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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of hypertension, hyperlipidemia, and the combination of both on acute and chronic myocardial ischemia were evaluated in a total of 30 male rabbits. After preliminary hypertension and/or hyperlipidemic load by loading of the abdominal aorta and/or cholesterol feeding, acute ischemia was produced by clipping of the left coronary artery. The banding produced elevation of carotid arterial pressure and left ventricular hypertrophy. Cholesterol feeding resulted in severe atheromatous changes in all sizes of coronary arteries. The intimal thickening was due to foam cell accumulation in all arteries examined. Animals pretreated with the combination of hypertension and hyperlipidemia displayed the most severe cardiolmegaly with advanced coronary atherosclerosis and chronic ischemic lesions of the myocardium, i.e., perivascular patchy fibrosis in the subendocardial area. Furthermore, electron microscopic detection of ultrastructural myocardial damage, involving glycogen depletion, sarcoplasmic edema, mitochondrial swelling, and contractile abnormalities, was also most frequent in this group. These changes were quantitated using the ischemic score. These results confirm the hypothesis that fatal ischemic injuries may occur clinically in human hearts with coronary insufficiency due to coexistence of hypertensive cardiomegaly and severe coronary atherosclerosis. They offer a model for further study of these combined effects.
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PMID:An ultrastructural study on ischemic lesions in rabbits' hearts with pressure overload and hyperlipidemia. 315 60

The plasma concentration of beta-thromboglobulin (BTG), a platelet-specific protein released during platelet aggregation, is considered a sensitive marker of in vivo platelet activity. The mean plasma level in 133 asymptomatic individuals was 32.3 +/- 1.1 ng/ml, and there was no difference between those with no risk factors (32.2 +/- 1.2 ng/ml, n = 56), those who smoked (31.8 +/- 1.8 ng/ml, n = 45), those with hyperlipidemia (32.8 +/- 1.7 ng/ml, n = 15), and those exposed to both of these risk factors (34.1 +/- 2.7 ng/ml, n = 17). The mean plasma BTG level in 104 patients with symptomatic ischemic heart disease was significantly elevated (40.9 +/- 1.4 ng/ml, p less than 0.01), but there was considerable overlap with normal levels. Although no difference was found between patients with no risk factors (38.1 +/- 4.0 ng/ml, n = 13) and those with only 1 risk factor (37.0 +/- 1.8 ng/ml, n = 44), patients with 2 or more risk factors ahd a significantly elevated plasma BTG level (45.2 +/- 2.2 ng/nl, n = 47, p less than 0.01). It is concluded that risk factors themselves do not increase platelet activity, but that patients with vascular disease have activated platelets that may contribute to the progression of the disease. Plasma BTG was also measured serially for 10 days in 29 patients after hospitalization with acute ischemic cardiac pain. Although the median plasma level was elevated above normal there were no acute changes in plasma BTG after either acute infarction (n = 22) or acute ischemia (n = 7), except in 2 patients in whom pericardial friction rubs developed. Thus, measurement of systemic plasma BTG did not detect platelet involvement in acute coronary occlusion or acute ischemia.
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PMID:Plasma beta-thromboglobulin as a measure of platelet activity. Effect of risk factors and findings in ischemic heart disease and after acute myocardial infarction. 618 69

A thirty-year-old woman, who had onset of nephrotic syndrome during the last part of her pregnancy, experienced recurrent acute ischemia of both lower limbs, leading to three conservative surgical procedures one month after delivery. Investigations disclosed no cause of embolism and were suggestive of thrombosis. The arteriography showed a diffuse reduction in diameter of the aorta and iliac vessels without localised stenosis or other vascular lesions. This complication is presumably related to several factors associated with the reduction in arterial diameter: hypovolemia, hyperfibrinemia, hyperlipidemia and abnormalities of hemostasis.
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PMID:[Acute ischemia of the lower limbs in nephrotic syndrome in a young woman]. 631 45

The authors examined 40 patients with chronic ischemic pancreatitis without concomitant pathology of the alimentary organs in order to define the features of the disease clinical picture and progress. It was found that patients with disseminated atherosclerosis, especially when it is coupled with essential hypertension, and with extravasal stenosis of the celiac trunk are predisposed to the development of chronic ischemic pancreatitis. Factors promoting pancreatic ischemia include abnormalities of the blood rheological properties seen in vascular pathology and alimentary hyperlipidemia.
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PMID:[Various characteristics of chronic ischemic pancreatitis]. 652 92

