[Factor VIII hyperactivity: an arterio-venous thrombogenic factor. Case report]. / Hyperactivité du facteur VIII: un facteur thrombogène artério-veineux. A propos d'un cas.

Thrombosis is the principal mechanism in vascular pathology, whether cerebral, coronary or peripheral. During the initial stages of infarction, coagulation contributes to vascular occlusion, the haemostatic factors playing a determining role in the development of atherothrombotic lesions. An increase in a coagulation protein, besides any lowering of anticoagulation protein levels, is a risk factor for thrombosis. Among these pro-coagulant factors, the pro-thrombogenic action of factor VIII has without doubt been studied the least. We report the case of a 62 year old patient with a personal and family history of many previous thrombotic episodes, both arterial and venous, in whom factor VIII hyperactivity was discovered after a myocardial infarction. This case underlines the association of the factor VIII complex with thrombosis, and its clinical repercussions, especially the incidence of coronary pathology.

[Incidence, causes and prognostic factors of hyponatremia in intensive care]. / Incidence, étiologies et facteurs pronostiques de l'hyponatrémie en réanimation.

PURPOSE: The incidence of hyponatremia is unknown, their causes are multiple. The higher mortality, especially in intensive care units, is currently unexplained. The objective of this article is to evaluate the incidence of hyponatremia, to assess their causes and to identify predictors of prognosis in intensive care units. METHODS: We included retrospectively all patients admitted at department of medical intensive care unit between January 1996 and February 2001, who presented at the admission, an hyponatremia (< 130 mmol/l). We excluded all patients who presented a hospital acquired hyponatremia, or hyponatremia associated with hyperglycemia > 13 mmol/l or with mannitol administration. Data were analysed by univariate methods, then by multivariate analysis. RESULTS: During the study period, 300 patients were identified among 2188: the incidence was 13.7% with 95% confidence interval (95% CI) between 9.8 % and 16.7%. Hypovolemic hyponatremia was observed in 25.7%, hypervolemic in 23.7% and normovolemic in 50.6%. In-hospital mortality was 37.7% (95% CI: 31.8% - 42.3%). Nine data were significantly associated with higher mortality in univariate analysis, but only 5 were identified as independant predictors of hospital mortality in multivariate analysis: hyponatremia < 125 mmol/l with a significant relative risk (RR) (RR = 2.10; 95% CI: 1.43-3.08; p < 0.001), Glasgow score < 9 (RR = 2.66; 95% CI: 1.25-5.66; p = 0.01), Glasgow score between 9 and 14 (RR = 1.94; 95% CI: 1.31-2.88; p < 0.001), shock (RR = 1.80; 95% CI: 1.10-3.05; p = 0.02) and blood urea concentration > 10 mmol/l (RR = 1.59; 95% CI : 1.08-2.34; p = 0.02). CONCLUSION: The frequency of hyponatremia is high; the normovolemic type represented 50%. Mortality is linked, in greater part, to organs dysfunction, but the severity of hyponatremia remained a significant predictor of mortality.

[Postpartum cardiomyopathy revealed by acute lower limb ischemia]. / Cardiomyopathie du péripartum révélée par l'ischémie aiguë d'un membre inférieur.

Peripartum cardiomyopathy is an uncommon disease defined as a dilated cardiomyopathy during puerperium, with left ventricular dysfunction (ejection fraction < 45%) without any other etiology. The etiology of this disease remains uncertain and it can be revealed in a variety of ways. Thrombo-embolic complications may be, although infrequently, the initial manifestation of peripartum cardiomyopathy, which is usually an intracardiac thrombosis. Lower extremity embolism is uncommon. The case reported is about a 39-year-old woman, multiparous, who presented, 40 days after delivery, a global heart failure with atrial fibrillation, revealed by left lower extremity thromboembolism. After echocardiographic and etiologic examinations, the diagnosis was established as peripartum cardiomyopathy. It evolved favourably after 2 months of medical treatment: the symptoms and cardiomegaly decreased, left ventricular systolic function was improved.