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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatic artery aneurysm is a rare vascular lesion that accounts for nearly 10% of hemobilia cases. Its etiology is most often atherosclerosis, trauma, or infection. Autoaggressive disorders are rarely associated with hepatic artery aneurysm as is thyroid dysfunction. Presented here is a case of hemobilia secondary to a rupture of one of multiple aneurysms of both right and left hepatic arteries in a women with a history of rheumatoid arthritis, hypothyroidism, and hypertension. Surgical intervention has been the rule in the past. Selective transcatheter embolization has gained clinical application in recent years, especially in the treatment of intrahepatic aneurysms. Its efficacy and safety are demonstrated by this case.
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PMID:Hemobilia in a patient with multiple hepatic artery aneurysms: a case report and review of the literature. 264 98

One of the leading causes of mortality in diabetics is myocardial disease. In the past few years this subject has generated a significant amount of interest with the result that myocardial problems associated with diabetes are far better understood. Though originally thought to occur as a result of atherosclerosis, various studies have shown that heart disease can occur in the absence of atherosclerosis, suggesting a diabetic cardiomyopathy. Using diabetic animals, it has been possible to characterize diabetes-induced myocardial abnormalities. Diabetic rat hearts do not respond to conditions of high stress as well as controls. The functional depression is accompanied by altered cardiac enzyme systems. A decrease in myosin ATPase activity which appears to be a result of diabetes-induced hypothyroidism is seen. Also, a depression of sarcoplasmic reticular calcium ATPase, along with a depression of calcium uptake by the SR, is seen in diabetic rat hearts. Na+, K+ ATPase activity has also been shown to be depressed and the depression appears to correlate with depressed atrial contractility. High levels of circulating fats in diabetics may alter the integrity of membranes leading to altered enzyme activities. Insulin treatment has been relatively successful at reversing or preventing myocardial changes in the diabetic rat. Other treatments that have been studied include thyroid hormone treatment, since the depression of myosin ATPase can be corrected by such treatment; and carnitine treatment, as the elevation of long chain acyl carnitines (LCAC) and the resulting depression of calcium uptake in the SR can be so normalized. These treatments have not been successful at normalizing cardiac function. A combination of the two treatments normalized function only partially, suggesting that factors besides myosin ATPase and SR calcium uptake are involved. Other treatments that have been tried include vanadate, methyl palmoxirate, and choline and methionine. Vanadate treatment has proved to be encouraging in that it normalizes both function and hyperglycemia. Methyl palmoxirate, a fatty acid analog, normalized only the elevation of LCAC but did not affect function. Methionine and choline were only partially successful in preventing the functional alterations of diabetic rat hearts. The purpose of the present article is to review our understanding of diabetes-induced myocardial problems and their possible causes. Findings from our laboratory and others are described in which attempts have been made to normalize cardiac function.
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PMID:Diabetes-induced abnormalities in the myocardium. 293 41

Exposure of rabbits for 12 weeks to 300 ppm carbon disulfide (CS2) for 6 h/day, 5 days/week, or to 25 mg/day of thiourea or 2% cholesterol in the diet, or to any combination thereof caused a significant reduction in the concentration of serum thyroxine (T4). The reduction of the concentration of serum T4 in rabbits by the treatments was completely offset by the inclusion of 0.1 mg/day of sodium levothyroxine in the diet. Ingestion of feed containing 2% cholesterol significantly increased the degree of atherosclerosis present in the aortic arch and significantly increased the oil red O positive lipid present in the heart and the aorta, with the aortic arch being the most severely affected. The response of the aorta and the heart to the 2% cholesterol diet was not significantly modified by concurrent exposure to CS2 by inhalation or by treatment with thiourea, a metabolite of CS2. We found no evidence that the development of cardiovascular lesions induced by a 2% cholesterol diet in rabbits was mediated by a mechanism involving a component of hypothyroidism.
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PMID:Failure of carbon disulfide and levothyroxine to modify the cardiovascular response of rabbits to a high-cholesterol diet. 308 26

