Biomechanical analysis of practitioner's gesture for peripheral venous catheter insertion.

Peripheral venous catheter insertion (PVCI) is one of the most common procedures performed by healthcare professionals but remains technically difficult. To develop new medical simulators with better representativeness of the human forearm, an experimental study was performed to collect data related to the puncturing of human skin and a vein in the antebrachial area. A total of 31 volunteers participated in this study. Force sensors and digital image correlation were used to measure the force during the palpation and puncturing of the vein and to retrieve the kinematics of the practitioner's gesture. The in vivo skin rupture load, vein rupture load, and friction loads for skin only and for both the skin and vein were (mean ± standard deviation) 0.85 ± 0.34 N, 1.25 ± 0.37 N, -0.49 ± 0.19 N, and -0.51 ± 0.16 N, respectively. The results of this study can be used to develop realistic skin and vein substitutes and mechanically assess them by reproducing the practitioner's gesture in a controlled fashion.

[Delays of treatment of acute myocardial infarction with ST elevation admitted to the CCU (coronary care unit) in Alsace]. / Délais de prise en charge de l'infarctus aigu du myocarde avec sus-décalage persistant du segment ST admis dans les USIC d'Alsace.

OBJECTIVE: to determine the time delay from symptom onset to diagnosis and treatment of patients with persistant ST segment elevation myocardial infarction (STEMI). DESIGN: prospective observational study. METHOD: patients with symptoms onset < 24 h admitted in all 10 cardiac intensive care units in one French administrative region (Alsace). Data were recorded by doctors on duty soon after hospital admission. Patients with STEMI during hospital stay or as a complication of cardiac interventional procedure were excluded. The Kruskal-Wallis test was used to assess statistical differences between the groups (p value < 0.05). RESULT: from April to October 2004, 326 patients were admitted for STEMI. Median time between the symptoms onset and the patient's call for medical help was 60 minutes. General practitioners were the first medical contact in 41%. The time from symptoms onset to first medical intervention and from first medical intervention to coronary care unit admission were markedly shorter in patients who had directly called the Emergency Medical Services (group 15-110 patients i.e. 33% of the study population): 44 min vs 75 min otherwise (p=0,003). Median transport time was 60 min. Sixty two percent of the pts were transported by the Emergency Medical Services. The median time from symptoms onset to initiation of reperfusion therapy was 240 min. It was significantly lower in group 15 (170 min vs 286 min - p < 0,001) and for thrombolytic therapy (190 min versus 245 min for primary angioplasty, p=0,007). When thrombolysis (THL) was used, 89% of the pts could be treated during 6 hours of symptoms onset and 44% in 3 hours. For angioplasty only 4% of the pts were treated in the first 90 minutes, 9% in the 2 hours and 30% in the 3 hours of symptoms onset. If the time delay is evaluated from the 1 st medical intervention, call to reperfusion intervention was significatly shorter for THL: 91 versus 157 min, p< 0,003. Angioplasty represented 75% of reperfusion strategy in our area and THL alone only 2,7% and combine therapy 5,4%. CONCLUSION: our study documents the beneficial effect of a direct call to Emergency Medical Services. Our results also underscore the need for an effort to reduce the time to offer the best appropriate reperfusion techniques in STEMI pts: speed up the admission in the cath-lab, think about pre-hospital thrombolysis followed by coronary angioplasty if necessary.

Comparative efficacy of a two-hour regimen of streptokinase versus alteplase in acute massive pulmonary embolism: immediate clinical and hemodynamic outcome and one-year follow-up.

