| 1. |
- Jönelid, Birgitta, 1965-
(författare)
-
Importance of peripheral arterial disease as a risk marker in patients with myocardial infarction
- 2019
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The purpose of this thesis was to describe the true prevalence of widespread arterial disease in a cohort with patients with a recent myocardial infarction (MI) to find valuable clinical methods to detect these patients. Our aim was also to investigate biomarker relationships with peripheral artery disease (PAD) and the importance of PAD in patients’ long-term outcomes.We studied patients with a recent MI in a prospective observational study, the REBUS ((Relevance of Biomarkers for Future Risk of Thromboembolic Events in Unselected Post-myocardial Infarction Patients) trial. A total of 421 patients were included in the study, 390 of whom had their ankle-brachial index (ABI) measured and a mean-time follow up of 5.5 years. Atherosclerotic changes were assessed in three arterial beds by coronary angiography, measuring the ABI and carotid ultrasound. Ninety-two biochemical biomarkers were assessed at baseline by a proximity extension assay (PEA) chip. 263 out of 421 filled in a self-administered Walking Impairment Questionnaire (WIQ). Polyvascular (PvD) disease was defined as pathological findings in all three arterial beds.We found that PAD and PvD are underdiagnosed in patients who suffered a recent MI. We also found the ABI to be a strong and useful method to identify patients with PAD as well as patients with more widespread arterial disease, such as PvD (paper I).The results of the scoring system, the WIQ, showed it is useful for finding patients with PAD and PvD, even when completed soon after an acute MI event (paper II).We also found that biochemical biomarkers associated with the inflammatory pathway – tumour necrosis factor receptor 1 (TNFR-1), tumor necrosis factor receptor 2 (TNFR-2) and growth differentiation factor 15 (GDF-15) – were able to predict pathological ABI, i.e. PAD, in these MI patients. These results could also be validated in another observational study and cohort of MI patients, the VaMIS cohort (paper III). Pathological ABI was also found to be a strong predictor for cardiovascular events of all-cause mortality, new ACS, and a composite endpoint of all-cause mortality, new ACS, new stroke/TIA or new PAD event. When evaluating the three inflammatory biomarkers as a surrogate marker for ABI, they showed a similar association with all-cause death and the composite endpoint (paper IV).
|
|
| 2. |
- Bergström, Ida
(författare)
-
Pro- and anti-inflammatory actions in coronary artery disease : with focus on CD56+ T cells and Annexin A1
- 2015
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- ¨The atherosclerotic process is considered to be driven by an imbalance between proand anti-inflammatory actions. Still, the inflammatory state in patients with coronary artery disease (CAD) remains to be clarified. Annexin A1 (AnxA1) is a glucocorticoidinduced protein which may have a key role in the anti-inflammatory response as a mediator of glucocorticoid effects.The general aim of this thesis was to deepen the knowledge of pro- and antiinflammatory mechanisms in CAD via phenotypic assessments of immune cell subsets, in particular CD56+ T cells, and exploration of AnxA1. The long-term goal is to reveal basic mechanisms that will lead to the development of biomarkers, which may be used for individualized treatment and monitoring.The AnxA1 protein was constitutively expressed in both neutrophils and peripheral blood mononuclear cells (PBMCs). However, it varied considerably across PBMC subsets, being most abundantly expressed in monocytes. The AnxA1 expression was also higher in CD56+ T cells than in CD56- T cells.The expression of total AnxA1 protein in neutrophils was higher in patients with stable angina (SA) compared with controls. However, this was not accompanied by altered neutrophil activation status. Instead, the neutrophils from patients exhibited an enhanced anti-inflammatory response to exogenous AnxA1, emphasizing the potential of AnxA1 as an inhibitor of neutrophil activity. Only patients with acute coronary syndrome (ACS) showed an increase in cell surface-associated AnxA1.CAD patients, independent of clinical presentation, had increased proportions of CD56+ T cells compared with controls, a phenomenon likely to represent immunological aging. The CD56+ T cells were found to exhibit a distinct proinflammatory phenotype compared with CD56- T cells. In all T cell subsets, the expression of cell surface-associated AnxA1 was significantly increased in ACS patients, while it tended to be increased in post-ACS patients. In addition, dexamethasone clearly inhibited activation of CD56+ T cells in in vitro assays, whereas AnxA1 did not. The findings highlight the need to clarify whether the role of AnxA1 is different in T cells than in innate immune cells.In PBMCs, the mRNA levels of AnxA1 were increased in CAD patients, particularly in ACS patients. Correspondingly, the monocytes in ACS patients exhibited increased AnxA1 protein levels, both totally and on the cell surface. However, only cell surface-associated AnxA1 in monocytes correlated with the glucocorticoid sensitivity of PBMCs ex vivo. We propose the expression of cell surfaceassociated AnxA1 to be a promising candidate marker of glucocorticoid sensitivity, which needs further investigations in larger cohorts and intervention trials. Furthermore, the fact that PBMCs in post-ACS patients exhibited pro-inflammatory activity but no increase in cell surface-associated AnxA1 allow us to speculate that the glucocorticoid action and/or availability might be insufficient in these patients.
