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Aims Major bleeding events in heart failure (HF) patients are poorly described. We sought to investigate the importance of major bleeding and its impact on outcomes in HF patients. Methods and results We analysed incident bleeding and ischaemic events during a 3 year follow‐up in 2910 HF outpatients included in a prospective multicentre registry. Major bleeding was defined as a Type ≥3 bleed using the Bleeding Academic Research Consortium definition. Ischaemic event was a composite of ischaemic stroke and myocardial infarction. Events were adjudicated by a blinded committee. At inclusion, most patients (89%) received at least one antithrombotic: anticoagulation (53.9%) and/or antiplatelet therapy (46.2%). Bleeding occurred in 111 patients {3 year cumulative incidence: 3.6% [95% confidence interval (CI) 3.0–4.3]} and ischaemic events in 102 patients [3 year cumulative incidence: 3.3% (95% CI 2.7–4.0)]. Most bleedings were Bleeding Academic Research Consortium 3a (32.5%) or 3b (31.5%). Most frequent sites of bleeding were gastrointestinal (40.6%) and intracranial (27.9%). Variables associated with bleeding were atrial fibrillation [hazard ratio (HR) = 2.63 (95% CI 1.66–4.19), P

A 72-year-old woman with history of breast cancer only treated surgically was referred to our department for pulmonary hypertension (PH) suspicion. Echocardiogram revealed elevated right ventricular systolic pressure. Computed tomography (CT) angiogram showed no pulmonary embolism (PE), but lung scan revealed two ventilation-perfusion mismatch areas. Right cardiac catheterization established precapillary PH. Despite treatment with PH specific therapy (sildenafil, ambrisentan, and epoprostenol), her condition worsened rapidly with acute right heart failure (RHF). She died 22 days after admission. Post-mortem microscopic examination showed a rare combination of PH etiologies consistent with metastasis of breast cancer in pulmonary vasculature including the rare pulmonary tumour thrombotic microangiopathy (PTTM).

Aims The clinical outcomes for patients with worsening chronic heart failure (WCHF) remain exceedingly poor despite contemporary evidence-based therapies, and effective therapies are urgently needed. Accumulating evidence supports augmentation of cyclic guanosine monophosphate (cGMP) signalling as a potential therapeutic strategy for HF with reduced or preserved ejection fraction (HFrEF and HFpEF, respectively). Direct soluble guanylate cyclase (sGC) stimulators target reduced cGMP generation due to insufficient sGC stimulation and represent a promising method for cGMP enhancement. Methods The phase II SOluble guanylate Cyclase stimulatoR in heArT failurE Study (SOCRATES) programme consists of two randomized, parallel-group, placebo-controlled, double-blind, multicentre studies, SOCRATES-REDUCED (in patients with LVEF

International audience; AIMS: To improve knowledge of epidemiological data, management, and clinical outcome of acute heart failure (AHF) in a real-life setting in France. METHODS AND RESULTS: We conducted an observational survey constituting a single-day snapshot of all unplanned hospitalizations because of AHF in 170 hospitals throughout France (the OFICA survey). A total of 1658 patients (median age 79 years, 55% male) were included. Family doctors were the first medical contact in 43% of cases, and patients were admitted through emergency departments in 64% of cases. Clinical scenarios were mainly acutely decompensated HF (48%) and acute pulmonary oedema (38%) with similar clinical and biological characteristics as well as outcome. Characteristics were different and severity higher in both shock and right HF. Infection and arrhythmia were the most frequent precipitating factors (27% and 24% of cases); diabetes and chronic pulmonary disease were the most frequent co-morbidities (31% and 21%). Over 80% of patients underwent both natriuretic peptide testing and echocardiography. LVEF was preserved (>50%) in 36% of patients and associated with specific characteristics and lower severity. Median hospital stay was 13 days; in-hospital mortality was 8.2%, and independent predictors were age, blood pressure, and creatinine. Treatment at discharge in patients with reduced LVEF included ACE inhibitors/ARBs, beta-blockers, and aldosterone inhibitors in 78, 67, and 27% cases. Non-surgical devices were reported in

Aim Peripartum cardiomyopathy (PPCM) is a rare cause of dilated cardiomyopathy responsible for heart failure toward the end of pregnancy, which can lead to chronic heart failure in 50% of cases. In this short report, we assessed the benefit of cardiac resynchronization in patients with PPCM and chronic systolic dysfunction despite optimal medical treatment. Methods and results For the last 10 years, we managed eight patients diagnosed with PPCM. Two of them presented severe systolic dysfunction, and medical treatment resulted in limited improvement from 10% to 25% and from 25% to 28% despite optimal treatment for 9 and 6 years, respectively. These two patients were porposed to receive an implantatable cardioverter defibrillator (ICD) and cardiac resynchronization therapy (CRT). Six months after ICD-CRT treatment, we observed a significant improvement in systolic function from 25% to 45% and 28% to 50%, respectively, and positive remodelling with reduction of left ventricular end-diastolic volume from 216 to 144 mL and from 354 to 105 mL, which represent a 34% and a 70% reduction, respectively. Conclusions Physicians in charge of patients with PPCM should offer the opportunity of CRT for patients whose cardiac function has not significantly improved under standard medical treatment.