OBJECTIVES: This study sought to compare the efficacy of 2-h regimens of alteplase and streptokinase in acute massive pulmonary embolism. The primary end point was immediate hemodynamic improvement, and secondary end points included early clinical efficacy and safety, as well as 1-year clinical outcome. BACKGROUND: Several thrombolytic regimens have been compared for the past 10 years in randomized studies, showing that 2-h infusion regimens of alteplase or urokinase lead to faster hemodynamic improvement than former 12- to 24-h administration protocols in acute massive pulmonary embolism. Many trials have focused on immediate hemodynamic and angiographic outcomes, but none has addressed long-term follow-up after thrombolysis. METHODS: Sixty-six patients with acute massive pulmonary embolism (Miller score > 17 and mean pulmonary artery pressure >20 mm Hg) were randomly assigned to receive either a 100-mg 2-h infusion of alteplase (n = 23) or 1.5 million IU of streptokinase over 2 h (n = 43). In both groups, heparin infusion was started at the end of thrombolytic infusion and adapted thereafter. Total pulmonary resistance was monitored over a 12-h period. Pulmonary vascular obstruction was assessed 36 to 48 h after thrombolytic therapy. One-year follow-up information included death, cause of death, recurrent pulmonary embolism, chronic thromboembolic pulmonary hypertension, stroke and bleeding. RESULTS: Both groups had similar baseline angiographic and hemodynamic characteristics of severity, with maintained cardiac output in 64 (97%) of 66 patients. The results (mean +/- SD) demonstrated that despite a faster total pulmonary resistance improvement observed at 1 h in the alteplase group compared with the streptokinase group (33+/-16% vs. 19 16%, p = 0.006), a similar hemodynamic efficacy was obtained at 2 h when both thrombolytic regimens were completed (38+/-18% vs. 31+/-19%). There was no significant difference in either pulmonary vascular obstruction at 36 to 48 h or bleeding complication rates. One-year event-free survival was similar in both groups, as most events were related to concomitant diseases. CONCLUSIONS: These results suggest that a 2-h regimen of streptokinase can be routinely used in patients with massive pulmonary embolism and maintained cardiac output without obviously compromising efficacy or safety.

Dupuytren's contracture, alcohol consumption, and chronic liver disease.

This prospective study was undertaken to assess the prevalence of Dupuytren's contracture (DC) and its relationship with possible causes, especially alcohol consumption and chronic liver disease. Four hundred thirty-two consecutively hospitalized patients were examined for evidence of DC. They were divided into five groups based on the following clinical, biologic, and histologic criteria: alcoholic cirrhosis (89 patients), noncirrhotic alcoholic liver disease (55 patients), chronic alcoholism without liver disease (46 patients), nonalcoholic chronic liver disease (68 patients), and a control group (174 patients). The prevalence of DC in these five groups of patients was 32.5%, 22%, 28%, 6%, and 12%, respectively; the prevalence of DC was higher in patients with cirrhotic or noncirrhotic alcoholic liver disease (25.5%) than it was in patients with nonalcoholic liver disease (6%), but it was not significantly different in alcoholic patients with or without liver disease. The relationship between DC and age, sex, manual labor, previous hand injuries, diabetes mellitus, alcohol consumption, and cigarette smoking was assessed by univariate and logistic regression methods. Nine variables were significantly different in patients with or without DC: age, sex, manual labor, previous hand injuries, diabetes mellitus, daily alcohol consumption, duration of alcohol consumption, total alcohol consumption, and duration of cigarette smoking. In our patients, variables that could explain DC were, in decreasing order, age, total alcohol consumption, sex (male), and previous hand injuries. In alcoholic patients, these variables were age and previous hand injuries; in nonalcoholic patients, these variables were age and cigarette smoking. These results emphasize the high prevalence of DC in alcoholic patients and the absence of a correlation between DC and chronic liver disease. Age and alcohol consumption are the best explanatory variables of DC in hospitalized patients.

Pharmacokinetics of ornidazole in patients with severe liver cirrhosis.

Pharmacokinetics of ornidazole, a nitroimidazole derivative, was studied after intravenous injection in 10 patients with severe alcoholic cirrhosis and 10 healthy volunteers. Plasma concentrations of ornidazole and its two major hydroxylated metabolites, M1 (alpha-(chloromethyl)-2-hydroxymethyl-5-nitroimidazole-1-ethanol) and M4 (3-(2-methyl-5-nitroimidazole 1-yl) 1,2 propane diol), were measured by HPLC. The t1/2 of ornidazole was 14.1 +/- 0.5 hours for normal subjects and 21.9 +/- 2.9 hours for patients with cirrhosis. Mean plasma clearance was 50.6 +/- 2.1 ml/min in control subjects and 34.9 +/- 4.9 ml/min in patients, whereas apparent V SS was not modified in hepatic insufficiency. In healthy volunteers, M1 and M4 levels are well below levels of the parent drug; in cirrhosis both metabolites accumulate in plasma as a result of decreased elimination. Hepatic cirrhosis prolongs ornidazole elimination, and to avoid cumulation the interval between repeated doses could be doubled.