Iatrogenic pathology of the optic nerve is examined according to a framework which distinguishes direct and indirect effects on the optic nerve. Direct effects due to toxic drugs should be suspected when unexplained, usually bilateral loss of visual acuity occurs. The 3 clinical stages of classical optic toxic neuropathy are 1) anomalies of color vision, 2) loss of visual acuity and narrowing field of vision, and 3) papillary palor corresponding to irreversible optic atrophy. Usually only the 1st stages are reversible, but the reversibility may be incomplete. The list of drugs which can cause such effects is lengthy and includes antiinfectious drugs such as sulfamides and derivatives of hydroxyquinoleins, chloramphenicol especially when used to treat cystic fibrosis of the pancreas in children, the antituberculins ethambutol in high doses and isoniazide, which occasion particular risks when combined; antiparasitics such as quinine and its derivatives chloroquine and hydroxychloroquine, which cause optic neuropathy through their effect on the retina; arsenic pentavalents such as tryparsamide, quinacrine, trecator and mystatin; drugs affecting the central nervous system such as monoamineoxydase inhibitors, laroxyl, phenothiazine and the barbituates; anticonvulsants such as phenytoin; antimitotics such as vincristine; digitalics, disulfiram; penicillamines, and pexid. The action of lasers on the optic nerve can have a similar effect. The optic nerve may be indirectly damaged during surgical procedures leading to hypotonia, acute ischemia of the head of the optic nerve or embolic accident after a local or regional injection. Damage may also be caused by radiotherapy of intracranial tumors and certain drugs which cause isolated papillary edema or edema associated with headaches, such as Tetracycline, large doses of vitamin A or D, corticoids, and oral contraceptive (OC) pills, which may cause papillary edema through cerebral pseudo-tumors that regress with discontinuation of treatment. This condition has been observed in women with uncontrolled hyperlipidemia. It is probable that an alteration ofaxonal transport is at the basis of the neuropathic mechanisms. The 1st step in therapy is the suppression of the toxin, or at least its discontinuation. Some success has been obtained with vitamin B therapy, corticotherapy, zinc, or isaxonine, depending on the specific condition.
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PMID:[Iatrogenic pathology of the optic nerve]. 676 92

Aseptic osteonecrosis is observed in 25% of cases after renal transplantation. This etiological variety of osteonecrosis is unusual in that it is frequently bilateral and has multiple localisations. Apart from the classical radiological signs, attention in attracted by isolated images of osteocondensation in the metaphyses and/or the diaphyses suggesting massive bony infarction and the appearances of fatigue fractures observed frequently (14%). In 43% of cases, the obvious necrosis was proceeded by early bone pain, around the 7 th day, during massive administration of corticosteroids in the prevention or cure of graft resection. This finding suggested to us that the best time to observe ischemia of the bone or marrow is very early and led us to undertake an experimental study in the rabbit. Two series of New Zealand White rabbits were treated with massive doses of corticosteroid and sacrificed between the 3rd and the 21st day. The treated animals presented an early peak of hyperlipemia from the 7th day onwards, and diffuse lesions of hepatic and renal steatosis. Fat emboli associated with appearances of parietal thrombosis were observed in most cases. In the same animals, there were also appearances of stage I or stage II necrosis. Referring to the description of bone marrow necrosis in stages by Arlet and Ficat, there was observed in all the series, a frequency of marrow lesions of all stages much higher in treated animals (16 out of 20) than in controls. Only one lesion of stage I was observed in controls; the difference was highly significant. (0,000001 < p < 0,00001). If one only considers necroses of stage II and III (10/20 in the treated group nil in controls) the frequency was still significant p < 0.001. The preliminary results of the fixation of tetracycline are reported.
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PMID:[Cortisone-induced osteonecrosis: knowledge acquired from observations in man and comparison with the results of animal experimentation]. 700 46

