The potential of disproportionate growth of tricuspid valve after decompression of the right ventricle in patients with pulmonary atresia and intact ventricular septa

ObjectiveTricuspid valve size is the major determinant of outcomes for patients with pulmonary atresia with intact ventricular septum. Lack of right ventricle–pulmonary artery continuity is associated with poor tricuspid valve growth (decrement in Z-value). However, most reports did not show evidence for disproportionate growth of the tricuspid valve after establishment of right ventricle–pulmonary artery continuity.MethodsWe studied 40 patients with pulmonary atresia with intact ventricular septum who underwent initial right ventricular decompression for planned staged repair. The initial Z-value of the tricuspid valve diameter (Zt1) was obtained from the echocardiography-derived normal value. The late Z-value (Zt2) was measured before definitive repair or the last available Z-value, if definitive repair was not yet reached. The factors associated with the changes of Z-values (Zt2 − Zt1) were analyzed.ResultsThe mean initial tricuspid Z-value (Zt1) was −6.2 ± 3.5. After treatment (Zt2), the mean Z-value was −6.0 ± 3.4 (n = 34). Overall, the tricuspid Z-values did not change. Individually, the change in Z-value (Zt2 − Zt1) was larger than +2 in 11 (32%) patients and smaller than −2 in 6 (18%) patients. Increases in Z-value (Zt2 − Zt1) were significantly associated with right ventricular pressure/left ventricular pressure ratio measured after initial palliation (r = −0.54; P = .001) and the initial tricuspid valve Z-value (Zt1) (r = −0.40; P = .02).ConclusionsDisproportional growth of the tricuspid valve can occur, especially in patients with small tricuspid valves and lower right ventricular pressures after decompression. The findings support the possibility of neonates with small tricuspid valves undergoing biventricular repair after right ventricular decompression surgery

A Newly Formed and Ruptured Atheromatous Plaque within Neointima after Drug-Eluting Stent Implantation: 2-Year Follow-Up Intravascular Ultrasound and Optical Coherence Tomography Studies

Late stent thrombosis (LST) which is a life threatening complication has emerged as a serious problem of drug-eluting stents (DES). Several studies have suggested that incomplete neointimal coverage of stent struts contributes to LST. Progressive atherosclerosis within the neointima is an another possible cause of LST, but this phenomenon has seldom been reported in DES. We present a case of LST following DES implantation after a period of 28 months due to ruptured atheromatous plaque, despite complete neointimal coverage of stent struts proven by optical coherence tomography

The Regulators of VEGF Expression in Mouse Ovaries

The objectives of this study were to explore whether ovarian vascular endothelial growth factor (VEGF) expression in mice can be regulated by IL-6 (interleukin-6), angiotensin II, FSH, and hCG; and to test whether the mouse ovarian VEGF expression can result in angiogenesis. The ICR mice were sacrificed, and their ovaries were recovered. Recovered ovaries were treated with IL-6, angiotensin II, FSH, and hCG separately and incubated for 24 hours in α-MEM. Expression of mRNA and protein of VEGF were assessed by RT-PCR and immunohistochemistry. The resulting angiogenesis was evaluated through immunohistochemical analysis for CD34. Treatment of mice ovaries with IL-6, FSH, and hCG resulted in a significant increase of VEGF mRNA, and IL-6 was the most potent inducer of VEGF. IL-6 and FSH resulted in increased neovascularization in the follicular phase of mouse ovaries. In contrast, angiotensin II could not increase VEGF expression or neovascularization. We documented an in vitro increase in VEGF expression by IL-6, FSH, and hCG; and reaffirmed that the proliferative response of murine ovarian endothelial cells paralleled an increase of VEGF expression

Alternative Functions of Core Cell Cycle Regulators in Neuronal Migration, Neuronal Maturation, and Synaptic Plasticity

Recent studies have demonstrated that boundaries separating a cycling cell from a postmitotic neuron are not as concrete as expected. Novel and unique physiological functions in neurons have been ascribed for proteins fundamentally required for cell cycle progression and control. These “core” cell cycle regulators serve diverse postmitotic functions that span various developmental stages of a neuron, including neuronal migration, axonal elongation, axon pruning, dendrite morphogenesis, and synaptic maturation and plasticity. In this review, we detail the nonproliferative postmitotic roles that these cell cycle proteins have recently been reported to play, the significance of their expression in neurons, mechanistic insight when available, and future prospects.National Institutes of Health (U.S.) (PO1 grant AG27916)National Institutes of Health (U.S.) (RO1 grant NS51876

Genetic Testing for Early Detection of Individuals at Risk of Coronary Heart Disease and Monitoring Response to Therapy: Challenges and Promises

Coronary heart disease (CHD) often presents suddenly with little warning. Traditional risk factors are inadequate to identify the asymptomatic high-risk individuals. Early identification of patients with subclinical coronary artery disease using noninvasive imaging modalities would allow the early adoption of aggressive preventative interventions. Currently, it is impractical to screen the entire population with noninvasive coronary imaging tools. The use of relatively simple and inexpensive genetic markers of increased CHD risk can identify a population subgroup in which benefit of atherosclerotic imaging modalities would be increased despite nominal cost and radiation exposure. Additionally, genetic markers are fixed and need only be measured once in a patient’s lifetime, can help guide therapy selection, and may be of utility in family counseling