Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One unit (500 ml) of 10% Intralipid (an intravenous soy bean oil-egg yolk lecithin preparation) was infused into 20 normal subjects over 4 hr. Serum triglyceride concentration and plasma optic density (at 700 nm) increased to maximal levels of 339 +/- 102 mg/100 ml and 1.14 +/- 0.41, respectively, at the completion of the infusion, and returned to basal levels in most subjects within 4 hr. Pulmonary membrane diffusion was decreased in six subjects at rest and with exercise at 25 and 50% maximum oxygen uptake. Only one subject showed a minor change in PO2 and none showed clinical signs of ischemia. The changes in pulmonary diffusion reverted to basal levels when serum lipids were cleared. Heparin (60 IU/kg) prevented the marked increase in serum lipids and, as a consequence, the changes in pulmonary function. Changes in pulmonary function from Intralipid-induced lipemia are similar to those known to result from diet-induced lipemia. The findings suggest that in the presence of normal vasculature and pulmonary function, Intralipid-induced lipemia should cause no clinical consequences. However, patients with preexisting pulmonary or vascular disease may be at greater risk after Intralipid-induced lipemia.
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PMID:Relationship between Intralipid-induced hyperlipemia and pulmonary function. 81 3

Atherosclerosis and insufficiency of the coronary arteries and their sequelae are summarized in the term "coronary heart disease". For the evaluation of the coronary arteries the knowledge of malformations, variants and supply areas is of importance. Extension and severity of atherosclerosis of the coronary arteries and their insufficiency is being influenced by hyperlipidemia, hypertension and diabetes mellitus. The process of atherosclerosis as a cause of the proliferation of vascular smooth muscle cells in complicated by ulceration, parietal and obliterative thrombosis as well by intramural hemorrhages. Relative ischemia leeds to disseminated cell necrosis; total ischemia causes large myocardial tissue necrosis, called infarction. Localization and extension of infarction and the later scars correspond to the caliber of the obliterated coronary artery and to the significance of the collaterals. Postmortem coronary angiography can detect cause and extension of the damaged cardiac area. Functional significance of chronic coronary heart disease is related to the "critical connective tissue content" of the heart. After surgical treatment qualitative and quantitative morphology may help to explain postoperative cardiac failure.
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PMID:[Morphology of coronary heart disease (author's transl)]. 126 48

This study was undertaken to study the effects of hyperlipidemia and hypertension on the coronary circulation and on the myocardium of Watanabe heritable hyperlipidemic (WHHL) rabbits. Surgery to induce hypertension by the one-kidney, one-clip technique was performed on the WHHL rabbits at 3 months of age. At 3 and 6 months after surgery, the right and left coronary arteries and the left ventricle and posterior papillary muscle from normotensive and hypertensive animals were assessed. Atherosclerotic involvement was found at the coronary origin in 94% of the arteries evaluated. Lesions were usually confined to the proximal 1-2 mm of the coronary artery. The prevalence of coronary atherosclerosis in the WHHL rabbit was found to be higher than previously reported in rabbits of the same age. Hypertension-induced muscular and vascular changes such as left ventricular hypertrophy, medial thickening of the arteries, and hyaline arteriolosclerosis were found in most of the hypertensive animals. These changes were rarely seen in the normotensive rabbits. Characteristics of ischemia and cell injury such as eosinophilic fibers, fiber vacuolization, and contraction band necrosis were found more often in hypertensive than in normotensive WHHL rabbits. Confluent areas of severe necrosis indicative of myocardial infarction were not found; myocardial damage was diffuse and involved individual cells and small microscopic areas. This model may be valuable in further studies of coronary artery disease and myocardial injury that result from the combination of hypercholesterolemia and hypertension.
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PMID:Effects of hypertension and hyperlipidemia on the myocardium and coronary vasculature of the WHHL rabbit. 138 26

Type-I-patients with silent myocardial ischemia (SMI) have a 2-4fold higher longterm-risk for coronary-events than healthy people. With increasing gravity and duration of ischemia type-II-patients have an increased event-risk. Reliable statements about prognosis of type-III-patients are very difficult. Therapy of SMI is equivalent to therapy of "loud" ischemia and comprises: 1) treatment of cardiovascular risk-factors (nicotine, arterial hypertension, hyperlipidemia, adiposis), 2) nitrates as effective straight at the coronary stenosis, 3) beta-blockers, which influence the circadian ischemic rhythm, 4) calcium-channel-blockers with especially for nifedipine little effect, 5) thrombocyte-aggregation inhibitors and 6) invasive therapeutical methods (percutaneous transluminal coronary angioplasty [PTCA] and aorto-coronary bypass grafting [ACBG]).
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PMID:[Silent myocardial ischemia. Current concepts of prognosis and therapy]. 176 84