|
|
| 3. |
- Szymanowski, Aleksander, 1973-
(författare)
-
Detection of apoptosis in patients with coronary artery disease : Assessment of temporal patterns and potential sources
- 2015
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The atherosclerotic process and its consequences are considered driven by an imbalance between pro- and ant-inflammatory actions. One contributing factor in this scenario is an altered regulation of apoptosis, which affects both immune, vascular and myocardial cells. The general aim of this thesis was to measure soluble markers of apoptosis in peripheral venous blood, in various clinical stages of coronary artery disease (CAD) and to further identify possible sources with specific focus on natural killer (NK) cell apoptosis and myocardial ischemia-reperfusion (IR)-injury.There was evidence of an increased apoptosis of NK cells, but not T cells, in the circulation of CAD patients. Spontaneous NK cell apoptosis and the cells´ sensitivity to oxidative stress in the form of oxidized lipids ex vivo, were increased. Findings were thus suggestive of an enhanced apoptosis contributing to the reduced NK cell activity seen in CAD. However, we could not verify that oxidative stress in the circulation was a driving force behind this loss.Soluble forms of the cell surface bound receptors of apoptosis include soluble (s) Fas and sFas ligand (L). They are detected in plasma and used as surrogate markers of apoptosis. Here we investigated the relationship between these markers and NK cell apoptosis and NK cell levels, in a 12 month longitudinal study on CAD patients. Plasma levels of sFasL correlated with increased susceptibility to NK cell apoptosis ex vivo but also with the levels of NK cells in the circulation after a coronary event. NK cells undergoing apoptosis ex vivo were also found to be a major source of sFasL themselves, indicating potential usefulness of sFasL in monitoring changes in NK cell levels.Apoptosis is suggested to be a key event in IR-injury, resulting in increased infarct size, left ventricular (LV) dysfunction, remodeling and heart failure. We investigated soluble markers of apoptosis in relation to these parameters in a ST-elevation myocardial infarction (STEMI) population. In addition to sFas and sFasL, we also measured tumor necrosis factor (TNF) receptor (R) I and II in this study. Acute phase levels of sTNFRI and sTNFRII, but not sFas or sFasL, correlated to cardiac MR (CMR) measures of infarct size and LV-dysfunction at 4 months after the ischemic event. Also, the soluble markers of apoptosis were correlated with matrix metalloproteinase (MMP)-2, a mechanistic trigger for cardiomyocyte apoptosis, further strengthening the role of apoptosis in IR-injury.Finally we explored the temporal patterns of soluble markers of apoptosis after an MI and, furthermore, investigated possible differences between patients presenting with a non(N)-STEMI versus STEMI. The sTNFRI/II and the sFas/sFasL pathways of apoptosis showed different temporal changes indicating diverse roles of these two systems. NSTEMI and STEMI patients however, shared these temporal patterns pointing to apoptosis as equally involved in either infarct type. Furthermore sTNFRs, but not sFas/sFasL correlated to levels of cytokine interleukin (IL)-6 illustrating the overlapping role TNF signaling in inflammation and apoptosis, while again suggesting differences between the TNF and the Fas/FasL systems during myocardial IR--‐injury.
