Percutaneous closure is the gold standard treatment for atrial septal defects, but the procedure can be complex in case of femoral thrombosis. Although unusual for congenital interventionists, transhepatic atrial septal defect closure is an attractive alternative to the internal jugular vein, especially when approaching the interatrial septum. Herein, we report the case of an adult patient with significant co-morbidities who had successful transhepatic atrial septal defect closure after a failed transjugular attempt. We describe the use of an absorbable haemostatic gelatin sponge to efficiently and safely achieve haemostasis after the use of a large vascular sheath with combined anticoagulation and antiplatelet therapy.

In many tropical areas schistosomiasis is a major health problem causing hepatosplenic, intestinal or urogenital complaints. Hepatosplenic schistosomiasis mansoni is also characterized by blood coagulation abnormalities. Liver pathology plays a role in the development of haemostatic changes and the parasitic infection may directly affect coagulation. However, these contributing factors cannot be studied separately in hepatosplenic schistosomiasis infections. This pilot study provides insight in haemostatic changes in urinary schistosomiasis by studying coagulation parameters in schistosomiasis haematobium-infected Gabonese schoolchildren. Selection on urinary schistosomiasis patients without hepatosplenic complaints allows for the investigation of the direct effects of the parasite on haemostasis. Levels of von Willebrand Factor (VWF) antigen, active VWF and osteoprotegerin were elevated, indicating inflammation-mediated endothelial activation. In contrast to hepatosplenic schistosomiasis, thrombin–antithrombin complex and D-dimer levels were not affected. Despite its small sample size, this study clearly indicates that Schistosoma haematobium directly alters the activation status of the endothelium, without initiation of coagulation.

n-3 Fatty acids (EPA and DHA, from fish oil) are essential fatty acids that are approved for the treatment of severe hypertriacylglycerolaemia and, in some countries, used for reducing the risk of CVD. Because of their inhibitory effects on platelet function, some practitioners have, perhaps unnecessarily, discontinued their use in patients undergoing invasive procedures or being treated with anti-platelet or anticoagulation drugs. Thus, the aim of the present study was to review the effects of n-3 fatty acids on bleeding complications in a wide variety of clinical settings, and to summarise their biochemical mechanism of action in platelet function and coagulation. We surveyed recent publications that either directly studied the effects of n-3 fatty acids on the risk of bleeding or focused on different end-points and also reported the effects on bleeding. n-3 Fatty acid treatment had no effect on the risk of clinically significant bleeding in either monotherapy or combination therapy settings. Although originally believed to operate primarily via the cyclo-oxygenase system, these fatty acids have been shown to affect multiple signalling pathways and thrombotic processes beyond simply affecting platelet aggregation. The present overview found no support for discontinuing the use of n-3 fatty acid treatment before invasive procedures or when given in combination with other agents that affect bleeding. On the contrary, the use of these fatty acids in several settings improved clinical outcomes.

We aimed to identify food intake patterns that operate via haemostatic and inflammatory pathways on progression of atherosclerosis among 802 middle-aged adults with baseline and 5-year follow-up ultrasound measurements of common (CCA) and internal carotid artery (ICA) intimal medial thickness (IMT). Food intake was ascertained with an FFQ. We derived food patterns using reduced rank regression (RRR) with plasminogen activator inhibitor 1 and fibrinogen as response variables. We explored the impact of various food pattern simplification approaches. We identified a food pattern characterised by higher intakes of less healthful foods (low-fibre bread and cereal, red and processed meat, cottage cheese, tomato foods, regular soft drinks and sweetened beverages) and lower intakes of more healthful foods (wine, rice and pasta, meal replacements and poultry). The pattern was positively associated with mean CCA IMT at follow-up (P = 0·0032), a 1 sd increase corresponding to an increase of 13 μm higher CCA IMT at follow-up, adjusted for demographic and cardiovascular risk factors. With increasing pattern quartile (Q), the percentage change in CCA IMT increased significantly: Q1 0·8 %; Q2 3·2 %; Q3 8·6 %; Q4 7·9 % (P = 0·0045). No clear association with ICA IMT was observed. All simplification methods yielded similar results. The present results support the contention that a pro-inflammatory and pro-thrombotic dietary pattern increases the rate of coronary artery atherosclerosis progression, independent of traditional cardiovascular risk factors. RRR is a promising and robust tool for moving beyond the previous focus on nutrients or foods into research on the health effects of broader dietary patterns.

