Background: Heart failure and diabetes are common coexisting diseases. Elevated levels of glucose in the blood caused by insulin resistance can damage blood vessels and nerves, and eventually lead to heart disease. A poor diet and obesity can also contribute to the progression of diabetes and heart disease. Objective: The purpose of this study was to determine if diet and lifestyle factors between adult heart failure patients with and without diabetes who are participating in the EducatioN, and Supportive Partners Improving Self-CaRE (ENSPIRE) study are associated with comorbidities such as diabetes, and if so then how current dietary recommendations in this population should be modified based on diabetes status. Methods: Using data collected from the EducatioN and Supportive Partners Improving Self-CaRE (ENSPIRE) study from 2006 to 2009 which was a prospective, randomized, controlled clinical trial, a secondary data analysis was conducted. Daily dietary intake of calories, sodium, carbohydrate, fat, sugar, and fiber was assessed via a 3-day food record. Differences in anthropometric measures, smoking history, education level and health literacy score between the two groups were also assessed. 117 heart failure patients were included in the analysis. Of these, 39% had diabetes. Statistical analysis: Statistical analyses included the t-test, Chi-square analysis, and Mann Whitney U test used to compare anthropometric data, lifestyle factors, and disease states. Results: Weight was higher in heart failure patients with vs. without diabetes (104.9 vs. 92.6 kg, respectively; P Conclusion: Weight was significantly higher in heart failure patients with diabetes and they consumed fewer carbohydrates than their non-diabetic counterparts. We recommend encouraging these individuals to closely monitor their macronutrient intake, specifically limiting fat in the diet. Meeting with a dietitian to ensure adequate nutrient intake is strongly recommended.

Primarily expressed by trophoblast cells, human leukocyte antigen-G (HLA-G) plays an essential role in maintaining maternal-fetal immune tolerance. Having previously been detected following heart transplantation, we sought to establish the value of HLA-G in identifying freedom from moderate or severe rejection post-heart transplant, and the capability of its expression in vitro. After assessing myocardial HLA-G expression through immunohistochemistry, we demonstrated that it was significantly more prevalent in non-rejecting than rejecting heart transplant recipients. Utilizing vascular endothelial and smooth muscle cell culture models, we also determined that while HLA-G expression remains tightly regulated, its expression in vitro can be induced following progesterone treatment in a dose-dependent manner. Hence, HLA-G may reliably identify patients with a low immunological risk of developing subsequent clinically significant rejection post-heart transplant. Furthermore, HLA-G expression can be induced in cultured endothelial and smooth muscle cells, which might represent a strategy to protect against allograft rejection and vasculopathy.

Primarily expressed by trophoblast cells, human leukocyte antigen-G (HLA-G) plays an essential role in maintaining maternal-fetal immune tolerance. Having previously been detected following heart transplantation, we sought to establish the value of HLA-G in identifying freedom from moderate or severe rejection post-heart transplant, and the capability of its expression in vitro. After assessing myocardial HLA-G expression through immunohistochemistry, we demonstrated that it was significantly more prevalent in non-rejecting than rejecting heart transplant recipients. Utilizing vascular endothelial and smooth muscle cell culture models, we also determined that while HLA-G expression remains tightly regulated, its expression in vitro can be induced following progesterone treatment in a dose-dependent manner. Hence, HLA-G may reliably identify patients with a low immunological risk of developing subsequent clinically significant rejection post-heart transplant. Furthermore, HLA-G expression can be induced in cultured endothelial and smooth muscle cells, which might represent a strategy to protect against allograft rejection and vasculopathy.

There is relatively little epidemiologic information about Ebstein anomaly (EA) ─ a rare congenital heart defect. Thus, we analyzed characteristics of EA in a geographically and ethnically diverse population. Data from the National Birth Defects Prevention Study were used to study infants born from 1997-2007 with EA. Birth prevalence and prevalence ratio (PR) estimates were derived from the number of affected infants per 10,000 live births in the catchment area. Case characteristics were examined, stratified by the presence of other cardiac and extracardiac defects. Predictive modeling using logistic regression was conducted to understand infant mortality risk factors. There were 249 cases with EA, for a birth prevalence of 0.55/10,000 live births. Other cardiac defects were present in 41.0% and extracardiac defects in 10% of cases. Prevalence was higher among multiple births compared to singletons (PR 2.41, 95% confidence interval (CI) 1.46-3.92) and preterm compared to term infants (PR 1.84, 95% CI 1.27-2.64). Compared to EA cases without other defects, those with additional defects were more likely to die (crude Odds Ratio (cOR) 4.07, 95% CI 1.71-9.93) or undergo cardiac surgery (cOR 6.06, 95% CI 2.78-13.49). Risk for death during infancy was increased by being small for gestational age (adjusted (a) OR 2.97, 95% CI 1.13-7.76) and having extracardiac defects (aOR 6.31, 95% CI 2.28-17.52). Some findings are consistent with previous work, but further studies of EA could clarify risk factors for occurrence and mortality. Knowing population characteristics could guide development of prevention strategies and may improve clinical care.

