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The results of this study show that a normal appendix can be depicted with US in 82% of asymptomatic children.

SummaryBackground Coagulation plays an important part in ischaemic cardiovascular disease. Results of studies have shown that extremes in hypocoagulability protect against ischaemic cardiovascular disease. We have investigated overall mortality and death from cardiovascular causes in carriers of haemophilia, who in most cases have mildly decreased coagulability without clinical signs.

A simple interview is useful as a screening tool for the dentist or surgeon. In a specialized hematology center with referred patients, however, the interview is of little value in identifying patients with a bleeding disorder.

Background-The results of a number of studies in pigs and mice suggest that absence of von Willebrand factor (vWF) protects against the development of atherosclerosis. We studied whether patients with a complete deficiency of vWF (type 3 von Willebrand disease [vWD]) develop fewer atherosclerotic vessel wall changes than healthy controls. Methods and Results-This study included 47 individuals with type 3 vWD and 84 healthy controls. Early atherosclerotic changes were assessed by measuring the thickness of the intima-media in the carotid and femoral arteries by B-mode ultrasonography. Advanced atherosclerotic changes were quantified by summing the maximal thickness of atherosclerotic plaques in the carotid and femoral arteries and were expressed as a plaque score. Established risk factors were determined to adjust for possible differences between the groups. We found no substantial difference in intima-media thickness between vWD patients and controls (adjusted difference for carotid artery 0.007 mm, 95% CI Ϫ0.022 to 0.036 mm; femoral artery 0.069 mm, 95% CI Ϫ0.056 to 0.19 mm). Similar proportions of patients and controls had atherosclerotic plaques (19% and 17%, respectively). No difference was found in the plaque score between groups (adjusted difference Ϫ0.22 mm, 95% CI Ϫ0.69 to 0.26). Among vWD patients, we found no effect of treatment with vWF concentrates on intima-media thickness or plaque score. Conclusions-The results of this study indicate that vWF does not play a substantial role in human atherogenesis.

Background-Hemostasis affects ischemic cardiovascular disease through its role in formation of occluding arterial thrombi. Several studies suggest that hemostasis also might play a role in atherogenesis. We investigated whether individuals with an inherited bleeding tendency are protected against development of atherosclerosis. Methods and Results-A total of 76 individuals with an inherited bleeding tendency (hemophilia and von Willebrand disease) and 142 healthy controls were included in the present study. Early atherosclerotic vessel-wall changes were quantified by measurement of intima-media thickness in the carotid and femoral arteries by B-mode ultrasonography.To validate intima-media thickness measurements, measurements also were performed in 77 individuals with clinically proven atherosclerosis and in 34 healthy, age-matched controls. A large difference in intima-media thickness was found between individuals with proven atherosclerosis and healthy controls, in particular for the femoral artery (difference for carotid artery, 0.16 mm; femoral artery, 0.53 mm). Comparison between patients with a bleeding tendency and healthy controls showed only minimally reduced intima-media in femoral artery in individuals with a bleeding tendency (adjusted difference, Ϫ0.078 mm; 95% CI, Ϫ0.17 to 0.018 mm). Subgroup analysis revealed that in subjects with moderate to severe hemophilia, vessel walls were thinnest (adjusted difference, Ϫ0.10 mm; 95% CI, Ϫ0.27 to 0.061 mm).

Objective. To determine the incidence, management, complications, and outcome in neonates with thrombotic events. Study Design. We performed a retrospective study of all neonates with thrombotic events admitted to our neonatal intensive care unit from January 2004 to July 2010. Results. Thrombotic events were identified in 32 of 4734 neonates (0.7%). Seven neonates were managed expectantly and 25 neonates received anticoagulant treatment. Complete resolution of the clot within 3 months of age was found in 68% (17/25) of the treated and in 86% (6/7) of the nontreated neonates. Major complications due to anticoagulant therapy occurred in 3/25 cases (12%) and included severe hemorrhage (n = 2) and abscess at the injection site (n = 1). Conclusion. Complete or partial clot resolution in neonatal thrombosis occurred in both the treated group and nontreated group. Randomized controlled trials are warranted to determine the optimal management in neonatal thrombosis.

Objective-Age is the strongest risk factor for venous thrombosis. Vessel wall changes such as thickening of venous valves may be one of the contributing mechanisms. We determined thickness and function of venous valves in the popliteal vein with ultrasound in 77 healthy individuals. Methods and Results-The study included 6 age groups ranging from 20 to 80 years old. Thickness of the valves was compared between age groups. Valve closure time was assessed as an indicator for valve function. In 69 of 77 participants, valve parameters could be measured. We found an increasing thickness of the valves with age, with a mean thickness of 0. Key Words: aging Ⅲ ultrasonic diagnosis Ⅲ venous thrombosis Ⅲ venous valves D eep-vein thrombosis (DVT) of the lower extremities is a disease with an annual incidence of 1 to 2 per 1000. 1,2 Risk factors for venous thrombosis can be divided into acquired and genetic risk factors. Among genetic risk factors are deficiencies of antithrombin, protein C, and protein S, which give a high risk for DVT but have low societal impact because of their low prevalence (Ͻ0.1%). 3 Risk factors such as the prothrombin 20210A and Factor V Leiden mutations are highly prevalent (3% to 8%) and are of intermediate strength. 4,5 Surgery and use of oral contraceptives are examples of highly prevalent acquired risk factors.Aging is the strongest risk factor for venous thrombosis. In people under the age of 40, the incidence is less than 1 per 10 000. 6 However, the incidence of venous thrombosis increases to 1 per 100 per year in elderly over the age of 75. 7 It is not clear why age is such an important risk factor. Explanations such as a decrease in mobility, an increase in prevalence of diseases with a high thrombotic risk (ie, malignancies, hip fractures), reduced venous compliance in the calf, and damaged venous valves have been suggested. 8 -10 Venous valves function to ensure that a proper inflow of blood reaches the heart during various cardiovascular adjustments. They can be regarded as flow modifiers that act and react constantly. 11,12 Venous valves are bicuspid and are positioned in a valve sinus, which is a local widening of the venous wall. The area between a valve leaflet and the vessel wall is called the valve pocket and is regarded as the place where thrombi originate. Low shear stress areas and stasis of blood flow predispose to thrombus formation. In the deepest part of the valve pockets, fluid circulates with very low velocities, creating a low shear field, thus allowing red cells to aggregate. Stagnation of blood leads to hypoxia, which subsequently causes endothelial damage. In case of nonpulsatile flow, a canine study showed that a thrombus was formed on a valve cusp after only 2 hours. 13 Age-related changes of the venous wall and valves have been described in renal veins. 14 Muscle fibers in the vessel wall atrophy with increasing age, whereas elastic fiber bundles hypertrophy. With respect to the valves, a gradual thickening with age was seen as a result of an increased number of ...