Risk factors of early and late complications in patients undergoing endovascular aneurysm repair.

OBJECTIVES: to identify pre-operative factors that could predict complications following from transluminal repair of abdominal aortic aneurysms (AAA). METHODS: during a 5-year period, 96 consecutive patients underwent elective endovascular treatment of a AAA. In all patients, helical CT and/or Magnetic Resonance Imaging (MRI), and plain abdominal roentgenogram were performed at 1, 3, 6, 12, 18, and 24 months and yearly thereafter. Angiography was performed systematically 1 year after the stent-graft implantation, or earlier if helical CT or MRI diagnosed an increase in the maximal transverse diameter or a high flow endoleak. RESULTS: early (<30 days) morbidity (12%) was significantly increased by pre-operative renal insufficiency (p < 0.01). Early mortality (2%) correlated with ASA score (p = 0.01). Median follow-up was 27 months (range 3-66). Mortality (12%) during follow-up was correlated to the pre-operative coronary status (p = 0.01). A type I endoleak was diagnosed in 18 patients (19%). Common iliac artery diameter was correlated with the presence of type I endoleak (p < 0.001). A type II endoleak was diagnosed in 47 (49%) patients. The diagnostic of type II endoleak was significantly increased (p = 0.001) in patients with pre-operative patent IMA associated with more than four patent lumbar arteries. The anatomic characteristics of the aneurysm were correlated to the additional endovascular procedures during stentgraft implantation (p = 0.01), and to the implantation of a complementary iliac limb extension during follow-up (p = 0.01). CONCLUSIONS: the risk factors determined by this statistical analysis could help surgeons to select more accurately patients suitable for endovascular treatment.     

Sneddon's syndrome: generalized livedo reticularis and cerebrovascular disease. Importance of hemostatic screening.

We report two cases of Sneddon's syndrome. Both cases had widespread livedo reticularis with repeated cerebrovascular accidents without persistent neurological deficit. In one case, hemostatic examination revealed an imbalance of plasminogen activator-inhibitor values, possibly related to the thrombogenic propensity of the syndrome. Treatment with acetylsalicylic acid led to normalization of hemostatic parameters and resulted in a symptom-free period of more than 10 months. The importance of hemostatic screening in patients with Sneddon's syndrome is discussed.     

Characteristics of apathy in Parkinson's disease.

The objective of this study was to use the Lille Apathy Rating Scale to assess apathy in a large population of Parkinson's disease (PD) patients and identify several different apathy profiles. One hundred fifty-nine patients with probable PD and 58 healthy controls participated in the study. Apathy was assessed using the Lille Apathy Rating Scale. Motor, cognitive, and depressive symptoms were rated on standardized scales. Data were analyzed using linear regression and multivariate analyses of variance. Thirty-two percent of the PD patients were classified as apathetic. Apathy was more frequent in patients with dementia. The four apathy dimensions contributed differently to the overall severity of the apathetic condition. Action initiation and intellectual curiosity had a marked influence. Linear regression analysis revealed that the apathy level was mainly determined by cognitive impairment, not associated with the severity of motor symptoms, and only associated with the apathy subcomponent of the Montgomery and Asberg Depression Rating Scale. Apathy is highly prevalent in PD patients. Apathy profiles vary according to the clinical presentation of PD. The high prevalence of apathy in PD suggests the involvement of frontal-subcortical circuits. Although the neurochemical substrate of apathy remains poorly characterized, the strong link between apathy and cognitive impairment observed in several studies suggests the participation of nondopaminergic circuits.     

Interleukin 1 alpha acts as an autocrine growth factor for RPMI 1788, an Epstein-Barr virus-transformed human B cell line

The Epstein-Barr virus-transformed B cell line RPMI 1788 constitutively produces autocrine growth factors with molecular masses of 17 kDa, 24 kDa and 35 kDa. All three molecular forms were completely neutralized with anti-interleukin (IL) 1 alpha antiserum. Although IL 1 alpha and IL 1 beta mRNA were both equally detectable by Northern blotting, no IL 1 beta activity was found in partially purified RPMI 1788 supernatant. The growth of low density-seeded RPMI 1788 cells is specifically dependent on the presence of either IL 1 alpha or IL 1 beta. Since no other cytokine was found to be capable of sustaining proliferation, this cell line is suitable for the identification and quantification of IL 1, even in the presence of other cytokines.     