Pharmacokinetics of ornidazole in patients with acute viral hepatitis, alcoholic cirrhosis, and extrahepatic cholestasis.

Pharmacokinetics of ornidazole, a nitroimidazole derivative, was investigated after intravenous injection in 3 groups of 10 patients with different hepatic diseases: hepatitis, noncholestatic cirrhosis and extrahepatic cholestasis. Plasma concentrations of ornidazole and its two major hydroxylated metabolites, M1 [alpha-(chloromethyl)-2-hydroxymethyl-5-nitroimidazole-1-ethanol] and M4 [3-(2-methyl-5-nitroimidazole 1-yl)-1,2-propane diol] were measured by HPLC assay. As a consequence of a decreased clearance (26% to 48%), the half-life and MRT are increased in all patients by 19% to 38% when compared with healthy volunteers. No clear difference could be established between the different groups. The volume of distribution remains the same in all patients and controls except those suffering from cancer. As previously shown in patients with severe liver cirrhosis, both metabolites accumulate in plasma as a result of decreased elimination; formation is no longer the rate-limiting step of their kinetics. This metabolite accumulation is in part due to decreased biliary excretion and to hepatocellular failure.

Ocular fluorophotometric and angiographic findings in toxemia of pregnancy.

Ocular fluorophotometry was performed in 24 patients with hypertension due to toxemia of pregnancy and in ten normal subjects. Patients showing features of accelerated hypertension in the fundus (eg, hemorrhage, cotton-wool spots, and disc edema) were excluded from the study. Fluorescein concentrations in the aqueous and posterior vitreous increased significantly in toxemic patients compared with those in normal subjects; the blood-aqueous barrier was disrupted earlier than the blood-retinal barrier. Nevertheless, these barriers were only disrupted when the arterial diameter was altered. Ocular fluorometric abnormalities disappeared after delivery in all but two cases.

Multicenter, double-blind, controlled comparison of zolpidem and triazolam in elderly patients with insomnia.

The efficacy and safety of zolpidem, a hypnotic of a new chemical class (the imidazopyridines), was compared with a reference benzodiazepine in elderly insomniac patients in a randomized, double-blind, multicenter trial. Hospitalized patients aged 58 to 98 years were randomized to receive zolpidem 5 mg (70 patients), zolpidem 10 mg (74 patients), or triazolam 0.25 mg (77 patients) at bed-time. (Three patients were excluded and 13 patients did not complete the study.) The 3-week active treatment period was preceded by 3 and followed by 7 days of placebo administration. Sleep quality was assessed by the patient via a questionnaire and visual analog scale. A clinician's global impression was also recorded. All measures of sleep quality were improved by both doses of zolpidem and by triazolam. The improvements between the end of the placebo phase and the end of the active treatment phase were significant for all treatments and assessment instruments. Moreover, the significant improvements in all measures were maintained during the week following withdrawal of both doses of zolpidem. The improvement in most sleep assessment parameters was maintained after withdrawal of triazolam. Tolerability of all treatments was excellent. The majority of patients reported no adverse effects. The reported adverse effects in all groups included nightmares, daytime drowsiness, and day- or nighttime agitation. There was no evidence of rebound insomnia; the therapeutic effect of zolpidem outlasted drug treatment. There were no signs of agitation or anxiety following cessation of treatment, which might be indicative of withdrawal phenomena. Confusion was recorded only in the triazolam group. These results suggest that zolpidem is at least as effective as triazolam in geriatric insomniac patients. Zolpidem 5 mg and 10 mg demonstrated a good safety profile. On the basis of these data, zolpidem 5 mg should be given as a starting dose in elderly patients, with a possible increase up to 10 mg in more severe cases of insomnia.

