| 1. |
- Andersson, Jonas, 1977-, et al.
(författare)
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C-reactive protein is a determinant of first-ever stroke: prospective nested case-referent study.
- 2009
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Ingår i: Cerebrovascular diseases (Basel, Switzerland). - : S. Karger AG. - 1421-9786 .- 1015-9770. ; 27:6, s. 544-51
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: C-reactive protein (CRP) is a determinant of stroke, but there are no prospective studies on CRP and first ischemic stroke divided into etiologic subtypes. Our primary aim was to study CRP as a determinant of ischemic stroke, classified according to Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria, and intracerebral hemorrhage (ICH) in a prospective study. A secondary aim was to study the relationship between the 1444C>T polymorphism, plasma levels of CRP and stroke. METHODS: The study was a prospective population-based case-referent study nested within the Northern Sweden Cohorts. We defined 308 cases of ischemic stroke and 61 ICH. Two controls for each case were defined from the same cohort. RESULTS: The OR for the highest (>3 mg/l) versus lowest group (<1 mg/l) of CRP was 2.58 (95% CI 1.74-3.84) for ischemic stroke and 1.63 (95% CI 0.67-3.93) for ICH. In a multivariate model including traditional risk factors, CRP remained associated with ischemic stroke (OR 2.06; 95% CI 1.29-3.29). Small-vessel disease was associated with CRP in the multivariate model (OR 3.88; 95% CI 1.10-13.7). The CRP 1444 (CC/CT vs. TT) polymorphism was associated with plasma levels of CRP but neither with ischemic stroke nor with ICH. CONCLUSIONS: This prospective population-based study shows that CRP is significantly associated with the risk of having a first ischemic stroke, especially for small-vessel disease. No significant associations were found between the CRP 1444C>T polymorphism and any stroke subtype.
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| 2. |
- Giang, Kok Wai, 1984, et al.
(författare)
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Long-term risk of stroke and myocardial infarction in middle-aged men with a hypertensive response to exercise : a 44-year follow-up study
- 2021
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Ingår i: Journal of Hypertension. - : Wolters Kluwer. - 0263-6352 .- 1473-5598. ; 39:3, s. 503-510
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Data on the prognostic value of hypertensive response to exercise in cardiovascular disease are limited. The aim was to determine whether SBP reactions during exercise have any prognostic value in relation to the long-term risk of stroke and myocardial infarction (MI).Patients and methods: A representative cohort of men from Gothenburg, Sweden, born in 1913, who performed a maximum exercise test at age 54 years, (n = 604), was followed-up for a maximum of 44 years with regard to stroke and MI. Results: Among the 604 men, the mean resting and maximum SBP was 141.5 (SD 18.8) and 212.1 (SD 24.6) mmHg, respectively. For maximum SBP, the risk of stroke increased by 34% (hazard ratio 1.34, 95% confidence interval 1.11-1.61) per 1-SD increase, while no risk increase was observed for MI. The highest risk of stroke among blood pressure groups was observed among men with a resting SBP of at least 140 mmHg and a maximum SBP of at least 210 mmHg with an hazard ratio of 2.09 (95% confidence interval 1.29-3.40), compared with men with a resting SBP of less than 140 mmHg and a maximum SBP of less than 210 mmHg, independent of smoking, blood glucose, cholesterol and BMI.Conclusion: Among middle-aged men with high resting and maximum blood pressure during maximum exercise workload, an increased risk of stroke was observed but not for MI. Further studies with larger sample sizes are needed to investigate the underlying mechanisms of the increased risk of stroke among individuals with hypertensive response to exercise.
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| 3. |
- Jood, Katarina, 1966, et al.