|
|
| 4. |
- Backteman, Karin, 1960-
(författare)
-
T Cells and NK Cells in Coronary Artery Disease : Longitudinal and methodological studies in humans
- 2014
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Coronary artery disease (CAD) is the leading cause of death worldwide and most often due to atherosclerosis. Atherosclerosis is a chronic inflammatory process that involves the arteries, inclouding those that supply blood to the heart muscle. Although inflammation is an important contributing factor to atherosclerosis, the mechanisms are not fully understood. One mechanism contributing to atherogenesis may involve some infectious microorganisms such as cytomegalovirus (CMV). In atherosclerosis, the arterial wall becomes infiltrated with lipids followed by different types of leukocytes and inflammatory mediators (atherogenesis). Leukocytes recirculate continuously between the blood and lymphoid organs, such as lymph nodes, where the adaptive immune response is started and regulated.The general aim of this thesis was to increase the understanding of associations between lymphocyte populations and different conditions of CAD (unstable and stable). To assess changes over time, a longitudinal follow up design was mostly used. Therefore, also perspectives of longitudinal variation were included in the thesis.Paper I showed that flow cytometric evaluation of lymphocyte populations is a robust technique that can be used in longitudinal studies, both in clinical and research settings. It was also shown that the time of sampling over the year did not have a major impact on the findings.In paper II, thoracic lymph nodes were investigated to assess whether CAD-associated changes were more prominent in comparison with blood. As expected, there were several major differences in lymphocyte composition between lymph nodes and blood. However, the analysis of thoracic lymph nodes did not reveal any further changes that were not detected in blood. Thus, blood is still the most reliable compartment for studies of lymphocyte populations in CAD since it is not possible to examine the local findings in the artery wall.Natural killer (NK) cells are innate lymphocytes with both regulatory and effector functions. In paper II and III we confirmed previous findings that CAD patients have lower proportions of NK cells in blood. However, the NK subtype and cytokine profile (paper III, measured by subtype markers and intra-cellular cytokine staining) did not differ between patients and controls. During a 12-month follow-up, the proportions of NK cells increased, although not in all patients. Failure to reconstitute NK cell levels was associated with several components of the metabolic syndrome and with a persistent low-grade inflammation as measured by plasma IL-6 levels. The findings support the notion of a protective role for NK cells in inflammation.CD4+ but not CD8+ T cells were significantly increased in patients with both unstable and stable conditions compared with healthy individuals (paper IV). Subpopulations of CD4+ T cells (CD4+CD28null) have previously been associated with CAD. However, we show that CD28null and CD28null57+ cells within the CD4+ and CD8+ T cell populations were similar in CAD patients and healthy controls. Instead, CMV seropositivity was the major determinant of expanded CD28null and CD57+ T cell fractions in both patients and healthy individuals. During the 1 year follow up the proportion of CD4+CD28null and CD8+CD28null cells increased in patients, which may reflect an accelerated immunological ageing occurring after the cardiac event.
|
|
| 5. |
- Garvin, Peter, 1976-
(författare)
-
Plasma levels of matrix metalloproteinase‐9 in a normal population : a psychoneuroendocrinological approach
- 2008
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Several large‐scale epidemiological studies have demonstrated the prognostic significance of psychosocial factors and stress for coronary artery disease (CAD). Observations of sudden changes in CAD incidence have led to the proposal of mechanisms regarding atherosclerotic plaque vulnerability. The collagen‐degrading enzyme matrix metalloproteinase-9 (MMP-9) is increased in rupture‐prone plaques with high inflammatory activity, and circulating levels of MMP-9 are raised in patients with acute coronary syndrome. However, the distribution of MMP‐9 levels and its relations to psychosocial factors and the stress hormone cortisol have not been previously explored in a normal population.The aim of this dissertation was to examine in a normal population the association of circulating levels of MMP-9 with traditional cardiovascular risk factors including levels of C-reactive protein (CRP), with psychosocial factors, and with saliva levels of cortisol. In addition, the reliability of a new method of ambulatory saliva sampling for assessment of cortisol levels was evaluated. A sub‐sample of the Life conditions, Stress, and Health (LSH)-study, a population based study exploring psychoneuroendocrinological pathways mediating the differences in CAD incidence over socioeconomic status, was used. Plasma levels of MMP-9 were examined in a sample randomly drawn from the LSH‐study (n=400), aged 45 to 69 years at enrollment.The main findings were: 1) there was a positive association between plasma MMP-9 levels and total risk load of cardiovascular risk factors. The findings were persistent after adjusting for CRP and could not be attributed to a single risk factor. 2) After adjusting for traditional cardiovascular risk factors and CRP, MMP-9 levels were positively associated with psychosocial risk factors and negatively associated with psychosocial resources. 3) Pooling saliva samples prior to laboratory analysis were as reliable as arithmetic means for assessment of diurnal cortisol variation in a field research setting. 4) There was a positive association between circulating levels of MMP‐9 and saliva levels of cortisol, both diurnal peak level and evening level of cortisol. The observed associations between MMP‐9 and traditional cardiovascular risk factors, psychosocial factors, and saliva cortisol levels suggest a psychoneuroendocrinological pathway linking stress to plaque vulnerability and provide increased understanding of the association between psychosocial factors and CAD.
