| 1. |
- Asciutto, Giuseppe, et al.
(författare)
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Treatment with beta-blockers is associated with lower levels of Lp-PLA2 and suPAR in carotid plaques.
- 2013
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Ingår i: Cardiovascular Pathology. - : Elsevier BV. - 1879-1336 .- 1054-8807. ; 22:6, s. 438-443
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To determine whether a long-term treatment with beta-blockers influences the inflammatory activity in carotid artery disease by reducing the carotid plaque levels of lipoprotein-associated phospholipase A2 (Lp-PLA2), its enzymatic products lysophosphatidylcholine (lysoPCs), and of soluble urokinase plasminogen activator receptor (suPAR). MATERIALS AND METHODS: One hundred and thirty-four patients with significant symptomatic or asymptomatic carotid stenosis undergoing surgery were prospectively included and divided into two groups (Group A or B) based on the absence or presence of an on-going long-term oral treatment with beta-blockers. The harvested carotid plaques were analyzed for the levels of lysoPCs using mass spectrometry and Lp-PLA2 and suPAR by Enzyme-linked immunosorbent assay (ELISA). RESULTS: Plaques of patients on long-term treatment with beta-blockers revealed lower levels of Lp-PLA2 (Group A 0.752±0.393 ug/g vs. Group B 0.644±0.445 ug/g, P=.049) as well as suPAR (Group A 0.044±0.024 μg/g vs. Group B 0.036±0.025 μg/g, P=.028). Levels of Lp-PLA2 and suPAR were positively correlated (r=.637, P<.0001). Lp-PLA2 and suPAR levels were also correlated (P<.0001) with the three lysoPC species tested (lysoPC 16:0, lysoPC 18:0. lysoPC 18:1). All the above-mentioned findings were confirmed after correction for age, gender, hypertension, coronary artery disease, and statin usage. CONCLUSIONS: The reduced levels of Lp-PLA2 and suPAR in human carotid plaques of subjects on long-term treatment with beta-blockers suggest their possible protective role in plaque inflammation. Our findings support an even more selective Lp-PLA2 and suPAR inhibition as a possible strategy for the prevention of cardiovascular disease.
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| 2. |
- Goncalves, Isabel, et al.
(författare)
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Activator protein-1 in carotid plaques is related to cerebrovascular symptoms and cholesteryl ester content
- 2011
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Ingår i: Cardiovascular pathology. - : Elsevier. - 1054-8807 .- 1879-1336. ; 20:1, s. 36-43
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Tidskriftsartikel (refereegranskat)abstract
- Transcription factor activator protein-1 regulates genes involved in inflammation and repair. The aim of this study was to determine whether transcription factor activator protein-1 activity in carotid plaques is related to symptoms, lipid accumulation, or extracellular matrix composition. Methods: Twenty-eight atherosclerotic carotid plaques were removed by endarterectomy and divided into two groups based on the presence or absence of ipsilateral symptoms (b1 month ago). Activator protein-1 DNA binding activity was assessed, and subunit (c-Jun, JunD, JunB, c-Fos, FosB, Fra-1, Fra-2) protein levels analyzed by immunoblotting. Distribution of c-Jun in plaques was analyzed by immunohistochemistry. Results: Plaques associated with symptoms had increased activator protein-1 activity and increased expression of c-Jun and JunD, as compared to asymptomatic plaques. Fra-1 and Fra-2 were present in equal amounts in both groups, whereas JunB, FosB, and c-Fos were undetectable. Activator protein-1 activity correlated with cholesteryl ester and elastin in plaques and decreased with age. Activator protein-1 activity did not correlate with collagen, calcified tissue, or proteoglycan content. Conclusions: Activator protein-1 is increased in plaques associated with symptoms. The correlation between activator protein-1 and cholesteryl esters suggests that high activator protein-1 is a marker of plaque vulnerability. Activator protein-1 expression can also reflect the activation of repair processes.
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| 3. |
- Mobini Far, Hamid Reza, et al.
(författare)
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Cardiac hypertrophy in deceased users of anabolic androgenic steroids : an investigation of autopsy findings
- 2012
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Ingår i: Cardiovascular pathology. - : Elsevier BV. - 1054-8807 .- 1879-1336. ; 21:4, s. 312-316
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND:The use of anabolic androgenic steroids (AASs) has been associated with hypertrophy of the left cardiac ventricle (LVH) as diagnosed by echocardiography. Case reports suggest that AAS-related LVH may lead to sudden death. We performed an investigation of the gross cardiac pathological findings in deceased male AAS users in order to further elucidate the proposed role of AAS in cardiac hypertrophy.METHODS:Eighty-seven deceased males who tested positive for AAS at autopsy and 173 age-adjusted control deceased males without suspected AAS use were studied for cardiac hypertrophy. The AAS-positive subjects had been examined at any of the six departments of forensic medicine in Sweden during the period from 1989 to 2009. Data were assessed employing multivariate analyses controlling for body weight, height, age, bleeding after trauma, and the impact of weight training.RESULTS: The analysis of the logarithm of heart mass by multivariate statistics implied that strong correlations existed between body mass and heart mass (P<.00001), height and heart mass (P<.02), age and heart mass (P<.00001), and trauma (bleeding) and heart mass (P=.00001). After controlling for these factors, a significantly higher heart mass (P=.0001) was found among the AAS-positive males.CONCLUSION: Our findings suggest that use of AAS may lead to cardiac hypertrophy with a direct cardiotropic effect.