(författare)
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Fibrinolytic gene polymorphism and ischemic stroke
- 2005
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Ingår i: Stroke. - 0039-2499 .- 1524-4628. ; 36:10, s. 2077-81
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: The tissue-type plasminogen activator (tPA) -7351C>T and the plasminogen activator inhibitor type 1 (PAI-1) -675 4G>5G polymorphisms influence transcriptional activity. Both variants have been associated with myocardial infarction, with increased risk for the T and 4G allele, respectively. In this study we investigated the possible association between these polymorphisms, the respective plasma protein levels, and ischemic stroke. METHODS: In the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), 600 patients with acute ischemic stroke aged 18 to 69 years and 600 matched community controls were recruited. Stroke subtype was determined using Trial of Org 10172 in Acute Treatment criteria. RESULTS: There were no associations between individual genetic variants and ischemic stroke. The multivariate-adjusted odds ratio for overall ischemic stroke was 1.11 (95% CI 0.87 to 1.43) for tPA T allele carriers, and 0.84 (95% CI, 0.64 to 1.11) for subjects homozygous for the PAI-1 4G allele. When genotypes were combined, a protective effect for the tPA CC/PAI-1 4G4G genotype combination was observed (odds ratio 0.65, 95% CI 0.43 to 0.98; P<0.05). Plasma levels of tPA and PAI-1 antigen at follow-up were independently associated with overall ischemic stroke. tPA-antigen differed by stroke subtype and was highest among those with large-vessel disease and cardioembolic stroke. CONCLUSIONS: Neither the tPA -7351C>T nor the PAI-1 to 675 4G>5G polymorphism showed significant association with ischemic stroke. For the tPA CC/PAI-1 4G4G genotype combination, a protective effect was observed. Collectively, these results are consistent with a more complex role for tPA and PAI-1 in the brain as compared with the heart.
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| 4. |
- Ladenvall, Claes, 1974, et al.
(författare)
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Serum C-reactive protein concentration and genotype in relation to ischemic stroke subtype
- 2006
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Ingår i: Stroke. - 0039-2499 .- 1524-4628. ; 37:8, s. 2018-23
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND PURPOSE: C-reactive protein (CRP) has evolved as an inflammatory risk marker of cardiovascular disease. Several single-nucleotide polymorphisms at the CRP locus have been found to be associated with CRP levels. The aim of the present study was to investigate CRP levels and genetic variants in etiological subtypes of ischemic stroke. METHODS: The Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS) comprises 600 consecutive ischemic stroke cases (18 to 69 years) and 600 matched controls from western Sweden. Stroke subtypes were defined by the TOAST classification. Serum CRP levels were determined by a high-sensitivity immunometric assay. RESULTS: CRP levels were significantly higher for all ischemic stroke subtypes compared with controls, both in the acute phase and at the 3-month follow-up. After adjustment for traditional risk factors, CRP at follow-up was related to higher odds ratios (ORs) of overall ischemic stroke (OR, 1.25; 95% CI, 1.09 to 1.43) and large-vessel disease (OR, 1.48; 95% CI, 1.09 to 2.00). The CRP -286C>T>A, 1059G>C, and 1444C>T single-nucleotide polymorphisms showed significant associations with CRP levels. However, neither CRP genotypes nor haplotypes showed an association to overall ischemic stroke. CONCLUSIONS: This is the first large study on CRP in different TOAST subtypes in a young ischemic stroke population. CRP levels differed between etiological subtypes of ischemic stroke both in the acute phase and at the 3-month follow-up. CRP at follow-up was associated with overall ischemic stroke and the large-vessel disease subtype. Genetic variants at the CRP locus were associated with CRP levels, but no association was detected for overall ischemic stroke.
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| 5. |
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| 6. |
- Ladenvall, Per, 1972, et al.
