Seminars in vascular medicine
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The number of pregnancies affected by neural tube defects has been estimated to be 4000/year in Europe, with a higher prevalence in Celtic populations and in women of low socioeconomic status. Since the 1980s, it has been shown that supplementation with folic acid during the periconceptual period reduces the risk of neural tube defects in the fetus. However, in view of the period during which supplementation should be taken (< 4 weeks before conception until 8-10 weeks after) and the fact that in some countries 30-50% of pregnancies are unplanned, a public health initiative based solely on increasing dietary folate intake or recommendations on use of folic acid supplements is likely to be insufficient. ⋯ A recent public health decision in Hungary stimulated flour fortification on a voluntary basis, but it remains the only European country to take this action. Many European countries have deferred a decision to introduce fortification because of concerns about possible masking of vitamin B (12) deficiency. This review advocates a proposal for combined fortification of folic acid and vitamin B (12) to address possible hazards of fortification with folic acid alone.
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Review Comparative Study
Obesity and cardiovascular disease: pathogenic mechanisms and potential benefits of weight reduction.
The prevalence of obesity in industrialized countries has reached epidemic proportions, with about one in three people being obese and another one in three people being overweight and at risk of developing obesity. In recent years, obesity has gained the traditional tetrad of cardiovascular risk factors of smoking: hypertension, dyslipidemia, and dysglycemia. ⋯ The objectives of this review are to summarize the effects of obesity on cardiovascular disease, and the possible mechanisms for these associations, and to investigate the effects of weight-loss interventions on the burden of cardiovascular disease. Large ongoing clinical outcome trials, such as the SOS study, the Look-AHEAD trial, or the SCOUT study, should provide important information on the effects of surgical and nonsurgical obesity treatment on cardiovascular morbidity and mortality.
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Current scientific evidence indicates that dietary fat plays a role in weight loss and maintenance. Meta-analyses of intervention trials find that fat-reduced diets cause a 3-4-kg larger weight loss than normal-fat diets. A 10% reduction in dietary fat can cause a 4-5-kg weight loss in individuals with initial body mass index of 30 kg m (-2). ⋯ Monounsaturated fatty acids may even be more fattening than polyunsaturated and saturated fats. No ad libitum dietary intervention study has shown that a normal-fat, high-monounsaturated fatty acid diet is comparable to a low-fat diet in preventing weight gain. Current evidence indicates that the best diet for prevention of weight gain, obesity, type 2 diabetes, and cardiovascular disease is low in fat and sugar-rich beverages and high in carbohydrates, fiber, grains, and protein.
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The number of patients anticoagulated with warfarin has rapidly increased over the last decade. Approximately 1% of these patients experience serious bleeding and 0.5% die annually from bleeding. ⋯ For life-threatening bleeding, the use of clotting factor concentrates is essential for immediate anticoagulation reversal, whereas for less severe bleeding intravenous vitamin K is the treatment of choice. Vitamin K (by the intravenous or oral route) should also be used in overanticoagulated patients who are not actively bleeding but who are at high risk of doing so if their anticoagulation is not, at least partially, corrected.
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This article focuses on the role of the tissue factor (TF)-thrombin pathway in cardiac ischemia-reperfusion (I/R) injury. We and others have used rabbit models of cardiac I/R injury to show that anti-TF therapy prevents the transient decrease in regional myocardial blood flow, reduces platelet and fibrin(ogen) accumulation, and reduces infarct size. At present, the mechanism by which TF-initiated coagulation contributes to myocardial injury is not established. ⋯ In contrast, inhibition of thrombin reduced infarct size to a similar extent as anti-TF therapy. We propose that the TF-thrombin pathway may contribute to myocardial injury by an additional mechanism that is not dependent on fibrin deposition but involves activation of protease activated receptor 1 (PAR-1) on vascular endothelial cells and cardiac myocytes. Anti-TF therapy would inhibit both thrombin-dependent fibrin deposition and thrombin-dependent PAR-1 signaling.