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Jonasson, Lena
Publications (10 of 93) Show all publications
Lundgren, O., Garvin, P., Kristenson, M., Jonasson, L. & Thylén, I. (2018). A journey through chaos and calmness: experiences of mindfulness training in patients with depressive symptoms after a recent coronary event - a qualitative diary content analysis.. BMC Psychology, 6(1), Article ID 46.
Open this publication in new window or tab >>A journey through chaos and calmness: experiences of mindfulness training in patients with depressive symptoms after a recent coronary event - a qualitative diary content analysis.
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2018 (English)In: BMC Psychology, E-ISSN 2050-7283, Vol. 6, no 1, article id 46Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Psychological distress with symptoms of depression and anxiety is common and unrecognized in patients with coronary artery disease (CAD). Efforts have been made to treat psychological distress in CAD with both conventional methods, such as antidepressant drugs and psychotherapy, and non-conventional methods, such as stress management courses. However, studies focusing on the experiences of mindfulness training in this population are still scarce. Therefore, the aim of this study was to explore immediate experiences of mindfulness practice among CAD patients with depressive symptoms.

METHODS: A qualitative content analysis of diary entries, written immediately after practice sessions and continuously during an 8-week long Mindfulness Based Stress Reduction course (MBSR), was applied.

RESULTS: Twelve respondents participated in the study. The main category: a journey through chaos and calmness captured the participants' concurrent experiences of challenges and rewards over time. This journey appears to reflect a progressive development culminating in the harvesting of the fruits of practice at the end of the mindfulness training. Descriptions of various challenging facets of mindfulness practice - both physical and psychological - commonly occurred during the whole course, although distressing experiences were more predominant during the first half. Furthermore, the diary entries showed a wide variety of ways of dealing with these struggles, including both constructive and less constructive strategies of facing difficult experiences. As the weeks passed, participants more frequently described an enhanced ability to concentrate, relax and deal with distractions. They also developed their capacity to observe the content of their mind and described how the practice began to yield rewards in the form of well-being and a sense of mastery.

CONCLUSIONS: Introducing MBSR in the aftermath of a cardiac event, when depressive symptoms are present, is a complex and delicate challenge in clinical practice. More nuanced information about what to expect as well as the addition of motivational support and skillful guidance during the course should be given in accordance with the participants' experiences and needs.

TRIAL REGISTRATION: The trial was retrospectively registered in clinicaltrials.gov (registration number: NCT03340948 ).

Place, publisher, year, edition, pages
BioMed Central, 2018
Keywords
Depressive symptoms, Mindfulness based stress reduction, Myocardial infarction, Qualitative content analysis, Unstable angina pectoris
National Category
Other Medical Sciences not elsewhere specified
Identifiers
urn:nbn:se:liu:diva-153226 (URN)10.1186/s40359-018-0252-1 (DOI)30213276 (PubMedID)2-s2.0-85053272711 (Scopus ID)
Available from: 2018-12-03 Created: 2018-12-03 Last updated: 2019-05-01Bibliographically approved
Lundgren, O., Garvin, P., Andersson, G., Jonasson, L. & Kristenson, M. (2018). Inverted items and validity: A psychobiological evaluation of two measures of psychological resources and one depression scale. Health psychology open, 5(1), Article ID 2055102918755045.
Open this publication in new window or tab >>Inverted items and validity: A psychobiological evaluation of two measures of psychological resources and one depression scale
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2018 (English)In: Health psychology open, ISSN 2055-1029, Vol. 5, no 1, article id 2055102918755045Article in journal (Refereed) Published
Abstract [en]

Psychological resources and risk factors influence risk of coronary heart disease. We evaluated whether inverted items in the Self-esteem, Mastery, and Center for Epidemiological Studies Depression scales compromise validity in the context of coronary heart disease. In a population-based sample, validity was investigated by calculating correlations with other scales (n = 1004) and interleukin-6 (n = 374), and by analyzing the relationship with 8-year coronary heart disease risk (n = 1000). Negative items did not affect the validity of the resource scales. In contrast, positive items from Center for Epidemiological Studies Depression showed no significant relationships with biological variables. However, they had no major impact on the validity of the original scale.