(författare)
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Low aerobic capacity in middle-aged men associated with increased mortality rates during 45 years of follow-up
- 2016
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Ingår i: European Journal of Preventive Cardiology. - : Oxford University Press (OUP). - 2047-4873 .- 2047-4881. ; 23:14, s. 1557-1564
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Tidskriftsartikel (refereegranskat)abstract
- Background Low aerobic capacity has been associated with increased mortality in short-term studies. The aim of this study was to evaluate the predictive power of aerobic capacity for mortality in middle-aged men during 45-years of follow-up. Design The study design was a population-based prospective cohort study. Methods A representative sample from Gothenburg of men born in 1913 was followed from 50-99 years of age, with periodic medical examinations and data from the National Hospital Discharge and Cause of Death registers. At 54 years of age, 792 men performed an ergometer exercise test, with 656 (83%) performing the maximum exercise test. Results In Cox regression analysis, low predicted peak oxygen uptake (VO2max), smoking, high serum cholesterol and high mean arterial blood pressure at rest were significantly associated with mortality. In multivariable analysis, an association was found between predicted VO2max tertiles and mortality, independent of established risk factors. Hazard ratios were 0.79 (95% confidence interval (CI) 0.71-0.89; p<0.0001) for predicted VO2max, 1.01 (1.002-1.02; p<0.01) for mean arterial blood pressure, 1.13 (1.04-1.22; p<0.005) for cholesterol, and 1.58 (1.34-1.85; p<0.0001) for smoking. The variable impact (Wald's (2)) of predicted VO2max tertiles (15.3) on mortality was secondary only to smoking (31.4). The risk associated with low predicted VO2max was evident throughout four decades of follow-up. Conclusion In this representative population sample of middle-aged men, low aerobic capacity was associated with increased mortality rates, independent of traditional risk factors, including smoking, blood pressure and serum cholesterol, during more than 40 years of follow-up.
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| 7. |
- Mirzada, Naqibullah, 1977, et al.
(författare)
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Multidisciplinary management of patent foramen ovale (PFO) and cryptogenic stroke/TIA
- 2013
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Ingår i: Journal of Multidisciplinary Healthcare. - 1178-2390. ; 6, s. 357-363
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: Patent foramen ovale (PFO) has been implicated as a risk factor for cryptogenic ischemic stroke (CS). However, there is still a lack of widely accepted, undisputed indications for PFO closure. The present study describes the concept of the multidisciplinary PFO conference and a decision making process for closure versus no closure that was developed into a formalized clinical algorithm, and presents the results of implementing these, in terms of number and proportion of PFO closures as well as repeat referrals. DESIGN: Five specialists in neurology, cardiology, internal medicine, thromboembolism, and echocardiography evaluated the clinical data of 311 patients at PFO conferences during 2006 to 2009. The main criteria for closure were patients with first-ever CS with PFO and atrial septal aneurysm, or patients with recurrent CS and PFO without atrial septal aneurysm. RESULTS: A total of 143 patients (46%) were accepted for closure and 167 patients were rejected. Patients accepted for closure were younger (mean 50 years versus 58 years) (P < 0.001). The acceptance rate for PFO closure was similar throughout these years, with an average of 45%. Three of 167 patients (1.8%) initially rejected for PFO closure were re-referred due to recurrent stroke, and the PFO closure was subsequently performed. CONCLUSION: The acceptance rate of less than 50% in the present study underscores the complex relationship between CS and PFO. Whatever the criteria used for PFO closure, any unit caring for these patients needs to have a rigorous process to avoid overtreatment as well as undertreatment and to ensure that personal preferences and economic incentives do not steer the selection process. Our algorithm provides a stable acceptance rate and a low rate of repeat referrals.
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| 8. |
- Mirzada, Naqibullah, 1977, et al.
(författare)
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Quality of life after percutaneous closure of patent foramen ovale in patients after cryptogenic stroke compared to a normative sample
- 2018
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Ingår i: International Journal of Cardiology. - : Elsevier BV. - 0167-5273. ; 257, s. 46-49
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Tidskriftsartikel (refereegranskat)abstract
- Aims: Despite the widespread use of percutaneous closure of patent foramen ovale (PFO) in patients after a cryptogenic stroke, little is known about its impact on health-related quality of life (HRQoL). The aim of this study was to assess HRQoL in these patients compared to PFO patients not considered candidates for percutaneous closure, and to a normal population. Methods and results: A total of 402 patients with cryptogenic stroke or transient ischaemic attack (TIA) who had been referred to our center for PFO closure were invited to a long-term clinical follow-up (mean follow-up 5.5 years; range 3-13 years). HRQoL was assessed using the SF-36 Health Survey and data were compared with an age-and gender-matched reference group from the Swedish SF-36 normative database. Fifteen patients had died and 43 did not answer the SF-36. Of the remaining 344 patients, 208 had undergone PFO closure, and 136 had not. The closure group and reference group reported similar HRQoL levels. However, the non-closure group showed significantly lower HRQoL in role limitation -physical, vitality, general health, mental health (p < 0.05) and social functioning (p = 0.05) than the reference group and also had significantly lower scores than the closure group, correcting for age differences, on physical functioning, role limitation - physical, vitality and general health (p < 0.05). Conclusions: Non-closure patients had lower HRQoL than their counterparts in the normal population and the closure group. Percutaneous PFO closure is associated with a favorable quality of life.