Effect of zolpidem on sleep in healthy subjects: a placebo-controlled trial with polysomnographic recordings.

The aims of this double-blind, placebo-controlled study, conducted in a group of healthy young adults with normal sleep patterns, were to ascertain the effect of various doses of zolpidem on polysomnographic variables and to determine whether zolpidem disrupts sleep architecture. Of the 15 subjects recruited, 8 were included in the final analysis. Subjects underwent four experimental sessions during three nights, of which the first night was used for adaptation, the second for zolpidem (10, 20, and 40 mg) or placebo administration, and the third for placebo administration. Sleep was assessed by conventional sleep parameters (latency, duration, wakefulness) and by subjective questionnaire. Polysomnographic recordings were analyzed for sleep stage, paradoxical sleep, graphic features, and longitudinally with reference to sleep stage. Zolpidem had little effect on polysomnographic variables, except for a trend toward a hypnotic effect and a slight, transient inhibition of paradoxical sleep at the highest dose. In particular, the clearcut reduction of stage 4 sleep and increase in spindle density often observed with benzodiazepine administration was not observed with zolpidem. Adverse effects were restricted to three reports of daytime drowsiness each after zolpidem 10 and 40 mg and placebo, and one amnesic episode after the highest dose (40 mg). There were no signs of ataxic symptomatology.

Von Willebrand factor in diabetic angiopathy.

Diabetes mellitus is a complex disease characterised by chronic hyperglycaemia responsible for complications affecting the kidneys, eyes, peripheral nerves and micro- and macrovascular systems. Von Willebrand factor (vWf), a multimeric glycoprotein mainly synthesised by endothelial cells, is involved in platelet adhesion and aggregation and acts as the carrier of coagulation factor VIII in plasma. Increased levels of vWf, reflecting activation of or damage to endothelial cells, have been described in association with atherosclerosis and diabetes. vWf appears to be a predictive marker of diabetic nephropathy and neuropathy, although not of retinopathy, which suggests that endothelial dysfunction precedes the onset of diabetic microangiopathy. This dysfunction could be especially involved in the pathogenesis of renal abnormalities of diabetes. vWf is not a predictive marker of macroangiopathy when diabetes is associated with atherosclerotic risk factors. In the presence of chronic diabetic complications, vWf levels are not associated with any grade of retinopathy but increase with the severity of nephropathy and would appear to be a risk factor for macrovascular mortality in these patients. The endothelial dysfunction of diabetes can generate atherosclerotic lesions responsible for damage to the arterial wall, atheroma and formation of platelet microaggregates. Concomitant with high vWf levels, other possible mechanisms of endothelial damage include reduced synthesis or release of nitric oxide, hyperglycaemic pseudohypoxia and protein kinase-C activation, increased synthesis of proteins bearing advanced glycosylation end-products or transforming growth factor-beta (TGF-beta) activation of coagulation and inhibition of fibrinolysis. At present, it is not known whether high vWf levels are inherent to the physiopathology of diabetes, nor whether diabetes induces endothelial dysfunction through other pathways. However, since angiopathy resulting from endothelial dysfunction is the main cause of morbidity and mortality in diabetic patients, appropriate therapy is necessary to reduce these complications. Glycaemic control seems to be insufficient to normalise plasma vWf, whereas a decrease can be obtained by ingestion of diets rich in oleic acid or by treatment with statins. Inhibition of the binding of vWf to the GPlba receptor by synthetic peptides, aurin tricarboxylic acid or monoclonal antibodies has been proposed to prevent the thrombosis induced by high levels of plasma vWf. Thus, vWf probably represents an interesting target for the inhibition of thrombosis in diabetes.

Sensitivity and long-term prognostic value of cardiac troponin-I increase shortly after percutaneous transluminal coronary angioplasty.

