Background-Although numerous signaling pathways are known to be activated in experimental cardiac hypertrophy, the molecular basis of the hypertrophic response inherent in human heart diseases remains largely unknown. Integrin-linked kinase (ILK) is a multifunctional protein kinase that physically links ␤-integrins with the actin cytoskeleton, suggesting a potential mechanoreceptor role. Methods and Results-Here, we show a marked increase in ILK protein levels in hypertrophic ventricles of patients with congenital and acquired outflow tract obstruction. This increase in ILK was associated with activation of the Rho family guanine triphosphatases, Rac1 and Cdc42, and known hypertrophic signaling kinases, including extracellular signal-related kinases (ERK1/2) and p70 S6 kinase. Transgenic mice with cardiac-specific expression of a constitutively active ILK (ILK S343D ) or wild-type ILK (ILK

Human fetal cardiac myocytes exhibit a uniquely adaptive transcriptional response to ischemia and reperfusion that is associated with an apoptosis-resistant phenotype. The stress-inducible fetal cardiac myocyte gene repertoire is a useful platform for identification of targets relevant to the mitigation of cardiac ischemic injury and highlights a novel avenue involving interleukin 6 modulation for preventing the cardiac myocyte injury associated with ischemia and reperfusion.

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This study demonstrates that self-renewing cardiospheres generated from human fetal cardiac cells are composed of cells exhibiting the properties of stem cells, including the capacity for self-renewal and multilineage differentiation. Our results suggest that integrin-linked kinase promotes stem cell amplification and can be applied therapeutically to overcome a major limitation in the field of cardiac regenerative medicine.

FIGURE 2. A, Huge LAAA. B, No anomaly of the 4 pulmonary veins. C, Postoperative computed tomography scan shows that LAAA was resected, and an annuloplasty ring was placed in the mitral annulus.

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A 34-year-old female with a gestational age of 38 weeks developed acute type A aortic dissection. Appearance of this patient was typical for Marfan s syndrome, and echocardiography revealed annuloaortic ectasia with mild aortic regurgitation, but pericardial effusion was absent. As her hemodynamic condition was stable, an emergency Caesarean section was carried out first. After careful observation in the ICU for half a day, she successfully underwent aortic valve reimplantation and replacement of the ascending aorta under deep hypothermic circulatory arrest. Intraoperative heparin use minimally impacted uterine bleeding. Both the mother and the neonate were discharged home 16 days later. We believe a two-stage strategy should be adopted whenever possible.

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