Purpose: The primary purpose of this study was to determine if a pedometer-driven physical activity (PA) intervention with individualized stepcount goals would be more efficacious in yielding greater amounts of PA than the usual time-based PA recommendations given to maintenance CR patients. Additionally, the secondary purpose of this study was to assess differences in stepcount activity on days attending maintenance CR and on non-rehab days. Methods: Subjects entering maintenance CR for the first referral were recruited for study participation and stratified into pedometer feedback (PF) and usual care (UC) groups. All subjects wore a New Lifestyles NL-1000 pedometer. PF subjects wore the pedometer for the duration of the 8-week study. For comparison, UC subjects wore the pedometer at baseline, week 4, and week 8.Both groups were encouraged to accumulate a minimum of 40 - 50 min/d at moderate intensity when attending maintenance CR. UC subjects were encouraged to follow-up with at least 30 min/d PA outside maintenance CR, while PF subjects were given daily stepcount goals. Stepcount goals were calculated as 10% of baseline stepcounts and added weekly to increase daily goal. All subjects completed a 6- minute walk test at baseline and week 8, and behavioral change questionnaires were completed at baseline, week 4, and week 8. Results: A total of 18 subjects (PF, n = 9, 53.7±8.0; UC, n = 9, 60.2±9.6 yrs) completed the 8-week study. There were no differences between groups at baseline. PF group increased daily stepcounts by week 4 (19%, 1,080±649 steps/d) and 8 (44%, 2,468±846 steps/d) in addition to days attending rehab by week 4 (14%, 1064±45 steps/d) and 8 (36%, 2,711±423 steps/d) and non-rehab days by week 8 (42%, 1,747±759 steps/d). PF subjects accumulated greater daily stepcounts compared to UC subjects at weeks 4 (26%, 1,405±393 steps/d) and 8 (48%, 2,612±284 steps/d). UC subjects accumulated greater stepcounts on rehab compared to non-rehab days, but no changes were found from baseline for daily stepcounts, rehab, or non-rehab days. There was a time effect for responses to social support from friends for all subjects (baseline to week 4) and a time by group effect for decision balance pro-questions by week 4 where PF significantly increased, UC significantly decreased, and both groups where significantly different. Conclusions: The results of this study suggest that a pedometer-driven PA intervention yields significantly greater stepcounts compared to time-based PA recommendations among maintenance CR patients. / School of Physical Education, Sport, and Exercise Science

Clinically, the modified Bruce protocol is widely used to predict functional capacity in cardiac patients. However, it has been suggested that cardiac patients have lower oxygen uptakes for standard workloads. In order to study this, we measured oxygen uptake (V02) and venous bloodV02 derived from lactic acid concentration during a modified Bruce treadmill protocol in 12 pest myocardial infarction (MI) and 12 normal males. During three stages of the protocol mean oxygen uptake was significantly lower (1.42 - 6.2 ml/kg.min; p < .001) for the pest MI than the normal males.However, venous blood lactic acid concentrations were not different at these stages. The MI patients' measured V02 for three stages of the protocol ranged from 1.8 - 7.3 ml/kg.min lower than the Bruce predictions for cardiacs. In addition, measured V02 (max) for cardiac patients were from 3.68 to 11.15 ml/kg.min lower than the predicted the normal subjects. These data suggest myocardial damage may slow oxygen kinetics and results in lower actual V02during treadmill testing. However, blood lactic acid concentrations failed to demonstrate an anaerobic compensation for the lower V02 in pest MI patients.

Chronic obstructive pulmonary disease (COPD) and chronic heart failure (CHF) patients show a marked reduction in exercise capacity compared to that of healthy age-matched individuals. While inadequate gas exchange and resulting hypoxemia appears as the primary factor in COPD, an impaired cardiac output is the predominant explanation for the reduced oxygen delivery in CHF. However, the extent of the contributions of other systemic factors remains unclear. In light of the potential interactions between cardiac output (Qc) and pulmonary hyperinflation, there is surprisingly little data thus far on ventilatory constraints in CHF and on the role of blood flow delivery in COPD which may further limit the exercise capacity. Thus, the purpose of this study was to compare the slope of the Qc versus oxygen uptake (VO2) response through several submaximal cycling loads in patients with moderately severe COPD and with that of moderate to severe CHF patients as well as age-matched healthy control subjects (CTRL). Also examined was the possibility that ventilatory constraints such as dynamic hyperinflation contribute to an abnormal stroke volume response in both diseases. Cardiac output was measured using the CO 2-rebreathing equilibrium technique during baseline conditions and cycling at 20, 40 and 65% of peak power in 17 COPD (Age: 64 +/- 8 yrs; FEV 1/FVC: 37 +/- 11%; FEV1: 41 +/- 15 % predicted), 10 CHF (Age: 57+/- 10 yrs; FEV1/FVC: 73.8 +/- 5.6%; FEV 1: 93 +/- 13% predicted) and 10 age-matched CTRL subjects. Inspiratory capacity (IC) was also measured for the determination of dynamic hyperinflation during the steady state exercise bouts. The results indicate that while the absolute Qc values are lower in COPD and in CHF than in CTRL during 65% peak power cycling (11.30 +/- 2.38 vs 12.40 +/- 2.08 vs 15.63 +/- 2.15 L&bull;min-1 respectively, p &lt; 0.01), likely due to their lower exercise metabolic demand. The Qc/VO2 response to increasing levels of exercise intensity was lower or normal in CHF patients compared to CTRL, while normal or hyperdynamic in most COPD patients. Indeed, the majority of patients with COPD exhibited Qc/VO2 slopes greater than 7.0, which may be indicative of a peripheral muscle bioenergetic disturbance that may drive the need for greater oxygen delivery, and thus result in an exaggerated central circulatory response.