Place, publisher, year, edition, pages
Sage Publications, 2018
Keywords
coronary heart disease, depressiveness, interleukin-6, mastery, self-esteem, wording effect
National Category
General Practice
Identifiers
urn:nbn:se:liu:diva-146087 (URN)10.1177/2055102918755045 (DOI)29479456 (PubMedID)
Available from: 2018-03-27 Created: 2018-03-27 Last updated: 2019-04-10Bibliographically approved
Jonasson, L. & Hansson, G. (2017). Inflammation och ateroskleros – sista pusselbiten är på plats: Inflammation är en aktör vid ateroskleros: nya fynd kan ge ny måltavla för effektiv läkemedelsterapi. Läkartidningen, 114
Open this publication in new window or tab >>Inflammation och ateroskleros – sista pusselbiten är på plats: Inflammation är en aktör vid ateroskleros: nya fynd kan ge ny måltavla för effektiv läkemedelsterapi
2017 (English)In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 114Article in journal, Editorial material (Refereed) Published
Abstract [en]

Inflammation and atherosclerosis - last piece of the puzzle has fallen into place Inflammation is a major component of atherosclerotic lesions and inflammatory biomarkers can be used to predict cardiovascular disease. Still, it has been unclear whether inflammation is a driving force in atherosclerosis, or merely an epiphenomenon. The recently published results of the CANTOS trial shows that treatment with canacinumab, a monoclonal antibody to the proinflammatory cytokine interleukin-1ß, led to a significantly lower rate of recurrent cardiovascular events, compared to placebo. Thus, it establishes beyond doubt that inflammation is a treatable pathogenetic mechanism in atherosclerosis.

Place, publisher, year, edition, pages
Stockholm, Sweden: Läkartidningen Förlag AB, 2017
National Category
Rheumatology and Autoimmunity
Identifiers
urn:nbn:se:liu:diva-146333 (URN)29292899 (PubMedID)
Available from: 2018-04-07 Created: 2018-04-07 Last updated: 2018-05-01Bibliographically approved
Hasib, L., Lundberg, A., Zachrisson, H., Ernerudh, J. & Jonasson, L. (2016). Functional and homeostatic defects of regulatory T cells in patients with coronary artery disease. Journal of Internal Medicine, 279(1), 63-77
Open this publication in new window or tab >>Functional and homeostatic defects of regulatory T cells in patients with coronary artery disease
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2016 (English)In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 279, no 1, p. 63-77Article in journal (Refereed) Published
Abstract [en]

ObjectiveRegulatory T cells (Tregs) are considered atheroprotective, and low levels have been associated with the acute coronary syndrome (ACS), particularly non-ST elevation (NSTE)-ACS. However, the functional properties as well as homeostasis of Tregs are mainly unknown in coronary artery disease (CAD). Here, we investigated the composition and functional properties of naive (n) and memory (m)Tregs in patients with NSTE-ACS and in patients 6-12months post-ACS. MethodsBased on the expression of CD25, FOXP3, CD127, CD45RA, CD39 and CTLA-4, Tregsubsets were defined by flow cytometry in whole blood or isolated CD4(+) T cells. The functional properties of nTregs and mTregs were examined in terms of proliferative capacity and modulation of cytokine secretion. To understand the potential consequences of Treg defects, we also investigated correlations with lipopolysaccharide (LPS)-induced cytokine secretion and ultrasound-defined carotid atherosclerosis. ResultsBoth NSTE-ACS and post-ACS patients exhibited reduced levels of nTregs (P<0.001) compared with healthy control subjects, but without compensatory increases in mTregs. Both nTregs and mTregs from patients showed significantly lower replicative rates and impaired capacity to modulate T-cell proliferation and secretion of interferon-gamma and IL-10. The Treg defect was also associated with LPS-induced cytokine secretion and increased burden of carotid atherosclerosis. ConclusionOur results demonstrate a functional and homeostatic Treg defect in patients with NSTE-ACS and also in stabilized patients 6-12months after ACS. Moreover, this defect was associated with a subclinical proinflammatory and atherogenic state. We believe that the failure to preserve Treg function and homeostasis reflects a need for immune-restoring strategies in CAD.

Place, publisher, year, edition, pages
WILEY-BLACKWELL, 2016
Keywords
acute coronary syndrome; coronary artery disease; immune homeostasis; inflammation; regulatory T cell
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-124108 (URN)10.1111/joim.12398 (DOI)000366606200006 ()26260103 (PubMedID)
Note

Funding Agencies|Swedish Medical Research Council; Swedish Heart-Lung Foundation

Available from: 2016-01-25 Created: 2016-01-19 Last updated: 2017-04-25
Alfredsson, J., Lindahl, T. L., Gustafsson, K. M., Janzon, M., Jonasson, L., Logander, E., . . . Swahn, E. (2015). Large early variation of residual platelet reactivity in Acute Coronary Syndrome patients treated with clopidogrel: Results from Assessing Platelet Activity in Coronary Heart Disease (APACHE).. Thrombosis Research, 136(2), 335-340
Open this publication in new window or tab >>Large early variation of residual platelet reactivity in Acute Coronary Syndrome patients treated with clopidogrel: Results from Assessing Platelet Activity in Coronary Heart Disease (APACHE).
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2015 (English)In: Thrombosis Research, ISSN 0049-3848, E-ISSN 1879-2472, Vol. 136, no 2, p. 335-340Article in journal (Refereed) Published
Abstract [en]

