L’hydrogène sulfuré est un gaz toxique rencontré dans de nombreuses industries (pétrole et mines) et dans les milieux professionnels en contact avec la décomposition de matières organiques. Il s’agit d’un toxique irritant responsable de lésions muqueuses parfois dramatiques, d’un poison de la respiration cellulaire, et d’un redoutable neurotoxique. À fortes doses (>1000 ppm), le décès est bien souvent inévitable avant la prise en charge. Pour les formes sévères, la démarche diagnostique regroupe des circonstances d’exposition, une atteinte des voies aériennes supérieures et des conjonctives ainsi qu’une défaillance multiviscérale progressive. La compréhension des effets toxiques de l’hydrogène sulfuré permet d’optimiser la prise en charge symptomatique et de discuter les différents traitements spécifiques proposés dans la littérature.

AbstractThe aim of this study was to define the use of a new cardiac troponin I (cTnI) assay for emergency patients with chest pain and no specific electrocardiographic changes consistent with the presence of ischemia. Patients (n=106) admitted in Emergency/Cardiology Departments for chest pain and suspicion of acute coronary syndrome (ACS) were randomized into two diagnosis groups (ACS or non-ACS) by two independent cardiologists. cTnI measurements were performed at admission, and 6 hours and 12 hours later with a new generation assay (Access AccuTnI, Beckman Coulter). Using an upper reference limit of 0.04 μg/l, 27 patients had a cTnI elevation not related to the final diagnosis of ischemia; the positive predictive value (PPV) was 67% with specificity 48%. The decisional value was re-defined and set at 0.16 μg/l, a concentration corresponding to the 99th percentile of the non-ACS patient group. Precision (coefficient of variation) was 8% at this level, PPV 97% and specificity 98%. This new decisional value is now used in our institution and could be included in standard care guidelines to improve the management of patients presenting chest pain in emergency departments.

Matrix metalloproteinases (MMPs) are implicated in multiple sclerosis where one of their roles may be to facilitate the transmigration of circulating leukocytes into the CNS. Studies have focused on only a few MMPs, and much remains unknown of which of the 23 MMP family members is/are critical to the multiple sclerosis disease process. Using quantitative real time polymerase chain reactions, we have systematically analysed the expression of all 23 MMP members in subsets of leukocytes isolated from the blood of normal individuals. We found a distinctive pattern of MMP expression in different cellular populations: MMP-11, MMP-26 and MMP-27 were enriched in B cells, while MMP-15, MMP-16, MMP-24 and MMP-28 were prominent in T lymphocytes. Of interest is the enrichment of a majority of MMP members in monocytes: MMP-1, MMP-3, MMP-9, MMP-10, MMP-14, MMP-19 and MMP-25. MMP-2 and MMP-17 were also significantly represented in monocytes, although B cells had significant amounts of these MMPs. In correspondence with their strong expression of many MMP members, monocytes migrated more rapidly across a model of the blood-brain barrier in culture than T or B lymphocytes. Finally, we found higher levels of two of the monocyte-expressed MMPs in multiple sclerosis patients compared with normal individuals: MMP-2 and MMP-14. Tissue inhibitor of metalloproteinases (TIMP)-2 was also elevated in monocytes from multiple sclerosis patients, providing a mechanism for the reported activation of MMP-2 by MMP-14 and TIMP-2. These results emphasize that monocytes are prominent contributors of the neuroinflammation in multiple sclerosis through a mechanism that involves their high MMP expression and that they identify specific MMP members as targets for novel therapeutics in the disease.

Valvular heart complications in Behcet's disease are rarely reported. Moreover, the risk of dehiscence in postoperative valvular replacement is high in Behcet's disease. We report a case of recurrent aortic prosthetic dehiscence revealing Behcet's disease in a young woman. Each disease exacerbation was concomitant to a Streptococcus agalactiae infection. This infection appears to act as a trigger for Behcet's disease exacerbation. The patient was successfully treated with immunosuppression plus antibiotic therapy.