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| 9. |
- Mirzada, Naqibullah, 1977, et al.
(författare)
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Recurrent stroke in patients with patent foramen ovale: An observational prospective study of percutaneous closure of PFO versus non-closure
- 2015
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Ingår i: International Journal of Cardiology. - : Elsevier BV. - 0167-5273. ; 195, s. 293-299
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Tidskriftsartikel (refereegranskat)abstract
- Aims: Observational studies favor percutaneous closure of patent foramen ovale (PFO) over medical therapy to reduce the risk of recurrent stroke, whereas randomized clinical trials have not shown significant differences. This study aims to compare long-term outcomes of PFO closure versus non-closure. Methods and results: Patients with PFO and stroke considered for PFO closure were invited to a long-term clinical follow-up. Of the 314 patients, 151 (48%) were accepted for closure and 163 (52%) were not accepted (mean age 50 vs. 58 years). The cumulative incidence of all-cause mortality, stroke or transient ischemic attacks (TIAs) for closure vs. non-closure under a mean follow-up time of five years was 10.6% (16 events) vs. 12.9% (21 events), p = 0.53. Six patients, 3.7% vs. 3.6%, died in each group, but no deaths were associated with PFO closure, recurrent stroke or TIA. The incidence of recurrent stroke or TIA for closure vs. non-closure was 6.6% (10 events) vs. 9.2% (15 events), p = 0.63. The respective event rates for stroke were 3.9% (6 events) vs. 5.5% (9 events), p = 0.50 and for TIA, 2.6% (4 events) vs. 3.7% (6 events), p = 0.59. Conclusion: PFO closure was associated with a low risk of recurrent events; however, compared to the non-closure group, no significant differences could be demonstrated. Careful patient selection can avoid under-as well as over-treatment of PFO patients. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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| 10. |
- Mirzada, Naqibullah, 1977, et al.
(författare)
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Seven-year follow-up of percutaneous closure of patent foramen ovale
- 2013
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Ingår i: IJC Heart and Vessels. - : Elsevier BV. - 2214-7632. ; 1, s. 32-36
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Tidskriftsartikel (refereegranskat)abstract
- Background: Observational studies favor percutaneous closure of patent foramen ovale (PFO) over medical treatment to reduce recurrent stroke while randomized trials fail to demonstrate significant superiority of percutaneous PFO closure. Few long-term studies are available post PFO closure. This study reports long-term clinical outcomes after percutaneous PFO closure. Methods: Between 1997 and 2006, 86 consecutive eligible patients with cerebrovascular events, presumably related to PFO, underwent percutaneous PFO closure. All 86 patients were invited to a long-term follow-up, which was carried out during 2011 and 2012. Results: Percutaneous PFO closure was successfully performed in 85 of 86 patients. The follow-up rate was 100%. No cardiovascular or cerebrovascular deaths occurred. Two patients (both women) died from lung cancer during follow-up. Follow-up visits were conducted for 64 patients and the remaining 20 patients were followed up by phone. The mean follow-up time was 7.3. years (5 to 12.4. years). Mean age at PFO closure was 49. years. One patient had a minor stroke one month after PFO closure and a transient ischemic attack (TIA) two years afterwards. One other patient suffered from a TIA six years after closure. No long-term device-related complications were observed. Conclusions: Percutaneous PFO closure was associated with very low risk of recurrent stroke and is suitable in most patients. We observed no mortality and no long-term device-related complications related to PFO closure, indicating that percutaneous PFO closure is a safe and efficient treatment even in the long term. © 2013 Elsevier B.V.