The relationship between myocardial ischemia and biochemical changes has been well documented. For example, hyperlipidemia is one of the largest risk factors for the development of coronary artery disease. Decreased coronary blood flow produces various changes in cardiac metabolism, which cause severe cardiac function abnormalities, including heart failure and arrhythmias. Many biochemical markers have been used for both diagnosis and evaluation of the severity of myocardial infarction. In this symposium the speakers have discussed: 1) the relationship between the changes in the ionic environments in the intra- and extra-cellular spaces and the genesis of cardiac arrhythmias, with special reference to the role of increased intracellular resistance in conduction delay during ischemia (Dr. Takao Fujino), 2) metabolic basis of ECG abnormalities in ischemic heart disease and the role of intra-coronary ECG recordings in the evaluation of cardiac ischemia (Dr. Tetsunori Saikawa), and 3) biochemical changes associated with exercise and other stresses, with special reference to the roles of increased catecholamines and decreased blood fluidity in the genesis of cardiac abnormalities (Dr. Takehiko Fujino). Prof. Takeshi Kanno gave a special lecture entitled "Approaches from clinical laboratory to hereditary variants". He showed an excellent model of approach from clinical laboratory medicine to detect important biochemical abnormalities which may be overlooked by routine daily analyses in the clinical laboratory.
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PMID:[Cardiac function abnormalities and biochemical changes in myocardial ischemia]. 192 Aug 72

Extracranial atherosclerotic cerebrovascular disease is a risk factor for myocardial infarction and stroke. Asymptomatic patients with evidence of disease may benefit from modification of risk factors for stroke (ie, hypertension, hyperlipidemia, diabetes mellitus, and cigarette smoking). Symptomatic patients with focal brain ischemia may benefit from antiplatelet therapy, anticoagulation, and surgery in addition to modification of risk factors.
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PMID:Extracranial atherosclerosis and cerebrovascular disease. Minimizing the risk of stroke. 200 Mar 53

Lupus anticoagulants and anticardiolipin antibodies are antiphospholipid antibodies (APLAb) with related antigenic specificities and are newly recognized markers for an increased risk of thrombosis. We studied 48 patients who presented with cerebral or visual dysfunction associated with APLAb to help clarify the diagnostic, clinical, laboratory, radiologic, and pathologic features in these patients. Most patients presented with transient cerebral ischemia or cerebral infarction. Recurrent and stereotypic events were frequent. Visual disturbances resulted from amaurosis fugax, retinal arterial or venous occlusion, occipital ischemia, diplopia, and migraine-like disturbances. Three patients presented with severe atypical classic migraine. Recurrent infarcts of brain and eye were significantly associated with the presence of cigarette smoking, hyperlipidemia, and a positive antinuclear antibody. During 44.4 patient-years of prospective follow-up, the combined stroke and systemic thrombotic event rate was 0.27 events per patient-year and was 0.54 events per patient-year if TIA and death were included. Forty (83%) of the patients did not have systemic lupus erythematosus (SLE). Thrombocytopenia was present in 15 (31%) and a false-positive VDRL in 11 (23%) of the patients. Cerebral angiography was normal or revealed large-vessel occlusion or stenosis without changes suggestive of vasculitis. Patients with only transient dysfunction generally had normal radiologic studies, including angiography. Organs and arterial vessels studied pathologically revealed thrombotic occlusive disease without vasculitis. APLAb are strongly associated with an immune-mediated thrombotic tendency, generally in the absence of SLE. Other stroke risk factors may add to the risk of recurrent ischemic events in patients with APLAb.
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PMID:Cerebrovascular and neurologic disease associated with antiphospholipid antibodies: 48 cases. 238 25