BACKGROUND: After successful coronary interventions, minor elevations of creatine kinase MB (CK-MB) identified a population with a worse long-term prognosis than that in patients without enzyme elevations. In that setting, cardiac troponin-I (cTn-I), a highly specific marker for myocardial injury, was considered for a small study; the results did not support the view that significant myocardial damage occurred during successful percutaneous transluminal coronary angioplasty (PTCA). HYPOTHESIS: The present study was designed to assess the rate of elevated values of cTn-I after successful PTCA and to determine its prognostic value. METHODS: CTn-I and CK-MB were measured in 44 patients before and daily for 3 days after PTCA. Two groups of patients were considered according to the presence or absence of elevated levels of cTn-I. The rate of free-event survival was estimated for the two groups using the Kaplan-Meier method and was compared with the log rank test. RESULTS: Globally, 36% of patients had an increase in cTn-I (normal values 0.35 ng/ml) and 9% had an increase in CK-MB, p = 0.002. The mean time to maximal enzyme level was 1.8 days for cTn-I and 2.2 days for CK-MB. Over a follow-up of 1375 +/- 416 days, 18% of patients experienced adverse events, and cTn-I did not identify a population of worse long-term prognosis. CONCLUSION: These results suggest that cTn-I is more sensitive than CK-MB in identifying minor myocardial damage after PTCA, but these elevated concentrations of cTn-I in the short-term aftermath of angioplasty do not seem to be a marker of worse long-term prognosis.

Effects of zolpidem versus diazepam and placebo on breathing control parameters in healthy human subjects.

The following study explores the possibility that zolpidem, a new hypnotic agent derived from imidopyridine, may induce changes in ventilatory function in normal subjects. The study, conducted double-blind on 16 subjects (eight men and eight women, aged 21 to 33 years) was undertaken in two successive phases: phase A with a cross-over, intended to compare the ventilatory effects of 10 mg oral dose of diazepam with a placebo, and then phase B, with a Latin square design, intended to compare the effects of 10 and 20 mg oral doses of zolpidem with 10 mg oral doses of diazepam and a placebo. Central inspiratory drive was assessed by occlusion pressure (P0.1) and breathing pattern in air and during carbon dioxide rebreathing. Measurements were performed one and three hours after each drug or placebo administration. Zolpidem did not affect tidal volume (Vt), slopes S1, S2 or P0.1, but decreased the duration of the phases of the respiratory cycle ti by 14% (p less than 0.01) and ttot by 15% (p = 0.03) after three hours post dosing without any change in ventilation, Vt/ti or ti/ttot. Nevertheless, these timing changes, although statistically significant, seem to have no clinical relevance to overall ventilation regulation in normal subjects. On the other hand, diazepam slightly changed S2 at three hours post dosing (0.14 +/- 0.07 versus 0.17 +/- 0.10 after the placebo; p = 0.06) without modifying the other parameters.

Mechanocardiographic evaluation of left ventricular diastolic function in hypertrophic cardiomyopathy and hypertensive cardiomyopathy.

Usefulness of computerized mechanocardiography and echocardiography in the diagnosis of impaired left ventricular diastolic function is shown in a study comparing 17 hypertrophic obstructive cardiomyopathy and 17 hypertensive cardiomyopathy patients to 20 normal subjects. Mechanocardiography allows the evaluation of three different parameters of diastolic function: isovolumic relaxation evaluated by S2a-O or better by t-dr/dt and dr/dt/A2 ratio, left ventricular compliance by the A/H ratio and time of rapid filling. All the parameters are impaired in both pathological populations. Isovolumic relaxation being more depressed in hypertensive cardiomyopathy and duration of rapid filling being prolonged especially in the hypertrophic obstructive cardiomyopathy patients. Although the differences are small indicating only trends computerized mechanocardiography gives some evidence for difference in the alteration of diastolic function in hypertrophic obstructive cardiomyopathy and hypertensive cardiomyopathy.

Ultrasonography, angiography, computed tomography and magnetic resonance in nodular regenerative hyperplasia of the liver: report of a pseudo-tumoral case.