INTRODUCTION: There is a large inter-individual variation in response to clopidogrel treatment and previous studies have indicated higher risk of thrombotic events in patients with high residual platelet reactivity (HRPR), but the optimal time-point for testing is not established. The aim of this study was to investigate the optimal time-point for aggregometry testing and the risk of major adverse cardiac events associated with HRPR.

METHOD AND RESULTS: We included 125 patients with ACS (73 with STEMI, and 71 received abciximab). The prevalence of HRPR varied substantially over time. The rate of HRPR in patients treated and not treated with abciximab were 43% vs 67% (p=0.01) before, 2% vs 23% (p=0.001) 6-8h after, 8% vs 9% (p=0.749) 3days after, and 23% vs 12% (p=0.138) 7-9 days after loading dose of clopidogrel. We found HRPR in 18% of the patients but only four ischemic events during 6months follow-up, with no significant difference between HRPR patients compared to the rest of the population. There were 3 TIMI major bleedings, all of which occurred in the low residual platelet reactivity (LRPR) group.

CONCLUSION: There is a large variation in platelet reactivity over time, also depending on adjunctive therapy, which has a large impact on optimal time-point for assessment. We found HRPR in almost 1 in 5 patients, but very few MACE, and not significantly higher in HRPR patients. In a contemporary ACS population, with low risk for stent thrombosis, the predictive value of HRPR for ischemic events will probably be low.

Place, publisher, year, edition, pages
Pergamon Press, 2015
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:liu:diva-119644 (URN)10.1016/j.thromres.2015.05.021 (DOI)000363953000026 ()26033398 (PubMedID)
Note

Funding agencies: Linkoping University; County Council of Ostergotland

Available from: 2015-06-24 Created: 2015-06-23 Last updated: 2019-02-11
Garvin, P., Jonasson, L., Nilsson, L., Falk, M. & Kristenson, M. (2015). Plasma Matrix Metalloproteinase-9 Levels Predict First-Time Coronary Heart Disease: An 8-Year Follow-Up of a Community-Based Middle Aged Population. PLoS ONE, 10(9), e0138290
Open this publication in new window or tab >>Plasma Matrix Metalloproteinase-9 Levels Predict First-Time Coronary Heart Disease: An 8-Year Follow-Up of a Community-Based Middle Aged Population
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2015 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 10, no 9, p. e0138290-Article in journal (Refereed) Published
Abstract [en]

Background The enzyme in matrix metalloproteinase (MMP)-9 has been suggested to be an important determinant of plaque degradation. While several studies have shown elevated levels in patients with coronary heart disease, results in prospective population based studies evaluating MMP-9 in relation to first time coronary events have been inconclusive. As of today, there are four published studies which have measured MMP-9 in serum and none using plasma. Measures of MMP-9 in serum have been suggested to have more flaws than measures in plasma. Aim To investigate the independent association between plasma levels of MMP-9 and first-time incidence of coronary events in an 8-year follow-up. Material and Methods 428 men and 438 women, aged 45-69 years, free of previous coronary events and stroke at baseline, were followed-up. Adjustments were made for sex, age, socioeconomic position, behavioral and cardiovascular risk factors, chronic disease at baseline, depressive symptoms, interleukin-6 and C-reactive protein. Results 53 events were identified during a risk-time of 6 607 person years. Hazard ratio (HR) for MMP-9 after adjustment for all covariates were HR = 1.44 (1.03 to 2.02, p = 0.033). Overall, the effect of adjustments for other cardiovascular risk factors was low. Conclusion Levels of plasma MMP-9 are independently associated with risk of first-time CHD events, regardless of adjustments. These results are in contrast to previous prospective population-based studies based on MMP-9 in serum. It is essential that more studies look at MMP-9 levels in plasma to further evaluate the association with first coronary events.