Heart failure has a significant impact on mortality and morbidity. Dilated cardiomyopathy (DCM) is the third most common cause of heart failure and the most common reason for heart transplantation. Familial DCM is known to be caused by mutations in the LMNA gene encoding lamins A and C. New methods to enhance cardiac contractility would be beneficial in the treatment or prevention of heart failure. The focus of this thesis was to evaluate the mechanisms of altered contractility in two mouse models: the LMNA knockout model (homozygous, Lmna-/-; heterozygous, Lmna+/-) generated by targeted deletion of the lmna gene, and the model of enhanced contractility due to cardiac alpha1A-adrenergic receptor (???1A-AR) overexpression (A1A1). Previous studies have found altered nuclear-desmin connections in lamin A/C deficient mice. It was proposed that these alterations result in ???defective force transmission???, which leads to DCM. Studies in this thesis have supported this hypothesis. Studies of isolated single cardiomyocytes from mice aged 4-6 weeks demonstrated abnormal cell morphology and contractile dysfunction in Lmna-/- cardiomyocytes, while Lmna+/- cells showed no overt phenotype. Excitation-contraction coupling experiments and forcecalcium studies in skinned fibers excluded altered calcium kinetics as a primary cause of DCM in this model, but there was evidence of reduced sarcomere numbers and reduced sarcomere lengths as a contributor to reduce force generation in Lmna-/- and Lmna+/- mice. Previous in vivo studies showed that A1A1 mice had enhanced contractility with the absence of hypertrophy. Studies on isolated single cardiomyocytes from A1A1 mice aged 8-12 weeks showed reduced contractility in the absence of ???1A-AR stimulation, but an exaggerated response to ???1A-AR stimulation. In contrast isolated isovolumic Langendorff perfused A1A1 hearts without ???1A-AR stimulation replicated the enhanced contractility observed in vivo. These studies are consistent with down-regulation of contractility due to the hyperactivity of the overexpressed ???1A-AR in vivo, which only becomes evident in isolated cells without ???1A-AR stimulation due to the loss of functional receptor numbers during isolation. Sufficient spontaneously active ???1A-ARs are preserved in the isolated Langendorff heart preparation to ensure maximum contractility driven by increase calcium release.

Thesis (M.S.)--Missouri State University, 2008. / "August 2008." Includes bibliographical references (leaves 44-45). Also available online.

Thesis (M.A. in communication)--Washington State University, August 2010. / Title from PDF title page (viewed on July 29, 2010). "Edward R. Murrow College of Communication." Includes bibliographical references (p. 58-62).

Coping strategies and causal attributions have been shown to be related to recovery and adjustment following illness. Certain coping strategies and causal attributions, such as avoidant coping and other blame have been found to be related to higher levels of distress while others, like behavioural self blame and attention coping have been shown to be related to lower distress. There have however, been few longitudinal studies of the process. The study described here examined coping strategies, causal attributions and levels of distress over a period of 1 year in 91 patients following a first myocardial infarction (MI). Coping strategies (measured by the COPE), causal attributions (measured by open ended questions and a check-list) and distress (measured by the HAD a measure of anxiety and depression with minimal somatic symptoms), were measured within 2 weeks of discharge and at 2, 6 and 12 months post MI. The main findings of the study showed that both coping strategies and causal attributions changed over time. Patients were most likely to use attention coping strategies early following the illness onset but more avoidant and religious coping later on. Patients made fewer attributions as time passed and the most commonly reported causal attributions were stress and smoking. Results further revealed that both coping strategies and causal attributions were either concurrently related to and/or predictive of levels of distress. Avoidant coping was related to higher distress at all assessment times. Furthermore, both characterological self blame and other blame were found to be concurrently related to higher distress, with characterological self blame also being predictive of subsequent higher distress. These findings have implications for care and rehabilitation of cardiac patients as they imply that certain causal attributions and coping strategies might be problematic as regards post MI distress. This points towards the importance of examining and if necessary, altering certain causal attributions and coping strategies in order for the patient to gain the best possible recovery.

