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Biomedical subjects

E Mazoyer

Publications and source records attributed to E Mazoyer.

At least 19 recordsLinked to original sources
PubMed2006

Recombinant activated factor VII efficacy and safety in a model of bleeding and thrombosis in hypothermic rabbits: a blind study.

BACKGROUND: Recombinant activated factor VII (rFVIIa) is increasingly used to secure hemostasis in hemorrhagic situations in trauma and surgical patients. Hypothermia is often observed in these clinical settings. OBJECTIVE: To study the efficacy and safety of rFVIIa in hypothermia in a rabbit model of bleeding and thrombosis. METHODS: Sixty-nine rabbits were anesthetized, ventilated and monitored for blood pressure, temperature and carotid flow. The Folts model was used: a stenosis (75%) and an injury were carried out on the carotid artery, inducing thrombosis. Blood flow decreased as thrombus size increased until the pressure gradient was such that the thrombus was released and local arterial blood flow was suddenly restored. This is known as a cyclic flow reduction (CFR). After counting baseline CFRs during a 20-min period (P1), rabbits were randomized blindly to one of four groups: normothermic (NT) placebo or rFVIIa (150 microg kg(-1)), hypothermic (HT) (34 degrees C) placebo or rFVIIa. Then CFRs were recorded over a second period (P2). At the end of the experiment, a hepato-splenic section was performed and the amount of blood loss was recorded. After each period, the following were measured: ear immersion bleeding time (BT), hemoglobin, platelet count, prothrombin time (PT), activated partial thromboplastin time (aPTT) and fibrinogen. RESULTS: Hypothermia increased BT and blood loss. These effects were reversed by rFVIIa. In NT rabbits, rFVIIa shortened BT but did not reduce blood loss. rFVIIa-treated rabbits bled similarly regardless of temperature. The incidence of CFRs was higher in treated than placebo animals regardless of temperature. rFVIIa decreased PT and aPTT without modifying platelet count or fibrinogen level. CONCLUSION: Hemostatic efficacy of rFVIIa was maintained in hypothermia. However, the number of CFRs was higher in the rFVIIa-treated group than in the placebo groups, whether for NT or HT rabbits.

Animals↗
PubMed2005

[Digestive surgery and varicose vein surgery].

The thromboembolic risk related to surgery may be considered as low for varicose vein surgery and non major digestive surgery. It could be defined as moderate in case of large dissection, long duration of procedures and emergency cases. The risk may be considered as high for major abdominal surgery involving cancer surgery or not and bariatric surgery. The absence of prophylaxis can be proposed for low risk surgery (grade B). However, elastic compression stocking are effective for all cases of digestive surgery and suggested to be used (grade A). There are no data concerning the moderate risk situation. Therefore, experts recommend the use of elastic compression stockings or low doses of LMWH (grade D). High-risk surgery requires the use of high doses of LMWH recommended for reasons of efficacy, tolerance, and easiness to use (grade A). Associated elastic stockings is efficious (grade B). The duration of prophylaxis lasts generally 7-10 days. Extension to 1 month is recommended for major abdominal cancer surgery (grade A).

Ambulatory Surgical Procedures↗
PubMed2005

Paracetamol: a haemorrhagic risk factor in patients on warfarin.

AIM: To quantify the effect of paracetamol on the anticoagulant effect of warfarin under normal clinical conditions. PATIENTS AND METHODS: In a prospective double-blind, cross-over, placebo-controlled study, 11 patients on stable warfarin therapy received in random order two 14-day regimens of paracetamol 4 g day(-1) or placebo, with a 14-day or more wash-out period in between, time necessary to fulfil the inclusion criteria. RESULTS: In patients on paracetamol, the mean maximum increase in the International Normalized Ratio (INR) observed was 1.04 +/- 0.55 vs. 0.20 +/- 0.32 in those on placebo (P = 0.003). The mean maximum INR observed was significantly higher with paracetamol than with placebo (3.47 vs. 2.61, P = 0.01). In patients receiving paracetamol, the mean observed INR was significantly increased after 4 days (+ 0.6 +/- 0.6, P < 0.001). CONCLUSION: Paracetamol at 4 g day(-1) induces a significant increase in INR in patients receiving a stable regimen of warfarin, increasing the risk of bleeding associated with warfarin.