Place, publisher, year, edition, pages
PUBLIC LIBRARY SCIENCE, 2015
National Category
Clinical Medicine Basic Medicine
Identifiers
urn:nbn:se:liu:diva-122112 (URN)10.1371/journal.pone.0138290 (DOI)000361791000022 ()26389803 (PubMedID)
Note

Funding Agencies|Swedish Research Council [2004-1881]; Swedish Heart and Lung Foundation [2004053]

Available from: 2015-10-19 Created: 2015-10-19 Last updated: 2018-01-11
Szymanowski, A., Alfredsson, J., Janzon, M., Lindahl, T. L., Swahn, E., Jonasson, L. & Nilsson, L. (2015). Soluble markers of apoptosis in myocardial infarction patients during acute phase and 6-month follow up.
Open this publication in new window or tab >>Soluble markers of apoptosis in myocardial infarction patients during acute phase and 6-month follow up
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2015 (English)Manuscript (preprint) (Other academic)
Abstract [en]

Objectives

The aim of the study was to investigate circulating markers of apoptosis in the acute phase and at follow8up in patients with ST8elevation myocardial infarction (STEMI) or non8ST8elevation myocardial infarction (NSTEMI).

Background

Myocardial cell death during acute MI results from necrosis, apoptosis and autophagy. An elevated rate of apoptosis can continue for several days after the acute event, contributing to an increased final infarct size. Moreover, a lower but still increased apoptosis can continue for months resulting in left ventricular (LV) dysfunction and heart failure. Few studies have analysed markers of apoptosis longitudinally in MI patients.  Also, it is not known whether STEMI and NSTEMI patients differ in regard to these markers. 

Methods

This study is a prespecified substudy of the APACHE trial. We included 61 STEMI and 40 NSTEMI patients. Blood samples for analysis of soluble tumor necrosis factor receptor (sTNFR) 1, sTNFR2, sFas, sFas ligand (sFasL) and IL86 were collected at baseline prior to PCI, at 3 days and at 6 months. High sensitivity troponin T (hsTnT) was measured at 688 hours and echocardiography was performed at 283 days after admission to hospital.

Results

STEMI compared to NSTEMI patients showed very similar temporal patterns for each of the markers of apoptosis analyzed. Levels of sTNFRs increased from baseline to day 3 and the absolute increase as well as day 3 levels correlated significantly with TnT. At 6 months, sTNFR1 had returned to baseline whereas levels of sTNFR2 were still elevated. Soluble Fas and sFasL did not change from baseline to day 3, and both markers were significantly lower in the acute phase compared to 6 months. Indeed, sFas at day 3 correlated negatively with TnT. At all time points, plasma sTNFRs were significantly higher in patients with reduced LV function, whereas no such associations with sFas or sFasL was observed. 

Conclusions

The TNF and Fas/FasL pathways of apoptosis, as reflected by soluble markers, show markedly different temporal changes after an acute MI, indicating diverse roles of these two systems. STEMI compared to NSTEMI patients showed very similar temporal patterns for all the analyzed markers, suggesting apoptosis to be equally involved in myocardial damage of either infarct type.

Keywords
Apoptosis, ST-elevation myocardial infarction, non- ST-elevation myocardial infarction
National Category
Cardiac and Cardiovascular Systems Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:liu:diva-121116 (URN)
Available from: 2015-09-07 Created: 2015-09-07 Last updated: 2016-04-14Bibliographically approved
Hovland, A., Jonasson, L., Garred, P., Yndestad, A., Aukrust, P., Lappegard, K. T., . . . Mollnes, T. E. (2015). The complement system and toll-like receptors as integrated players in the pathophysiology of atherosclerosis. Atherosclerosis, 241(2), 480-494
Open this publication in new window or tab >>The complement system and toll-like receptors as integrated players in the pathophysiology of atherosclerosis
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2015 (English)In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 241, no 2, p. 480-494Article, review/survey (Refereed) Published
Abstract [en]

Despite recent medical advances, atherosclerosis is a global burden accounting for numerous deaths and hospital admissions. Immune-mediated inflammation is a major component of the atherosclerotic process, but earlier research focus on adaptive immunity has gradually switched towards the role of innate immunity. The complement system and toll-like receptors (TLRs), and the crosstalk between them, may be of particular interest both with respect to pathogenesis and as therapeutic targets in atherosclerosis. Animal studies indicate that inhibition of C3a and C5a reduces atherosclerosis. In humans modified LDL-cholesterol activate complement and TLRs leading to downstream inflammation, and histopathological studies indicate that the innate immune system is present in atherosclerotic lesions. Moreover, clinical studies have demonstrated that both complement and TLRs are upregulated in atherosclerotic diseases, although interventional trials have this far been disappointing. However, based on recent research showing an intimate interplay between complement and TLRs we propose a model in which combined inhibition of both complement and TLRs may represent a potent anti-inflammatory therapeutic approach to reduce atherosclerosis. (C) 2015 The Authors. Published by Elsevier Ireland Ltd.

