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Biomedical subjects

Lena Jonasson

Publications and source records attributed to Lena Jonasson.

9 recordsLinked to original sources
PubMed2006

Effects of simvastatin on human T cells in vivo.

OBJECTIVE: The use of statins has shown several anti-inflammatory actions, including modulatory effects on T cells in vitro. Since the effects on human T cells in vivo are less clarified, our aim was to investigate the effects of simvastatin on human T cells in vivo and ex vivo. METHODS AND RESULTS: A randomized, double-blind, placebo-controlled study design was applied. Eighty volunteers with mild to moderate hypercholesterolemia received either simvastatin 40 mg or placebo for 6 weeks. The serum levels of C-reactive protein (CRP) were significantly reduced by simvastatin. The proportions of CD4+ and CD8+ T cell subsets expressing early (CD25) or late (HLA-DR) activation markers, as assessed by flow cytometry, were not changed by simvastatin. However, simvastatin tended to increase the density of HLA-DR and L-selectin per CD8+ T cell. The T helper(h)1/Th2 response was evaluated by stimulatory assays followed by intra-cellular staining of interferon-gamma and interleukin-4. Simvastatin treatment did not affect the Th1 response but the results indicated a potential to suppress Th2. CONCLUSION: Simvastatin treatment resulted in a few discrete changes as regards peripheral T cells. However, the findings do not provide evidence that simvastatin-induced anti-inflammatory actions are related to any significant modulatory effects on human T cells in clinically healthy men with hypercholesterolemia.

Adult↗
PubMed2006

Low plasma levels of oxygenated carotenoids in patients with coronary artery disease.

BACKGROUND AND AIMS: Low circulating levels of carotenoids have been associated with cardiovascular disease. The distribution of different carotenoids in blood may have an impact on the cardioprotective capacity. The aim of the present study was to determine the plasma levels of 6 major carotenoids in patients with coronary artery disease (CAD) and relate the findings to clinical, metabolic and immune parameters. METHODS AND RESULTS: Plasma levels of oxygenated carotenoids (lutein, zeaxanthin, beta-cryptoxanthin) and hydrocarbon carotenoids (alpha-carotene, beta-carotene, lycopene) were determined in 39 patients with acute coronary syndrome, 50 patients with stable CAD and 50 controls. Serological assays for inflammatory activity and flow cytometrical analysis of lymphocyte subsets were performed. Both patient groups had significantly lower plasma levels of oxygenated carotenoids, in particular lutein+zeaxanthin, compared to controls. Low levels of oxygenated carotenoids were associated with smoking, high body mass index (BMI), low high density lipoprotein (HDL) cholesterol and, to a minor degree, inflammatory activity. Plasma levels of lutein+zeaxanthin were independently associated with the proportions of natural killer (NK) cells, but not with other lymphocytes, in blood. CONCLUSION: Among carotenoids, lutein+zeaxanthin and beta-cryptoxanthin were significantly reduced in CAD patients independent of clinical setting. The levels were correlated to a number of established cardiovascular risk factors. In addition, the relationship between NK cells and lutein+zeaxanthin may indicate a particular role for certain carotenoids in the immunological scenario of CAD.

Acute Disease↗
PubMed2006

Increased plasma concentration of matrix metalloproteinase-7 in patients with coronary artery disease.

BACKGROUND: Plaque rupture is often associated with breakdown of the extracellular matrix in the shoulder region of a plaque. We tested whether plasma concentrations of various matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase-1 (TIMP-1) could serve as markers for plaque instability as well as relationships between plasma MMPs and inflammatory markers. METHODS: The study group included 65 men with angiographically verified CAD (45 with stable and 20 with unstable CAD) and 28 healthy controls. Circulating MMP, TIMP-1, C-reactive protein, and cytokine concentrations were measured by ELISA. Leukocyte subtype counts in whole blood were determined, and T-cell subsets and natural killer cells were measured by flow cytometry. Differences in continuous variables between groups were tested by ANOVA with the Scheffé F-test used as a post hoc test, and correlations were analyzed by a linear regression method. RESULTS: The plasma concentration of MMP-7 was increased in patients with stable and unstable CAD, whereas MMP-2 and -3 concentrations were decreased. The plasma concentration of TIMP-1 was significantly increased in patients with unstable CAD. MMP-2, -3, and -7 showed no correlations with established markers of inflammation. However, MMP-2 correlated positively with the number of natural killer cells in patients with stable and unstable CAD. CONCLUSION: Plasma concentrations of MMPs and TIMPs may be markers of CAD but appear to be differentially regulated.

