Practical guide on left atrial appendage closure for the non-implanting physician: an international consensus paper.

A significant proportion of patients who suffer from atrial fibrillation (AF) and are in need of thromboembolic protection are not treated with oral anticoagulation or discontinue this treatment shortly after its initiation. This undertreatment has not improved sufficiently despite the availability of direct oral anticoagulants which are associated with less major bleeding than vitamin K antagonists. Multiple reasons account for this, including bleeding events or ischaemic strokes whilst on anticoagulation, a serious risk of bleeding events, poor treatment compliance despite best educational attempts, or aversion to drug therapy. An alternative interventional therapy, which is not associated with long-term bleeding and is as effective as vitamin K anticoagulation, was introduced over 20 years ago. Because of significant improvements in procedural safety over the years, left atrial appendage closure, predominantly achieved using a catheter-based, device implantation approach, is increasingly favoured for the prevention of thromboembolic events in patients who cannot achieve effective anticoagulation. This management strategy is well known to the interventional cardiologist/electrophysiologist but is not more widely appreciated within cardiology or internal medicine. This article introduces the devices and briefly explains the implantation technique. The indications and device follow-up are more comprehensively described. Almost all physicians who care for adult patients will have many with AF. This practical guide, written within guideline/guidance boundaries, is aimed at those non-implanting physicians who may need to refer patients for consideration of this new therapy, which is becoming increasingly popular

Cause of Death and Predictors of All-Cause Mortality in Anticoagulated Patients With Nonvalvular Atrial Fibrillation : Data From ROCKET AF

M. Kaste on työryhmän ROCKET AF Steering Comm jäsen.Background-Atrial fibrillation is associated with higher mortality. Identification of causes of death and contemporary risk factors for all-cause mortality may guide interventions. Methods and Results-In the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF) study, patients with nonvalvular atrial fibrillation were randomized to rivaroxaban or dose-adjusted warfarin. Cox proportional hazards regression with backward elimination identified factors at randomization that were independently associated with all-cause mortality in the 14 171 participants in the intention-to-treat population. The median age was 73 years, and the mean CHADS(2) score was 3.5. Over 1.9 years of median follow-up, 1214 (8.6%) patients died. Kaplan-Meier mortality rates were 4.2% at 1 year and 8.9% at 2 years. The majority of classified deaths (1081) were cardiovascular (72%), whereas only 6% were nonhemorrhagic stroke or systemic embolism. No significant difference in all-cause mortality was observed between the rivaroxaban and warfarin arms (P=0.15). Heart failure (hazard ratio 1.51, 95% CI 1.33-1.70, P= 75 years (hazard ratio 1.69, 95% CI 1.51-1.90, P Conclusions-In a large population of patients anticoagulated for nonvalvular atrial fibrillation, approximate to 7 in 10 deaths were cardiovascular, whereasPeer reviewe

Crit. Care

Aim: Postoperative effusions and edema and capillary leak syndrome in children after cardiac surgery with cardiopulmonary bypass constitute considerable clinical problems. Overshooting immune response is held to be the cause. In a prospective study we investigated whether preoperative immune status differences exist in patients at risk for postsurgical effusions and edema, and to what extent these differences permit prediction of the postoperative outcome. Methods: One-day preoperative serum levels of immunoglobulins, complement, cytokines and chemokines, soluble adhesion molecules and receptors as well as clinical chemistry parameters such as differential counts, creatinine, blood coagulation status (altogether 56 parameters) were analyzed in peripheral blood samples of 75 children (aged 3-18 years) undergoing cardiopulmonary bypass surgery (29 with postoperative effusions and edema within the first postoperative week). Results: Preoperative elevation of the serum level of C3 and C5 complement components, tumor necrosis factor-alpha, percentage of leukocytes that are neutrophils, body weight and decreased percentage of lymphocytes (all P 86% of the patients with postoperative effusions and oedema were correctly predicted using two different classification algorithms. Data mining by both methods selected nine partially overlapping parameters. The prediction quality was independent of the congenital heart defect. Conclusion: Indicators of inflammation were selected as risk indicators by explorative data analysis. This suggests that preoperative differences in the immune system and capillary permeability status exist in patients at risk for postoperative effusions. These differences are suitable for preoperative risk assessment and may be used for the benefit of the patient and to improve cost effectiveness

