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

The role of the blood platelets in the aetiogenesis of arterial lesions has been underlined in recent years by studies of platelet elastase and above all the mitogenic factor of smooth muscle cells. A truly thrombogenic theory of atherosclerosis can now be envisaged. In the context of arterial thromboses, it is interaction between the damaged vessel wall, the lesion most often being atherosclerosis, and blood platelets which gives rise to the thrombus. In certain conditions such as diabetes abnormalities in the interaction between platelets and vessel walls may favour the development of vascular lesions and thromboses. With regard to venous thrombosis, the participation of the vessel and/or platelets is less clear. However, recently described platelet procoagulant activities could activate coagulation mechanisms. Knowledge of diseases of primary haemostasis has benefited from studies of platelet-vessel interaction. Whilst the spontaneous haemorrhagic syndrome of major thrombocytopaenia remains mysterious, platelet membrane molecular abnormalities in thrombopathies such as Bernard Soulier syndrome or thrombasthenia offer an explanation for their mechanisms. By their interaction with the vessel, platelets finally participate in mechanisms of inflammation, immunological conflicts, disseminated intravascular coagulation and metastatic dissemination.
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PMID:[Interactions between the platelets and the vessel wall. Part 2: physiopathology (author's transl)]. 746 76

Phytosterolaemia (beta-sitosterolaemia), a rare, autosomal recessive disorder, has not hitherto been reported in Southern Africa. We report four new homozygous patients, from three unrelated families with significant beta-sitosterolaemia (6.6-11.3%), campesterolaemia (2.2-4.6%) and clearly detectable, though unquantified, levels of cholestanol. Three of the four patients had characteristic cutaneous and tendinous xanthomas within the first decade of life. The fourth patient, a 5 year old, was free of xanthomas despite persistently elevated concentrations of plant sterols in her plasma. All our patients were female bringing the male:female ratio in reported cases to 8:23. All were at or below the 50th percentile for height and weight, and presented at some stage with borderline, hypochromic anaemia associated with red cell abnormalities and thrombocytopaenia. The oldest patient showed suggestive clinical evidence of atherosclerosis affecting her aorta, ileofemoral bifurcation and possibly coronary arteries. All homozygotes responded to a diet restricted in phytosterols and the administration of cholestyramine with falls in plasma sterols of up to 68%. The recent discovery of a possible inherited defect in the synthesis of HMG CoA reductase in patients with phytosterolaemia makes this disorder a model system for studying the biological role of this enzyme in regulating the absorption and clearance of sterols other than cholesterol, and the factors governing the sterol composition of cell membranes.
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PMID:Phytosterolaemia in three unrelated South African families. 797 27

The objective of this study was to determine the prevalence and clinical significance of elevated antiphospholipid antibodies (APA) in a large series of patients admitted to a department of Internal Medicine. At the end of entry phase, 1014 patients were tested (488 males-526 females, mean age: 66.7 years, range 18-97). Seventy-two (7.1%) patients were found APA positive at least once: 44 males and 28 females, mean age 69 years, range 23 to 94. Twenty fulfilled the criteria of Primary Antiphospholipid Antibody Syndrome: 10 patients were referred for deep vein thrombosis, 3 had history of deep vein thrombosis, 1 had both arterial thrombosis and a history of venous thrombosis; 2 had thrombocytopenia; 3 had stroke, 1 had a history of a stroke. One patient had SLE according to ARA classification. The most frequent associated disease was cancer: 14 patients, 9 had evolutive malignant disease, 5 were in clinical remission of neoplasia. Other clinical conditions included chronic and/or acute alcoholic intoxication (n = 8), severe atherosclerosis (n = 4), leg ulcer (n = 4). Insufficient data are available about the evolution, but 7 patients died in the year following diagnosis. Eight patients had fluctuations in APA detection: 2 initially APA positive became negative, 5 initially negative became positive and 1 patient was alternatively positive, negative and positive without steroid treatment. Thus, as expected, APA occur in a variety of clinical disorders. The association with cancer or alcoholic intoxication deserves further investigations.
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PMID:A prospective epidemiological study on the occurrence of antiphospholipid antibody: the Montpellier Antiphospholipid (MAP) Study. 798 47

