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Peripartum cardiomyopathy (PPCM) is a rare cause of heart failure. Only half of the patients recover normal cardiac function. We assessed the usefulness of magnetic resonance imaging (MRI) and late enhancement imaging to detect myocardial fibrosis in order to predict cardiac function recovery in patients with peripartum cardiomyopathy. Among a consecutive series of 1,037 patients referred for heart failure treatment or prognostic evaluation between 1999 and 2006, eight women had confirmed PPCM. They all underwent echocardiography and cardiac MRI for assessment of left ventricular anatomy, systolic function and detection of myocardial fibrosis through late enhancement imaging. Mean (+/- SD) baseline left ventricular ejection fraction (LVEF) was 28 +/- 4%. After a follow-up of 50 +/- 9 months, half the patients recovered normal cardiac function (LVEF = 58 +/- 4%) and four did not (LVEF = 35 +/- 6%). None of the eight patients exhibited abnormal myocardial late enhancement. No difference in MRI characteristics was observed between the two groups. Patients with PPCM do not exhibit a specific cardiac MRI pattern and particularly no myocardial late enhancement. It suggests that myocardial fibrosis does not play a major role in the limitation of cardiac function recovery after PPCM. [ABSTRACT FROM AUTHOR]

Aim: To determine whether pancreatitis associated protein (PAP) is a marker for cystic fibrosis which could be used in neonatal screening for the disease.Methods: PAP was assayed on screening cards from 202,807 neonates. Babies with PAP > or = 15 ng/ml, or > or = 11.5 ng/ml and immunoreactive trypsinogen (IRT) > or = 700 ng/ml were recalled for clinical examination, sweat testing, and cystic fibrosis transmembrane regulator (CFTR) gene analysis.Results: Median PAP value was 2.8 ng/ml. Forty four cases of cystic fibrosis were recorded. Recalled neonates (n = 398) included only 11 carriers. A receiver operating characteristic curve analysis showed that PAP above 8.0 ng/ml would select 0.76% of babies, including all those with cystic fibrosis, except for one with meconium ileus and two with mild CFTR mutations. Screening 27,146 babies with both PAP and IRT showed that only 0.12% had PAP > 8.0 ng/ml and IRT > 700 ng/ml, including all cases of cystic fibrosis.Conclusion: PAP is increased in most neonates with cystic fibrosis and could be used for CF screening. Its combination with IRT looks promising. [ABSTRACT FROM AUTHOR]

The aetiological role of biliary lithiasis for chronic pancreatitis remains controversial. Previous studies based on pancreatographic studies reported changes in the pancreatic duct system caused by biliary lithiasis. This study analysed retrospectively the endoscopic retrograde cholangiopancreatography of 165 patients presenting with biliary lithiasis and of 53 controls. Among the 165 patients, 113 had choledochal stones (53 with gall bladder stones, 50 had had a cholecystectomy, 10 with a normal gall bladder), 35 had gall bladder stones without choledochal stones, 17 had cholecystectomy for gall bladder stones. Pancreatograms were analysed by measuring the diameter of the pancreatic duct in the head, the body, and the tail of the pancreas, and evaluating the regularity of the main pancreatic duct and the presence of stenosis, the regularity or the dilatation of secondary ducts, and the presence of cysts. In addition, we established a score, based on the above parameters, by which pancreatograms were classified as normal or with mild, intermediate, moderate or severe abnormalities. A multivariate analysis (stepwise multiple discriminant analysis) was performed for age, sex, presence of gall stones, presence of choledochal stones. Patients were comparable with controls for sex, alcohol consumption but were younger (55 v 68 years, p < 0.01). In patients and in controls, the frequency of pancreatographic abnormalities increased significantly with age. The pancreatographic features of patients and controls were not significantly different. In the multivariate analysis, age was the only factor with significant predicting value for pancreatographic abnormalities. In conclusion, biliary lithiasis in itself is not an aetiological factor for chronic pancreatitis, older age being responsible for the abnormalities seen by pancreatography of patients with biliary lithiasis. [ABSTRACT FROM PUBLISHER]