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| 11. |
- Burgess, S., et al.
(författare)
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Bayesian methods for meta-analysis of causal relationships estimated using genetic instrumental variables
- 2010
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Ingår i: Statistics in medicine. - : Wiley. - 1097-0258 .- 0277-6715. ; 29:12, s. 1298-311
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Tidskriftsartikel (refereegranskat)abstract
- Genetic markers can be used as instrumental variables, in an analogous way to randomization in a clinical trial, to estimate the causal relationship between a phenotype and an outcome variable. Our purpose is to extend the existing methods for such Mendelian randomization studies to the context of multiple genetic markers measured in multiple studies, based on the analysis of individual participant data. First, for a single genetic marker in one study, we show that the usual ratio of coefficients approach can be reformulated as a regression with heterogeneous error in the explanatory variable. This can be implemented using a Bayesian approach, which is next extended to include multiple genetic markers. We then propose a hierarchical model for undertaking a meta-analysis of multiple studies, in which it is not necessary that the same genetic markers are measured in each study. This provides an overall estimate of the causal relationship between the phenotype and the outcome, and an assessment of its heterogeneity across studies. As an example, we estimate the causal relationship of blood concentrations of C-reactive protein on fibrinogen levels using data from 11 studies. These methods provide a flexible framework for efficient estimation of causal relationships derived from multiple studies. Issues discussed include weak instrument bias, analysis of binary outcome data such as disease risk, missing genetic data, and the use of haplotypes.
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| 12. |
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| 13. |
- Fasth, Oskar, et al.
(författare)
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Age in relation to comorbidity and outcome in patients with high-risk TIA or minor ischemic stroke : A Swedish national observational study
- 2021
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Ingår i: European Stroke Journal. - : Sage Publications. - 2396-9873 .- 2396-9881. ; 6:1, s. 53-61
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Recent trials report positive results for preventing vascular events with dual antiplatelet therapy (DAPT) in patients with high-risk TIA or minor ischemic stroke. We aimed to investigate this population regarding influence of age on vascular risk factors, hospital stay and mortality.Patients and methods: Data on patients aged 40-100 years with TIA or ischemic stroke in the Swedish Stroke Register during 2012-13 were linked with national registers. To identify patients with high-risk TIA (ABCD(2) >= 6) or minor ischemic stroke (NIHSS <= 5) eligible for DAPT, we excluded patients with atrial fibrillation, anticoagulant use, prior major bleeding, or unknown stroke severity.Findings: We identified 10,053 potential DAPT-candidates (mean age 72.6 years, 45.2% female, 16.4% with TIA). With advancing age, most vascular risk factors increased. Antiplatelet treatment increased from 31.9% before the event to 95.5% after discharge. Within 1 year following index event, the proportion of patients with >= 1 re-admission increased with age (29.2% in 40-64 year-olds; 47.2% in 85-100 year-olds). All-cause death per 100 person-years was 6.9 (95% CI 6.4-7.4) within 1 year, and highest in the first 30 days (15.2; 95% CI 12.8-18.2). For each year of increased age, the risk of death increased with 3.5% (p = 0.128) in patients 40-64 years and with 11.8% (p < 0.001) in those >= 85 years.Conclusions: While in theory representing a subset of patients with mild injury, our observational study highlights substantial use of health-care resources and high mortality rates among patients with high-risk TIA or minor ischemic stroke assumed eligible for DAPT.