An eighty-four-year-old man was admitted to the hospital because of pain at rest in the lower extremities. On physical examination, trophic changes of the skin and petechiae in the limbs were observed. Computed tomographic scan of the abdomen showed focal renal infarctions and calcification of the descending aorta. Moreover, radionuclide imaging of the arterial system revealed complete obstructions of the two right iliac arteries and the left external iliac artery, where collateral flows were observed. Laboratory examination showed a severe thrombocytopenia caused by immunoglobulin G (IgG)-type autoantibody against platelets. He was diagnosed as having arteriosclerosis obliterans complicated by idiopathic thrombocytopenic purpura, although no known risk factors promoting atherosclerosis other than age were evident. In such a case with hemorrhagic diathesis, a hemorheologic agent and the vasodilator prostaglandin could confer advantages in relieving and controlling the ischemic leg pain without hemorrhagic complications. Moreover, small doses of the initial prednisolone therapy for ITP might also be recommended to avoid thrombus formations in the atherosclerotic lesions.
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PMID:A rare case of arteriosclerosis obliterans without prominent risk factors complicated by idiopathic thrombocytopenic purpura. A case report. 861 16

We analysed the causes of 67 deaths, over a 4 y period, in our oriental population with systemic lupus erythematosus (SLE). The median disease duration was 48 +/- 60.5 months (range 1-250 months). The mean age at diagnosis and death were 30 and 35.1 y respectively. SLE alone accounted for death in 30 patients (44.8%), infection in 27 (40.3%), pulmonary embolism in 5 (7.5%), malignancy in 4 (5.9%) and rheumatic heart disease in 1 (1.5%). The major organ involvement in those with active disease at death were SLE related thrombocytopenia (n = 23/44, 52.3%), nephritis (n = 21/44), 47.7%), cerebral lupus (n = 16/44, 36.4%), and pulmonary haemorrhage (n = 12/44, 27.3%). As in other series, SLE and infection were the principal causes of death in our population. During this 4 y period, there was no late death due to atherosclerosis.
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PMID:SLE mortality in an oriental population. 911 15

Pure cortical arterial injury is defined as an acute subdural hematoma (ASDH) due to micro laceration of the cortical artery without cerebral contusion. We analyzed this peculiar ASDH in 14 cases. This ASDH has the following characteristics. 1) This disease develops in elderly persons after minor head trauma. 2) After a relatively long lucid interval, the consciousness level of these patients decreases rapidly to semicoma or deep coma. 3) Brain atrophy, atherosclerosis and a tendency to bleed (drugs, hemodialysis, thrombocytopenia, etc.) are involved in this hematoma. 4) The clinical outcome is generally poor because of systemic complications. The authors infer the mechanism of pure cortical arterial injury to be as follows. Minor hemorrhage occurs due to direct impact damage after trivial head trauma, but physiological hemostatic actions are set in motion. After a lucid interval, rebleeding from the injured cortical artery causes massive subdural hemorrhage.
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PMID:[Acute subdural hematoma due to pure cortical arterial injury: analysis of 14 cases]. 933 Mar 92

Antiphospholipid syndrome (APLS), is defined as the presence of antiphospholipid antibodies (APLA) associated with clinical phenomena of arterial or venous thrombosis, recurrent spontaneous abortions and thrombocytopenia. APLA represent the family of antibodies of different specificity. They are mostly directed to various anionic phospholipids (cardiolipin, phosphatidylcholine, phosphatidylserine, phosphatidyl acid and phosphatidyl ethanolamine). The part of APLA is directed towards epitope at the structurally changed beta-2-GPI, the so-called anti beta-2-GPI antibodies and the hypothesis was established that the subgroup of APLA was directed towards complex of beta-2-GPI with the phospholipids and oxidized lipoproteins of high and very low density. This could explain the clinically observed association of mutual onset of thrombosis and atherosclerosis. The most frequent target tissues for APLA are endothelial cells, thrombocytes, monocytes, natural anticoagulant system and placenta. APLA can be detected in a serum with one of the following assays: testing of lupus anticoagulant presence, determination of anticardiolipin antibodies (ACLA) concentration by ELISA and by testing the false positivity of VDRL test (standard test for syphilis). The pathological base for so-called vasculopathy in APLS are arterial and venous thrombosis. Clinical manifestations of APLS are mainly the result of blood vessels' occlusion but the thrombotic mass deposition on the surface of the heart valves may also occur. Clinically APLS can be divided into primary and secondary one, and manifestations of the secondary APLS are mainly expressed in the patients with SLE. Some clinical and serological variants of primary APLS were also described. The tendency for thrombotic process as a crucial characteristic of the syndrome and the lack of inflammation, imposes the choice of antithrombotic and anticoagulant therapy.
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PMID:[The antiphospholipid syndrome--yesterday, today, tomorrow]. 962 52