Frequent consumption of nuts lowers the risk of CHD. While lowering blood lipids is one of the mechanisms for cardioprotection, the present study sought to determine whether monounsaturated fat-rich almonds also influence other CHD risk factors such as inflammation and haemostasis. This was a randomised, controlled, crossover feeding study with twenty-five healthy adults (eleven men; fourteen women), age 22–53 years. Following a 2 week run-in phase (34 % energy from fat), subjects were assigned in random order to three diets for 4 weeks each: a heart-healthy control diet with no nuts ( < 30 % energy from fat), low-almond diet and high-almond diet (10 % or 20 % isoenergetic replacement of control diet with almonds, respectively). Serum E-selectin was significantly lower on the high-almond diet compared with the control diet. E-selectin decreased as the percentage of energy from almonds increased (P < 0·0001). C-reactive protein (CRP) was lower in both the almond diets compared with the control diet. A clear dose response was not observed for either E-selectin or CRP. There was no effect of diet on IL-6 or fibrinogen. Tissue plasminogen activator antigen was significantly lower on the control and high-almond diets compared with the low-almond diet, although the values were within normal range. In conclusion, consumption of almonds influenced a few but not all of the markers of inflammation and haemostasis. A clear dose response was not observed for any of the markers studied.

Ticks are blood-feeding arthropods widely distributed in the world and vectors of several diseases. As haematophagy demands evasion strategies and repeatedly infested hosts develop protective immune responses, we investigated the mechanisms of the Rhipicephalus (Boophilus) microplus saliva anti-haemostatic activity and the possible relationship between the acquired natural anti-tick host resistance and anti-haemostatic action. For this purpose, we studied the effects of R. microplus saliva on different pathways of haemostasis and tested whether repeated infested bovine sera (RIBS) are able to abolish salivary anti-haemostatic activities. R. microplus saliva (i) displays inhibitory activity upon collagen-induced platelet aggregation; (ii) inhibits the induction of endothelial pro-coagulant state; and (iii) reduces thrombogenesis in vivo. RIBS were shown to be able to partially block the delay of coagulation and the anti-thrombotic effect of saliva, and to totally abolish the modulation of endothelium activation. Conversely, RIBS has no effect on the inhibition of platelet aggregation. These results show, for the first time, the neutralization ability of sera from acquired resistance hosts against tick anti-haemostatics. Moreover, this is the first report of a haematophagous parasite able to modulate endothelial cell pro-coagulant state, and addresses the presence of anti-platelet and anti-thrombotic activity in R. microplus saliva.

The present paper provides a comprehensive review of the literature pertaining to the impact of alcohol intake on cardiovascular disease. Both cross-sectional and prospective studies have disclosed a negative association between moderate intake of alcoholic beverages and cardiovascular disease. The relationship appears to be present for both wine, beer and spirits. Effects of alcohol itself and also the role of different cardio-protective substances in alcoholic beverages are discussed. Alcohol has been suggested to beneficially affect the blood lipid profile, as it increases plasma HDL-cholesterol level. Furthermore, it may inhibit thrombogenesis by reducing thromboxan formation and decreasing the plasma level of fibrinogen. However, high blood concentrations of alcohol may impair fibrinolysis by increasing plasma plasminogen activator inhibitor-1 level. This action could contribute to explaining the ‘U’-shaped association between alcohol intake and cardiac events. Alcohol seems to promote abdominal fat distribution, but the importance of this effect in non-obese individuals is uncertain. Wine in particular, but also beer, contains polyphenols which act as antioxidants. Their action could maintain the integrity of the endothelial function by reducing the formation of superoxide. Moreover, these antioxidants may protect against LDL oxidation and modulate the macrophage attack on the endothelium. Although the cardio-protective effect of alcohol can hardly be addressed in healthy individuals by intervention studies with hard end points, there are many observational and experimental findings indicating that moderate alcohol drinking possesses properties preventive of cardiovascular disease.

Homocysteine, derived from the demethylation of the ammo acid methionine, is either further catabolised by trans-sulfuration to cysteine or remethylated to methionine. Remethylation to methionine requires the cofactors, folate and vitamin B12. Folate is an effective homocysteine-lowering agent and, thus, homocysteine and folate status are inversely related. Hyperhomocysteinaemia is a strong independent risk factor for venous thromboembolism (VTE) and is associated with adverse pregnancy outcomes such as pre-eclampsia, placental abruption, early pregnancy loss and neural-tube defects. Pregnancy is a risk factor for VTE as a result of prothrombotic changes in levels of haemostatic factors. However, despite this hypercoagulable state, the incidence of pregnancy-associated VTE is relatively low. Hyperhomocysteinaemia is associated with abnormalities in markers of coagulation activation, and recent research suggests that folic acid supplementation, as well as lowering homocysteine, lowers markers of coagulation activation and increases levels of coagulation inhibitors. Tissue factor (TF) is the initiator of blood coagulation in vivo, and homocysteine induces TF expression in vitro. During pregnancy, monocyte TF expression is lower than that in the non-pregnant state, and this lowering of TF may act to counterbalance increases in coagulation activation. Furthermore, despite a high folate requirement, several studies have reported that homocysteine is lower in normal pregnancy than in the non-pregnant state. Although the exact mechanism of homocysteine lowering during pregnancy is unclear, one possible outcome of lower homocysteine may be the protection of women from pregnancy complications and VTE, and thus lower homocysteine may contribute to maintaining homeostasis in haemostasis.