Acetaminophen↗
PubMed2003

[Direct and indirect effects of epoietin alpha in an experimental model of thrombosis and bleeding in the rabbit].

OBJECTIVES: To study direct and indirect effects of EPO on haemostasis. STUDY DESIGN: Experimental, randomised. ANIMALS: Forty-eight New Zealand rabbits. METHOD: Animals were anaesthetised, ventilated and monitored continuously for blood pressure, heart rate, body temperature, and carotid blood flow variations and were randomised into four groups: control, EPO bolus 2400 IU kg(-1), fractionated EPO (one injection a week of 600 IU kg(-1) for 4 weeks), homologous red blood cell transfusion to reach the Ht level of the fractionated EPO group. A compression injury and a 75% stenosis of the carotid artery triggered a series of cyclic flow reductions (CFRs). CFRs were observed for a 20 min period in each group. Ear immersion bleeding time (BT) and hepato-splenic bleeding were performed at the end of the experiment. Biology was performed at the end of the thrombosis period: blood cells count, Hte, activated partial thromboplastin time, fibrinogen, arachidonic-induced platelet aggregation, EPO dosages. RESULTS: No significant increase in thrombosis (CFRs) in the two EPO groups and in the transfused group. Increase in Hte in the fractionated EPO group versus control. Group EPO bolus: decrease in BT and hepato-splenic bleeding versus control; decrease in hepato-splenic bleeding versus fractionated EPO group, increase in platelet aggregation velocity versus control. CONCLUSION: EPO did not increase the thrombotic risk in this rabbit model. EPO bolus decreased BT and hepato-splenic bleeding.

Animals↗
PubMed2002

D-dimer: a characteristic of the coagulation state of each patient with chronic atrial fibrillation.

BACKGROUND AND OBJECTIVE: It is accepted that patients with atrial fibrillation (AF) are characterised by increased levels of plasmatic D-dimers, with a wide inter-individual variability depending on the patients and therapeutic characteristics, but it has not been established if this level was predictive of the risk of arterial thromboembolic event. In order to answer such a question, it has to be established if the D-dimer level in a given patient is characteristic of such a patient (stable over time) if also fluctuating with time (and useless to characterise the patient). METHODS AND RESULTS: One hundred thirty clinically stable patients with chronic AF were recruited (anticoagulant: group 1, antiaggregant aspirin: group 2, no antithrombotic: group 3). During the follow-up of patients without clinical events (n=63), it is notable that in patients with D-dimer levels <500 ng/ml, these remained <1000 ng/ml, in patients with levels between 500 and 1000 ng/ml, these did not reach 1590 ng/ml, and in those with D-dimers >1000 ng/ml, the levels remained relatively stable. Mean age and D-dimer levels were lower in group 1 (74.4 years and 509.1 ng/ml, respectively) than in group 2 (82.4 years, p=0.0003 and 1015.7 ng/ml, p<0.0001, respectively) and in group 3 (79.3 years and 1289.3 ng/ml, p<0.0001, respectively). The effect of the antithrombotic therapy was independent of the age of patients (p=0.017). CONCLUSION: D-dimer levels in patients with chronic AF remain in the same range over time. They are lower on anticoagulant therapy than on antiaggregant or no antithrombotic therapy, irrespective of age. Thus, D-dimers appear to be a useful parameter for assessing the degree of hypercoagulability of patients whatever their age.

Age Factors↗
PubMed1999

Risk factors and outcomes for atherothrombotic disease in French patients: the RIVAGE study. RIsque VAsculaire Group d'Etude.