Ultrasonographic, computed tomographic, and angiographic abnormalities of nodular regenerative hyperplasia have been described in very few cases. We report here the case of a 50-year-old man with round, well-limited hypoechogenic lesions involving the two lobes of the liver, and hypervascular, poorly delineated angiographic lesions. Computed tomography and magnetic resonance of the liver were normal. Histological examination of large liver specimens provided by intraoperative biopsy allowed the diagnosis of nodular regenerative hyperplasia. Such a pseudo-tumoral ultrasonographic and angiographic pattern must be recognized in order to avoid diagnostic and therapeutic mistakes, especially since percutaneous liver biopsy usually fails to diagnose this disease.

Long-term treatment of insomnia with zolpidem: a multicentre general practitioner study of 107 patients.

The effects of zolpidem, an imidazopyridine derivative, were studied in 107 patients suffering from insomnia, 60.9% of whom were over 60 years of age, in a 6-month, single-blind, flexible dose, general practitioner study. Comparison was made between baseline, last day of treatment and 10 days after the end of treatment to assess efficacy and rebound insomnia. An improvement in all efficacy parameters--time taken to fall asleep, total amount of nocturnal sleep and number of nocturnal awakenings--was reported by the investigator and the patients; the improvement was evident from the first evaluation day and was maintained throughout the trial. Improvement was also maintained during the washout period with a lack of rebound insomnia. There was no sign of withdrawal symptoms and tolerance to zolpidem did not develop over the 6-month treatment period. Adverse events were mild and infrequent, and tended to resolve with a dose reduction. It is concluded that 10 mg/day zolpidem is an appropriate starting dose and is effective and safe for the treatment of sleep disturbances of different origins.

Pilot controlled double-blind study of the hypnotic effects of zolpidem in patients with chronic 'learned' insomnia: psychometric and polysomnographic evaluation.

In a pilot double-blind trial in 21 patients with learned or idiopathic insomnia (DSM-IIIR), patients received placebo for 1 week (nights 1-7), either active (zolpidem, 10 mg) or placebo treatment for 2 weeks (nights 8-21) and then placebo for a further week (nights 22-28). Variables to measure efficacy, rebound and withdrawal were assessed daily from day 1 to day 28. Polysomnographic recordings together with sleep cycle analysis were performed on nights 7, 21 and 28. Patients treated with 10 mg zolpidem for 2 weeks had significantly improved sleep efficiency at the end of the randomised double-blind phase compared with the placebo group. Fractionated sleep-cycle analysis showed an increase in slow-wave sleep during the first 2-hour cycle after sleep onset. During the withdrawal placebo week, most of the main sleep variables remained relatively stable in the zolpidem group (nights 22-28), and deteriorated further in the placebo group. At the end of the withdrawal phase, there was a statistically significant difference between groups, in favour of the zolpidem treatment, in sleep efficiency, total sleep time, absolute and percentage of time awake, and percentage of REM sleep. REM sleep, which was normal in both groups at baseline, decreased significantly in the placebo group between nights 22 and 28 (during the withdrawal placebo week) compared with the zolpidem treatment group, and the number of periods of time awake increased. Minor subjective complaints were recorded under zolpidem and were comparable with those under placebo. Zolpidem seemed to improve some important sleep variables, when assessed both objectively and subjectively. The sleep cycle analysis suggested a possible shift of slow-wave sleep to an earlier period of the night, with a more physiological sleep structure. There was no evidence for withdrawal or rebound after stopping the 2 weeks of zolpidem treatment, but rather signs that the effect of zolpidem outlasted active treatment. The present pilot study justifies a prospective confirmatory comparison of zolpidem with benzodiazepines in an adequate number of patients and withdrawal after 6-8 weeks of treatment.

The safety and efficacy of zolpidem in insomniac patients: a long-term open study in general practice.

The safety and efficacy of 10 or 20 mg/day zolpidem, a new hypnotic belonging to the imidazopyridine class, were studied over a 180-day period in 96 patients with sleep disorders. The treatment was continued for a further 180 days by 49 of these patients. Follow-up information from 21 patients who discontinued treatment after 180 days showed no rebound insomnia or withdrawal signs. Efficacy of treatment with respect to reduction of sleep onset latency and number of nocturnal wakenings, and improvement in duration of sleep, quality of sleep and morning wakenings was found in nearly 90% of patients and was maintained in those patients who continued treatment for 360 days. This efficacy was achieved with a stable percentage of patients receiving 10 mg/day and 20 mg/day zolpidem from day 30 to the final visit. Zolpidem, therefore, has been shown to be an effective and safe hypnotic, and to be devoid of rebound and withdrawal effects.

