Abstract-Our aim was to determine the usefulness of circulating oxidized low density lipoprotein (LDL) in the identification of patients with coronary artery disease (CAD). A total of 304 subjects were studied: 178 patients with angiographically proven CAD and 126 age-matched subjects without clinical evidence of cardiovascular disease. The Global Risk Assessment Score (GRAS) was calculated on the basis of age, total and high density lipoprotein cholesterol, blood pressure, diabetes mellitus, and smoking. Levels of circulating oxidized LDL were measured in a monoclonal antibody 4E6 -based competition ELISA. Compared with control subjects, CAD patients had higher levels of circulating oxidized LDL (PϽ0.001) and a higher GRAS (PϽ0.001). The sensitivity for CAD was 76% for circulating oxidized LDL (55% for men and 81% for women) compared with 20% (24% for men and 12% for women) for GRAS, with a specificity of 90%. Logistic regression analysis revealed that the predictive value of oxidized LDL was additive to that of GRAS (PϽ0.001). Ninety-four percent of the subjects with high (exceeding the 90th percentile of distribution in control subjects) circulating oxidized LDL and high GRAS had CAD (94% of the men and 100% of the women Key Words: atherosclerosis Ⅲ coronary artery disease Ⅲ diagnosis Ⅲ lipoproteins M ajor independent risk factors for coronary artery disease (CAD) are advancing age, elevated blood pressure, elevated serum total and LDL cholesterol levels, low serum HDL cholesterol level, diabetes mellitus, and cigarette smoking. 1-3 The Framingham Heart Study 1 has elucidated the quantitative relationship between these risk factors and CAD. It has shown that the major risk factors are additive in predictive power. Accordingly, the total risk of a person can be estimated by a summing of the risk imparted by each of the major risk factors. Recently, the American Heart Association and the American College of Cardiology issued a scientific statement that assessed the Global Risk Assessment Scoring (GRAS) as a guide to primary prevention. 4 GRAS is based on age, total and HDL cholesterol levels, systolic blood pressure, diabetes mellitus, and smoking. Predisposing factors such as obesity, physical inactivity, and family history of premature CAD are not included in GRAS.Elevated levels of oxidized LDL have previously been detected in the plasma of CAD patients. 5-7 Therefore, we determined the predictive value of circulating oxidized LDL for CAD. Logistic regression analysis was used to determine whether the predictive value of circulating oxidized LDL was additive to that of GRAS. Finally, the correlation between circulating oxidized LDL and major cardiovascular risk factors in subjects without clinical evidence of CAD was studied. Methods Study DesignThe present study included 304 subjects (aged Ͼ45 years). Seventyeight patients with angiographically proven CAD have previously been described. 6 Blood samples from these patients were collected from 1993 to 1994 and were analyzed within 1 month after collection. Bl...
Of 732 consecutive patients admitted to an acute geriatric ward, 178 (24%) were found to be anaemic (haemoglobin of 115 g/l or below). An appropriate cause responsible for anaemia was identified in 83 %. The anaemia of chronic disorders (ACD) (35%) and iron deficiency anaemia (15%) were the commonest causes. The spectrum of disorders associated with ACD is much broader than the classical category of infectious, inflammatory and malignant disorders. The relatively high prevalence of the myelodysplastic syndrome (5%) is striking and this syndrome as a cause of anaemia in geriatric patients deserves more attention than it has so far received. No obvious cause was found in 17 %. The clinical significance of this finding remains unclear.
The aim of our study was to evaluate the results of catheter-directed thrombolysis and complementary procedures to treat acute iliofemoral deep vein thrombosis (DVT). A total of 24 consecutive patients with acute iliofemoral DVT underwent intrathrombus drip infusion of alteplase (3 mg/h; mean dosage 86 mg, range 45-174 mg), while intravenous heparin (1000 U/h) was continued. Complementary procedures were hydrodynamic thrombectomy in 3 and primary insertion of a Wallstent in 9 patients. Patency of 19 thrombosed veins (79 %) was restored with prompt symptomatic relief. An underlying anatomical anomaly or lesion was present in 13 patients: iliac vein compression syndrome (n = 8), absent (n = 2) or obstructed (n = 1) vena cava or venous stenosis (n = 2). Ten of the abnormalities were unknown before lysis and eight were relieved by stent deployment. Puncture site bleeding was the only complication but led to transfusion in 6 patients (25 %). Symptomatic reocclusion occurred in 4 patients. Catheter thrombolysis of iliofemoral vein thrombosis revealed many anatomical abnormalities which may predispose to thrombosis and are often amenable to stenting.
SUMMARY Adenosine and the adenine nucleotides caused a greater relaxation of strips of canine saphenous vein and tibial artery when they had been contracted by nerve stimulation than by exogenous norepinephrine. An infusion of adenosine into the dogs' lateral saphenous vein, perfused at constant flow, caused a greater relaxation of this vein when constricted by electrical stimulation of the lumbar sympathetic chain than by exogenous norepinephrine. That this difference was due to inhibition by these compounds of the output of neurotransmirter from the sympathetic nerve endings was demonstrated by column chromatographic analysis of the radioactivity in the supervision fluid of vein strips, previously incubated with tritiated norepinephrine. Both adenosine and adenosine triphosphate (10"' M) reduced the efflux of 3 H-norepinephrine during nerve stimulation with electrical impulses. Adenosine also reduced the efflux caused by potassium (30 mM), but not that caused by tyramine (6 x 10~6 M). Theophylline antagonized the inhibitory effect of adenosine on the sympathetic neurotransmission. We found that at 4 x 10 4 M adenosine triphosphate still caused a decreased efflux of neurotransmitter during electrical stimulation, but with adenosine the 3 H-norepinephrine efflux no longer decreased and the overflow of deaminated compounds increased. Furthermore, the same concentration of adenosine increased the efflux of 3 H-norepinephrine and deaminated compounds in unstimulated strips, and the increase of 3 H-norepinephrine was enhanced after monoamine oxidase inhibition. Thus, we conclude that at higher concentrations adenosine increases the intraneuronal leakage of norepinephrine out of the storage vesicles.ADENOSINE and the adenine nucleotides by a local action on blood vessels cause their dilation. This has been demonstrated both in vivo and in vitro. '" 3 There is evidence that these substances can inhibit neuromuscular transmission in the rat phrenic nerve-diaphragm and frog sartorius preparations 4 ' 5 and cholinergic neurotransmission in the intestinal wall. 6 The present experiments were performed to determine whether adenosine and related nucleotides inhibit adrenergic neurotransmission in canine blood vessels. Methods STUDIES IN VITROHelical strips of lateral saphenous veins and anterior tibial arteries, isolated from dogs (15-25 kg) anesthetized with sodium pentobarbital (30 mg/kg, iv), were placed in an organ bath filled with Krebs-Ringer solution (NaCl, 118.2 mM; KC1, 4.7 mM; MgSO 4 , 1.2 mM; KH 2 PO 4 , 1.2 mM; CaCl 2 , 2.5 mM; NaHCO 3 , 25 mM; calcium disodium ethylenediaminetetraacetate (EDTA) 0.026 mM; and glucose, 5.5 mM) maintained at 37°C and aerated with a 95% O 2 -5% CO 2 mixture. The strips were attached to a force transducer (Grass FT 03C) for isometric tension recording. The transducer was mounted on a movable support allowing fine adjustments of the strip length and connected to a pen writing recorder (Gould Brush 220). For electrical stimulation of the preparations, two rectangular platinum electr...
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