Place, publisher, year, edition, pages
ELSEVIER IRELAND LTD, 2015
Keywords
The complement system; Toll-like receptors; Atherosclerosis; Inflammation
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-121437 (URN)10.1016/j.atherosclerosis.2015.05.038 (DOI)000360100700026 ()26086357 (PubMedID)
Available from: 2015-09-18 Created: 2015-09-18 Last updated: 2017-12-04
Lappegard, K. T., Gaffed, P., Jonasson, L., Espevik, T., Aukrust, P., Yndestad, A., . . . Hovland, A. (2014). A vital role for complement in heart disease. Molecular Immunology, 61(2), 126-134
Open this publication in new window or tab >>A vital role for complement in heart disease
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2014 (English)In: Molecular Immunology, ISSN 0161-5890, E-ISSN 1872-9142, Vol. 61, no 2, p. 126-134Article, review/survey (Refereed) Published
Abstract [en]

Heart diseases are common and significant contributors to worldwide mortality and morbidity. During recent years complement mediated inflammation has been shown to be an important player in a variety of heart diseases. Despite some negative results from clinical trials using complement inhibitors, emerging evidence points to an association between the complement system and heart diseases. Thus, complement seems to be important in coronary heart disease as well as in heart failure, where several studies underscore the prognostic importance of complement activation. Furthermore, patients with atrial fibrillation often share risk factors both with coronary heart disease and heart failure, and there is some evidence implicating complement activation in atrial fibrillation. Moreover, Chagas heart disease, a protozoal infection, is an important cause of heart failure in Latin America, and the complement system is crucial for the protozoa-host interaction. Thus, complement activation appears to be involved in the pathophysiology of a diverse range of cardiac conditions. Determination of the exact role of complement in the various heart diseases will hopefully help to identify patients that might benefit from therapeutic complement intervention.

Place, publisher, year, edition, pages
Elsevier, 2014
Keywords
Complement system; Myocardial infarction; Coronary heart disease; Heart failure; Atrial fibrillation; Chagas disease
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-111600 (URN)10.1016/j.molimm.2014.06.036 (DOI)000342265300010 ()25037633 (PubMedID)
Available from: 2014-10-27 Created: 2014-10-27 Last updated: 2017-12-05
Jonasson, L., Guldbrand, H., Lundberg, A. K. & Nyström, F. H. (2014). Advice to follow a low-carbohydrate diet has a favourable impact on low-grade inflammation in type 2 diabetes compared with advice to follow a low-fat diet. Annals of Medicine, 46(3), 182-187
Open this publication in new window or tab >>Advice to follow a low-carbohydrate diet has a favourable impact on low-grade inflammation in type 2 diabetes compared with advice to follow a low-fat diet
2014 (English)In: Annals of Medicine, ISSN 0785-3890, E-ISSN 1365-2060, Vol. 46, no 3, p. 182-187Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Inflammation may play an important role in type 2 diabetes. It has been proposed that dietary strategies can modulate inflammatory activity.

METHODS: We investigated the effects of diet on inflammation in type 2 diabetes by comparing a traditional low-fat diet (LFD) with a low-carbohydrate diet (LCD). Patients with type 2 diabetes were randomized to follow either LFD aiming for 55-60 energy per cent (E%) from carbohydrates (n = 30) or LCD aiming for 20 E% from carbohydrates (n = 29). Plasma was collected at baseline and after 6 months. C-reactive protein (CRP), interleukin-1 receptor antagonist (IL-1Ra), IL-6, tumour necrosis factor receptor (TNFR) 1 and TNFR2 were determined.

RESULTS: Both LFD and LCD led to similar reductions in body weight, while beneficial effects on glycaemic control were observed in the LCD group only. After 6 months, the levels of IL-1Ra and IL-6 were significantly lower in the LCD group than in the LFD group, 978 (664-1385) versus 1216 (974-1822) pg/mL and 2.15 (1.65-4.27) versus 3.39 (2.25-4.79) pg/mL, both P < 0.05.

CONCLUSIONS: To conclude, advice to follow LCD or LFD had similar effects on weight reduction while effects on inflammation differed. Only LCD was found significantly to improve the subclinical inflammatory state in type 2 diabetes.

Place, publisher, year, edition, pages
Informa Healthcare, 2014
National Category
General Practice
Identifiers
urn:nbn:se:liu:diva-107718 (URN)10.3109/07853890.2014.894286 (DOI)000335584000011 ()24779961 (PubMedID)
Available from: 2014-06-19 Created: 2014-06-19 Last updated: 2018-01-11Bibliographically approved
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