Lipids are transported in the blood in four major classes of lipoproteins. The triacylglycerol-rich lipoproteins are chylomicrons and very-low-density lipoproteins (VLDL) which are produced by the small intestine and liver, respectively. These lipoproteins mainly carry fatty acids to adipose tissue and muscle where the triacylglycerol is hydrolysed by lipoprotein lipase. The resulting particles that remain in the blood are chylomicron remnants and low-density lipoprotein (LDL), respectively. The remnant is taken up by the liver via endocytosis which is mediated by a specific receptor for apolipoprotein E (apoE). LDL, which are rich in cholesterol, can also be taken up by the liver or extrahepatic tissues by a receptor-mediated endocytosis that specifically recognises apoB or apoE. 'Nascent' high-density lipoprotein (HDL) particles are secreted by the liver and intestine and then undergo modification to become HDL3 and then HDL2 as they acquire cholesterol ester. They facilitate the reverse transport of cholesterol back to the liver. Little is known of the hormonal regulation of lipoprotein uptake by the liver. Recently, we have shown that insulin and tri-iodothyronine (T3) increase the specific binding of LDL to cultured hepatocytes whereas dexamethasone (a synthetic glucocorticoid) has the opposite effect. The changes in binding produced by insulin and dexamethasone are paralleled by alterations in the rate of degradation of apoB. These findings may in part explain the hypercholesterolaemia and increased risk of premature atherosclerosis that can be associated with poorly controlled diabetes or hypothyroidism.
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PMID:The biochemistry of lipoproteins. 314 85

The control of coronary heart disease (CHD) depends primarily on its prevention at an early stage. It is generally agreed that this depends upon the elimination or treatment of the known risk factors for CHD. Among these, hyperlipidaemia occupies a central position. The diagnosis and treatment of this condition is the subject of this statement. Before initiating therapy for primary hyperlipidaemia the common causes of secondary hyperlipidaemia are sought and dealt with, including diabetes, hypothyroidism, over-use of alcohol, renal and liver diseases and certain drugs. Next, an assessment of all risk factors for CHD is carried out, i.e. family history of CHD, smoking, hypertension, high density lipoprotein (HDL) cholesterol measurement, diabetes mellitus and overweight. More intensive therapy is called for in patients with multiple risk factors than in those with lone hyperlipidaemia, and also after successful bypass operation or after coronary angioplasty. Evaluation of hyperlipidaemia in the patient's family is often appropriate. The diagnosis and follow-up of the hyperlipidaemic patient depend on reliable and well-controlled laboratory support. The primary hyperlipidaemias include several distinct diseases that are characterized by elevated serum levels of cholesterol and/or triglyceride with or without abnormally low levels of HDL cholesterol. From these measurements, low-density lipoprotein (LDL) cholesterol levels are calculated [except when triglyceride levels are greater than 500 mg dl-1 (5.6 mmol l-1)]. Elevated LDL levels are causally important in atherosclerosis, and occur in three disorders: familial hypercholesterolaemia, familial combined hyperlipidaemia and common hypercholesterolaemia. The finding of elevated serum triglyceride without marked hypercholesterolaemia may occur in familial hypertriglyceridaemia and sometimes in familial combined hyperlipidaemia. Elevation of serum cholesterol and triglyceride can have several genetic bases, including remnant (type III) hyperlipidaemia and familial combined hyperlipidaemia. The characteristic feature of remnant (type III) hyperlipidaemia (demonstrated by ultracentrifugation in a specialized laboratory) is the presence of cholesterol and triglyceride-rich very low density lipoproteins (VLDL), whereas combined (mixed) hyperlipidaemia is diagnosed when both VLDL (of normal composition) and LDL levels are elevated. Investigation of other family members is necessary to make the diagnosis of familial combined hyperlipidaemia. It depends on the identification of different lipoprotein profiles in affected members of the same family.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The recognition and management of hyperlipidaemia in adults: A policy statement of the European Atherosclerosis Society. 340 74