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| 14. |
- Ladenvall, Per, 1972
(författare)
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Genetic variation at the human tissue-type plasminogen activator locus
- 2002
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Tissue-type plasminogen activator (tPA) is the key initiator of intravascular fibrinolysis. Family studies suggest that tPA release is regulated by hereditary factors. The aim of the present thesis was therefore to test the hypothesis that a neutral polymorphism at the tPA locus is associated with vascular release of tPA, and if so search the tPA locus for functional polymorphisms that could explain this finding. An identified genetic marker of vascular tPA release was then investigated in an association study of myocardial infarction.Vascular tPA release rates were assessed in 51 healthy males by the perfused forearm model. By this invasive procedure blood samples were simultaneously drawn from the brachial artery and vein. Net release of tPA was defined as the venoarterial plasma concentration difference times local plasma flow. In an initial study, subjects were typed for an Alu insertion polymorphism in intron eight of the tPA gene. A significant association with both basal and stimulated tPA release rates was observed. As the Alu polymorphism is neutral, this finding prompted us to search the tPA locus for putative functional variations, that could explain our observation. Regulatory and coding regions of the tPA gene were re-sequenced in 30 chromosomes and eight single nucleotide polymorphisms (SNPs) were discovered. All SNPs were typed in the 51 subjects who had taken part in invasive experi-ments as well as in 240 subjects in whom plasma levels of tPA had been determined. The results showed a high level of linkage disequilibrium among the majority of SNPs and thus, only a few common haplotypes were observed. Three of the SNPs showed a significant association with vascular release rates of tPA, but were not significantly associated with plasma levels of tPA. The closest association was observed for tPA -7,351C>T, which is located in an enhancer region upstream of the gene. Initial in vitro studies suggested a preferential binding of the transcription factor Sp1 to the C allele, which is the allele that was associated with a high tPA release rate. Since it was recently shown that Sp1 mediates induction of tPA gene transcription through the enhancer, this finding indicates that tPA -7,351C>T is functional. This SNP was therefore tested in a prospective nested case-control study on myocardial infarction in northern Sweden, which included 61 cases with a first myocardial infarction and 120 controls matched for age, sex, and geographical region. The results showed that both tPA -7,351C>T and plasma tPA antigen were associated with myocardial infarction and this association was independent of traditional risk factors. Carriers of the T allele had an increased risk of myocardial infarction.In conclusion, eight novel SNPs were identified at the tPA locus. The enhancer -7,351C>T variant, which was associated both with vascular tPA release rates and myocardial infraction, is of putative functional importance. Thus, the genetic variation at this locus appears important for physiological regulation of tPA.
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| 15. |
- Ladenvall, Per, 1972, et al.
(författare)
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Genetic variation at the human tissue-type plasminogen activator (tPA) locus: haplotypes and analysis of association to plasma levels of tPA.
- 2003
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Ingår i: European journal of human genetics : EJHG. - : Springer Science and Business Media LLC. - 1018-4813 .- 1476-5438. ; 11:8, s. 603-10
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Tidskriftsartikel (refereegranskat)abstract
- Tissue-type plasminogen activator (tPA) plays a key role in thrombus dissolution and plasma levels of tPA have been associated with cardiovascular disease. We have previously resequenced regulatory and coding regions of the human tPA gene (PLAT) and identified eight single-nucleotide polymorphisms (SNPs). In a small experimental study, four common variants were associated with invasively determined vascular tPA release rates. The aim of the present study was to investigate whether there is an association between genetic variants at this locus and plasma levels of tPA. To this end, 240 Swedish individuals without cardiovascular disease were typed for the eight SNPs and an Alu insertion polymorphism at the PLAT locus, as well as for a polymorphism in the plasminogen activator inhibitor type 1 (PAI-1) promoter (PAI-1 -675 4G>5G). Stepwise regression analysis, with established predictors of plasma tPA including plasma PAI-1 and genetic variants, showed that neither genotypes nor haplotypes were major contributors to plasma tPA. The results also showed that the level of linkage disequilibrium was high at the PLAT locus, as demonstrated by the fact that only three haplotypes had a frequency above 5%. In conclusion, in the present study neither genetic variation at the PLAT locus nor the PAI-1 -675 4G>5G polymorphism was strong predictors of plasma tPA levels, which suggests that variations in other genes contribute to the heritability of this phenotype. The results also show that three haplotypes at the PLAT locus accounted for nearly 90% of the chromosomes and that they could be defined by typing only two SNPs.
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| 16. |
- Ladenvall, Per, 1972, et al.
(författare)
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Tissue-type plasminogen activator -7,351C/T enhancer polymorphism is associated with a first myocardial infarction.
