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PubMedDate not supplied

Instrument development: cardiac diet and exercise self-efficacy.

Self-efficacy has been documented as a strong predictor of health behaviors. Unfortunately, availability of reliable and valid measures of self-efficacy for a range of health behaviors is still limited. This study validated two measures of cardiac risk factor self-efficacy: the Cardiac Diet Self-Efficacy Instrument (CDSEI) and the Cardiac Exercise Self-Efficacy Instrument (CESEI). A sample of 370 cardiac rehabilitation participants provided data for principal factor analyses showing the unidimensionality of each instrument. Known groups construct validity was supported by a comparison of CDSEI and CESEI scores for cardiac rehabilitation participants and marathon runners. The value of CDSEI and CESEI scores in predicting subsequent exercise and diet performance was demonstrated with a third group of cardiac rehabilitation participants. Stability and internal consistency estimates in the .80s and .90s, respectively, support the scales' reliabilities.

Adult↗
PubMed2003

Amphibian in vitro heart induction: a simple and reliable model for the study of vertebrate cardiac development.

Amphibian embryos are an excellent model system for analyzing the mechanisms of vertebrate cardiogenesis. Studies of heart development in Xenopus have, for example, revealed that the inductive interaction of the heart primordia with the adjacent underlying endoderm and dorsal lip starts at the early stages of gastrulation. However, the molecular basis of those early inductive events and the genes expressed during the early phases of heart differentiation remain largely unknown. Amphibian blastula embryos contain pluripotent cells in their ectodermal region, called the "animal cap," which fortunately can be exploited for understanding a variety of organogenesis processes. Despite an enormous potential for analysis, the use of this system in cardiogenesis research has languished due to a lack of information concerning appropriate culture methods. Herein we report conditions for generating an in vitro heart induction system and present evidence from two types of in vivo transplantations, that the cultured heart rudiment can develop and function in the adult organism. It is expected that the fundamental principles established in this model system will provide a versatile research platform for a variety of organ engineering projects, including modifying in vitro organ growth with exogenous components (e.g. various growth factors) and developing methods for preparing tissue for transplantation.

Activins↗
PubMed2005

Novel targets for cardiac antiarrhythmic drug development.

Cardiac arrhythmias remain a major source of morbidity and mortality in developed countries. Antiarrhythmic drug therapy was traditionally the mainstay of cardiac arrhythmia treatment; however, drug therapy of cardiac arrhythmias has been plagued by incomplete efficacy and by potentially serious adverse reactions, of which the most worrisome has been a potential for malignant proarrhythmia and related effects to increase cardiac mortality. This article reviews the principal arrhythmia mechanisms and their ionic determinants, and discusses potential innovative approaches to new antiarrhythmic drug development, including the consideration of novel ionic targets, potential biophysical approaches and non-channel components involved in composing the arrhythmic substrate.

Action Potentials↗
PubMed2002

Allograft inflammatory factor-1 expression correlates with cardiac rejection and development of cardiac allograft vasculopathy.

BACKGROUND: Standard morphological features of endomyocardial biopsy specimens do not necessarily correlate with the efficacy of immunotherapy or development of cardiac allograft vasculopathy (CAV). We hypothesized that expression of allograft inflammatory factor-1 (AIF-1), a cytokine-inducible, calcium-binding protein associated with vascular smooth muscle cell proliferation, would be associated with allograft rejection and development of CAV. METHODS AND RESULTS: A total of 157 endomyocardial biopsy specimens from 26 patients with heart transplants were examined for expression of AIF-1 mRNA by semiquantitative reverse transcription-polymerase chain reaction. A significant relation was found between the International Society for Heart and Lung Transplantation rejection grade and expression of AIF-1 (P<0.001). The calculated odds ratio indicates that a biopsy has 2.5 times the chance of AIF-1 expression per grade of rejection. The relative concentrations of AIF-1 and GAPDH mRNA were calculated and the resulting ratios indicated that the amount of AIF-1 mRNA expression is relative to the rejection grade (P<0.02). In grade 1 biopsy specimens, AIF-1 was localized to infiltrating immune cells. In grade 3 biopsy specimens, AIF-1 was observed in immune cells and myocytes. AIF-1 is expressed in vascular and immune cells in coronary arteries with CAV, and persistent expression of AIF-1 in the allograft correlates with development of CAV (P<0.002). CONCLUSIONS: Expression of AIF-1 in cardiac allografts correlates with rejection, and the amount of AIF-1 expressed correlates with the severity of rejection. AIF-1 is expressed in coronary arteries with CAV, and persistent expression of AIF-1 in the cardiac allograft is associated with development of CAV.

Calcium-Binding Proteins↗
PubMed2003

Inhibition of E2F abrogates the development of cardiac myocyte hypertrophy.