Recent in vitro studies on isolated coronary and mesenteric arteries have shown that hyperlipidemia appears to hypersensitize the vascular arterial smooth muscle to drugs such as ergonovine and that this increased contractility seems to be mediated by a serotinergic mechanism. This results in vasospasm with exposure to certain vasoactive drugs such as serotonin or norepinephrine. However, in vivo quantification of this observed phenomenon has not been done. In the present study we used Watanabe hereditary hyperlipidemic (WHHL) rabbits (cholesterol level 459 +/- 216 mg/dL) and the normal lipidemic New Zealand white (NZW) rabbit (cholesterol level 35 +/- 19) as a control in the study of hyperlipidemia and blood flow changes in response to various vasoactive drugs. Blood flow measurements were made by the video dilution technique (VDT) following catheterization of the superior mesenteric artery. The serotinergic vasoactive drug ergonovine maleate was injected into the superior mesenteric artery at low dose (0.002) mg/kg) and high dose (0.004 mg/kg). A significant decrease (p less than .05) in blood flow was observed in response to high-dose ergonovine maleate in WHHL rabbits compared to the NZW rabbits. This in vivo experiment confirms the in vitro studies showing that hyperlipidemia sensitizes mesenteric arteries in the presence of serotinergic stimuli. The vasodilators verapamil hydrochloride and calcitonin gene-related peptide (CGRP) injected into the superior mesenteric artery caused a marked increase in flow in both the WHHL and the normal lipidemic NZW rabbits. This model can be used in the assessment of superior mesenteric artery ischemia and its reversal.
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PMID:Superior mesenteric artery vasoactivity in hyperlipidemic Watanabe rabbits versus normal lipidemic New Zealand controls. 248 10

Major risk factors have been identified that enhance the chances of cardiovascular morbidity and mortality. These include such modifiable factors as hypertension, hyperlipidemia, obesity, diabetes mellitus, smoking and hyperuricemia. Other factors that also increase risk are not modifiable and include advancing age, male gender and black race. The development of left ventricular (LV) hypertrophy imposes another significant risk for increased morbidity and mortality. Development of LV hypertrophy may be produced by hemodynamic as well as nonhemodynamic mechanisms. Included in the latter group are some of the same factors that in and of themselves participate in the production of increased LV mass (i.e., aging, gender and race, obesity, coronary disease, diabetes and the underlying mechanisms that subserve the hypertensive disease). This article discusses the concept, drawn from clinical and experimental studies, that demonstrate that the additional increased risk of LV hypertrophy may be ascribed to loss of reserve cardiac function, accelerated atherosclerosis, development of abnormal cardiac rhythm secondary to ischemia, fibrosis or drug-induced hypokalemia, inherent predisposition to ventricular dysrhythmias and sudden death, risks directly or coincidentally related to associated diseases or perhaps even the paradoxical risk of beneficial antihypertensive therapy.
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PMID:Potential mechanisms explaining the risk of left ventricular hypertrophy. 294 82

The problem of caring for patients undergoing reoperative coronary revascularization is one that cardiac anesthesiologists will face with increasing frequency. Many thousands of CABG procedures continue to be performed annually with ever-increasing survival rates. Consequently, the population at risk for reoperative CABG is growing, while surgical intervention necessarily follows apace. As one recent long-term, retrospective study showed, patients surviving 12 years after CABG have a reoperative rate of 17.3%. Physicians caring for these patients must recognize that they are not seeing patients with routine CAD, but with a different entity: coronary graft disease (CGD). These patients with CGD are different in many ways from those with native CAD, and these differences must be taken into account when planning for their perioperative care. Cardiologists have strived to check the growth of CGD by aggressive emphasis on modification of coronary risk factors such as tobacco use, hypertension, and hyperlipidemia. In addition, recent interest has been focused on a pharmacologic approach via the platelet-prostaglandin system. Surgeons have also attempted to reduce the incidence of CGD by recognition that significantly improved long-term patency rates can be achieved by the use of the internal thoracic artery as a bypass conduit. Consequently, an expanded role for this vessel in the form of free, sequential, and bilateral ITA grafting is currently being advocated as a surgical solution to the problem of CGD. In contrast, the anesthesiologist probably has little to add to the prevention of CGD, but may be able to contribute to a favorable outcome at reoperation. The medical variables and preoperative characteristics that make reoperative CABG patients different from those presenting for primary CABG should be recognized. A firm appreciation of the nature of graft disease, as well as the surgical intricacies required for correction, can only serve to improve the care offered during these often complex operations. Aggressive, invasive hemodynamic monitoring, constant vigilance for signs of early ischemia, and preparedness for prebypass hemorrhage and postbypass ventricular dysfunction should be made. Furthermore, if anesthesiologists are to contribute to an improved outcome in these patients, strategies must be developed to attenuate cerebral and myocardial damage resulting from hemorrhage and atheroembolic catastrophies that appear to be frequent complications in these challenging surgical patients.
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PMID:Reoperation for coronary artery bypass grafting: anesthetic challenge. 1717


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