Uncoupling between beta-adrenoceptors and adenylate cyclase in dog ischemic myocardium

Summary We evaluated the effects of ischemic injury on the myocardial adenylate cyclase system, 5 h after ligation of the left anterior descending coronary in 5 anesthetized dogs. Crude cardiac membrane preparations were isolated from control and ischemic areas of ventricular myocardium and tested for: 1. L-(¹²⁵I)iodocyanopindolol binding, in the absence and presence of ±-isoprenaline and GTP, and 2. adenylate cyclase activity. The density of beta-adrenoceptors increased by 35% in membranes from ischemic areas while the proportion of receptors in a high affinity state for ±-isoprenaline decreased from 43% to 20%. Adenylate cyclase activities in the basal state and under stimulation with NaF, forskolin, Gpp(NH)p, ±-isoprenaline and VIP were all markedly and similarly reduced, being only about 30% of comparable activities in membranes from control areas. The ±-isoprenaline subsensitivity of cardiac adenylate cyclase can, thus, be attributed to a defective enzymatic system and not to a reduction in the number of beta-adrenoceptors implying that the internal components of the system were more sensitive to acute ischemia than the outward oriented hormone receptors. It is tempting to ascribe this uncoupling to a functional depletion in the guanine nucleotide-binding regulatory protein Ns that might reflect a loss of high energy phosphate stores including GTP.Abbreviations CYP cyanopindolol - Gpp(NH)p 5-guanyl imidodiphosphate - VIP vasoactive intestinal peptide - Ns guanine nucleotide-binding regulatory protein     

Brain stem infarction, systemic lupus erythematosus and circulating lupus anticoagulant

A 30 year old man admitted with a brain stem infarct presented with intellectual deterioration. A diagnosis of systemic lupus erythematosus (S.L.E.) was based on the presence of five A.R.A. criteria :photosensitivity, arthralgia, leukopenia and thrombopenia, false positive syphilitic serology, antinuclear factors on immunofluorescence. A lupus type circulating anticoagulant (L.C.A.) was no longer detected after corticotherapy. This appears to be a case of the "hematologic" form of S.L.E. in which the presence of L.C.A. predisposes towards thrombosis, not only of veins--which is typical--but also of arteries. These may be isolated and reveal the underlying disease as in the present case. The L.C.A. is an antibody possessing antiphospholipid specificity which explains the anticoagulant action in vitro and the thrombogenic effect in vivo. Some authors consider this to be sufficient justification for administration of anticoagulants and/or antiplatelet agents, but corticotherapy may be effective.     

Cellular and molecular mechanisms involved in insulin's potentiation of glycogen synthase activity by metformin.

By taking advantage of the Xenopus oocyte model, we recently confirmed the in vitro enhancing effect of metformin (MET) on glycogen synthase (GS) activity when induced by insulin (INS). We now investigated some mechanistic aspects of its modulatory role upon the hormonal regulation of this rate-limiting enzyme. The action of 20 microM MET (approximately 3.3 microg/mL) was measurable at early steps in the intracellular metabolic pathway: the amount of adenosine 3',5'-cyclic monophosphate (cAMP) was markedly decreased in the presence of the biguanide plus 50 nM INS (to about 60% of control vs 25% with INS alone). The injection of tyrphostin B46, a potent inhibitor of insulin receptor (IR)-associated tyrosine kinase activity, led to a drastic reduction in MET-stimulated GS activity in the presence of INS. MET failed to increase the activity of type 2 protein phosphatases whether INS was present or not. However, a specific inhibitor of type 1 phosphatases, when microinjected, blocked both the hormonal effect on GS and its potentiation by MET. The salient feature of this study was that there was almost no accumulation of radiolabeled MET in oocytes: less than 0.1% was found in the cytosol of cells which had been exposed to MET at a therapeutic dose (10 microM) for up to 16 hr. Moreover, a lack of detectable intracellular MET after a 60-min incubation nevertheless correlated with its sustained action on INS-regulated GS activity. From these results, it could be inferred that the major site of MET action may reside within some membrane components of a signaling complex most likely linked to the IR, but in any case located upstream of the branching of reactions which tightly control GS activity.     

Effect of bronchodilation on regional lung function measured by 133Xe and gamma camera

Using ¹³³Xe, a gamma camera and off-line data handling the effect of inhaled Salbutamol on regional lung function was measured in six patients with chronic obstructive lung disease and associated bronchospasm.After bronchodilation only minor changes were obtained in regional ventilation or in the arterial hypoxemia, although the overall airways obstruction improved markedly. These findings suggest that the bronchodilating agent had an effect mainly on the larger airways and almost did not influence the function of the more peripheral lung units responsible for gas exchange. Also, a slight but direct effect on the perfusion was demonstrated. The effect on the ¹³³Xe ventilation-perfusion ratio was not correlated with that on the hypoxemia, indicating that the first is not a good representation of the latter.Supported by a grant from the Fonds voor Geneeskundig Wetenschappelijk Onderzoek