Diets high in monounsaturated fatty acids (MUFA) are increasingly being recommended as a highly-effective cholesterol-lowering strategy in populations at risk of CHD. However, the need for a re-appraisal of the benefits of diets rich in MUFA became apparent as a result of recent studies showing that meals high in olive oil cause greater postprandial activation of blood coagulation factor VII than meals rich in saturated fatty acids. The present review evaluates the evidence for the effects of MUFA-rich diets on fasting and postprandial measurements of haemostasis, and describes data from a recently-completed long-term controlled dietary intervention study. The data show that a background diet high in MUFA has no adverse effect on fasting haemostatic variables and decreases the postprandial activation of factor VII in response to a standard fat-containing meal. Since the same study also showed a significant reduction in the ex vivo activation of platelets in subjects on the high-MUFA diet, the overall findings suggest that there is no reason for concern regarding adverse haemostatic consequences of high-MUFA diets.

Interest in the Mediterranean diet (MD) has grown worldwide. Despite the high complexity of its nutrients composition, olive oil emerges as its principal food, since it provides the higher percentage of energy and a lot of bioactive compounds.

The intake of long-chain n-3 PUFA, including DHA (22:6n-3), is associated with a reduced risk of CVD. Schizochytrium sp. are an important primary source of DHA in the marine food chain but they also provide substantial quantities of the n-6 PUFA docosapentaenoic acid n-6; DPA). The effect of this oil on cardiovascular risk factors was evaluated using a double-blind randomised placebo-controlled parallel-design trial in thirty-nine men and forty women. Subjects received 4g oil/d for 4 weeks; the active treatment provided 1·5g DHA and 0·6g DPA. Active treatment increased plasma concentrations of arachidonic acid, adrenic acid, DPA and DHA by 21, 11, 11 and 88mg/l respectively and the proportions of DPA and DHA in erythrocyte phospholipids by 78 and 27% respectively. Serum total, LDL- and HDL-cholesterol increased by 0·33mmol/l (7·3%), 0·26mmol/l (10·4%) and 0·14mmol/l (9·0%) compared with placebo (all p≤0·001). Factor VII (FVII) coagulant activity increased by 12% following active treatment (P=0·006). There were no significant differences between treatments in LDL size, blood pressure, plasma glucose, serum C-reactive protein, plasma FVII antigen, FVII activated, fibrinogen, von Willebrand factor, tocopherol or carotenoid concentrations, plasminogen activator inhibitor-1, creatine kinase or troponin-I activities, haematology or liver function tests or self-reported adverse effects. Overall, the oil was well tolerated and did not adversely affect cardiovascular risk.

The objective of the present study was to investigate the postprandial metabolism of two starches with contrasting rates of hydrolysis in vitro. Characterized using the Englyst method of in vitro starch classification, C*Set 06 598 contained predominantly rapidly digestible starch and C*Gel 04 201 contained predominantly slowly digestible starch. Each test starch, naturally enriched with 13C, was fed to ten healthy female volunteers as part of a moderate fat test meal (containing 75 g test starch and 21 g fat), in a double-blind randomized crossover design. The metabolic response to each starch was measured after an overnight fast, in an acute 6 h study, before and after 14 d of daily consumption of 75 g test starch. During each acute study, blood samples were taken at 15 min intervals for the first 2 h and at 30 min intervals for the remaining 4 h. Breath 13CO2 enrichment was measured at the same time points and indirect calorimetry was performed for 20 min every 40 min immediately before and throughout the study. Significantly more rapid, greater changes in postprandial plasma glucose, NEFA and serum insulin concentrations were observed after consumption of the rapidly digestible starch. Breath 13CO2 output over the first 3–4 h rose rapidly then began to decline following consumption of the rapidly digestible starch, but plateaued for the slowly digestible starch. The 14 d adaptation period did not affect any of the glycaemic or lipaemic variables but there was a reduction in postprandial plasminogen activator inhibitor-1 concentrations. These data confirm that starches characterized as predominantly rapidly digestible versus slowly digestible by the Englyst procedure provoke distinctly different patterns of metabolism postprandially.