Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The anomalous finding that very low density lipoprotein levels are relatively normal in patients with familial hyperchylomicronaemia has never been satisfactorily explained, particularly in view of the marked reduction or absence of peripheral lipoprotein lipase activity characteristic of this condition. I propose that the discrepancy between the plasma levels of the two triglyceride-rich lipoprotein fractions in these patients is due to the secretion by the liver of triglyceride in the form of chylomicron-like particles, rather than as very low density lipoprotein. The proposed "switch" in the spectrum of lipoproteins secreted by the liver is probably contingent upon the activity of the hepatic lipase present on the liver cell plasma membrane.
Atherosclerosis 1979 Sep
PMID:Why very low density lipoprotein levels are normal in familial hyperchylomicronaemia. 22 32

Fourteen patients with prostatic carcinoma were treated with 1.0-0.5 mg ethinyl estradiol orally daily and 160-80 mg polyestradiol phosphate im monthly. Lipid concentrations were determined in plasma and the high density lipoprotein fraction, and the plasma lecithin-cholesterol acyl transfer rate was measured before and 1 and 6 months after the start of therapy. During treatment, the concentration of total cholesterol was unchanged while there was a 60% increase of high density lipoprotein-total cholesterol. Triglyceride (TG) concentration increased 40%, indicating an augmented level of very low density lipoprotein concentration. The plasma lecithin-cholesterol acyl transfer rate increase 20-35%, indicating that an increased rate of production and turnover of TG, cholesteryl esters, and very low density lipoproteins probably was a main cause of the elevated TG concentration. The potential effects on the development of atherosclerosis by the plasma lipid changes during estrogen treatment are discussed.
J Clin Endocrinol Metab 1978 Sep
PMID:Changes of plasma lipid metabolism in males during estrogen treatment for prostatic carcinoma. 23 77

Aortocoronary vein grafts removed at autopsy of 182 patients who died up to 5 years after the bypass operation were examined by light and electron microscopy. During the first month after surgery, graft occlusion was due to thrombi, some of them recent, some organized and recanalized. Intimal proliferation of the graft first appeared 4 weeks after the bypass surgery; several cases of total occlusion of the lumen by this process were seen within 6 months of the operation. A change in the morphological features of the intimal thickening from cellular to fibrotic and hylain-like was observed in several grafts implanted for more than 1 year. Typical atherosclerosis developed in vein grafts in three of the six patients surviving the operation for more than 3 years.
Circulation 1977 Sep
PMID:The spectrum of pathologic changes in aortocoronary saphenous vein grafts. 30 96

Intralysosomal accumulation of lipid has been implicated as an important mechanism in the pathogenesis of atherosclerosis. Although atherosclerosis develops frequently in organ transplants maintained on a long-term basis, to our knowledge no studies to date have demonstrated the intracellular localization of the lipid in this setting. Light and electron microscopic study of a renal artery branch from a transplanted kidney maintained for 3 1/2 years demonstrates that the lipid is sequestered within intimal smooth muscle cell lysosomes. The features of the atherosclerotic plaque in long-term transplantation appear to be identical to spontaneous lesions or those induced experimentally.
Arch Pathol Lab Med 1977 Sep
PMID:Intralysosomal lipid in long-term maintenance transplant atherosclerosis. 32 1

Heart disease continues to be a major cause of disablement and death in Canada. Elevated serum cholesterol concentrations, hypertension and cigarette smoking are among the standard risk factors associated with ischemic heart disease. Research attention has also been directed at the role of behavioural factors in the development of atherosclerosis and myocardial infarction. Experimental findings support a conceptual approach to the interplay of psychologic stress, the type A "coronary"-prone behaviour pattern and pathophysiologic mechanisms that have been implicated in the development of coronary artery disease. It is concluded that type A behaviour and stress contribute substantially to the pathogenesis of cardiovascular disease. However, assessment of the manner in which these two variables influence the pathophysiology of ischemic heart disease requires further research, with systematic examination of physiologic and biochemical processes. Potential strategies for modifying type A behaviour are reviewed. However, unequivocal support for the preventive efficacy of behavioural approaches must await future research.
Can Med Assoc J 1978 Sep 23
PMID:Behavioural prevention of ischemic heart disease. 36 Nov 91

Hypercholesterolemia was induced in rabbits by feeding Purina Chow supplemented with cholesterol (5 g/kg body weight/day). The serum cholesterol levels of these rabbits increased progressively and after 3 to 5 months were 4 to 9-fold greater than those of the control animals. Decrease in total hemolytic complement was not apparent during the feeding regimen. Morphologic examination of aortae of these hypercholesterolemic rabbits showed typical atherosclerotic intimal plaques. Immunofluorescent microscopy with fluorescein (F)-labeled anti-rabbit C3 showed deposition of C3 in the intimal and inner medial layers as early as 3 months on high cholesterol diet. C3 deposits were also observed in the renal glomeruli and in the walls of coronary arteries. However, fluorescent studies failed to demonstrate the presence of IgG, IgM, and C4 at these sites. Tissues from control animals fed normal diets were negative for immunoglobulins, C3, and C4. These results suggest that the complement system may be implicated in the pathogenesis of cholesterol-induced atherosclerosis in rabbits.
J Immunol 1979 Sep
PMID:C3 deposition in cholesterol-induced atherosclerosis in rabbits: a possible etiologic role for complement in atherogenesis. 38 17