Via the delivery of blood, heart transfers oxygen and nutrients to various organs and is thus a highly influential for circulatory system. To adapt to the variation of physiological conditions, the intensity and frequency of heart beats change with time. Careful observation finds that the time intervals between heartbeats are often different even if the body is at rest. Such heart rate variability (HRV) has been used to estimate the activity of the autonomic nervous system which can be divided into sympathetic and parasympathetic subsystems both of which can significantly affect the physiology of the human body. As a result, HRV has been used as a physiological indicator to assist doctors in making diagnostic decisions. Many studies have used HRV to analyze the ECG signal via studying the QRS complex waveform to determine the time intervals between R-peaks and analyze the R-R intervals from time and frequency domains. Different from the conventional R-R Interval based approach, this work introduces new HRV feature variables by computing spectrogram of the ECG signal waveform. In particular, based on the harmonics of the spectrum, we introduce the concepts of modes. By find the relative amount of energy associated with each mode and degree-of-energy-concentration associated with each mode, this work introduces two sets of new HRV features. In addition, we also investigate how these variables change with time and the correlations between these features. To demonstrate the potential of the proposed features, the differences of the values of the proposed features are compared for healthy individuals versus OSA patients, young versus old and male versus female. The experimental results show the differences between many of the tested features are statistically significant.

Aging is characterized by a progressive decline in cardiac function. A critical contributor to the age-related impairment in heart function is the loss of cardiac myocytes through ??apoptosis??, or programmed cell death. A dramatic increase in the rate of apoptosis has been reported with aging in the rat left ventricle. In contrast, exercise training not only improves cardiac function, but also reduces the risk of heart disease. However, the ability of exercise training to modulate apoptotic signaling and apoptosis in the aging heart remains unknown. Therefore, the purpose of this study was to determine the effects of exercise training on apoptotic signaling and apoptosis in the aging heart. We hypothesized that (1) aging would increase pro-apoptotic signaling and apoptosis in the rat left ventricle, and (2) exercise training would ameliorate upregulation of Bcl-2 family-driven apoptosis in the heart. Four and 25 month old Fischer-344 rats were assigned to four groups: young control (YC), young trained (YT), old control (OC), and old trained (OT). Exercise training groups ran on a treadmill for 60 min/day at 15 m/min (15˚ incline), 5 d/wk for 12 wk. Protein expression of Bax, Bcl-2, caspase-9, and cleaved caspase-3 was measured using Western immunoblot analysis. Apoptosis (DNA fragmentation) was assessed using a cell death detection ELISA. Bax levels in OC were dramatically higher (+176.0%) compared to YC. In contrast, exercise training resulted in a significant decrease (-53.4%) in Bax in OT compared to OC. Bcl-2 levels in OC were lower (-26.3%) compared to YC. Conversely, exercise training significantly increased Bcl-2 levels by 117.8% in OT compared to OC. Caspase-9 levels were higher (+98.7%) in OC than YC, while exercise training significantly reduced caspase-9 levels in YT (-52.6%) and OT (-76.9%), respectively. Aging resulted in a dramatic increase (+122.8%) in cleaved caspase-3 levels and a significant decrease (-32.9%) with exercise training. Finally, apoptosis (DNA fragmentation) significantly increased (+163.8%) with aging and decreased (-43.9%) with exercise training. These novel data indicate that aging increases pro-apoptotic signaling and apoptosis in the left ventricle, while exercise training is effective in diminishing pro-apoptotic signaling and apoptosis in the aging heart.

According to the American Heart Association, there are currently 5 million Americans diagnosed with congestive heart failure and that number is steadily increasing (AHA, 2003). The alarming problem of congestive heart failure and other related medical complications has created a need for devices that not only assist the heart but also help the heart to grow and remodel back to its normal configuration. Currently, there are several direct cardiac compression devices (DCCDs) that do assist the heart, however, they do not help the heart to grow and remodel correctly. Dr. John C. Criscione of Texas A&M University has proposed a novel DCCD, in which the compression of the device reinforces the natural curvature of the heart, helping it to grow and remodel correctly. It is hypothesized that with the support of the device, the cells of the heart will be stimulated to grow and remodel back to their normal size and return to their proper function. Two key components necessary to the novel DCCD were designed and constructed for this study. The first component was an adjustable outer shell which enabled the device to become smaller as the failing heart returned to normal size. The second component was an inflatable inner membrane that applies direct pressure to the outer wall of the heart in a way that promotes physiological stress and strain patterns.

Thesis (Ph. D.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 296-319).

Thesis (Th. M.)--Western Seminary, Portland, OR, 2007. / Abstract. Typescript. Description based on print version record. Includes bibliographical references (leaves 148-152).

Thesis (M. Med. Sc.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 53-67).