
quadrant is the gold standard for the diagnosis of stones in the gallbladder.
Endoscopic retrograde cholangiopancreatography (ERCP) is the gold standard for
the diagnosis of stones in the common bile duct. Oral cholecystogram (OCG) helps
select patients who have noncalcified, floating stones that may be dissolved
with bile acids or methyl tertiary butyl ether (MTBE). Therapy with chenodiol
has been a disappointment because of a low complete response rate. The ideal
candidate for attempted dissolution with chenodiol would be a thin woman with
hypercholesterolemia and a small number of symptomatic, small, floating,
radiolucent gallstones. Ursodeoxycholic acid (Urso), when it is available, will
have all of the attributes of chenodiol and virtually none of the side effects.
Rapid dissolution of gallstones with MTBE shows great promise of being a
generally available means of dissolving gallstones. Extracorporeal shock wave
lithotripsy also shows promise, but its general availability may be limited by
the cost of the equipment needed. As of now, the treatment of choice for
symptomatic gallstones remains cholecystectomy, unless there is a compelling
reason not to operate.
- Language of Publication
- English
- Unique Identifier
- 88307464
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- MeSH Heading (Major)
- Cholelithiasis|AN/*TH; Cholesterol|*AN
- MeSH Heading
- Chenodeoxycholic Acid|TU; Cholecystectomy; Ethers|TU; Human; Lithotripsy;
Risk Factors; Solvents|TU; Support, Non-U.S. Gov't; Ursodeoxycholic Acid|TU
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0002-9629
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Ethers); 0 (Solvents); 128-13-2 (Ursodeoxycholic Acid); 1634-04-4 (methyl
tert-butyl ether); 474-25-9 (Chenodeoxycholic Acid); 57-88-5 (Cholesterol)
Record 23 from database: MEDLINE
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- Title
- Reliability of lipid, lipoprotein, and apolipoprotein measurements.
- Author
- Naito HK
- Address
- Department of Biochemistry, Cleveland Clinic Foundation, OH 44195.
- Source
- Clin Chem, 1988, 34:8B, B84-94
- Abstract
- The National Heart, Lung, and Blood Institute national awareness program on
cholesterol and heart disease has placed new demands on laboratorians to utilize
and perform more reliable measurements of lipids, lipoproteins, and
apolipoproteins. The general public's awareness and the clinicians' concerns
about the reliability of laboratory testing make it paramount that the
analytical problems and issues are identified and solutions are provided to
increase the current state of reliability of the measurement of these blood
constituents. To accomplish this, the initial step is to assess the current
state of reliability of lipid, lipoprotein, and apolipoprotein measurements in
the clinical laboratories. Accuracy and precision of measurements of total
cholesterol, triglycerides, high-density lipoprotein cholesterol, and
apolipoproteins A-I and B are extensively discussed, and general as well as some
specific recommendations are provided for some of the apparent problems.
- Language of Publication
- English
- Unique Identifier
- 88295453
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- MeSH Heading (Major)
- Apolipoproteins|*BL; Lipids|*BL; Lipoproteins|*BL
- MeSH Heading
- Autoanalysis; Cholesterol|BL; Human; Lipoproteins, HDL|BL; Lipoproteins, HDL
Cholesterol|BL; Triglycerides|BL
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0009-9147
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Apolipoproteins); 0 (Lipoproteins); 0 (Lipoproteins, HDL Cholesterol); 0
(Lipoproteins, HDL); 0 (Triglycerides); 57-88-5 (Cholesterol)
Record 24 from database: MEDLINE
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- Title
- Cholesterol, lipoproteins, and coronary heart disease in women.
- Author
- Bush TL; Fried LP; Barrett-Connor E
- Address
- Department of Epidemiology, Johns Hopkins University, School of Hygiene and
Public Health, Baltimore, MD.