Atheroarteriosclerosis closely resembling that in humans was induced in normocholesterolemic and hypercholesterolemic chickens by infection with Marek's disease herpesvirus (MDV). Four comparably sized groups of chickens were used. Each group was initially fed a diet relatively poor in cholesterol. Group I and II were inoculated intratracheally at 2 days of age with MDV. At 15 weeks, one group of virus-infected chickens (Group II) and one group of uninfected controls (Group IV) were fed a 2% cholesterol supplement for an additional 15 weeks. Group I, infected, and III, uninfected, were continued on a cholesterol-poor diet. All groups were killed at 30 weeks. Striking grossly visible atherosclerotic lesions were seen in large coronary arteries, aortas, and major aortic branches of both Groups I and II but not in those of Groups III and IV. Microscopically, arterial changes in infected animals were characterized by occlusive fibromuscular intimal thickening, which formed fibrous caps overlying areas of atheromatous change. This change closely resembled chronic atherosclerosis in humans. These results may be important to our understanding of human arteriosclerosis, since there is widespread and persistent infection of human populations with as many as five herpesviruses.
Am J Pathol 1979 Sep
PMID:Atheroarteriosclerosis induced by infection with a herpesvirus. 38 68

To determine the effect atherosclerosis has on myocardial contractility, we studied the contractile properties of right ventricular papillary muscles from 34 atherosclerotic and 17 control rabbits. We produced atherosclerosis by feeding for 2 to 8 months a diet of 5% lard, 5% peanut oil, 0.5% cholesterol, and 89.5% rabbit pellets. The controls received only rabbit pellets during the same time interval. Contracting isometrically 12 times per minute at 25 degrees C, muscles from the atherosclerotic rabbits developed tension at a lower maximum rate (max dT/dt), had a longer latency, and required longer to develop tension at the maximum rate and to develop peak tension. In isotonic contractions, they shortened with lower maximum velocities and required longer to accelerate to maximum velocity and to shorten maximally. We found no evidence that developed tension or distance shortened differed between the two groups of muscles. Raising the contraction frequency to 24 contractions per minute between the two groups of muscles. Raising the contraction frequency to 24 contractions per minute brought performance of the two groups of muscles closer in both types of contraction. Norepinephrine (1.5 x 10-5 M) nearly abolished differences between performance of the two groups. The loss of contractility correlates poorly with coronary and aortic atherosclerosis. It occurred early in the feeding of the atherogenic diet. We think it was due to a lipid-induced defect in the cardiac cell's handling of calcium.
Circ Res 1979 Sep
PMID:Decreased myocardial contractility in papillary muscles from atherosclerotic rabbits. 45 99

An 86-year-old man with previous normal renal function was hospitalized because of renal insufficiency. He had a long history of atherosclerotic heart disease, mild hypertension and pulmonary embolism, requiring anticoagulant therapy. In view of the normal-sized kidneys and absence of casts in the urinary sediment, a diagnosis of atheroembolic renal disease was made. The patient's renal function deteriorated, but he refused hemodialysis. Death occurred within a few weeks. At autopsy, severe aortic atherosclerosis was observed and atheroembolic renal disease was confirmed as the cause of renal failure. Occasionally, renal failure can be the sole manifestation of spontaneous atheroembolic disease. This possibility should be considered if the physician is called upon to establish the diagnosis when renal insufficiency develops in atherosclerotic patients.
J Am Geriatr Soc 1979 Sep
PMID:"Spontaneous" atheroembolic disease as a cause of renal failure in the elderly. 46 53

Thirteen of 1,250 patients required a second operation for recurrent stenosis following carotid endarterectomy performed at the Cleveland Clinic between 1958 and 1978. Two other patients underwent reoperation because of recurrent stenosis following primary operations at other institutions. Thirteen of the 15 patients experienced neurologic symptoms caused by recurent stenosis, while two patients remained asymptomatic. Atherosclerosis was responsible for recurrent stenosis in 12 patients and appeared to be related to hypercholesterolemia. Three of the patients had myointimal fibroplasia. Eleven of the 16 reoperations for recurrent stenosis of the carotid artery consisted of carotid endarterectomy with vein patch angioplasty. Three patients had carotid endarterectomy with closure of the primary arteriotomy. One patient with occlusion of the internal carotid artery underwent endarterectomy of the external carotid artery because of amaurosis fugax, and a saphenous vein interposition graft was used to replace a previous Dacron graft in one patient with anastomotic stenosis. One patient had a stroke during reoperation manifest as multiple retinal emboli. Fourteen patients have remained asymptomatic from one to 70 months following reoperation. One patient with occlusion of the contralateral internal carotid artery has experienced persistent vertebrobasilar symptoms.
Surg Gynecol Obstet 1979 Sep
PMID:Recurrent stenosis after carotid endarterectomy. 47 95


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