Pancreatic stones of patients with chronic calcifying pancreatitis (CCP) are mostly made up of CaCO3 crystals. Formation and growth of such crystals is inhibited in vitro by lithostathine, a protein present in normal pancreatic juice. Decreased lithostathine activity was therefore suspected in patients with CCP, but comparison by immunoassay of lithostathine concentrations in the pancreatic juices of patients and controls led to conflicting results. This study shows that these discrepancies might have been caused in part by a remarkably high susceptibility of the protein to trypsin like cleavage, resulting in important structural changes and concomitant modifications of the epitopes. A novel lithostathine assay in juice was developed, based on separation of secretory proteins by high performance liquid chromatography. The chromatographic separation of lithostathine was based on hydrophobic interactions at pH 5.0 using a Phenyl-TSK column. This study showed with this assay that lithostathine concentrations (microgram/mg of total protein) were similar in CCP patients with alcoholic aetiology (mean (SD) 6.3 (2.7)) and other aetiologies (7.2 (3.7)), but one third of those estimated in patients without pancreatic disease (16.7 (4.3)). Similar concentrations were found, however, in chronic alcoholic patients without CCP (6.6 (3.3)) and in patients with CCP. It was concluded that decreased lithostathine concentration is associated with CCP, although such a decrease is not sufficient by itself for the disease to occur. [ABSTRACT FROM PUBLISHER]

It has been shown recently that longterm but not short term heavy drinking of alcohol frequently results in increased serum activities of pancreatic enzymes suggesting subclinical pancreatic injury. Serum pancreatitis associated protein (PAP) is a novel protein, whose synthesis in the acinar cells and release into serum is specifically induced by acute pancreatic damage. This study was performed to further characterise the alcohol induced subclinical pancreatic injury by using serum PAP measurements. Three groups were studied: (1) control group (n = 25), (2) short term drinking group (n = 20), who consumed 2.0 g of ethanol per kg body weight during four hours, and (3) longterm drinking group (n = 32), who were admitted to withdrawal clinic after a median 30 months heavy drinking period. Serum PAP concentration was low in the control group (8 (5 to 12) micrograms/l, geometric mean (95% confidence intervals)). In the short term drinking group serum PAP was in the range of the control group values during 56 hours after drinking. Longterm drinking induced at least a 10-fold increase in serum PAP, the highest concentrations being seen on day 2 after drinking had ended (106 (61 to 184) micrograms/l). The patients did not develop abdominal symptoms, increased blood white cell count, or increased serum C reactive protein concentration. These results further support the suggestion that heavy longterm drinking often induces subclinical pancreatic damage, but not clinical pancreatitis. [ABSTRACT FROM PUBLISHER]

An abstract of the article "Is exercise echocardiography usefull in evaluation of pulmonary artery pressure in patients with systemic sclerosis?," by J. Dagorn is presented.

Chronic heart failure remains a frequent, severe and costly disease. Despite encouraging data from different countries, heart failure clinics are scarce in France. We have analyzed the impact of a heart failure clinic (UTIC of Pontoise) in terms of reduction of rehospitalizations and in hospitalization costs in 4855 consecutive patients. In our study, heart failure clinic management dramatically reduces HF related hospitalizations (RRR: -28 %, P=0.001) and HF related costs (55% reduction, P<0.001) regardless of comorbidities or disease severity. HF clinics have to be developed in France in order to optimize management of CHF and reduce the HF related costs., (Copyright © 2015 Elsevier Masson SAS. All rights reserved.)

Heart failure is a frequent and severe disease. The rate of avoidable hospitalizations due to lack of treatment adherence is estimated at 30% and, makes this disease a prime target for patient education. Implementation of such education initially began as a function of the local possibilities and willingness, which has led to great variety in the programs (only some of which meet the criteria set forth in the National Authority for Health guidelines) and the tools used. More recently, regional and even national programs, such as ICARE, sponsored by the two principal learned societies (The French Society and French Federation of Cardiology) have helped more than 200 private and public hospitals to set up field patient education programs based upon common concepts and tools.

Pancreatic adenocarcinoma, with an incidence/death ratio of 0.99, has the worst prognosis of all cancers. Risk factors associated with the sporadic form of pancreatic adenocarcinoma are unknown and less than 10% of patients receive curative treatment (surgery associated with radiation therapy or chemotherapy) with a low 5-year survival rate (10 to 20%). In more than 90% of patients, the tumor discovered at diagnosis is not resectable or has already metastasized. Thus, a better understanding of the etiology of pancreatic cancer is essential to identify new prognostic markers and new therapeutic targets. There is a wealth of data on the identification of genetic alterations associated with pancreatic cancer and their role in its development. This review will focus on the current knowledge of genetic alterations associated with two pancreatic lesions that can potentially evolve into pancreatic adenocarcinoma, Pancreatic Intraepithelial Neoplasia (PanIN) and Intraductal Papillary Mucinous Neoplasm (IPMN). These two lesions share a large panel of typical genetic alterations which are close to those found in pancreatic adenocarcinoma. A better understanding of these alterations may lead to therapeutic targets that could help prevent the progression of PanIN and IPMN to cancer.