|
|
| 6. |
- Eriksson, Maria, 1965-
(författare)
-
Adipocyte-derived hormones and cardiovascular disease
- 2010
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Obesity is increasing globally and related to major changes in lifestyle. This increase is associated with an increased risk of cardiovascular disease (CVD). Knowledge about adipose tissue as a metabolic-endocrine organ has increased during the last few decades. Adipose tissue produces a number of proteins with increased body weight, many of which are important for food intake and satiety, insulin sensitivity, and vessel integrity, and aberrations have been related to atherosclerosis. Notably, the risk for developing CVD over the course of a lifetime differs between men and women. In Northern Sweden, men have a higher risk for myocardial infarction (MI). However, the incidence is declining in men but not in women. These sex differences could be due to functional and anatomical differences in the fat mass and its functions. The primary aim of this thesis was to evaluate associations between the adipocyte-derived hormones leptin and adiponectin, and fibrinolysis and other variables associated with the metabolic syndrome, and particularly whether these associations differ between men and women. Another aim was to evaluate these associations during physical exercise and pharmacological intervention (i.e. enalapril). Finally, whether leptin and adiponectin predict a first MI or sudden cardiac death with putative sex differences was also investigated. The first study used a cross-sectional design and included 72 men and women recruited from the WHO MONICA project. We found pronounced sex differences in the associations with fibrinolytic variables. Leptin was associated with fibrinolytic factors in men, whereas insulin resistance was strongly associated with all fibrinolytic factors in women. The second study was an experimental observational study with 20 men exposed to strenuous physical exercise. During exercise, leptin levels decreased and adiponectin levels increased, and both were strongly associated with an improved fibrinolytic capacity measured as decreased PAI-1 activity. Changes in insulin sensitivity were not associated with changing adiponectin levels. The third study was a randomised, double-blind, single centre clinical trial including 46 men and 37 women who had an earlier MI. The study duration was one year, and participating subjects were randomised to either placebo or ACE inhibitor (i.e. enalapril). Circulating leptin levels were not associated with enalapril treatment. During the one-year study, changes in leptin levels were associated with changes in circulating levels of tPA mass, PAI-1 mass, and tPA-PAI complex in men, but not vWF. These associations were found in all men and men on placebo treatment. In women on enalapril treatment there was an association between changes in leptin and changes in vWF. In the fourth study, the impact of leptin, adiponectin, and their ratio on future MI risk or sudden cardiac death was tested in a prospective nested casecontrol study within the framework of the WHO MONICA, Västerbotten Intervention Project (VIP), and Västerbotten Mammary Screening Program (MSP). A total 564 cases (first-ever MI or sudden cardiac death) and 1082 matched controls were selected. High leptin, low adiponectin, and a high leptin/adiponectin ratio independently predicted a first-ever MI, possibly with higher risk in men in regards to leptin. The association was found for non-fatal cases with ST-elevation MI. Subjects with low adiponectin levels had their MI earlier than those with high levels. In conclusion, the adipocyte-derived hormones leptin and adiponectin are related to the development of CVD with a sex difference, and fibrinolytic mechanisms could be possible contributors to CVD risk.