Viscoelastic properties of human whole blood were measured in 338 subjects: 110 persons (75 F, 35 M) following total thyroidectomy but without substitution therapy over three weeks as well as 228 healthy control subjects (124 F, 104 M) were investigated in this study. Subjects with other variable factors were excluded. The viscous and the elastic portion of apparent whole blood viscosity -the latter subdivided into red cell aggregation and red cell rigidity were determined by using a newly developed oscillating capillary rheometer and densitymeter at the real hematocrit value and at a computed hematocrit of 40%. Serum viscosity, hematocrit (Hct), hemoglobin (Hb), mean corpuscular volume of red blood cells (MCV), free triiodothyronine (fT3), free thyroxine (fT4) and serum-thyrotropin (bTSH) were evaluated as well. In a further subgroup of 80 subjects (40 patients with hypothyroidism, 40 healthy control persons) additional plasma viscosity and sedimentation rate were determined. Red cell aggregation and blood viscosity especially at shear-rates below 10/sec increased significantly in hypothyroid patients. There was no significant difference of red cell rigidity, serum viscosity, plasma viscosity and sedimentation rate as against euthyroids. So new aspects of thyroid dysfunction could be described probably with consequences for therapy and for considerations about the development of atherosclerosis and ischemic disorders.
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PMID:Hypothyroidism and the influence on human blood rheology. 341 Oct 87

The endogenous lipoprotein system (very low-density lipoprotein [VLDL], intermediate-density lipoprotein [IDL], low-density lipoprotein [LDL] cascade) holds the key to understanding the mechanisms by which hormones, diet, and drugs interact to regulate the plasma cholesterol level. Crucial components of this system are hepatic LDL receptors that mediate the uptake and degradation of plasma LDL. With experimental animals, it has been possible to demonstrate that hepatic LDL receptors are sensitive to hormonal, dietary, and pharmacologic manipulation. The decrease in number of hepatic LDL receptors in hypothyroidism or after cholesterol feeding leads to elevation of plasma LDL cholesterol levels. Conversely, the increase in number of hepatic LDL receptors results in lowering of plasma LDL cholesterol levels. This can be observed in hyperthyroidism, during administration of pharmacologic doses of 17 alpha-ethinyl estradiol, or during treatment with cholesterol-lowering drugs such as the bile acid-binding resins and cholesterol-synthesis inhibitors. Since cholesterol excretion from the body occurs via the liver, the increased efficiency of disposal of plasma cholesterol by increasing hepatic LDL receptors will ultimately lead to depletion of excessive body cholesterol. Pharmacologic regulation of hepatic LDL receptors should be a valuable tool in the prevention and therapy of atherosclerosis.
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PMID:Regulation of plasma cholesterol by hepatic low-density lipoprotein receptors. 354 61

Hypercholesterolemia associated with hypothyroidism is due partly to increased plasma LDL and partly to increased HDL cholesterol concentrations. The increase in LDL cholesterol has been shown to be secondary to reduced plasma clearance of LDL. To determine which catabolic route was thyroid dependent, the present study examined the effects of hypothyroidism on the receptor-mediated pathway and the 'receptor-independent' pathway of LDL metabolism. Wistar rats (327 +/- 22 g; mean +/- SD) were made hypothyroid by feeding propylthiouracil (0.1%, w/w) and rat 131I-LDL (rLDL; d = 1.019-1.050) and 125I-methylated-LDL (rLDL-CH3) were simultaneously injected i.v. after which the rates of clearance of labelled LDL in plasma were determined over 0-54 h. Total LDL and 'receptor-independent' clearances were represented by clearance of 131I-rLDL and 125I-rLDL-CH3 respectively and the difference between the two represented high affinity receptor-mediated clearance. The data were analyzed using Matthews' model and the fractional catabolic rates (FCR) were calculated. The FCR of rLDL clearance via the receptor-mediated pathway was 0.1042 +/- 0.0112 pools/h (n = 6) in controls vs. 0.0613 +/- 0.0079 pools/h (n = 6) in hypothyroid animals (P less than 0.01). The FCR via the 'receptor-independent' pathway was 0.0642 +/- 0.0040 pools/h (n = 6) in controls vs. 0.0561 +/- 0.0036 pools/h (n = 6) in hypothyroid animals (not significant). The plasma HDL cholesterol concentration was also increased in hypothyroid rats (70.4 +/- 6.7 mg/dl) compared to control (53.3 +/- 3.1 mg/dl) (P less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1987 Aug
PMID:HDL clearance and receptor-mediated catabolism of LDL are reduced in hypothyroid rats. 363 63

