1/11. The use of antioxidants in retarding atherosclerosis: fact or fiction?The proposal that antioxidants may retard the progression of atherosclerosis is not new. Published studies examining the effect of antioxidants on experimental antioxidants extend back to 1940. The results have all been inconsistent. However, the data regarding the beneficial effects of retarding atherosclerotic progression are strong enough to warrant continued research on the lipoprotein oxidation theory or atherosclerosis. However, caution is needed to avoid embracing a concept without proof. It should be noted that the National Cholesterol education Program does not recommend the use of antioxidant vitamin supplements to reduce CAD. Atherogenesis is produced by multiple factors. To believe that all such factors are mediated by uncontrolled oxidative events is, to say the least, naive. Finally, should antioxidants prove to be effective in retarding coronary atherosclerosis, their place on the therapeutic ladder of CAD prevention would be low. The overwhelmingly proven evidence favors the following factors that have been proven to lower morbidity and mortality due to atherosclerosis: (a) treatment of hypertension, (b) cessation of tobacco use, (c) treatment of dyslipidemia, (d) achieving a normal weight, (e) regular exercise, (f) treatment of homocystinuria, especially in cases with renal disease, and (g) antioxidants.- - - - - - - - - - ranking = 1keywords = atherosclerosis (Clic here for more details about this article) |
2/11. A case of marked hyperlipoprotein(a)emia associated with nephrotic syndrome and advanced atherosclerosis.In 1989, we encountered a 68-year-old male patient with marked hyperlipoprotein(a)emia (hyperLp(a)emia), who was being treated for hypertension and arteriosclerotic obliterans (ASO) at an outpatient clinic of our hospital. He began to develop leg edema in 2002 and was referred to the Department of internal medicine. It was determined that he had severe hyperlipidemia (total cholesterol, 362 mg/dl), proteinuria, and hypoalbuminemia, suggesting the presence of nephrotic syndrome. On lipoprotein analysis, he was found to have very high levels of Lp(a) in the plasma (329 mg/dl). Severe atherosclerosis was also found: that is, abdominal aortic aneurysm (AAA) and coronary artery disease (CAD) were detected, in addition to ASO. After remission of the nephrotic syndrome, the plasma Lp(a) level decreased to 204 mg/dl and the total cholesterol concentration decreased to 179 mg/dl, while very high levels of Lp(a) persisted. We estimate that the markedly elevated Lp(a) plasma levels in this patient may have played some role in the progression of atherosclerosis.- - - - - - - - - - ranking = 0.75237340033491keywords = atherosclerosis, artery disease, artery (Clic here for more details about this article) |
3/11. Molecular basis of lipid transfer protein deficiency in a family with increased high-density lipoproteins.plasma high density lipoproteins (HDL) are a negative risk factor for atherosclerosis. Increased HDL is sometimes clustered in families, but a genetic basis has never been clearly documented. The plasma cholesteryl ester transfer protein (CETP) catalyses the transfer of cholesteryl ester from HDL to other lipoproteins and therefore might influence HDL levels. Using monoclonal antibodies, we show that CETP is absent in two Japanese siblings who have markedly increased and enlarged HDL. Furthermore, they are homozygous for a point mutation in the 5'-splice donor site of intron 14 of the gene for CETP, a change that is incompatible with normal splicing of pre-messenger RNA. The results indicate that the family has an inherited deficiency of CETP due to a gene splicing defect, and illustrate the key role that CETP has in human HDL metabolism.- - - - - - - - - - ranking = 0.125keywords = atherosclerosis (Clic here for more details about this article) |
4/11. Recurrent tendinitis and achilles tendon nodule with positively birefringent crystals in a patient with hyperlipoproteinemia.We describe a patient with hypercholesterolemia and premature coronary artery disease. Positively birefringent suspected lipid crystals were aspirated from a retrocalcaneal bursa and an achilles tendon nodule. These crystals may have been a factor in the tendinitis and could be confused with calcium pyrophosphate dihydrate crystals.- - - - - - - - - - ranking = 0.0023734003349128keywords = artery disease, artery (Clic here for more details about this article) |
5/11. Hyperlipoproteinemia with albumin-lipid complex: a novel type of hyperlipoproteinemia associated with insulin-resistant diabetes mellitus.We describe a new phenotype of hyperlipoproteinemia in two members of a family with a high degree of consanguinity. Both have a history of uncontrolled diabetes mellitus without ketoacidosis, and a family history of coronary artery disease at a relatively early age. A high degree of insulin resistance was found. The abnormal lipoprotein(s) has alpha-lipoprotein mobility on cellulose acetate electrophoresis and has a relative density of less than 1.006 as determined by ultracentrifugation of serum collected after a short fast. The fraction isolated by ultracentrifugation contains about half of the serum cholesterol and triglycerides and most of the phospholipids; the major protein component is albumin. immunoelectrophoresis showed low concentrations of beta-lipoproteins in both sera, and two abnormal precipitin bands against monospecific antiserum to antilipoprotein A; a third member of the family showed only one abnormal precipitin band against the same antibody. We tentatively propose an abnormal gene(s) as the underlying mechanism. The insulin-resistant diabetes mellitus, probably inherited separately, may aggravate the hyperlipidemia.- - - - - - - - - - ranking = 0.0023734003349128keywords = artery disease, artery (Clic here for more details about this article) |