|
|
| 7. |
- Hellman, Urban, 1966-
(författare)
-
About hyaluronan in the hypertrophic heart : studies on coordinated regulation of extracellular matrix signalling
- 2010
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Background. Myocardial hypertrophy is a risk factor for cardiovascular morbidity and mortality. Independent of underlying disease, the cardiac muscle strives in different ways to compensate for an increased workload. This remodelling of the heart includes changes in the extracellular matrix which will affect systolic and diastolic cardiac function. Furthermore, signal transduction, molecular diffusion and microcirculation will be affected in the hypertrophic process. One important extracellular component is the glycosaminoglycan hyaluronan. It has been shown to play a major role in other conditions that feature cellular growth and proliferation, such as wound healing and malignancies. The aim of this thesis was to investigate hyaluronan and its role in both an experimental rat model of cardiac hypertrophy as well as in cultured mouse cardiomyocytes and fibroblasts. Methods. Cardiac hypertrophy was induced in rats by aortic ligation. Hyaluronan concentration was measured and expression of genes coding for hyaluronan synthases were quantified after 1, 6 and 42 days after operation, in cardiac tissue from the left ventricular wall. Localization of hyaluronan and its receptor CD44 was studied histochemically. Hyaluronan synthesis was correlated to gene transcription using microarray gene expression analysis. Cultures of cardiomyocytes and fibroblasts were stimulated with growth factors. Hyaluronan concentration was measured and expression of genes coding for hyaluronan synthases were detected. Hyaluronan size was measured and crosstalk between cardiomyocytes and fibroblasts was investigated. Results. Increased concentration of hyaluronan in hypertrophied cardiac tissue was observed together with an up-regulation of two hyaluronan synthase genes. Hyaluronan was detected in the myocardium and in the adventitia of cardiac arteries whereas CD44 staining was mainly found in and around the adventitia. Hyaluronan synthesis correlated to the expression of genes, regulated by transcription factors known to initiate cardiac hypertrophy. Stimulation of cardiomyocytes by PDGF-BB induced synthesis of hyaluronan. Cardiomyocytes also secreted a factor into culture media that after transfer to fibroblasts initiated an increased synthesis of hyaluronan. When stimulated with hyaluronan of different sizes, a change in cardiomyocyte gene expression was observed. Different growth factors induced production of different sizes of hyaluronan in fibroblasts. The main synthase detected was hyaluronan synthase-2. Cardiomyocytes were also shown to secrete microvesicles containing both DNA and RNA. Isolated microvesicles incubated with fibroblasts were observed by confocal microscopy to be internalized into fibroblasts. Altered gene expression was observed in microvesicle stimulated fibroblasts. Conclusion. This study shows that increased hyaluronan synthesis in cardiac tissue during hypertrophic development is a part of the extracellular matrix remodelling. Cell cultures revealed the ability of cardiomyocytes to both synthesize hyaluronan and to convey signals to fibroblasts, causing them to increase hyaluronan synthesis. Cardiomyocytes are likely to express receptors for hyaluronan, which mediate intracellular signalling causing the observed altered gene expression in cardiomyocytes stimulated with hyaluronan. This demonstrates the extensive involvement of hyaluronan in cardiac hypertrophy.