Objective An algorithm for the detection of pulmonary arterial hypertension (PAH), based on the presence of dyspnea and the findings of Doppler echocardiographic evaluation of the velocity of tricuspid regurgitation (VTR) and right-sided heart catheterization (RHC), which was applied in a large multicenter systemic sclerosis (SSc) population, estimated the prevalence of PAH to be 7.85%. The aim of this observational study was to investigate the incidence of PAH and pulmonary hypertension (PH) during a 3-year followup of patients from the same cohort (the ItinerAIR-Sclerodermie Study). Methods Patients with SSc and without evidence of PAH underwent evaluation for dyspnea and VTR at study entry and during subsequent visits. Patients in whom PAH was suspected because of a VTR of 2.8–3.0 meters/second and unexplained dyspnea or a VTR of >3.0 meters/second underwent RHC to confirm the diagnosis. Results A total of 384 patients were followed up for a mean ± SD of 41.03 ± 5.66 months (median 40.92 months). At baseline, 86.7% of the patients were women, and the mean ± SD age of the patients was 53.1 ± 12.0 years. The mean ± SD duration of SSc at study entry was 8.7 ± 7.6 years. After RHC, PAH was diagnosed in 8 patients, postcapillary PH in 8 patients, and PH associated with severe pulmonary fibrosis in 2 patients. The incidence of PAH was estimated to be 0.61 cases per 100 patient-years. Two patients who exhibited a mean pulmonary artery pressure of 20–25 mm Hg at baseline subsequently developed PAH. Conclusion The estimated incidence of PAH among patients with SSc was 0.61 cases per 100 patient-years. The high incidence of postcapillary PH highlights the value of RHC in investigating suspected PAH.

Aims Recent studies have shown that prescription rates and doses of recommended drugs for chronic heart failure (CHF) are not optimal in daily practice. The aim of the Impact-Reco programme was to analyse prescription rates of CHF drugs in stable outpatients with CHF related to left ventricular (LV) systolic dysfunction in two similar surveys in France. Methods and results The two surveys, which included 1917 and 1974 patients, were performed between September 2004 to March 2005 and September 2005 to May 2006, respectively. Prescription rates of angiotensin-converting enzyme-inhibitors (ACE-I) remained stable (71 vs. 68%, respectively), whereas the proportion of patients receiving angiotensin receptor blockers (21 vs. 30%, P < 0.0001) and beta-blockers (65 vs. 70% P < 0.0001) increased significantly. Doses of ACE-I and beta-blockers increased significantly between the two surveys. However, the improvement was of lesser magnitude in some subgroups of patients, such as elderly patients or patients with renal failure. Conclusion The Impact-Reco programme found an improvement in prescription rates and in the dosage of neurohumoral antagonists in French outpatients with stable CHF. However, there is still room for improvement, especially regarding the doses of medications and the treatment of some subgroups of patients such as the elderly and patients with renal failure.

Background: Patients with chronic heart failure (CHF) due to left ventricular systolic dysfunction (LVSD) may develop pulmonary hypertension at rest and during exercise. The cardiac correlates of pulmonary hypertension have been ascertained in the resting state, but seldom during exercise in these patients. Aims: We sought to determine the cardiac correlates of exercise induced pulmonary hypertension in patients with LVSD by monitoring the estimated pulmonary artery systolic pressure (PASP) by continuous Doppler echocardiography during semirecumbent bicycle exercise. Methods: Eighty-five patients (mean age 57 ± 13 years, 75% male) with CHF due to LVSD (LV ejection fraction [EF]

Cognitive impairment has seldom been investigated in patients with chronic heart failure (CHF). The authors' aim was to assess the prevalence and determinants of cognitive impairment in patients hospitalized for CHF decompensation. The authors prospectively performed the Folstein Mini-Mental State Examination (MMSE) and completed a standardized questionnaire for cerebrovascular accidents (CVA) and transient ischemic attacks (TIA) in patients hospitalized for CHF decompensation during a 3-month period. A total of 83 patients were studied: 15 had a history of CVA or TIA, 51 (61%) had an MMSE scoreor = 28 (oror = 26 if schoolingor = 8 years), and 26 (31%) had an MMSE score24. Factors associated with an MMSE score24 were atrial fibrillation/flutter (odds ratio [OR], 8.1; 95% confidence interval [CI], 1.9-34.6), New York Heart Association functional class IV (OR, 4.1; CI, 1.0-16.4), and schooling8 years (OR, 0.2; CI, 0.0-0.8). Adjusting for history of CVA or TIA or excluding patients with a history of CVA or TIA did not affect the findings. Cognitive impairment is frequent in patients hospitalized for CHF decompensation whether or not they have a past history of CVA or TIA. The severity of cognitive impairment parallels that of CHF. The question of whether this cognitive impairment decreases adherence to treatment and contributes to a worse outcome in CHF patients should be explored.

