Intérêt du test d'effort cardiorespiratoire dans la sténose aortique asymptomatique

Objectifs de l étude : Le remplacement valvulaire aortique chez les patients présentant une sténose aortique sévère asymptomatique reste controversé. Les recommandations récentes de l ESC et de l AHA/ACC proposent une stratification du risque basée sur l évaluation de l évolutivité de la sténose et les résultats du test d effort. Cependant, l apparition d une dyspnée non spécifique durant le test d effort est fréquemment observée. Différencier une dyspnée physiologique d une dyspnée pathologique est parfois difficile. La valeur pronostique du test d effort cardiorespiratoire est bien établie dans l insuffisance cardiaque. Il a récemment été proposé de l utiliser afin de mieux quantifier la capacité fonctionnelle des patients porteurs de valvulopathies. Le but de cette étude était d évaluer l intérêt du test d effort cardiorespiratoire dans la sténose aortique sévère apparemment asymptomatique. Méthodes et résultats : Entre 2007 et 2013, 44 patients consécutifs (32 hommes ; moyenne d âge 69+-13 ans) sans symptomatologie fonctionnelle et avec une sténose aortique au moins modérée (surface valvulaire aortique<1.5 cm et surface valvulaire aortique indexée <= 0.6 cm /m ) ont prospectivement bénéficié d un test d effort cardiorespiratoire. 12 (27%) patients ont eu un test d effort anormal avec apparition de symptômes (dyspnée chez 11 patients, angor chez 1 patient). Le test d effort cardiorespiratoire a mis en évidence une réduction objective de la capacité fonctionnelle (pic de VO2<80% de la valeur prédite) chez 28/44 patients (64%). Le suivi moyen était de 28+-31 mois après le test d effort cardiorespiratoire. Durant le suivi, 21/44 (48%) ont eu un remplacement valvulaire aortique (20 chirurgies et 1 TAVI), la plupart dans la première année après le test d effort cardiorespiratoire (15/21 ; 71%). La FEVG (p=0.04), la pente VE/VCO2>34 (p=0.003), un pic de VO2 <=14ml/kg/min (p=0.06), le diamètre télésystolique du ventricule gauche (p=0.01), la surface aortique (p=0.03) et un test d effort anormal montrant des symptômes (p=0.0001), étaient associés à un remplacement valvulaire aortique durant le suivi. Une pente VE/VCO2>34 (HR=7.10; 95% CI: [2.35 24.818], p=0.002); un pic de VO2 <=14ml/kg/min (HR=3.40; 95% CI: [1.02 11.41], p=0.047) et un test d effort anormal (HR=6.13; 95% CI: [1.86 20.22], p=0.003) étaient des facteurs prédictifs indépendants de remplacement valvulaire aortique durant le suivi. Conclusions: Le test d effort cardiorespiratoire a un intérêt pour mieux caractériser la dyspnée durant le test d effort chez les patients porteurs d une sténose aortique apparemment asymptomatique. Un pic de VO2 <= 14ml/kg/min et une pente VE/VCO2 >34 sont associés à un test d effort anormal avec apparition de symptômes et par la suite à des remplacements valvulaires aortiques plus fréquents durant le suivi.AMIENS-BU Santé (800212102) / SudocSudocFranceF

Analysis of phosphatidylcholine oxidation products in human plasma using quadrupole time-of flight mass spectrometry

We report here an application of the previous method for the analysis ofphosphatidylcholine (PC) and lysophosphatidylcholine (lysoPC) oxidation products inhuman plasma using quadrupole time of flight (Q-TOF) mass spectrometry withelectrospray ionization. We separated these products using an HPLC C8 column witha gradient of methanol and 10 mM aqueous ammonium acetate. Monohydroperoxides,epoxyhydroxy derivatives, oxo derivatives, and trihydroxides of palmitoyl-linoleoyl(C16:0/C18:2) PC and stearoyl-linoleoyl (C18:0/C18:2) PC were detected mainly asMH+ and [M+Na]+ ions in the plasma of alcoholic patients. Using standard syntheticPC-OH (C16:0/C18:2-OH), the lipid extract component was identified as(C16:0/C18:2-OH) PC based on the product ions of ESI-MS-MS. Using standardsynthetic PCOOH (C16:0/C18:2-OOH) as a reference, the PCOOH concentration inplasma was quantified. Two oxidatively modified lysoPCs were also detected. This isthe first report showing the presence of epoxyhydroxy derivatives,monohydroperoxides, oxo derivatives, and trihydroxides of (C16:0/C18:2) PC and(C18:0/C18:2) PC, and PC-OH (C16:0/C18:0-OH) in human plasma

Autopsy case of acute pulmonary thromboembolism with neurosyphilis

Abstract Background Syphilis is caused by the bacterium Treponema pallidum. Syphilis is a multistage disease, and the clinical stages of syphilis are divided to primary, secondary, and tertiary syphilis, where the tertiary stage is classified as neurosyphilis, cardiovascular syphilis, or gummatous syphilis. Here, we describe an autopsy case of acute pulmonary thromboembolism with neurosyphilis. Case presentation A male in his early 40s began to complain of hallucinations. He was admitted to a psychiatric hospital as an emergency case 4 days before death. He was physically restrained to control agitation and aggressiveness. The patient was severely obese (BMI 36.45). At autopsy, large thromboembolic masses filled the pulmonary trunk and both pulmonary arteries. Thrombi were also noted in the right popliteal vein and bilateral gastrocnemius and soleus veins, suggesting bilateral lower extremity deep vein thrombosis. Dissection of the brain, which weighed 1457 g, revealed no noteworthy macroscopic findings. Histological examination showed lymphocyte infiltration into the perivascular space of the brain tissue with no vasculitis. Immunohistochemical staining of T. pallidum was negative, the fluorescent treponemal antibody-absorption test was positive, the rapid plasma reagin titer was 1:4, and the T. pallidum hemagglutination assay titer was 1:10,240. Real-time PCR assay of the brain tissue detected low copy numbers of T. pallidum genes. Altogether, the cause of death was acute pulmonary thromboembolism resulting from bilateral lower extremity deep vein thrombosis. The patient also had early-stage meningovascular neurosyphilis. Conclusion An autopsy case of acute pulmonary thromboembolism with meningovascular neurosyphilis is presented, including histopathological examination, serological assessment, and genetic testing. Forensic pathologists should pay attention to a myriad of syphilitic manifestations. The contributing factors for thrombosis in the present case included severe obesity, probable dehydration, and physical restraints implemented to control meningovascular neurosyphilis-induced neuropsychiatric symptoms

Free radicals in alcoholic myopathy: Indices of damage and preventive studies

Chronic alcoholic myopathy affects up to two-thirds of all alcohol misusers and is characterized by selective atrophy of Type If (glycolytic, fast-twitch, anaerobic) fibers. In contrast, the Type I fibers (oxidative, slow-twitch, aerobic) are relatively protected. Alcohol increases the concentration of cholesterol hydroperoxides and malondialdehyde-protein adducts, though protein-carbonyl concentration levels do not appear to be overtly increased and may actually decrease in some studies. In alcoholics, plasma concentrations of a-tocopherol may be reduced in myopathic patients. However, a-tocopherol supplementation has failed to prevent either the loss of skeletal muscle protein or the reductions in protein synthesis in alcohol-dosed animals. The evidence for increased oxidative stress in alcohol-exposed skeletal muscle is thus inconsistent. Further work into the role of ROS in alcoholic myopathy is clearly warranted. (C) 2002 Elsevier Science Inc