Hypothyroidism results in decreased platelet aggregation and has unique effects on the development of atherosclerosis and angina pectoris. Because prostacyclin and thromboxane A2 profoundly influence platelet function and vascular tone and are thought to be important in the development of atherosclerosis and angina pectoris, we studied the effects of hypothyroidism in rats on the in vitro elaboration of prostacyclin passively by aortic tissue and of thromboxane A2 by thrombin-stimulated whole blood. Hypothyroidism induced by iodine 131 (given at age 7 weeks) persistently caused a mild decrease in platelet count (P less than 0.01) and 30% decrease in immunoreactive thromboxane B2 (the hydrolysis product of thromboxane A2) generation per platelet (P less than 0.01) compared with age-matched euthyroid rats. Between 20 and 23 weeks of age immunoreactive 6-ketoprostaglandin F1 alpha (the hydrolysis product of prostacyclin) generation decreased by 30% in euthyroid rats. In hypothyroid rats less than 23 weeks of age, 6-ketoprostaglandin F1 alpha production was the same as that of age-matched euthyroid rats. With further aging, 6-ketoprostaglandin F1 alpha production did not decrease as it did in euthyroid rats. Hypothyroid rats more than 20 weeks old had, therefore, significantly greater 6-ketoprostaglandin F1 alpha production than age-matched euthyroid rats (P less than 0.005). L-Thyroxine given daily for 28 days to 23-week-old hypothyroid rats caused a rapid increase in platelet count and a delayed normalization of the thromboxane synthetic abnormality. 6-Ketoprostaglandin F1 alpha production transiently increased in response to L-thyroxine, but decreased to the euthyroid level after 28 days of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of hypothyroidism and short-term aging on whole blood thromboxane and arterial prostacyclin synthesis. 366 59

Atherosclerosis was diagnosed on necropsy in 21 dogs in a 14-year period. Nine dogs died and 12 were euthanatized because of complications associated with the disease. The mean age was 8.5 +/- 0.5 years; 18 dogs were male. Three breeds (Miniature Schnauzer, Doberman Pinscher, and Labrador Retriever) had a higher prevalence of the disease than other breeds in the canine necropsy population of The Animal Medical Center. Most common clinical signs were lethargy, anorexia, weakness, dyspnea, collapse, and vomiting. Hypercholesterolemia, lipidemia, and hypothyroidism were common in affected dogs tested, and protein electrophoresis revealed high values for alpha 2 and beta fractions in all dogs tested. Electrocardiography indicated conduction abnormalities and myocardial infarction in 3 of 7 dogs. Necropsy revealed that affected arteries (including coronary, myocardial, renal, carotid, thyroidal, intestinal, pancreatic, splenic, gastric, prostatic, cerebral, and mesenteric) were yellow-white, thick and nodular, and had narrow lumens. Myocardial fibrosis and infarction also were observed in the myocardium. Histologically, affected arterial walls contained foamy cells or vacuoles, cystic spaces, mineralized material, debris with or without eroded intima, and degenerated muscle cells.
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PMID:Clinical and pathologic findings in dogs with atherosclerosis: 21 cases (1970-1983). 374 84


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