Objective Screening allows for early management of pulmonary arterial hypertension (PAH), a severe complication of systemic sclerosis (SSc). Since no consensus has been reached on the method and criteria for optimal screening, we sought to develop an algorithm based on symptoms, Doppler echocardiography, and right heart catheterization (RHC) for application to a nationwide multicenter SSc population in France. Methods This prospective study was conducted from September 2002 to July 2003 by experts at 21 SSc centers. At each center, SSc patients without severe pulmonary function abnormalities underwent Doppler echocardiography by an experienced cardiologist. Patients with a peak velocity of tricuspid regurgitation (VTR) of >3 meters/second or 2.5–3 meters/second with unexplained dyspnea were asked to undergo RHC to confirm PAH according to international guidelines. Results Of the 599 patients analyzed, 29 had known PAH and 33 had suspected PAH, based on Doppler echocardiography, and underwent RHC. Of these 33, 18 were found to have PAH, 3 had left ventricular dysfunction, and 12 had no PAH. Newly diagnosed cases of PAH were of mild severity (mean ± SD pulmonary artery pressure [mPAP] 30 ± 9 mm Hg, mean ± SD total pulmonary resistance [TPR] 524 ± 382 dynes × second/cm5). Hemodynamic findings in patients with known PAH were mPAP 49 ± 17 mm Hg and TPR 1,007 ± 615 dynes × second/cm5. The estimate of PAH prevalence was 7.85% (95% confidence interval 5.70–10.00). Conclusion This screening algorithm, based on dyspnea, Doppler echocardiographic evaluation of VTR, and RHC, enabled early detection of PAH at a mild stage. Whether mild PAH will evolve to severe PAH in reported cases and whether this early diagnosis translates into improved prognosis for patients with mild PAH will be evaluated in the ongoing 3-year followup of this cohort.

Beta-adrenergic receptor blockade is an established treatment of chronic heart failure (HF). Previous studies have suggested a potential pharmacogenetic interaction between beta-blocker therapy and the angiotensin-converting enzyme (ACE) I/D polymorphism in patients with HF.We designed this study to analyze changes in myocardial function of HF patients in response to beta-blocker therapy as a function of the ACE I/D polymorphism.We studied 199 consecutive patients with chronic HF not treated with beta-blockers. Before initiation of beta-blockers and 3 months after the maximal tolerated dose was reached, patients underwent echocardiography, radionuclide angiography, and a cardiopulmonary exercise test. We extracted genomic DNA from white blood cells and determined the ACE I/D polymorphism. Thirty-five (18%) patients had the II genotype, 86 (43%) the ID genotype and 78 (39%) the DD genotype. A significant and similar improvement in left ventricular ejection fraction (LVEF) was observed in II (from 0.30+/-0.10 to 0.41+/-0.13; P0.0001), ID (from 0.29+/-0.11 to 0.39+/-0.13; P0.0001) and DD patients (from 0.31+/-0.11 to 0.40+/-0.13; P0.0001). Peak Vo(2) before and after beta-blockade was similar among the three groups. The proportion of responders to beta-blockers (patients without cardiac events during titration who had an increase in LVEF5% after beta-blockers) was similar among the three groups (II: 65.9%%, ID: 60.6%%, DD: 65.9%; P=NS). During a median follow-up of 933 days, there was no evidence for any effect of ACE I/D polymorphism on cardiac survival.We observed no evidence of pharmacogenetic interaction between the ACE I/D polymorphism and the effects of beta-blockade on LVEF and other prognostic parameters in patients with chronic HF. Our results support the initiation of beta-blockers in HF patients with the II or the ID genotype as well as in those with the DD genotype.

We read with great interest the case report of Habedank et al.1 We would like to bring to your attention the fact that the authors overstate the efficacy of bromocriptine in their case report, and prematurely conclude with the indication of bromocriptine in the situation of peripartum cardiomyopathy. The authors report the case of a young patient presenting with acute heart failure within days following delivery of healthy twins. The clinical description along with the left ventricular dysfunction assessed through both echocardiography and cardiac MRI are clearly in favour of peripartum cardiomyopathy. Following the improvement in left ventricular ejection fraction assessed by MRI, from 15% after delivery to 60% two months later, the authors claim the efficacy of bromocriptine, prescribed for 6 weeks after delivery. However, bromocriptine was prescribed with the usual combination of a beta-blocker and ACE inhibitor. Even though low ejection fraction and left ventricular dilation at the acute phase of heart failure are pejorative for short-term left ventricular function recovery, it has been clearly demonstrated that such improvement can occur in some patients. We and others have reported cases of patients with initially very low ejection fraction and ventricular dilatation, who recovered normal cardiac function under beta-blocker and ACE inhibitor combination.2,3 The reasons underlying this left ventricular alteration after the acute phase remain unexplained. The hypothesis of potential treatment of patients with bromocriptine has recently been proposed by Hilfiker-Kleiner et al.,4 and is currently under clinical evaluation. Until the results of randomized trials are reported, this option should not be used routinely, and cautionary issues have already been raised.5 Even though we obviously cannot say that bromocriptine did not improve cardiac function in the case reported by Hadebank et al., the contrary is also true: unless the authors can show that the improvement was not related to usual beta-blocker and ACE-inhibitor treatment, their conclusion should be more balanced.