This prospective observational study was designed to delineate the course of atherosclerotic disease in a representative group of French patients receiving standard medical care and to look for clinical and laboratory factors predictive of recurrent cardiovascular events. The 2416 study patients (75.2% men and 24.8% women) had diagnoses of peripheral arterial disease (stage II or III), ischemic heart disease (stable angina or myocardial infarction), or cerebrovascular disease (transient ischemic attack or stroke); 2004 patients (82.9%) had only one of these diagnoses, and 412 (17.1%) had more than one. Among patients with a given stage of peripheral arterial disease, mean age was older in the women than in the men. Coronary disease and cerebrovascular disease were more severe in the men. During the 18-month follow-up, 408 cardiovascular events were recorded in 380 patients (15.7% of the overall study group). In patients who had a single clinical event at inclusion, subsequent clinical events usually occurred in the same vascular bed. The incidences of coronary and cerebral events were correlated with age and the incidence of peripheral events with smoking status. Fatal events were correlated with age but not with the baseline diagnosis, except for a weak relationship with peripheral arterial disease. In a subset of 411 patients who had laboratory tests, plasma fibrinogen level was the only independent predictor of recurrence for all cardiovascular events; this parameter was more closely correlated with fatal events than with all events.

Aged↗
PubMed1998

[The role of thrombotic and hemostatic mechanisms in the initial phases of atherosclerosis].

The factors of thrombosis (endothelium, haemostasis, coagulation, fibrinolysis) are implicated from the initiating phase of atherosclerotic lesions. Their participation is more established (and studied) in the later phases of intraluminal evolution of atherosclerosis, of thromboembolic complications of the lesions and interventional procedures. The traditional theory of response to physical lesions of the endothelium as an initiating factor of atherosclerotic lesions, which gave platelets an essential role, has been replaced by that linking an early functional lesion of the endothelium and a cellular response by monocytes infiltrating the vessel wall, becoming macrophages. The macrophages participate in changes of the LDL in the wall, ingest the lipids at the same time as the smooth muscle cells which have migrated and proliferated from the media to the intima. The lipid overload, especially with oxidised LDL, is intracellular at first in these foam cells, then extracellular as the cells die. During the early stages, all the tissue factors of activation and development of coagulation are present in the vessel wall and then within the lesion. This intra-cellular coagulation results in the production of thrombi in the tissues and the transformation of fibrinogen to fibrin. These stages precede and participate in cellular proliferation and extracellular lipid deposits. Factors of tissular thrombolysis (the uPA pathway) play a part in cellular immigration and proliferation. It is only at a later stage that the lesion activates intravascular coagulation and fibrinolysis which, in conditions of variable equilibrium, will result in the clinical complications of the atherosclerotic process. All these factors therefore participate firstly in the tissues and then within the lumen, in the progression and complications of atherosclerosis which for these reasons is often called atherothrombotic disease. The comprehension of these mechanisms is essential for the development and interpretation of tests and treatment applied to different stages of the disease, which is all the more complex given that in a given patient at a given time, lesions at different stages are present in the arterial network.

Arteriosclerosis↗
PubMed1997

Infants with Kasabach-Merritt syndrome do not have "true" hemangiomas.