Cardiac troponin I release after transcatheter atrial septal defect closure depends on occluder size but not on patient’s age

Objective: To examine whether transcatheter closure of secundum atrial septal defect (ASD) with the Amplatzer septal occluder leads to more myocardial injury in children than in adults. Design: In a prospective study with children and adults cardiac troponin I (cTnI) serum concentrations were determined by immunoassay (AxSYM, Abbott Laboratories) before, during, and up to 20 months after surgical or transcatheter ASD closure. Patients: Four groups of patients were studied: transcatheter ASD closure (group 1: 22 children, age range 3.26–14.7 years; group 2: 22 adults, 18.0–67.3 years), surgical ASD closure (group 3: 18 children, 3.12–13.5 years), and diagnostic catheterisation (group 4: 12 children, 2.68–15.0 years). Results: cTnI concentrations were significantly increased after occluder implantation with higher serum concentrations in children than in adults (immediately after implantation: group 1, 3.2 (4.4) μg/l; group 2, 1.1 (4.2) μg/l; four hours after implantation: group 1, 4.8 (5.0) μg/l; group 2, 1.7 (2.3) μg/l; both p < 0.01, group 1 v group 2; one day after implantation: group 1, 3.0 (5.7) μg/l; group 2, 2.2 (5.2) μg/l) but were less than 20% of those after surgical ASD closure (group 3; p < 0.001) where the highest cTnI concentration was found (37.1 (26.3) μg/l). Diagnostic catheterisation (group 4) was not associated with detectable cTnI increase. From the cTnI concentrations the total amount of cTnI released after ASD closure was estimated for each patient. This was dependent on the size of the occluder (p < 0.05) but not on the patient’s age or procedural duration. Conclusion: In regard to interventional ASD closure our data do not provide evidence that the child’s myocardium is more vulnerable. Transcatheter ASD closure induces minor myocardial lesion, the extent of which depends on the size of the Amplatzer septal occluder but is irrespective of the patient’s age

Platelet glycoprotein GP VI 13254C allele is an independent risk factor of premature myocardial infarction

Aim The purpose of this study was to asses the impact of haemostatic and platelet receptor gene polymorphisms as an inherited risk factor for premature onset of myocardial infarction (MI).&lt;p&gt;&lt;/p&gt; Methods Polymorphisms of platelet receptors - GP Ia (807C&#62;T, rs1126643), GP VI (13254T&#62;C, rs1613662), GP IIIa (HPA-1, rs5918), PAR -1 (IVS -14A&#62;T; rs168753), P2Y12 (34C&#62;T, rs6785930 and H1/H2 haplotype, rs2046934), and genetic variations of the gene coding for cyclooxygenase-1 (COX-1) ( -842A&#62;G, rs10306114 and 50C&#62;T, rs3842787) were investigated. Mutations in the genes coding for coagulation factor V (Q506R (Leiden) mutation, rs6025) and factor II (prothrombin G20210A, rs1799963) were also determined. The prevalence of gene polymorphisms was investigated in 105 consecutive patients with premature MI. This was compared with the same gene polymorphism prevalence in a group of 132 patients in which coronary artery disease had been excluded. Genotyping was done using PCR, followed by melting curve analysis with specific fluorescent hybridization probes.&lt;p&gt;&lt;/p&gt; Results A significant association between GP VI 13254C allele carriers and premature MI was found (p = 0.025). No other differences in prevalence of the investigated polymorphisms between the compared patient populations reached statistical significance. In a logistic regression, which took other cardiovascular risk factors into account, the significance of the GP VI 13254C allele and vascular risk was suggested (OR 1.888, 95% C.I. 1.029 to 3.464, p = 0.040). In a binary logistic regression the positive relationship between the GP VI genotype and female gender was observed (0R 3.676; 95% C.I. 1.159 to 11.628; p = 0.027). The frequencies of GP VI and GP Ia gene polymorphisms were independent of one another (p = 0.836).&lt;p&gt;&lt;/p&gt; Conclusion The presence of the GP VI 13254C allele is an independent predictor of premature MI