Cardiovascular diseases, including atherosclerosis and myocardial ischemia, occur as a result of a complex set of genetic and environmental factors. During periodontitis, dental plaque microorganisms may disseminate through the blood to infect the vascular endothelium and contribute to the occurrence of atherosclerosis and risk of myocardial ischemia and infarction. Myocardial ischemia and infarction are often preceded by acute thromboembolic events. In an in vitro model of thrombosis, certain dental plaque bacteria induce platelets to aggregate. Aggregation of platelets is induced by the platelet aggregation-associated protein [PAAPJ expressed on plaque bacteria, including Streptococcus sanguis and Porphyromonas gingivalis. Intravenous infusion of S. sanguis into rabbits has been shown previously to cause changes in the electrocardiogram (ECG), heart rate, blood pressure, and cardiac contractility. These changes are consistent with the occurrence of myocardial infarction. The ECG changes are now shown to begin within 30 seconds after infusion of PAAP+ S. sanguis, followed by alterations in blood pressure and respiratory rate. These changes occurred intermittently over a 30-minute period and changed within one heartbeat to a normal pattern and suddenly back to abnormal. Intermittent ECG abnormalities were seen in 13 of 15 rabbits, including left axis deviation, ST-segment depression, preventricular contractions, alternans, and bigemnia. Dose-dependent thrombocytopenia, accumulation of 111Indium-labeled platelets in the lungs, and tachypnea also occurred. No changes occurred with the PAAp- strain. The data indicated that PAPP+ S. sanguis interacts with circulating platelets, inducing thromboemboli to cause the pulmonary and cardiac abnormalities. During periodontitis, therefore, PAAP+ S. sanguis and P. gingivalis bacteremia may contribute to the chance of acute thromboembolic events.
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PMID:Dental plaque, platelets, and cardiovascular diseases. 972 99

The recent CAPRIE trial (clopidogrel versus aspirin in patients at risk of ischaemic events) compared clopidogrel with aspirin in reducing the risk of vascular events in 19,185 patients with clinical manifestations of atherosclerosis. Participants were randomized to receive daily oral clopidogrel (75 mg) or aspirin (325 mg). Treatment periods ranged from 1 to 3 years. The primary outcome measurement was an aggregate of myocardial infarction, ischemic stroke and vascular death. Event rates of 5.32% and 5.83% were associated with clopidogrel and aspirin therapy, respectively. Clopidogrel therapy resulted in a relative risk reduction of 8.7% (CI 0.3-16.5%) compared with aspirin therapy (p = 0.043). Gastrointestinal hemorrhages occurred in 1.99% of patients treated with clopidogrel and 2.66% of patients treated with aspirin (p < 0.002). There were no significant treatment-based differences in the rates of intracerebral hemorrhages and hemorrhagic deaths or thrombocytopenia. These results indicate that clopidogrel is more effective and safer than aspirin in reducing adverse cardiovascular events in patients with atherosclerosis.
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PMID:Results of the CAPRIE trial: efficacy and safety of clopidogrel. Clopidogrel versus aspirin in patients at risk of ischaemic events. 989 20

The paper summarizes the results of over 30-year studies dealt with dyslipidemias and autoimmune diseases. The teaching of the antiphospholipid syndrome (APS) has aroused interest in the problem. The experience gained shows changes in the blood cholesterol transport system. Patients with systemic lupus erythematosus (SLE) have higher levels of low density lipoprotein cholesterol and lower concentrations of high density lipoprotein (HDL) cholesterol, apolipoprotein A than the controls. The quantitative and qualitative changes in particles result in decreased acceptance of cholesterol from the membrane of a cell and tissues, which promotes the development of vascular diseases. Lipoprotein (a) may be an additional risk factor for thrombosis chiefly of coronary arteries, in patients with SLE and APS. Increased levels of oxidized low density proteins having atherogenic activity were found mainly in patients with SLE. The use of corticosteroids causes the changes in the spectrum of blood lipids, which together with other factors (thrombosis, vasculopathy, thrombocytopenia, etc.) create good conditions for the development of atherosclerosis, which determines the necessity of correcting the parameters of blood lipid transport not only to prevent vascular disorders but to improve the general life prognosis in SLE patients.
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PMID:[Dyslipidemias and autoimmune diseases]. 998 60


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