|
|
| 8. |
- Jönsson, Simon, 1983-
(författare)
-
Leukocyte-derived matrix metalloproteinase-9 in patients with coronary artery disease : Associations with psychological stress and glucocorticoid sensitivity
- 2015
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Inflammation is closely associated with development of atherosclerosis. The proteolytic enzyme matrix metalloproteinase (MMP)-9 is considered to play a prominent role in this process. MMP-9 has also been introduced as a marker for plaque vulnerability. Still, the possible mechanisms behind altered levels of MMP-9 and its tissue inhibitors (TIMPs) in patients with atherosclerotic disease remain unclear. The general aim of this thesis was to compare leukocyte-derived MMP-9 and TIMPs in patients with coronary artery disease (CAD) and healthy controls and to further relate the findings to psychological stress and glucocorticoid sensitivity.Levels of leukocyte-derived MMP-9 and TIMP-1 showed a significant difference between CAD patients and controls. Neutrophils in CAD patients were more prone to release MMP-9 and furthermore, PBMCs in patients expressed higher levels of MMP-9 and TIMP-1 and -2 mRNA than PBMCs in controls while there were no differences in plasma or serum levels. The increase in leukocyte-derived levels of MMP-9 and TIMPs indicate the presence of preactivated leukocytes in CAD.Inflammation has been proposed as a mechanistic link between cardiovascular risk and depressive symptoms. We investigated whether the overexpression of leukocyte-derived MMP-9 and TIMPs in CAD patients was associated with psychological factors. Patients exhibited sustained elevations in depressive symptoms, however, these symptoms were not related to any MMP-9 or TIMP variables. The findings suggest that overexpression of leukocyte-derived MMP-9 and TIMPs and elevated depressive scores represent two parallel phenomena in CAD.Chronic inflammation may be associated with reduced glucocorticoid sensitivity. We found that PBMCs in CAD patient expressed significantly increased levels of glucocorticoid receptor (GR)-α mRNA, whereas GR-β mRNA levels did not differ between patients and controls. Moreover, in ex vivo assays, dexamethasone efficiently suppressed MMP-9 and TIMPs equally or even more in patients compared to controls. The findings provide evidence for enhanced glucocorticoid sensitivity in CAD patients and also suggest that a state of relative hypocortisolism may contribute to the overexpression of leukocyte-derived MMP-9 and TIMPs.Lastly, we explored the release of MMP-9, TIMPs and cortisol in response to acute mental stress in CAD patients. Patients who exhibited a significant stress-induced increase in serum MMP-9 also exhibited an altered cortisol response. Moreover, the susceptibility to stressinduced increase in serum MMP-9 was associated with shorter leukocyte telomere length and atherosclerotic plaque burden. The findings highlight the existence of a high-risk group which may be in need of improved diagnostic and therapeutic strategies.
|
|
| 9. |
- Lundgren, Oskar, 1979-
(författare)
-
Psychological Resources and Risk Factors in Coronary Heart Disease : Assessment, Impact and the Influence of Mindfulness Training
- 2018
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- There is strong evidence for the observation that psychological risk factors, such as depressive symptoms, hopelessness, and anxiety are associated with higher risk of developing coronary heart disease (CHD), and also contribute to a worse prognosis among CHD patients. Much less is known about psychological resources, such as Mastery, and their role in cardiovascular medicine. Although the current state of science about the importance of psychological factors has advanced during the last decades, the mental health status of patients is often neglected in clinical practice. The reason behind this gap is multifaceted, including unawareness of the current state of science among professionals and a lack of clear guideline, which in turn, results from a lack of evidence-based ways to address the issues. Furthermore, the measurement of psychological resources is complex and a debated topic in psychology. The aim of this thesis was to investigate: 1) If the use of inverted items in three questionnaires that measure psychological resources and risk factors represent a validity risk in the context of CHD. 2) If psychological resources and risk factors are independently associated with incidence in CHD. 3) If an eight-week course in Mindfulness-Based Stress Reduction (MBSR) is a feasible psychological intervention, as an addition to cardiac rehabilitation. 4) How CHD patients experience the practices of mindfulness and yoga in MBSR.In Study I and II, data from 1007 participants randomly selected from a Swedish community sample, aged 45-69 at baseline (50 % women), were analysed. To study the validity of the self-report instruments Mastery, Self-esteem and Centre for Epidemiological Studies Depression scale (CESD), subscales with only positive and negative items were created. The new subscales were evaluated against three criterion measures; cross-sectional against each other and the circulatory marker of inflammation interleukine-6 (IL-6) (concurrent construct validity); prospectively against 8-year incidence in CHD (predictive validity), and in addition, a factor analysis was used to investigate construct dimensionality. The instruments seemed to be valid measures of psychological resources and risk factors in the context of CHD risk. The new subscales showed the same associations as the original scales, except for the positive items in CES-D. However, this did not have a major influence on the full scale. In Study II a prospective analysis of the impact of psychological factors on 8-year incidence in CHD was performed. The psychological resources Mastery and Self-esteem were negatively associated with CHD, also after adjustment for nine traditional cardiovascular risk factors in Cox proportional hazard models. The protective effect of the two resources, and the increased risk of Hopelessness, remained after adjustment for depressive symptoms. In Study III and IV, a group of CHD patients with depressive symptoms (n=79) was invited to participate in MBSR as a complement to cardiac rehabilitation. Twenty-four patients started MBSR and 16 completed it. The results were compared with a reference group (n=108) of patients from the same clinic, which showed stability in psychological variables over 12 months. MBSR was appreciated by the patients and improvements in psychological risk factors (e.g., depressive symptoms), and an increase in Mastery were observed. Study IV made use of a qualitative content analysis of diary entries written by patients immediately after practice sessions throughout MBSR. Participants described difficulties, both physical and psychological, during the whole course, but as the weeks passed they more frequently described an enhanced ability to concentrate, relax and deal with distractions. From the combined findings in Study III and IV, we conclude that MBSR could be a promising complement to cardiac rehabilitation for a selection of patients.The overall picture, emerging from this thesis, strengthens the argument that psychological factors should be recognized and addressed in clinical practice. It also encourages further studies of how psychological resources could be built, which could inform the development of effective prevention and treatment strategies for CHD patients with psychological distress and also contribute to improved public health interventions.