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| 4. |
- Quintana, Hedley Knewjen, et al.
(författare)
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Comorbidities in relation to fatali of first myocardial infarction
- 2018
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Ingår i: Cardiovascular pathology. - : ELSEVIER SCIENCE INC. - 1054-8807 .- 1879-1336. ; 32, s. 32-37
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Present knowledge concerning potential associations between comorbidities and the fatality of a first myocardial infarction (MI) is limited.Aim: To identify comorbidities in 45-70-year-old individuals who suffered a first MI and died within 7 days in Stockholm County from 1992-1994. In addition, to assess how each of the comorbidities identified, as well as the number of hospitalizations during the 10-year period prior to the MI, was associated with MI fatality.Methods: The data collected on our inception cohort of 1984 first Ml, of which 524 were fatal within 7 days, were primarily self-reported, proxy-reported by questionnaire and/or extracted from comprehensive national registers. Comorbidilies among fatal cases with a prevalence >2% were identified. Risk ratios (with 95% confidence intervals) for the association of Ml fatality with number of prior hospitalizations and specific comorbidities were calculated using binomial regression with log link. A structured review of autopsy reports on fatal cases was performed in order to identify additional indicators of comorbidities.Results: After adjusting for sex, age and disposable income, the number of previous hospitalizations was associated with 7-day Ml fatality. Of the comorbidities identified as prevalent in fatal cases, the following were associated with 7-day fatality in crude analysis: epilepsy, heart failure, stroke, alcoholism, cancer, renal diseases, asthma, psychiatric diseases, diabetes, and rheumatoid arthritis. Indicators of comorbidities identified from autopsy data included a silent MI, severe atherosclerosis of the abdominal aorta, and hepatic steatosis. Adjustments for sex and age (although not possible for epilepsy and alcoholism), did not substantially alter results.Conclusions: Our current findings indicate that in connection with a first MI, particular attention should be paid to those with repeated prior hospitalizations and/or epilepsy, heart failure, stroke, alcoholism, cancer, renal diseases, asthma, psychiatric diseases, diabetes and rheumatoid arthritis.
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| 5. |
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| 6. |
- Terzian, Zaven, et al.
(författare)
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Peristrut microhemorrhages : a possible cause of in-stent neoatherosclerosis?
- 2017
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Ingår i: Cardiovascular pathology. - : Elsevier. - 1054-8807 .- 1879-1336. ; 26:1, s. 30-38
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Tidskriftsartikel (refereegranskat)abstract
- Background: In-stent neoatherosclerosis is characterized by the delayed appearance of markers of atheroma in the subintima, but the pathophysiology underlying this new disease entity remains unclear. Methods and results: We collected 20 human coronary artery stents by removal from explanted hearts. The mean duration of stent implantation was 34 months. In all samples, neoatherosclerosis was detected, particularly in peristrut areas. It consisted of foam cells and cholesterol clefts, with or without calcification, associated with neovascularization. Iron and glycophorin-A were present in peristrut areas, as well as autofluorescent ceroids. Moreover, in response to neoatherosclerosis, tertiary lymphoid organs (tissue lymphoid clusters) often developed in the adventitia. Some of these features could be reproduced in an experimental carotid stenting model in rabbits fed a high-cholesterol diet. Foam cells were present in all samples, and peristrut red blood cells (RBCs) were also detected, as shown by iron deposits and Bandeiraea simplicifiola isolectin-B4 staining of RBC membranes. Finally, in silico models were used to evaluate the compliance mismatch between the rigid struts and the distensible arterial wall using finite element analysis. They show that stenting approximately doubles the local von Mises stress in the intimal layer. Conclusions: We show here that stent implantation both in human and in rabbit arteries is characterized by local peristrut microhemorrhages and finally by both cholesterol accumulation and oxidation, triggering together instent neoatherosclerosis. Our data indicate that these processes are likely initiated by an increased mechanical stress due to the compliance mismatch between the rigid stent and the soft wall. (C) 2016 The Authors. Published by Elsevier Inc.
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| 7. |
- Wallby, Lars, et al.