OBJECTIVES:This study was designed to assess the prognostic value of a new variable derived from a cardiopulmonary exercise test, the circulatory power, a surrogate of cardiac power, at peak exercise, in patients with chronic heart failure.BACKGROUND:Peak exercise cardiac power and stroke work are invasive parameters with recently proven prognostic value. It is unclear whether these variables have better prognostic value than peak oxygen uptake (VO(2)).METHODS:The study population comprised 175 patients with chronic heart failure (ejection fraction <45%) who underwent a cardiopulmonary exercise test. Circulatory power and circulatory stroke work were defined as the product of systolic arterial pressure and VO(2) and oxygen pulse, respectively. Prognostic value was assessed by survival curves (Kaplan-Meier method) and uni- and multivariate Cox analyses.RESULTS:With a mean follow-up of 25+/-10 months, ejection fraction, heart rate, systolic arterial pressure, peak VO(2), VCO(2), the anaerobic threshold, minute ventilation, the ventilatory equivalents of oxygen and carbon dioxide, the half times of VO(2) and VCO(2) recoveries, and the circulatory stroke work and power predicted outcome. Multivariate analysis demonstrated that the peak circulatory power (chi-square=19.9, P<0.001) (but not peak circulatory stroke work) was the only variable predictive of prognosis.CONCLUSION:The prognostic value of cardiopulmonary exercise tests in heart failure patients can be improved by assessing a new variable, the circulatory power - a surrogate of cardiac power - at peak exercise.

Les bêtabloquants, longtemps contre-indiqués, se sont révélé ces dernières années comme le traitement le plus efficace de l’insuffisance cardiaque. Plusieurs essais font maintenant état d’une réduction de mortalité de l’ordre de 35 %, en sus du traitement classique. Néanmoins, la conduite de ce traitement reste complexe et nécessite des règles strictes.

Background Myocyte death could play a role in heart failure (HF) irrespective of the presence of coronary artery disease. The study aimed to assess this hypothesis by use of the cardiac troponin I (cTnI) assay. Methods and Results Seventy-one patients with nonischemic HF, New York Heart Association (NYHA) class II-IV, with a normal coronary angiogram and after exclusion of myocardiopathies were evaluated in the study. The control group included 9 healthy subjects and 15 patients hospitalized for severe noncardiac dyspnea. Cardiac TnI concentrations were determined at admission with a research reagent (cTnIus) characterized by a detection limit of 0.026 ng/mL and a high analytic sensitivity of 0.002 ng/mL. cTnIus levels were more than 0.026 ng/mL in 19 HF patients, ranging between 0.027 and 0.463 ng/mL, whereas no cTnIus level was detectable in the control group. With use of a reference assay, only 2 HF patients had abnormal cTnI values. Severe HF was observed in 17 of these 19 patients, assessed by NYHA class IV or by the presence of pulmonary edema. Patients with an increased cTnIus level had a more restrictive mitral Doppler pattern (P <.001) and a more distinctive left ventricular (LV) concentric remodeling (P <.0001), whereas LV ejection fraction was similar in both HF groups. The increased cTnIus level was also associated with a LV wall strain biologic marker (ie, an increased brain natriuretic peptide plasma level) (P <.001). Conclusions cTnI assay is a promising biochemical method for detecting cardiac myolysis in HF, independent of the presence of coronary artery disease. This subtle myolysis could be in part related to the severely increased LV wall strain. (Am Heart J 2001;141:247-53.)