Objective: Yersinia pseudotuberculosis causes ileitis and mesenteric lymphadenitis by mainly invading the Peyer's patches that are positioned in the terminal ileum. Whereas toll-like-receptor 2 (TLR2) controls mucosal inflammation by detecting certain microbiota-derived signals, its exact role in protecting Peyer's patches against bacterial invasion has not been defined., Design: Wild-type, Tlr2-, Nod2- and MyD88-deficient animals were challenged by Y pseudotuberculosis via the oral or systemic route. The role of microbiota in conditioning Peyer's patches against Yersinia through TLR2 was assessed by delivering, ad libitum, exogenous TLR2 agonists in drinking water to germ-free and streptomycin-treated animals. Bacterial eradication from Peyer's patches was measured by using a colony-forming unit assay. Expression of cryptdins and the c-type lectin Reg3 beta was quantified by quantitative reverse transcriptase polymerase chain reaction analysis., Results: Our data demonstrated that Tlr2-deficient mice failed to limit Yersinia dissemination from the Peyer's patches and succumbed to sepsis independently of nucleotide-binding and oligomerisation domain 2 (NOD2). Recognition of both microbiota-derived and myeloid differentiation factor 88 (MyD88)-mediated elicitors was found to be critically involved in gut protection against Yersinia-induced lethality, while TLR2 was dispensable to systemic Yersinia infection. Gene expression analyses revealed that optimal epithelial transcript level of the anti-infective Reg3 beta requires TLR2 activation. Consistently, Yersinia infection triggered TLR2-dependent Reg3 beta expression in Peyer's patches. Importantly, oral treatment with exogenous TLR2 agonists in germ-free animals was able to further enhance Yersinia-induced expression of Reg3 beta and to restore intestinal resistance to Yersinia. Lastly, genetic ablation of Reg3 beta resulted in impaired clearance of the bacterial load in Peyer's patches., Conclusions: TLR2/REG3 beta is thus an essential component in conditioning epithelial defence signalling pathways against bacterial invasion.

Background: Previous studies, with limited number of patients, have tried to determine the predictors of left ventricular ejection fraction (LVEF) improvement after beta-blockade. No study has demonstrated that LVEF improvement was an independent predictor of cardiac survival., Methods: The aims of the study were to determine in a large group of patients with stable chronic heart failure associated with reduced LVEF the predictors of LVEF improvement (difference in LVEF [deltaLVEF], ie, the value after beta-blockade minus the value before beta-blockade) after beta-blockade and to analyze prognostic impact of deltaLVEF. Three hundred fourteen consecutive patients underwent an echocardiogram, a radionuclide angiogram, and a maximum cardiopulmonary exercise test before and 3 months after maximal tolerated doses of beta-blockers have been reached., Results: After beta-blockade, LVEF improved from 30% +/- 11% to 40% +/- 13%. In the whole population, independent predictors of deltaLVEF were nonischemic etiology, baseline LVEF (negative correlation), and baseline heart rate (positive correlation). In ischemic patients, independent predictors of deltaLVEF were absence of history of myocardial infarction, baseline heart rate, and baseline LVEF; whereas in nonischemic patients, independent predictors were baseline LVEF and baseline QRS width (negative correlation). After 1082 days of follow-up, there were 53 cardiovascular deaths and 2 urgent transplantations. Left ventricular ejection fraction improvement (defined as an absolute increase in LVEF > 5%) was an independent predictor of cardiac survival. Patients who had an LVEF < or = 45% after beta-blockade with a deltaLVEF < or = 5% represented a high-risk subgroup., Conclusions: In patients with chronic heart failure, predictors of LVEF improvement after beta-blockade were different according to etiology. Left ventricular ejection fraction improvement was an independent predictor of cardiac survival.