Thesis (MTech (Biomedical Technology))--Cape Peninsula University of Technology, 2016. / Type 2 diabetes mellitus (T2DM) is a metabolic disorder which is characterised by insulin resistance, defective insulin secretion or both. The chronic state of hyperglycemia in diabetes is associated with microvascular complications and macrovascular complications which account for an estimated 80% of deaths as a result of cardiovascular complications. Type 2 diabetes mellitus is an inflammatory disease and pro- inflammatory stimuli in the form of activated endothelial cells, render the vascular endothelial surface attractive for both platelets and leukocytes. Activated platelets bind to the exposed extracellular matrix (ECM) and also to each other in both physiological haemostasis and pathological thrombosis. They can also adhere to leukocytes. Platelet leukocyte interactions are divided into 3 stages; these include the initiation of the interaction, stabilization of the aggregates and amplification of leukocyte activation. This study attempts to contribute to the current knowledge of T2DM by investigating the percentage of monocytes and neutrophils forming aggregates with platelets in pre-diabetes and diabetes and comparing this to non- diabetes individuals as well as the up regulation of pro-thrombotic and activation antigens on the surface of monocytes and neutrophils (Tissue Factor and CD69). Levels of platelet activation and function will be determined by both plate monocyte aggregates (PMA) and platelet neutrophil aggregates (PNA). A total of 124 individuals were recruited from Bellville South, Cape Town, South Africa. This comprised of diabetes (DM) (n=15), pre-diabetes (pre-T2DM) (n=25) and controls (n=84). All individuals were screened for diabetes using the oral glucose tolerance test (OGTT). Platelet leukocyte measurements were performed using the Navios 8-colour flow cytometer. The median percentage of circulating platelets bound to monocytes (%PMAs) was significantly increased in the T2DM 49.04[36.78-62] and the Pre-T2DM 48.96[36.72-61.2],groups, compared to the control group 7.2[5.4-9], p<0.0001. The median %PNAs, which show interactions between neutrophils and platelets, were significantly increased in the T2DM group 13.56[10.17-16.95] compared to the control group 6.01[4.51-7.51] p<0.0001. Platelet monocyte aggregates (PMAs) were higher in both the pre-T2DM and T2DM groups when compared to the control group indicating increased interactions between platelets and monocytes. In addition to forming aggregates with leukocytes, the platelets were able to initiate activation and phenotypic change to the leukocytes by increasing the expression of CD69 and TF (CD142). This finding provides further evidence that there is a link between the inflammatory process and the prothrombotic activity evident in diabetes and pre-diabetes individuals. Furthermore, we describe elevated levels of circulating activated neutrophils which directly correlate with increased PNA formation in both the pre-T2DM and T2DM group. / South African Medical Research Council

M.Cur. (Intensive General Nursing) / The rehabilitation of the coronary artery bypass patient should be a continuation of the contact which exists during the hospitalisation phase, with specific reference to the pre-dismissal phase. As a member of the health team, the nurse makes the most important inputs during this phase because she is the one who is in constant contact with the patient and his family. The purpose of this study is to determine, by means of set criteria and within a nursing perspective, the contributions that are made by various support groups to the rehabilitation of persons who have undergone coronary artery bypass surgery.

Congenital heart defects (CHD) are the largest class of birth defects in humans and are a major cause of infant mortality and morbidity. Deciphering the molecular and genetic etiologies central for heart development and the pathogenesis of congenital heart diseases (CHD) is a challenging puzzle. We have previously demonstrated that the zinc-finger kruppel-like transcription factor KLF13, expressed predominantly in the atria, binds evolutionarily conserved regulatory elements known as CACC-boxes and transcriptionally activates several cardiac promoters. KLF13 loss of function in Xenopus embryos was associated with cardiac developmental defects underscoring its critical role in the heart. In the current study, using in vivo and in vitro approaches, we examined KLF13’s mechanisms of action and its interaction with other cardiac regulators. To test the evolutionary conserved role in the mammalian heart, we deleted the Klf13 gene in transgenic mice using homologous recombination. Mice with homozygote deletion of Klf13 were born at reduced frequency owing to severe heart defects. We also report the existence of a novel isoform of KLF13, referred to here as KLF13b. Furthermore, we report that KLF13 interacts biochemically and genetically with the T-box transcription factor TBX5 which is a key regulator of heart development. Our data provide novel insight into the role of KLF13 in cardiac transcription and suggest that KLF13 maybe a genetic modifier of congenital heart disease. Furthering our knowledge of protein-protein interactions and gene transcription will enhance genotype-phenotype correlation and contribute to better understanding of the etiology of CHD.