Long-term polysomnographic study of the efficacy and safety of zolpidem in elderly psychiatric in-patients with insomnia.

The effects of 20 mg zolipidem were studied in an open, polysomnographically-monitored 179 day trial in 14 elderly psychiatric patients suffering from severe insomnia. After a placebo run-in of 7 days, zolpidem was given for 179 days followed by a 30-day wash-out period. Polysomnographic recordings (PSG) were performed just before active treatment; 30, 90 and 179 days into the treatment period; and at the end of the wash-out period. Statistically significant improvements in total sleep time, sleep efficiency and percentage of rapid eye movement sleep were observed after 30 days, all of which were maintained at 179 days. Sleep stages 1-4 all changed, with a significant decrease in percentage of stage 1, and a significant increase in both percentages of stage 2 and 3, and duration of stages 3 and 4 at the end of active treatment. After a 90-day follow-up period, only stage 3 sleep and sleep efficiency were no longer significantly changed compared to baseline, all other criteria showing maintenance of efficacy. Slow-wave sleep, which was increased during active treatment, decreased in the follow-up period. No serious adverse events were observed. These results suggest that, contrary to other hypnotics, zolpidem, after long-term administration, improves objective sleep parameters and may normalize a disturbed sleep architecture.

[Use of heparin in unstable angina and non-Q-wave infarction]. / Utilisation des héparines dans l'angor instable et l'infarctus sans onde Q.

The limitations of conventional treatment by non-fractionated heparin (NFH) in unstable angina and non-Q wave infarction with a serious adverse event rate (infarction and/or death) of 7 to 9% at 30 days have led to research in the use of low molecular weight heparin (LMWH). In 1995, Gurfinkel et al reported the superiority of the association aspirin-LMWH (Nadroparine) over a more classical treatment with aspirin alone or the association of aspirin-NFH in unstable angina and non-Q wave infarction. In 1996, the FRISC trial confirmed the value of LMWH (Dalteparine). However, this trial compared the LMWH with placebo. In 1997, the FRIC trial showed that dalteparine was equivalent to NFH. However, the ESSENCE and TIMI 11B trials reported the superiority of LMWH (Enoxaparine) over NFH in unstable angina and non-Q wave infarction. Compared with NFH, a significant 20% reduction in the composite criterion (death-non-fatal infarction) was observed with enoxaparine from the 2nd day up to day 43, without an increase in serious haemorrhagic complications. More recently, FRISC II showed the value and indicated the duration of treatment of LMWH, dalteparine, with respect to the chosen "invasive" or "non-invasive" strategies of revascularisation. The subcutaneous administration, absence of biological controls, the predictability of the anticoagulation and the better tolerance of the LMWH are powerful arguments in favour of their use in unstable angina and non-Q wave infarction. Thus, the LMWH have taken their place in the treatment of unstable coronary disease where the therapeutic arsenal is in constant evolution.

[Aneurysm of the interatrial septum. Apropos of a retrospective study of 41 cases]. / Anévrysme du septum interauriculaire. A partir d'une série rétrospective de 41 cas.

The authors undertook a retrospective study of 41 patients in whom an atrial septal aneurysm (ASA) had been diagnosed at transoesophageal echocardiography performed for ischaemic cerebrovascular events in 26 cases. No significant differences in this size, thickness or mobility of the ASA or the associated cardiac abnormalities were demonstrated in this context. However, patients presenting with cerebrovascular accidents were older, had several cardiovascular risk factors and more cardiac arrhythmias. These arrhythmias were usually related to other cardiac pathology such as ventricular hypertrophy or chronic cor pulmonale. Moreover, the probability of the cerebrovascular accident being related to the ASA was only acknowledged in 11 cases. These results mean a certain degree of discretion in diagnostic investigation and therapeutic management of these cases.