Aims: To determine the potential adjunct of high-sensitivity (hs) C-reactive protein for risk stratification in patients with stable congestive heart failure (CHF)., Methods and Results: We studied 546 consecutive patients clinically stable with an ejection fraction <45% who were referred to our centre for evaluation of left ventricular dysfunction. hs C-reactive protein levels were determined on blood samples obtained on entry into the study. Clinical follow-up (median 972 days) was obtained for 545 patients. Cardiovascular mortality was significantly increased (P=0.001) in patients with hs C-reactive protein >3 mg/L. By multivariable analysis, including clinical, biological, and echocardiographic variables, hs C-reactive protein >3 mg/L was an independent predictor of cardiovascular mortality [HR=1.78 (1.17-2.72); P=0.008]; the strongest predictive parameter in this model was B-type natriuretic peptide (BNP) (P=0.005). When peak VO(2) was included into the model, hs C-reactive protein >3 mg/L remained an independent predictor of cardiovascular mortality [HR=1.55 (1.02-2.38); P=0.04]; the strongest predictive parameter in this model was peak VO(2) (P<0.0001). In patients with ischaemic CHF, cardiovascular mortality was significantly increased in patients with hs C-reactive protein >3 mg/L (P=0.001), whereas in patients with non-ischaemic CHF, hs C-reactive protein >3 mg/L was not associated with cardiovascular mortality (P=0.098). By multivariable analysis, hs C-reactive protein >3 mg/L was an independent predictor of cardiovascular mortality in ischaemic patients [HR=2.16 (1.23-3.78)] but not in non-ischaemic patients [HR=1.05 (0.52-2.11)]., Conclusion: Cardiovascular mortality is increased in CHF patients with hs C-reactive protein >3 mg/L. The impact of hs C-reactive protein is independent of usual prognostic parameters, in particular BNP and peak VO(2). The interest of hs C-reactive protein determination appears to be especially marked in patients with ischaemic cardiomyopathy.

Background: Recent experimental studies have suggested that the angiogenic cytokines hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) may play a role in the pathogenesis of congestive heart failure (CHF). The aim of the present study was to test the hypothesis that HGF and VEGF concentrations may vary according to the different markers of CHF severity and to analyze the impact of HGF and VEGF concentrations on the cardiovascular mortality of patients with CHF., Methods: We studied 529 consecutive patients who were referred to our center for an evaluation of left ventricular dysfunction. Hepatocyte growth factor and vascular endothelial growth factor levels were determined on blood samples obtained on entry into the study. Clinical follow-up (median 988 days) was obtained for 528 patients., Results: Hepatocyte growth factor concentrations were strongly associated with age, diabetes mellitus, and all markers of CHF severity; by contrast, baseline characteristics did not differ among VEGF tertiles. Cardiovascular survival rates at 1, 2, and 3 years were 91%, 87%, and 80%, respectively. The survival curves indicated a worse outcome for patients with high HGF concentrations at baseline (P < .0001); by contrast, cardiovascular survival was similar across the tertiles of VEGF (P = .37). Hepatocyte growth factor concentrations were higher in the 109 patients with a cardiovascular event (1001 [741-1327] pg/mL) than in the 419 patients without (773 [610-1045] pg/mL, P < .0001). By multivariate analysis, a baseline HGF concentration >802 pg/mL was associated with an increased cardiovascular mortality (hazard ratio = 1.85, 95% CI 1.09-3.13, P = .02); other variables retained into the final model were B-type natriuretic peptide (P < .0001), peak oxygen consumption (P = .0002), and ischemic etiology (P = .0005)., Conclusions: Hepatocyte growth factor levels correlate with CHF severity and are associated with an increased cardiovascular mortality during follow-up.

Objectives: The aim of this study was to compare the prognostic value of peak oxygen consumption (VO(2)) and B-type natriuretic peptide (BNP) in patients with stable congestive heart failure (CHF)., Background: Previous studies have demonstrated that both peak VO(2) and BNP are useful for risk stratification in patients with CHF. No study has compared the respective prognostic value of these two parameters in a large series of patients receiving a combination of angiotensin-converting enzyme inhibitors and of beta-blockers., Methods: Patients with stable CHF underwent radionuclide angiography, echocardiography, 24-h Holter monitoring, and a cardiopulmonary exercise test. Blood samples were drawn for standard measurements and for hormonal determinations., Results: After a median follow-up period of 787 days, there were 75 cardiac-related deaths and three urgent transplantations. Independent predictors of cardiac survival were percent of maximal predicted VO(2) (%VO(2), relative risk [RR] = 2.84 [95% confidence interval, CI = 1.73 to 4.65], p < 0.00001), BNP (RR = 3.17 [95% CI 1.68 to 5.96], p = 0.0004), left atrial diameter (LAD) (RR = 2.04 [95% CI 1.25 to 3.34], p = 0.004), age (RR = 1.93 [95% CI 1.22 to 3.05], p = 0.005), and aldosterone (RR = 1.84 [95% CI 1.12 to 3.00], p = 0.015). In patients with infra-median levels of BNP (<109 pg/ml), age was the only independent predictor of cardiac survival. However, in patients with supra-median levels of BNP, independent predictors of cardiac survival were %VO(2) (RR = 3.76 [95% CI 2.19 to 6.45], p < 0.00001) and LAD (RR = 1.90 [95% CI 1.10 to 3.28], p = 0.02)., Conclusions: B-type natriuretic peptide, in combination with %VO(2), improves risk stratification of patients with stable CHF.