- Source
- Clin Chem, 1988, 34:8B, B60-70
- Abstract
- In the United States, coronary heart disease is the major cause of death and
disability in women and in men. Despite this, little is known about the risk
factors, including cholesterol and lipoprotein concentrations, for coronary
disease in women. In this paper we review the determinants of cholesterol and
lipoprotein concentrations in women, assess whether values for total cholesterol
and lipoproteins (HDL and LDL) are associated with the occurrence of coronary
heart disease in women, and evaluate the evidence that suggests that modifying
the concentrations of lipids in women is associated with changing the risk of
coronary disease. Besides genetic determinants, dietary cholesterol, dietary
fat, total caloric intake, alcohol consumption, cigarette smoking, and physical
activity are known to influence concentrations of lipids in women. Some of the
strongest determinants of cholesterol and lipoprotein concentrations in women
are sex hormones, including estrogen and progestin. Exogenous use of both of
these hormones markedly influences HDL and LDL cholesterol; additional evidence
suggests that endogenous sex hormones also influence lipid and lipoprotein
concentrations. The few studies that have examined the association of total
cholesterol with coronary heart disease occurrence and mortality in women have
consistently shown that (a) women have much lower rates of coronary heart
disease than men at the same values for cholesterol, and (b) clearly elevated
risk for coronary heart disease in women is evident only at relatively high
values of total cholesterol (i.e., greater than 260 mg/dL). There also appears
to be an age effect, with total cholesterol concentrations being more predictive
in older than in younger women.
- Language of Publication
- English
- Unique Identifier
- 88295450
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- MeSH Heading (Major)
- Cholesterol|*BL; Coronary Disease|BL/*EP/GE/MO; Lipoproteins|*BL
- MeSH Heading
- Adult; Age Factors; Aged; Contraceptives, Oral, Hormonal|AE; Epidemiologic
Methods; Female; Human; Male; Menopause; Middle Age; Risk Factors; Sex Factors;
United States
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0009-9147
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins); 57-88-5 (Cholesterol)
Record 25 from database: MEDLINE
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- Title
- Cholesterol and risk of coronary heart disease and mortality in men.
- Author
- Kannel WB
- Address
- Section of Preventive Medicine and Epidemiology, Boston University School of
Medicine, MA.
- Source
- Clin Chem, 1988, 34:8B, B53-9
- Abstract
- Extensive data implicate cholesterol in the atherosclerotic process
responsible for coronary disease. Of the atherosclerotic disease outcomes, serum
cholesterol is most strongly related to coronary disease. A significant
relationship of serum cholesterol to all clinical manifestations of coronary
heart disease has been demonstrated in the Framingham Study, after adjusting for
coexistent risk factors. Cholesterol and blood pressure exert similar influences
on the occurrence of coronary heart disease. Risk of coronary heart disease
associated with serum cholesterol is continuous, graded, and strong, with ideal
values for cholesterol probably in the 130-190 mg/dL range. The impact of serum
cholesterol diminishes with advancing age, but the predictive value of
cholesterol is restored when fractionated into its atherogenic LDL and
protective HDL components. The predictive value of total cholesterol in serum at
all concentrations, including values less than 200 mg/dL, can be enhanced by
taking HDL cholesterol into account. The total/HDL cholesterol ratio is a
practical, efficient means for evaluating the joint effect of the two-way
cholesterol traffic. Other cardiovascular risk factors such as blood pressure,
glucose, cigarette smoking, fibrinogen, and left ventricular hypertrophy
markedly influence the risk associated with measured concentrations of serum
cholesterol. In correcting hypertension or diabetes, lipid values are an
important consideration in determining the urgency, type, and efficacy of
treatment used. In contrast to coronary mortality, rates of overall mortality
show a quadratic relationship to total cholesterol in serum, with excessive
mortality at concentrations greater than 160 mg/dL.
- Language of Publication
- English
- Unique Identifier
- 88295449
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- MeSH Heading (Major)
- Cholesterol|*BL; Coronary Disease|BL/EP/*MO
- MeSH Heading
- Adult; Age Factors; Aged; Epidemiologic Methods; Female; Human;
Lipoproteins|BL; Lipoproteins, HDL Cholesterol|BL; Lipoproteins, LDL
Cholesterol; Male; Middle Age; Risk Factors; United States
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0009-9147
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipoproteins); 0 (Lipoproteins, HDL Cholesterol); 0 (Lipoproteins, LDL
Cholesterol); 57-88-5 (Cholesterol)
Record 26 from database: MEDLINE
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- Title
- Chemistry, biochemistry, and pharmacology of HMG-CoA reductase inhibitors.
- Author
- Endo A
- Address
- Department of Agricultural and Biological Chemistry, Tokyo Noko University,
Japan.
- Source
- Klin Wochenschr, 1988 May 16, 66:10, 421-7
- Abstract
- After an extensive searching for a microbial product that inhibits
cholesterol synthes
