Clinico-histopathological correlation of symptomatic left main coronary artery electrocardiographic ischemia pattern in a young child with hypertrophic cardiomyopathy.

The specific electrocardiographic (ECG) pattern of left main coronary artery ischemia is exceptionally rare in children and under recognized. Occasional reports are bereft of a detailed mechanistic ECG description and limited to dissection, spasm, or anomalous origin of the left main coronary artery. An association with pediatric hypertrophic cardiomyopathy (HCM) is hitherto unreported. We furbish a detailed electrocardiographic description of this entity in the unusual setting of a 4-year-old child with HCM with a restrictive phenotype and exertional symptoms consistent with myocardial ischemia. Heart transplant was performed for this rare indication. Histopathology of the explanted heart in particular revealed left main coronary artery narrowing and provided us with a unique window of opportunity to correlate with clinical findings. The pathophysiology was also likely exacerbated by diffuse sub endocardial ischemia in the milieu of left ventricular hypertrophy with elevated end diastolic pressures. We anticipate that this illustrative case will help contextualize this as well as pediatric scenarios in which the 'left main ischemia' ECG pattern can be encountered and foster an accurate electrocardiographic recognition of this entity in children.

The regulation of tumor suppressor protein, p53, and estrogen receptor (ERα) by resveratrol in breast cancer cells.

Resveratrol (RES) is a natural antioxidant found abundantly in grapes, peanuts, and berries, and is known to possess anti-tumorigenic properties. However, there is a noticeable lack of studies on the mechanistic effects of Resveratrol on tumor suppressors. Previous studies from our laboratory have shown the tumor suppressor protein p53 and estrogen receptor-alpha (ERα) to be possible molecular targets for RES. In this study, the anti-estrogenic effects of RES were analyzed on the expression of ERα and p53. The breast cancer cells grown in stripped serum were treated with 60 µM RES, as the optimum concentration based on data obtained from a concentration study using 1-100 µM RES. Our studies indicate that RES caused a decrease in the levels of protein expression of p53 and ERα as compared to the control. Increasing concentrations of RES caused a four-fold decrease in cell number in comparison to estradiol. RES, in conjunction with ICI 182,780 (ICI), caused a down-regulation of both p53 and ERα as compared to the control. These observed effects on cell proliferation and regulation of both p53 and ERα by RES may lead to further understanding of the relationship between tumor suppressor proteins and steroid receptors in breast cancer cells.