This study defined the patterns of investigation and treatment of serum lipids and other modifiable risk factors for atherosclerosis among 3,304 hospitalized patients at high risk for future cardiovascular events. There were 2,161 men and 1,143 women; 1,955 were aged < 70 years, and 1,349 were aged > or = 70 years. Acute (61%) and chronic (65%) cardiac ischemia was the most prevalent reason for high-risk status, followed by cardiac revascularization (46%) and diabetes (28%). Only 28% of patients had lipid measurements recorded during their hospital stay, or recorded at any time between 1988 and 1993. A lipid-lowering diet or drugs were prescribed for 22% and 8% of all patients, respectively, and an adjustment in lifestyle in only 5% of all patients. Moreover, measurement and therapy of lipid risk were recorded less frequently in older patients (p < 0.01), and less often in women (p < 0.01). Logistic regression analysis revealed admission for revascularization, preadmission lipid-lowering or lifestyle therapies, and history of hyperlipidemia or diabetes to be associated with increased likelihood of in-hospital lipid measurement; age > or = 70 years was associated with reduced likelihood of lipid determinations (p < 0.01). The overall investigation and therapy of serum lipids and other risk factors in acute care patients at high risk for cardiovascular events appear less than optimal. Moreover, there is significantly fewer measurements and less treatment of risk factors in women and older patients. Improvement in these practice patterns would improve patient outcomes for the most important diseases in society.
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PMID:Low incidence of assessment and modification of risk factors in acute care patients at high risk for cardiovascular events, particularly among females and the elderly. The Clinical Quality Improvement Network (CQIN) Investigators. 767 79

A retrospective community-wide survey identified 109 patients younger than 40 years of age with lower extremity ischemia: 72 men and 37 women, mean age 36 years (range 25 to 40 years), black-to-white ratio-1:1. Initially, 66 patients had claudication and 43 had severe ischemia. Cardiovascular risk factors were smoking (85%), hypertension (47%), coronary artery disease (30%), hyperlipidemia (27%), diabetes (25%), and visceral arteriopathy (17%). Unique risk factors included hypercoagulability (15%) and clinical arterial hypoplasia (15%). Twenty-three (21%) patients were treated medically; 74 (68%) underwent primary revascularization and 12 (11%) primary major limb amputation. Forty-six (53%) patients required secondary procedures, of which 34 (74%) were performed within 1 year of primary intervention. A total of 29 (27%) patients ultimately required amputation (10 bilateral). Women had higher prevalence of diabetes (p < 0.01), arterial hypoplasia (p < 0.05), and tendency for more severe ischemia (p = 0.11). No racial differences in severity of symptoms or outcome of treatment were found. By multiple logistic regression analysis, typical cardiovascular risk factors did not predict severity of symptoms, need for surgical treatment, or outcome. However, diabetes was associated with tissue loss (p < 0.05) and primary amputation (p < 0.001). Further, adjusted odds ratios indicate that arterial hypoplasia had a protective effect on distal vasculature (p < 0.05) and predicting need for revascularization (p < 0.05), but not on treatment failure. Hypercoagulability had the highest predictive value for presence of severe ischemia (p < 0.05), need for primary amputation (p < 0.01), and early failure of surgical treatment (p < 0.05).
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PMID:Lower extremity ischemia in adults younger than forty years of age: a community-wide survey of premature atherosclerotic arterial disease. 817 42

A higher prevalence of stroke is found in the patient with both diagnosed and undiagnosed diabetes and glucose intolerance. Because of local cerebral acidosis caused by ischemia and hyperglycemia, morbidity and mortality from a stroke are increased. Most studies show that individuals with admission serum glucose > 120 mg/dl (6.7 mM) have a higher morbidity and mortality from a stroke. The prevalence of cerebral infarcts, especially lacunar infarcts, is increased and the prevalence of subarachnoid hemorrhage, cerebral hemorrhage, and transient ischemic attacks are decreased in the diabetic patient. Age, race, hypertension, and the presence of diabetic nephropathy and coronary and peripheral vascular disease are risk factors for stroke in the diabetic patient, whereas obesity, smoking, hyperlipidemia, and glycemic control are not. Investigation and treatment of the diabetic patient with a stroke is discussed.
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PMID:Stroke in the diabetic patient. 817 50

The risk factors predominating in patients with peripheral arterial occlusive disease are cigarette smoking and diabetes. Moreover, hypertension and hyperlipidemia play an important role. Especially younger patients profit from elimination or treatment (primary or secondary prevention), whereas in elderly patients these measures are no longer crucial. In patients with intermittent claudication, the quality of life may be improved by physical training, vasoactive medicaments, optimal management of concomitant diseases and the different modalities of catheter therapy. According to the special situation in critical ischemia, surgical or catheter revascularization is preferred. If these two techniques cannot be used, intra-arterial or intravenous prostanoids are still promising. Aspirin and in second priority ticlopidine are suited for secondary prevention of arteriosclerosis not only in the extracranial, but also in the peripheral vascular region. After endarterectomy and catheter therapy, aspirin improves the long-term outcome by reducing the incidence of restenoses. Better results are obtained by oral anticoagulation in patients with emboli and after local thrombolysis.
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PMID:[Treatment strategies in arterial occlusive diseases]. 827 1


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