|
|
| 10. |
- Sandberg, Camilla, 1971-
(författare)
-
Physical performance, physical activity, body composition and exercise training in adults with congenital heart disease
- 2016
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Background Adults with congenital heart disease (CHD) is a growing population and related to advances in surgical and medical treatment, they now outnumber the children with corresponding lesions. Since a congenital heart lesion often results in reduced exercise capacity, this population is a potential target for physiotherapy. To what extent this reduction in exercise capacity is caused by abnormal cardiovascular anatomy and physiology or to what degree insufficient physical activity contributes is not known. To support the advancements in paediatric cardiac care, increased knowledge regarding physical performance, physical activity level, body composition and the effects of exercise training among adults with CHD is required.Methods In a cross-sectional study skeletal- and respiratory muscle function, physical activity level and exercise self-efficacy was investigated among 85 adults with various forms of CHD and 42 control subjects. A second study was conducted to analyse height, weight and body mass index (BMI) in 538 adults with complex CHD and 1886 adults with simple CHD. Data were extracted from the Swedish registry on congenital heart disease (SWEDCON) and compared to data from a national population survey. In a third study, factors associated with self-reported quality of life (QoL) were analysed using SWEDCON data on 315 adults with congenital aortic valve disease. Finally, a randomised controlled trial was conducted to investigate the effects of interval exercise training among adults with complex CHD.Results Adults with complex CHD showed impaired muscle function compared to both patients with simple CHD and controls. In addition, patients with complex CHD had a lower exercise self-efficacy compared to controls. Patients with CHD were equally active at moderate-to-vigorous level as the controls. However, approximately 50% of both patients and controls failed to reach the recommended physical activity level. In general patients with CHD had the same height, weight and BMI, as the general population. However, compared to the general population, men with CHD were more commonly underweight and less commonly overweight/obese. Additionally, especially male patients with complex CHD were shorter compared to the general population. Among adults with congenital aortic valve disease, a higher physical activity level was associated with better QoL. Furthermore, interval training increased exercise capacity and endurance among adults with complex CHD.Conclusion A higher physical activity level was associated with better self-reported QoL in patients with congenital aortic valve disease which implies that QoL might be possible to improve, by adopting a physically active life-style. Adults with CHD were equally active as controls at a moderate-to-vigorous physical activity level. However, approximately half of both groups were insufficiently physically active based on current recommendations. This indicates that low physical activity, on group level, does not explain the lower exercise capacity commonly found among patients with CHD. In addition, this is consistent the finding that the majority of patients followed the same pattern regarding BMI as seen in the general population. However, impaired muscle function in combination with the shorter stature and higher prevalence of underweight found in men, especially with complex CHD, implies an altered body composition in this group. The findings of the present thesis suggests an indication for physiotherapy targeting increased physical activity level and individualized exercise training in this patient population. Moreover, regular evaluation of muscle function, exercise self-efficacy and QoL, in addition to exercise capacity, might be useful for monitoring disease development over time.
|
|