- 2002
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Ingår i: Thrombosis and haemostasis. - 0340-6245. ; 87:1, s. 105-9
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Tidskriftsartikel (refereegranskat)abstract
- We recently identified a polymorphic Sp1 binding site in an enhancer at the tissue-type plasminogen activator (tPA) locus (tPA -7,351C/T), which was associated with vascular tPA release. Subjects homozygous for the -7,351C allele had twice the tPA release rate compared to subjects carrying the -7,351T allele. In this study we tested the hypothesis that the tPA -7,351C/T polymorphism is associated with myocardial infarction (MI). In a population-based prospective nested case-control study within northern Sweden, genotypes were determined among 61 MI cases and 120 controls. In a multivariate model, the tPA -7,351C/T polymorphism (OR 2.68 for T allele carriers; 95% CI 1.31-5.50), tPA antigen (OR 1.16; 95% CI 1.07-1.25) and apo A-I (OR, 0.997; 95% CI 0.995-0.999) were independently associated with a first MI. These findings suggest that genetic markers of local tPA release and circulating steady-state tPA levels carry independent prognostic information.
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| 17. |
- Mirzada, Naqibullah, 1977, et al.
(författare)
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Absence of significant aortic regurgitation seven years after closure of patent foramen ovale
- 2014
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Ingår i: International journal of cardiology. Heart & vessels. - : Elsevier BV. - 2214-7632. ; 4, s. 59-62
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Tidskriftsartikel (refereegranskat)abstract
- Background It has been suggested that there is an increase in aortic regurgitation (AR) in the short and medium term after percutaneous closure of patent foramen ovale (PFO). The aim of this study is to determine the long-term effect of percutaneous closure of PFO on the prevalence of AR. Methods Patients with cryptogenic stroke or transient ischemic attack who had undergone percutaneous closure of PFO more than five years before the study were invited to an echocardiographic examination. Results Out of 83 invited patients, 64 accepted the invitation and were examined with echocardiography. Mild AR was found in one patient (2%), but this was already evident in the patient's echocardiographic result before PFO closure. Trace AR was detected in 11 patients (17%). No case of moderate or severe AR was detected. Patients with AR were more often hypertensive (six out of 12 patients with AR, compared to nine of the 52 without AR, p = 0.025), and the indexed sinus of Valsalva was larger in patients with AR (18.6 mm/m2, SD 1.6, as compared to 17.3 mm/m2, SD 1.6, p = 0.02). Conclusion In this long-term study with a minimum follow-up of 5.6 years and a mean of 7.1 years, we found negligible levels of AR. Where present, AR was associated with hypertension and mild dilatation of the aortic root, but there was no indication that device closure per se increased the risk of developing AR.
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| 18. |
- Tjärnlund, Anna, 1974, et al.
(författare)
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Rapid genotyping of haemostatic gene polymorphisms using the 5' nuclease assay.
- 2003
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Ingår i: Thrombosis and haemostasis. - 0340-6245. ; 89:5, s. 936-42
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Tidskriftsartikel (refereegranskat)abstract
- Hemostatic gene polymorphisms have been shown to be associated with arterial and venous thrombotic disease. To date these polymorphisms have mainly been detected by labor-intensive conventional gel based methods. Aim of the present study was to design and optimize high throughput 5' nuclease assays for the detection of a set of 10 single-nucleotide polymorphisms (SNP) in genes of importance for hemostasis: plasminogen activator inhibitor type 1 -675 4G>5G, thrombin activatable fibrinolysis inhibitor Ala147Thr and 1,542C>G, beta-fibrinogen -455G>A, von Willebrand factor -1,051A>G, factor VII Arg353Gln, factor XIII Val34Leu, prothrombin 20,210G>A, tissue factor pathway inhibitor -287T>C, and methylenetetrahydrofolate reductase 1,298A>C. Specificity of each genotyping assay was confirmed by sequence-based typing and reproducibility was evaluated by repeated genotyping. The genotyping protocols presented here may serve as a valuable tool for clinical researchers interested in exploring associations between these SNPs and thrombotic disease.
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