C-Reactive Protein↗
PubMed2005

Decreased plasma CXCL16/SR-PSOX concentration is associated with coronary artery disease.

OBJECTIVES: To investigate for the first time whether the plasma CXCL16 concentration is altered in coronary artery disease (CAD) patients. BACKGROUND: Accumulating evidence suggests that the novel chemokine/scavenger receptor CXCL16/SR-PSOX is involved in the development of atherosclerosis and CAD. METHODS: Using ELISA we assessed the plasma CXCL16 concentration in 40 stable angina pectoris (SAP) patients, 17 unstable angina pectoris/non-ST-elevation myocardial infarction (UAP/non-STEMI) patients, 387 survivors of a first myocardial infarction (MI) and healthy control subjects (44 controls for SAP and UAP/non-STEMI patient groups and 387 controls for post-MI patients). RESULTS: SAP patients exhibited significantly lower median CXCL16 levels (2111 pg/ml) than the corresponding control subjects (2678 pg/ml) (P=0.0012). UAP/non-STEMI patients also appeared to have lower CXCL16 levels (2192 pg/ml) compared with controls (NS). Patients investigated 3 months after MI tended (P=0.07) to have lower CXCL16 levels (2529 pg/ml) than the corresponding controls (2638 pg/ml). There were no significant correlations between CXCL16 levels and different measures of CAD severity determined by quantitative coronary angiography in post-MI patients. Neither patients nor controls exhibited significant correlations between CXCL16 levels and plasma lipoprotein fractions, inflammatory cytokines, C-reactive protein or numbers of inflammatory cells in peripheral blood. CONCLUSIONS: The finding that lower plasma CXCL16 concentration is associated with CAD might indicate a potential atheroprotective function of CXCL16.

Blood Chemical Analysis↗
PubMed2005

Loss of natural killer cell activity in patients with coronary artery disease.

BACKGROUND: Natural killer (NK) cells are important components of the innate immune system and have a potential role in the regulation of autoimmunity. In the present study, we evaluated the NK cells in patients with coronary artery disease (CAD) and related the findings to clinical and laboratory parameters of the disease. METHODS AND RESULTS: We studied 45 patients with acute coronary syndrome (ACS), 50 patients with stable angina and angiographically verified CAD (SA) and 50 healthy controls. The distribution of NK cell subsets was determined by flow cytometry and NK cell-mediated cytotoxicity was quantified ex vivo. Both ACS and SA patients had significantly reduced numbers of CD56(dim) NK cells compared with controls. The patients also exhibited a significant decrease in NK cell activity. The loss in NK cell function was not related to inflammatory activity or metabolic status. CONCLUSION: Both stable and unstable conditions of CAD were associated with a redistribution of circulating lymphocytes, comprising a significant reduction of CD56(dim) NK cells and a concomitant loss of NK cell function. The findings suggest the presence of a persistent immune aberration in CAD patients independent of their clinical setting or systemic inflammatory state.

C-Reactive Protein↗
PubMed2005

Circulating levels of proinflammatory cytokines and neutrophil-platelet aggregates in patients with coronary artery disease.

