Outcome of aortic valve repair in children with congenital aortic valve insufficiency

OBJECTIVE: Surgical aortic valvotomy has a long history of providing excellent palliation for aortic stenosis in infancy and childhood. The fate of aortic valve repairs for dominant aortic regurgitation in this same age group is considerably less clear. METHODS: From 1990 to 2000, a total of 21 patients underwent aortic valve repair for aortic regurgitation at our institution. Seventeen patients were younger than 17 years at the time of repair (3-17 years, mean 8.1 +/- 3.7 years). Of these 17 children, 6 (35%) had bicuspid valves and 11 (65%) had tricuspid valves. Type of repair varied with valve type, but repair generally consisted of commissure resuspension, partial commissure closure, triangular resection of redundant leaflets, or some combination. RESULTS: There were no deaths. Follow-up ranged from 1 to 11 years (mean 5.3 +/- 2.4 years). At present 3 of 17 (17.6%) have mild aortic regurgitation according to echocardiography and 6 (35.2%) have moderate aortic regurgitation. In 8 of 17 cases (47.1%) the repair clearly failed, requiring reoperation from 0.5 to 73 months after the original operation (mean 18.9 months). Reoperation consisted of 6 Ross procedures and 2 mechanical aortic valve replacements. There were no deaths at the secondary operation. CONCLUSION: Aortic valve repair in children with a dominant feature of aortic insufficiency tended to fail progressively and at a high rate. Leaflet thickening was associated with higher risk of repair failure in this series. The threshold for aortic valve replacement should remain low.     

Predictive factors of atrial fibrillation in mitral stenosis. Clinical and echocardiographic study

The objective of this study was to define the predictive factors of atrial fibrillation in pure or very predominant mitral stenosis in a series of 472 consecutive patients divided into 2 groups according to the presence (group I: n = 113) or absence (group II: n = 359) of permanent atrial fibrillation. Univariate analysis showed that predictive factors for atrial fibrillation in mitral stenosis are age (40.3 +/- 9 years vs 31.4 +/- 9.5, p < 0.0001), history of commissurotomy or mitral angioplasty (13 cases vs 10, p < 0.01), functional class III or IV (36 cases vs 43, p < 0.01), history of valvular heart disease (8.4 +/- 7.3 years vs 6.4 +/- 9.2, p < 0.05), left atrial diameter (53.3 +/- 10.3 mm vs 46.5 +/- 8.5, p < 0.0001) and mitral surface area (1.1 +/- 0.4 cm2 vs 1.3 +/- 0.4, p < 0.0001). On multivariate analysis, age and left atrial dilatation were independent predictive factors of atrial fibrillation in mitral stenosis.     

Foxc1 and Foxc2 deletion causes abnormal lymphangiogenesis and correlates with ERK hyperactivation

The lymphatic vasculature is essential for maintaining interstitial fluid homeostasis, and dysfunctional lymphangiogenesis contributes to various pathological processes, including inflammatory disease and tumor metastasis. Mutations in FOXC2 are dominantly associated with late-onset lymphedema; however, the precise role of FOXC2 and a closely related factor, FOXC1, in the lymphatic system remains largely unknown. Here we identified a molecular cascade by which FOXC1 and FOXC2 regulate ERK signaling in lymphatic vessel growth. In mice, lymphatic endothelial cell–specific (LEC-specific) deletion of Foxc1, Foxc2, or both resulted in increased LEC proliferation, enlarged lymphatic vessels, and abnormal lymphatic vessel morphogenesis. Compared with LECs from control animals, LECs from mice lacking both Foxc1 and Foxc2 exhibited aberrant expression of Ras regulators, and embryos with LEC-specific deletion of Foxc1 and Foxc2, alone or in combination, exhibited ERK hyperactivation. Pharmacological ERK inhibition in utero abolished the abnormally enlarged lymphatic vessels in FOXC-deficient embryos. Together, these results identify FOXC1 and FOXC2 as essential regulators of lymphangiogenesis and indicate a new potential mechanistic basis for lymphatic-associated diseases.     

Mechanisms of oxidative stress-induced increase in salt sensitivity and development of hypertension in Sprague-Dawley rats

High salt intake produces vascular changes that contribute to the development of hypertension in salt-sensitive individuals. Because reactive oxygen species play a role in the pathogenesis of cardiovascular diseases, we investigated whether oxidative stress contributes to salt-sensitive hypertension. Sprague-Dawley rats were divided in different groups and received tap water (vehicle), 30 mmol/L of l-buthionine sulfoximine ([BSO] an oxidant), high salt ([HS] 1% NaCl), and BSO plus HS without and with antioxidant tempol (1 mmol/L) in drinking water for 12 days. Compared with vehicle, BSO treatment caused oxidative stress and mild increase in blood pressure. Thoracic aortic rings from BSO-treated rats exhibited decreased response to endothelium-independent vasorelaxants. In HS-treated rats, the response to vasoactive agents, as well as blood pressure, was unaffected. Concomitant treatment of rats with BSO and HS produced a marked increase in blood pressure and a decreased response to both endothelium-dependent and endothelium-independent vasorelaxants with an increase in EC(50). Incubation of aortic tissue from BSO-treated rats with sodium nitroprusside showed decreased cGMP accumulation, whereas HS rats had decreased basal NO synthase activity. Tempol decreased oxidative stress, normalized blood pressure, and restored NO signaling and responses to vasoactive compounds in BSO and BSO plus HS rats. We conclude that BSO increases oxidative stress and reduces NO signaling, whereas HS reduces NO levels by decreasing the NO synthase activity. These phenomena collectively result in reduced responsiveness to both endothelium -dependent and endothelium- independent vasorelaxants and may contribute to salt-sensitive hypertension.     

Multifocal osseous tuberculosis involving hand and feet

A rare case of multifocal cystic tuberculosis of hands and feet is presented in an adolescent female. The presence of multiple lytic areas mimicked secondary metastases and biopsy remained the mainstay for final diagnosis.     

The use of radiation therapy after breast-conserving surgery in hormonally treated breast cancer patients is dependent on patient age, geographic region, and surgeon specialty

BACKGROUND: The use of radiation therapy (RT) after breast-conserving surgery (BCS) is inconsistent in patients treated with hormonal therapy (HT). We sought to identify factors influencing the decision to use RT in this setting. METHODS: Patients in the North American Fareston vs. Tamoxifen Adjuvant (NAFTA) trial who had BCS were evaluated for factors influencing the use of RT using univariate and multivariate analyses. RESULTS: Of the 1,811 patients enrolled in the NAFTA trial, 1,222 (67.4%) had BCS. Of these, 241 (19.7%) did not have RT. There were no significant differences in tumor grade, lymphovascular invasion, estrogen receptor status, or nodal status between those who received RT and those who did not. On univariate analyses, patients who did not receive RT were more likely to be older (median 72 versus 66 years, P < .001), have larger tumors (median 1.35 versus 1.10 cm, P = .009), and be progesterone negative (18.3% versus 13.1%, P = .048). Surgeons in the West were most likely to omit RT, whereas those in the Midwest were least likely to omit it (26.7% versus 7.2%, P < .001). Surgical oncologists were more likely to omit RT after BCS than general surgeons (21.8% versus 13.7%, P < .001). Academic affiliation (P < .001), number of breast procedures performed per year (P = .017), and the percentage of breast practice (P = .019) also correlated with whether or not RT was used. On multivariate analysis, patient age (P < .001), geographic region (P = .006), and surgeon specialty (P = .027) remained significant. CONCLUSION: Patient age, geographic region, and surgeon training influence the decision to use RT after BCS in patients receiving HT.