6/11. Cerebrovascular arteriopathy (arteriosclerosis) and ischemic childhood stroke.The aim of this report is to describe the intracranial cerebrovascular abnormalities and clinical status of 8 children who had familial lipoprotein disorders and evidence of thromboembolic cerebrovascular disease. Six of the 8 children had low levels of plasma high density lipoprotein cholesterol, two had high triglyceride levels, and all came from kindreds characterized by familial lipoprotein abnormalities and premature cardio- and/or cerebrovascular atherosclerosis. Vascular occlusion, irregularities of the arterial lumen, beading, tortuosity, and evidence of collateralization were consistently noted. We speculate that cerebrovascular arteriosclerosis in pediatric ischemic stroke victims who have familial lipoprotein abnormalities may be related to lipoprotein-mediated endothelial damage and thrombosis formation, or to the failure to restore endothelial cells' integrity following damage. The apparent association of lipoproteins and strokes in children and their families merits further exploration, particularly when assessing cerebral angiograms in pediatric ischemic stroke victims. In children with unexplained ischemic cerebrovascular accidents, the diagnostic possibility of occlusive arteriosclerosis with thrombosis must be entertained.- - - - - - - - - - ranking = 0.125keywords = atherosclerosis (Clic here for more details about this article) |
7/11. myocardial infarction in familial hyper-alpha and hypo-beta-lipoproteinaemia.This is the documentation of an acute myocardial infarction in a 45-year-old woman with familial hyper-alpha- and hypo-beta-lipoproteinaemia. This dyslipoproteinaemia has been rarely associated with clinical evidence of ischaemic heart disease. documentation of angiographically normal coronary arteries in this patient is consistent with the concept that increased alpha-lipoprotein (HDL) and low beta-lipoprotein (LDL) may prevent atherosclerosis. Thus, myocardial infarction in patients with this dys-lipoproteinaemia should be attributable to factors other than coronary atherosclerosis.- - - - - - - - - - ranking = 0.25keywords = atherosclerosis (Clic here for more details about this article) |
8/11. Massive lower extremity arterial thrombosis and acute hepatic insufficiency in a young adult with premature atherosclerosis associated with hyperlipoprotein(a)emia and antiphospholipid syndrome. A case report.The authors describe a healthy young male smoker with familial history of recurrent thromboembolism who presented with severe, rapidly progressive lower limb ischemia and abnormal results from liver function tests. An arteriogram of the lower extremities showed bilateral infrainguinal atherosclerotic arterial occlusions. The laboratory findings, in addition to abnormal liver function findings, included moderately elevated antiphospholipid antibodies and hemostatic abnormalities involving elevated fibrinogen, lipoprotein (a) levels, and deficient fibrinolysis. He underwent bilateral femoral thrombectomy, which was followed by a meticulous anticoagulation, and had gradual improvement of ischemic symptoms and liver functions. This is, to their knowledge, the first reported case in the English literature of premature lower extremity atherosclerosis and antiphospholipid syndrome associated with elevated lipoprotein (a) levels and documented complex hemostatic abnormalities contributing to systemic thrombosis.- - - - - - - - - - ranking = 0.625keywords = atherosclerosis (Clic here for more details about this article) |
9/11. Diffuse arterial thrombosis in a young man with elevated lipoprotein(a) and minimal atherosclerosis.An increased incidence of premature atherosclerotic arterial occlusive disease was recently reported in young adults. This condition is characterized by early occurrence of severe symptoms, lower incidence of typical cardiovascular risk factors for atherosclerosis, different natural course of arterial disease vis-a-vis older population, and poor outcome of a standard treatment. This report describes a young man with aggressive arterial occlusive disease in the lower extremities and symptom-free occlusions of coronary and renal arteries in association with high levels of lipoprotein(a). Microscopic early atherosclerotic changes were noted in the occluded arteries of the amputated leg. Premature atherosclerotic arterial occlusive disease in young adults has different clinical and pathological patterns, necessitating a different approach for evaluation and treatment.- - - - - - - - - - ranking = 0.625keywords = atherosclerosis (Clic here for more details about this article) |
10/11. Hyperlipoprotein(a)aemia in nephrotic syndrome.The nephrotic syndrome is frequently associated with hyperlipidaemia and hyperfibrinogenaemia, leading to an increased coronary and thrombotic risk, which may be enhanced by high lipoprotein (a) [Lp(a)] concentrations. We followed the quantitative and qualitative pattern of plasma lipoproteins over 18 months in a patient with nephrotic syndrome suffering from premature coronary artery disease and with elevated level of Lp(a) (470 mg dL-1). Analysis of kinetic parameters after heparin-induced extracorporeal plasma apheresis revealed a reduced fractional catabolic rate for both low-density lipoprotein (LDL) and Lp(a). After improvement of the nephrotic syndrome, Lp(a) decreased to 169 mg dL-1 and LDL concentrations were normalized. The decrease of Lp(a) was associated with an increase in plasma albumin concentrations. Analysis of apo(a) isoforms in the patient showed the presence of isoform S2 (alleles 10 and 19). Consequently, the authors' present strategy is to normalize the elevated Lp(a) and fibrinogen levels. For this purpose heparin-mediated extracorporeal LDL precipitation (HELP) apheresis is a promising regimen, helping to reduce the thrombotic risk and prevent coronary and graft atherosclerosis as well as the progression of glomerulosclerosis in our patient.- - - - - - - - - - ranking = 0.12737340033491keywords = atherosclerosis, artery disease, artery (Clic here for more details about this article) |
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