Growth of the post-natal mammalian heart occurs primarily by cardiac myocyte hypertrophy. Previously, we and others have shown that a partial re-activation of the cell cycle machinery occurs in myocytes undergoing hypertrophy such that cells progress through the G1/S transition. In this study, we have examined the regulation of the E2F family of transcription factors that are crucial for the G1/S phase transition during normal cardiac development and the development of myocyte hypertrophy in the rat. Thus, mRNA and protein levels of E2F-1, 3, and 4 and DP-1 and DP-2 were down-regulated during development to undetectable levels in adult myocytes. Interestingly, E2F-5 protein levels were substantially up-regulated during development. In contrast, an induction of E2F-1, 3, and 4 and the DP-1 protein was observed during the development of myocyte hypertrophy in neonatal myocytes treated with serum or phenylephrine, whereas the protein levels of E2F-5 were decreased with serum stimulation. E2F activity, as measured by a cyclin E promoter luciferase assay and E2F-DNA binding activity, increased significantly during the development of hypertrophy with serum and phenylephrine compared with non-stimulated cells. Inhibiting E2F activity with a specific peptide that blocks E2F-DP heterodimerization prevented the induction of hypertrophic markers (atrial natriuretic factor and brain natriuretic peptide) in response to serum and phenylephrine, reduced the increase in myocyte size, and inhibited protein synthesis in stimulated cells. Thus, we have shown that the inhibition of E2F function prevents the development of hypertrophy. Targeting E2F function might be a useful approach for treating diseases that cause pathophysiological hypertrophic growth.

3T3 Cells↗
PubMed2002

Overexpression of apolipoprotein B in the heart impedes cardiac triglyceride accumulation and development of cardiac dysfunction in diabetic mice.

The heart secretes apolipoprotein B (apoB) containing lipoproteins. Herein, we examined whether the overexpression of a human apoB transgene in the heart affects triglyceride accumulation and development of cardiac dysfunction in streptozotocin-treated diabetic mice. Blood glucose, plasma free fatty acids, and plasma triglycerides were similarly affected in diabetic wild type mice and diabetic apoB transgenic mice as compared with non-diabetic mice of the same genotype. After 12 weeks, heart triglycerides were increased by 48% in diabetic wild type mice. These mice displayed an increased expression of brain natriuretic peptide and deterioration of heart function on echocardiography. In diabetic apoB transgenic mice, heart triglyceride levels were identical to those in non-diabetic wild type and apoB transgenic mice, and brain natriuretic peptide expression as well as echocardiographic indexes of heart function were only marginally affected or unaffected. The findings suggest that triglyceride accumulation in the heart is important for development of diabetic cardiomyopathy in mice, and that lipoprotein formation by cardiomyocytes plays an integrated role in cardiac lipid metabolism.

Animals↗
PubMed1997

Twin-reversed arterial perfusion (TRAP) sequence: case reports and review of literature.

The twin reversed-arterial-perfusion (TRAP) sequence found in monozygotic twins is a consequence of primary or secondary cardiac development disruption and direct arterioarterial and venovenous placental anastomoses. Associated findings include the presence of a single umbilical artery (66%) and chromosomal abnormalities in the acardiac twin (33%). Morphological abnormalities in the acardiac twin are consistent with perfusion of tissues supplied by the common iliac and lower branches of the aorta with deoxygenated blood. The pump or donor twin may develop cardiac failure because of the anomalous perfusion circuit. Polyhydramnios is significantly associated with presence of renal tissue in the acardiac twin. An acardiac pump twin weight ratio (> 50%) is associated with the development of polyhydramnios and preterm labour. Identified high-risk factors for poor obstetrical outcome include: acardiac anceps, polyhydramnios, acardiac twin with ears, and pump twin cardiac failure. Management options include elective termination, observation (serial cardiotocography (CTG), ultrasonography and echocardiography) and selective nonsurgical interventions (indomethacin, digitalis, tocolysis). Additionally, surgical interventions (hysterotomy with selective delivery of the acardiac twin or ligation of the acardiac twin's umbilical cord), and ultrasound-guided embolization of the acardiac twin's umbilical artery with absolute alcohol, platinum coils, or thrombogenic coils have been reported. The most appropriate interventions for the various clinical presentations of this disorder are as yet undetermined, and conservative nonintervention is often appropriate. Long-term follow-up data on surviving pump twins are lacking. It is anticipated that centres with active study protocols for these conditions will best serve patient care and clinical research needs.

Female↗
PubMed2005

The heart of children with steroid-resistant nephrotic syndrome: is it all podocin?

Mutations in the gene NPHS2 encoding podocin are responsible for a recessive form of steroid-resistant nephrotic syndrome (SRNS). The common phenotype is of massive proteinuria in early childhood that tends to progress to end-stage renal failure. Extrarenal manifestations have not been described. Twenty-two children with SRNS from six unrelated Arab families were found to be homozygous for the R138X mutation in NPHS2. Eighteen patients underwent cardiac evaluation at diagnosis of SRNS while they had normal BP and preserved renal function. Cardiac anomalies were detected in 16 (89%) children: Left ventricular hypertrophy in eight, pulmonary stenosis in six, discrete subaortic stenosis in two, and Ebstein anomaly and ventricular septal defect in one each. The remaining four affected individuals were assessed only once they had end-stage renal failure. They had severe left ventricular hypertrophy and experienced repeated episodes of heart failure. Two control groups were equally evaluated. The first consisted of 37 siblings without nephrotic syndrome, of whom only one carrier had a cardiac defect (P < 0.001). None of the second group, which included 22 children with persistent nephrotic syndrome as a result of other causes, had a cardiac anomaly (P < 0.001). Cardiac disorders in homozygotes for mutations in NPHS2 cannot be attributed to an association by chance or to a state of persistent nephrotic syndrome. Because human podocin mRNA is expressed in fetal heart, it is speculated that it may have a role in normal cardiac development. Cardiac evaluation is recommended at the time of diagnosis of SRNS due to mutations in podocin.

Child, Preschool↗