OBJECTIVE: In 1940 Kasabach and Merritt described an infant with a vascular anomaly, extensive purpura, and thrombocytopenia; they called his lesion "capillary hemangioma." Hemangioma is a benign tumor that grows in infancy and is characterized by proliferation of endothelial cells and regression during childhood. Although Kasabach-Merritt syndrome (KMS) is frequently mentioned as a possible complication of hemangioma, our experience suggests that the anatomic vascular lesion underlying the thrombocytopenia is not a "true," classic, involuting type of hemangioma of infancy and childhood. STUDY DESIGN: We reviewed the clinical and hemostasis data and the response to treatment in 22 cases of KMS, and we analyzed the biopsy specimens of 15 of them. RESULTS: Clinically none of the 22 patients had classic hemangioma. There was no female preponderance. All patients had severe thrombocytopenia (lowest platelet count = 3000/mm3) and consumption of fibrinogen. Histologically, none had the typical "capillary," involuting type of hemangioma of infancy: they exhibited either a tufted angioma or a kaposiform hemangioendothelioma pattern; all specimens also contained numerous abnormal lymphatic-like vessels; lymphatic malformation was the major component in two patients. The infants exhibited a heterogeneous response to a number of therapeutic regimens, as noted in other reports. Severe morbidity was present; three of our patients died, and one had leg amputation. "Residua" were, in fact, residual vascular neoplasia, variable in duration, and not a stable fibrofatty residuum, as in classic involuted hemangioma; only the hematologic phenomenon was "cured" after a period of years. CONCLUSIONS: KMS is a distinctive disease of infancy, but the underlying vascular lesion is not a "true," classic, involuting type of hemangioma of infancy. This is a different vascular tumor with a resemblance pathologically to either tufted angioma or kaposiform hemangioendothelioma in association with lymphatic-like vessels. Whether the underlying lesion in KMS is a single anatomic entity or heterogeneous cannot be definitely concluded from this study. We need a better understanding of the pathogenesis of KMS to improve our therapeutic management.

Biopsy↗
PubMed1997

Extensive pure venous malformations in the upper or lower limb: a review of 27 cases.

BACKGROUND: Extensive pure venous malformations (VMs) involving the entire lower or upper limb and adjacent trunk form a particular group of rare vascular malformations. OBJECTIVE: Our purpose was to review 27 cases of extensive limb VMs and describe their characteristics and management. METHODS: Cases of extensive limb VMs were investigated, treated, and observed for a mean of 7 years. RESULTS: Eleven cases involved the upper limbs and 16 involved the lower limbs. All involved skin and muscle. In 81% of cases in the lower limb there was also knee joint involvement that created severe functional impairment. Ultrasonography with Doppler (duplex scans), computed tomographic scans, and magnetic resonance imaging were helpful noninvasive diagnostic procedures in these patients, whereas arteriography and phlebography were less informative. Muscle involvement was present in 100% of patients and bone abnormalities in 63%. Leg length was either normal or there was slight limb undergrowth, except in three patients who had minor overgrowth of the affected limb. Coagulation profiles demonstrated localized intravascular coagulation in 88% of patients. The majority of patients had conservative management (elastic stockings). In a few, percutaneous sclerotherapy or partial excision of skin and muscle VMs was beneficial. Knee joint involvement required synovectomy and VM excision during childhood in 7 of 16 patients. CONCLUSION: Extensive limb VMs are characterized by diffuse involvement of the skin, muscle, and joints, and by a specific localized intravascular coagulopathy with general consequences. This group of vascular malformations should be separated from the Klippel-Trenaunay and Parkes Weber syndromes.

Abnormalities, Multiple↗
PubMed1995

[Antiphospholipid antibodies: cause of thrombosis or an epiphenomenon?].

Antiphospholipid antibodies (aPL) present in systemic lupus erythematosus and the primary antiphospholipid syndrome are a well-known risk factor for thrombosis. Most of them require the presence of a cofactor, beta 2-glycoprotein I for anticardiolipin antibodies, prothrombin for lupus anticoagulant. These aPL are of the "immune" type. APL are also found in various non-immunological conditions, in which repeated endothelial or membranous damages appear to be frequent, but thromboses are rare. Most of these aPL are cofactor-independent, except those induced by chlorpromazine, and might belong to "natural" antibodies.

Animals↗
PubMed1995

Characterization of an antithrombotic peptide from kappa-casein in newborn plasma after milk ingestion.

Bovine and human kappa-caseinoglycopeptides, two antithrombotic peptides derived from the corresponding kappa-caseins, were detected in physiologically active concentrations in the plasma of 5-d-old newborn infants after ingestion of cow's-milk-based formula or human milk respectively. It is suggested that these two bioactive peptides are released from milk proteins during digestion.

Amino Acid Sequence↗