(författare)
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Role of inflammation in non-rheumatic, regurgitant heart valve disease : A comparative, descriptive study regarding apolipoproteins and inflammatory cells in non-rheumatic heart valve disease
- 2007
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Ingår i: Cardiovascular pathology. - : Elsevier BV. - 1054-8807 .- 1879-1336. ; 16:3, s. 171-178
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Tidskriftsartikel (refereegranskat)abstract
- Background: Nonrheumatic aortic stenosis is the predominant cause of heart valve surgery in the Western world. Aortic and mitral regurgitation account for a lesser amount of the heart valve surgery. During the 1990s, inflammatory cell infiltrates have been demonstrated in nonrheumatic stenotic aortic valves. These findings suggest an inflammatory component in the pathogenesis of nonrheumatic aortic valve stenosis. However, nonrheumatic regurgitant aortic and mitral valves have not been investigated in this respect. The aim of this study was to compare nonrheumatic regurgitant aortic and mitral valves with stenotic aortic valves regarding the presence of T lymphocytes, macrophages, apolipoprotein B, and apolipoprotein A-I. Methods: Valve specimens were obtained from 42 patients referred to hospital for surgery because of significant heart valve disease. From these patients, 29 aortic stenotic valves, 9 aortic regurgitant, and 6 mitral regurgitant valves, all nonrheumatic, were obtained for the study. Fourteen valves collected from subjects undergoing clinical/medicolegal autopsy were used as control. In order to identify mononuclear inflammatory cells and apolipoproteins, sections were investigated with immunohistochemical analyses and then categorized semiquantitatively. Results: Regurgitant and control valves showed a significantly lower degree of inflammatory cell infiltrate and a lower degree of apolipoprotein deposition as compared to stenotic aortic valves. Conclusions: The signs of inflammation seen in nonrheumatic aortic stenosis are not prominent features in the nonrheumatic, regurgitant valves. This is consistent with the multi-factorial pathogenesis of these conditions.
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| 8. |
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| 9. |
- Palao, Teresa, et al.
(författare)
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Thrombospondin-4 mediates cardiovascular remodelling in angiotensin II-induced hypertension
- 2018
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Ingår i: Cardiovascular Pathology. - : Elsevier BV. - 1054-8807. ; 35, s. 12-19
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Tidskriftsartikel (refereegranskat)abstract
- Thrombospondin 4 (TSP-4) expression is induced in the heart and vasculature under pathological conditions, including myocardial infarction, myocardial pressure overload, and hypertension. TSP-4 is linked to remodelling processes, where it may affect extracellular matrix protein organization. In previous work, we studied the role of TSP-4 in small arteries during hypertension using Ang II-treated Thrombospondin 4 knockout (Thbs4−/−) mice. We reported increased heart weight, as well as the occurrence of aortic aneurysms in the Ang II-treated Thbs4−/− animals. In the present study, we further characterized the hearts and aortas from these animals. Hypertrophy of cardiomyocytes, together with perivascular fibrosis and inflammation was observed in the Ang II-treated Thbs4−/− hearts. In the aortas, an increase in the aortic wall cross-sectional area (CSA) and wall thickness of the Ang II-treated Thbs4−/− mice was found. More detailed investigation of the Ang II-treated Thbs4−/− aortas also revealed the appearance of aortic dissections in the outer medial layer of the arteries, as well as pronounced inflammation. No differences were found in several other extracellular matrix-related parameters, such as number of elastin breaks or stress–strain relationships. However, at the ultrastructural level, collagen fibers showed alterations in diameter in the media and adventitia of the Ang II-treated Thbs4−/− mice, in the area prone to dissection. In conclusion, we identified TSP-4 as an important protein in the development of cardiac hypertrophy and aortic dissections in Ang II-induced hypertension.
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| 10. |
- Tse, Yuet-Tung, et al.
(författare)
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Quantitative analysis and risk assessment to full-size microplastics pollution in the coastal marine waters of Hong Kong
- 2023
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Ingår i: Science of the Total Environment. - : Elsevier BV. - 0048-9697 .- 1879-1026. ; 879
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Tidskriftsartikel (refereegranskat)abstract
- Given the potential risk to the ecosystem, attention has increased in recent decades to the contamination of the aquatic environment by microplastics (MPs). Due to the limitations of conventional analysis methods of MPs, little is known about the size distribution and abundance of a full-size MPs from 1 μm to 5 mm. The present study quantified MPs with size ranges of 50 μm – 5 mm and 1–50 μm in the coastal marine waters from twelve locations in Hong Kong using fluorescence microscopy and flow cytometry respectively, during the end of wet (September 2021) and dry (March 2022) seasons. The average abundance of MPs with size ranges of 50 μm – 5 mm and 1–50 μm from twelve sampling locations marine surface waters were found ranging from 27 to 104 particles L−1 and 43,675–387,901 particles L−1 in the wet season respectively, and 13–36 particles L−1 and 23,178–338,604 particles L−1 in the dry season respectively. Significant temporal and spatial variations of small MPs abundance might be observed at the sampling locations, which were contributed by the influences of the estuary of Pearl River, sewage discharge points, land structure, and other anthropogenic activities. Based on the MPs abundance information, ecological risk assessment was conducted and revealed that the small MPs (< 10 μm) in coastal marine surface waters may pose potential health risks to aquatic organisms. Additional risk assessments are needed in order to determine whether or not the MPs exposure would cause health risks to the public.
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