[Epicardial adipose tissue and atrial fibrillation]. / Tissu adipeux épicardique et fibrillation auriculaire.

Atrial fibrillation (AF) is the most common arrhythmia encountered in adults; it is associated with a significant morbidity and mortality. Obesity is a risk factor contributing to AF occurrence. Recently, interest has focused on epicardial adipose tissue (EAT), defined as a fatty deposit located between the epicardium and the visceral pericardium. Its characteristics are distinct from classic adipose deposits: it infiltrates the epicardial myocardium and secretes cytokines, which modulate cardiomyocyte electrophysiology and cardiac remodeling. Different studies show that EAT can be an independent risk factor for AF and that EAT thickness, as measured by CT or MRI, could predict the presence, severity and recurrence of AF.

La fibrillation auriculaire (FA) est l'arythmie la plus fréquemment rencontrée chez l'adulte ; elle est associée à une morbi-mortalité importante. L'obésité est un facteur de risque contribuant à sa survenue. Récemment, l'intérêt s'est porté sur le tissu adipeux épicardique (TAE), défini comme un dépôt adipeux situé entre l'épicarde et le péricarde viscéral. Ses caractéristiques sont distinctes des dépôts adipeux classiques : il infiltre le myocarde épicardique et sécrète des cytokines modulant l'électrophysiologie des cardiomyocytes et provoquant un remodelage fibro-adipeux cardiaque. Différentes études montrent que le TAE peut être un facteur de risque indépendant de survenue de FA. L'épaisseur du TAE mesurée par CT-scan ou par IRM pourrait être utilisée comme facteur prédictif de la présence, de la gravité et de la récidive de FA.

Unprovoked internal jugular vein thrombosis: a case report and literature review.

BACKGROUND: Managing thrombosis in rare sites is challenging. Existing studies and guidelines provide detailed explanations on how to overcome lower-limb thromboses and pulmonary embolisms, but few studies have examined thrombosis in rare sites. Lack of data makes clinical practice heterogeneous. Recommendations for diagnosing, treating, and following-up internal jugular vein thrombosis are not clearly defined and mostly based on adapted guidelines for lower-limb thrombosis. CASE PRESENTATION: A 52-year-old Caucasian woman came to the Emergency Department with chest, neck, and left arm pain. Computed tomography imagery showed a left internal jugular vein thrombosis. An extensive workup revealed a heterozygous factor V Leiden gene. Therapy was initiated with intravenous unfractionated heparin, then switched to oral acenocoumarol, which resolved the symptoms. Based on this case presentation and a literature review, we summarize the causes, treatment options, and prognosis of unprovoked internal jugular vein thrombosis. CONCLUSIONS: Managing internal jugular vein thrombosis lacks scientific data from large randomized clinical trials, partly because such thromboses are rare. Our literature review suggested that clinical treatments for internal jugular vein thrombosis often followed recommendations for treating lower-limb thrombosis. Future specific studies are required to guide clinicians on the modalities of diagnosis, screening for thrombophilia or oncologic disease, treatment duration, and follow-up.

Circadian rhythm of blood cardiac troponin T concentration.

INTRODUCTION: High-sensitivity cardiac troponin assays have significantly improved the sensitivity of myocardial infarction detection by using cutoff values and early absolute changes. However, variation in repeated measures also depends on biological variability. This study aimed to assess the potential circadian component of this biological variability. METHODS: 17 healthy volunteers were recruited, and standardized conditions for physical activity, meals, exposure to light and duration of sleep were imposed. Blood samples were collected every 4 h and high-sensitivity troponin T assay with a limit of detection of 3 ng/l and a 99th percentile of 14 ng/l were used. Circadian variations were analyzed using the cosinor method. RESULTS: Statistically significant circadian variations were observed for body temperature, heart rate, and systolic/diastolic arterial blood pressures (p < 0.01 using both a non-adjusted cosinor model and a gender- and BMI-adjusted cosinor model). The amplitudes of the circadian variations were 18.93, 6, 15.35, and 1.92%, respectively. A statistically significant circadian biological variation of troponin blood concentrations was evidenced (p < 0.01 in both the non-adjusted cosinor model and the gender- and BMI-adjusted cosinor), with an amplitude of 20.5% (average: 4.39 ng/l; amplitude: 0.9 ng/l; peak at 06:00 and nadir at 18:00). DISCUSSION: This study demonstrates a circadian biological variation in blood troponin concentration in a healthy population. The amplitude of this variation challenges the cutoff value for instant rule-out of the rapid rule-in/rule-out of the recent European guidelines for the management of acute coronary syndromes. These findings deserve further investigation in a population at risk of myocardial infarction.