Several lines of evidence indicate that increased inflammatory activity in peripheral blood is associated with the acute coronary syndrome. Systemic inflammation in clinically stable conditions of coronary artery disease has been less studied. We examined cytokine profiles in 20 patients who had acute coronary syndrome, 45 who had angiographically verified coronary artery disease and stable angina pectoris, and 45 healthy controls. Circulating levels of C-reactive protein, interleukin-1 receptor antagonist, interleukin-2 receptor, interleukin-6, interleukin-10, and interleukin-18 were determined. Subpopulations of peripheral immune cells, including neutrophil-platelet aggregates, were analyzed by 3-color flow cytometry using a panel of monoclonal antibodies. Patients who had acute coronary syndrome and stable angina pectoris had significantly higher levels of C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist than did controls, whereas levels of interleukin-2 receptor, interleukin-10, and interleukin-18 were similar across groups. Patients had significantly more neutrophils, and the numbers of neutrophil-platelet aggregates were particularly large in patients who had stable angina pectoris. High levels of C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist in patients were significantly related to numbers of neutrophils and neutrophil-platelet aggregates but not to other immune cell subpopulations. The data suggest that the interaction between neutrophils and platelets is an important component of proinflammatory activity seen in peripheral blood of stable and unstable forms of coronary artery disease.

Angina Pectoris↗
PubMed2005

Denial in patients with a first-time myocardial infarction: relations to pre-hospital delay and attendance to a cardiac rehabilitation programme.

BACKGROUND: Survival of a myocardial infarction and subsequent prognosis are highly dependent on the time between onset of symptoms and medical intervention. DESIGN: This cross-sectional study examines whether patients who used the psychological defence mechanism of denial when faced with symptoms of a first-time myocardial infarction tended to also show a prolonged delay in going to the hospital and to be less willing to participate in a cardiac rehabilitation programme. METHODS: One hundred and seven patients, 78 men and 29 women, were enrolled in this study. The sample was divided into two groups depending on whether the patients sought medical help within 4 h after they began experiencing myocardial infarction symptoms (non-delayers) or whether they waited longer (delayers). Denial was measured with the Hackett and Cassem semi-structured interview 3-5 days after the patients entered the hospital. Data on participation (attenders) or not (non-attenders) in the rehabilitation programme was also obtained. RESULTS: Forty-nine patients exhibited a prolonged delay and 76 patients did not attend the rehabilitation programme. Both prolonged delay and a lesser readiness to attend the rehabilitation programme that was offered were related to a greater use of denial. In addition, the great majority of the patients categorized as being high deniers were found to also be both delayers and non-attenders. CONCLUSIONS: The results suggest denial to increase the health risks of persons potentially prone to myocardial infarction. If our knowledge about this psychological defence mechanism is increased, we might be able to reach more patients in alternative and individually based cardiac rehabilitation programmes.

Adult↗
PubMed2002

Effect of thoracic epidural analgesia on refractory angina pectoris: long-term home self-treatment.

OBJECTIVES: To evaluate the effects of long-term home self-treatment with thoracic epidural analgesia (TEA) on angina, quality of life, and safety. DESIGN: Prospective consecutive pilot study. SETTING: Department of Cardiology, Heart Center, Linköping University Hospital. PARTICIPANTS: Between January 1998 and January 2000, 37 consecutive patients with refractory angina began treatment with TEA, using a subcutaneously tunnelled epidural catheter. INTERVENTIONS: The patients were trained to provide self-treatment at home with intermittent injections of bupivacaine. Data were collected until January 2001, and the follow-up for each patient was 1 to 3 years. MEASUREMENTS AND MAIN RESULTS: All but 1 of the patients improved symptomatically. The improvement was maintained throughout the treatment period (4 days to 3 years). The Canadian Cardiovascular Society angina class decreased from 3.6 to 1.7, frequency of anginal attacks decreased from 46 to 7 a week, nitroglycerin intake decreased from 32 to 5 a week, and the overall self-rated quality of life assessed by visual analog scale increased from 24 to 76 (all p < 0.001). No serious catheter-related complications occurred; however, 51% of the catheters became displaced and a new one had to be inserted during the study. CONCLUSION: Long-term self-administered home treatment with TEA seems to be an effective and safe adjuvant treatment for patients with refractory angina. It produces symptomatic relief of angina and improves the quality of life.

Aged↗