with “BD SST 1 double centrifugation” (P ,0.0001, paired t-test). Deming regression analysis yielded the following: slope 5 1.16 [95% confidence interval (95% CI), 1.03–1.29]; intercept 5 0.04 mg/L (95% CI, 0.02– 0.06 mg/L). Table 1 shows the assay values of the six apparently falsepositive results. These results prompted a second phase, during which the BD Thrombin sample was also centrifuged twice. Nineteen additional patients were included. The difference between the results (cTnI range, 0.01–24 mg/L, 32% above threshold) was not statistically significant as analyzed by the paired t-test and the Deming regression [slope 5 1.04 (95% CI, 0.93–1.14); intercept 5 20.03 mg/L (95% CI, 20.08 to 0.02 mg/L)]. We conclude that a single centrifugation of collection tubes containing thrombin as a clot activator is insufficient to avoid false-positive cTnI results on the ACCESS analyzer. Repeat centrifugation eliminates false-positive results. The presence of thrombin in collection tubes does not significantly affect cTnI results by this assay. Roberts et al. (3 ) published similar results.

Acute cardiogenic pulmonary oedema is a medical emergency. It generally result from an acute left ventricular insufficiency, itself resulting from systolic or diastolic dysfunction (alteration in relaxation or distensibility). Clinical presentation may be atypical, especially in the elderly. Treatment is based on oxygen, diuretics and nitrates. In severe cases, mechanical ventilation may be required.

Cardiac troponin I (cTnI) has become a major marker in the diagnosis and monitoring of myocardial damage. On the ACCESSTM analyzer (Beckman Coulter), serum is the biological fluid compatible with both myoglobin and cTnI tests (1). However, residual fibrin (2) and microparticles (2) have been reported to interfere with one or more cTnI assays. Some of these interferences can be avoided with repeat centrifugation of the sample and/or the use of a clot activator (3). The BD VacutainerTM HemogardTM Thrombin glass evacuated blood collection tube (BD Thrombin) contains thrombin as a …

Brain natriuretic peptide (BNP) is a recently discovered peptide, secreted by the atria and ventricles in response to parietal distension. It was recently proposed as a screening test for left ventricular failure. The authors assayed this peptide at rest in 37 patients with chronic heart failure due to left ventricular systolic dysfunction and another 20 patients with various diseases (respiratory failure, cirrhosis, heart transplantation, "diastolic" heart failure) but normal left ventricular systolic function. A significant increase compared to normal values was observed not only in the group of heart failure patients, but also in patients with all other diseases. BNP was significantly higher in NYHA class IV patients. The relationship between plasma BNP levels and ejection fraction was not significant. On the other hand, a good correlation was observed between BNP and left ventricular filling parameters evaluated by cardiac Doppler: E wave deceleration time (r = -0.53, p = 0.001), E/A ratio: r = 0.57 p = 0.005) or VO2 max (r = -0.55, p < 0.005).

Studies conducted over recent years have definitively confirmed beta-blockers as the major treatment for heart failure. However, they are difficult to use and, to date, only carvedilol has been granted a Marketing Authorisation for this indication. The practical aspects of treatment with carvedilol in these patients are reviewed.

Le peptide natriuretique cerebral (BNP: brain natriuretic peptide) est un peptide recemment decouvert, secrete par les oreillettes et les ventricules en reponse a la distension parietale. Il a ete recemment propose comme test de depistage de l'insuffisance ventriculaire gauche. Nous avons dose ce peptide au repos chez 37 insuffisants cardiaques chroniques par dysfonction systolique ventriculaire gauche ; et 20 autres patients avec des pathologies variees (insuffisance respiratoire, cirrhose, transplantes cardiaques, insuffisance cardiaque «diastolique») mais une fonction systolique ventriculaire gauche normale. Une augmentation significative par rapport aux valeurs normales a ete retrouvee non seulement dans le groupe des insuffisants cardiaques, mais aussi dans l'ensemble des autres pathologies. Le BNP etait significativement plus eleve chez les patients en classe IV de la NYHA. La relation entre le taux plasmatique de BNP et la fraction d'ejection n'etait pas significative. Il existait par contre une bonne correlation entre le taux de BNP et les parametres de remplissage ventriculaire gauche evalues par le doppler cardiaque: temps de deceleration de l'onde E (r= -0,53, p=0,001), rapport E/A: r=0,57; p=0,005) ou la VO 2 max (r=-0,55, p<0,005).