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- 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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- 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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- 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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- Berglund, Lisa, et al.
(författare)
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Glucose-Dependent Insulinotropic Polypeptide (GIP) Stimulates Osteopontin Expression in the Vasculature via Endothelin-1 and CREB.
- 2016
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Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 65:1, s. 239-254
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Tidskriftsartikel (refereegranskat)abstract
- Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone with extrapancreatic effects beyond glycemic control. Here we demonstrate unexpected effects of GIP signaling in the vasculature. GIP induces the expression of the pro-atherogenic cytokine osteopontin (OPN) in mouse arteries, via local release of endothelin-1 (ET-1) and activation of cAMP response element binding protein (CREB). Infusion of GIP increases plasma OPN levels in healthy individuals. Plasma ET-1 and OPN levels are positively correlated in patients with critical limb ischemia. Fasting GIP levels are higher in individuals with a history of cardiovascular disease (myocardial infarction, stroke) when compared to controls. GIP receptor (GIPR) and OPN mRNA levels are higher in carotid endarterectomies from patients with symptoms (stroke, transient ischemic attacks, amaurosis fugax) than in asymptomatic patients; and expression associates to parameters characteristic of unstable and inflammatory plaques (increased lipid accumulation, macrophage infiltration and reduced smooth muscle cell content). While GIPR expression is predominantly endothelial in healthy arteries from human, mouse, rat and pig; remarkable up-regulation is observed in endothelial and smooth muscle cells upon culture conditions yielding a "vascular disease-like" phenotype. Moreover, a common variant rs10423928 in the GIPR gene associated with increased risk of stroke in type 2 diabetes patients.
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- Johnston, S. Claiborne, et al.
(författare)
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The Acute Stroke or Transient Ischemic Attack Treated with Ticagrelor and Aspirin for Prevention of Stroke and Death (THALES) trial : Rationale and design
- 2019
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Ingår i: International Journal of Stroke. - : SAGE Publications. - 1747-4930 .- 1747-4949. ; 14:7, s. 745-751
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Tidskriftsartikel (refereegranskat)abstract
- RationaleIn patients with acute cerebral ischemia, the rate of stroke, myocardial infarction, or death during 90 days was reported to be non-significantly lower with ticagrelor compared with aspirin, with no increase in major hemorrhage. Dual antiplatelet therapy may be more effective in this setting.AimTo investigate whether ticagrelor combined with aspirin are superior to aspirin alone in preventing stroke or death in patients with non-severe, non-cardioembolic ischemic stroke or high-risk transient ischemic attack.DesignThe Acute Stroke or Transient Ischemic Attack Treated with Ticagrelor and Aspirin for Prevention of Stroke and Death (THALES) trial is a randomized, placebo-controlled, double-blind, event-driven study. Patients will be randomized within 24 h of onset of acute ischemic symptoms. THALES is expected to randomize 13,000 at ∼450 sites worldwide, to collect 764 primary outcome events. Study treatments are ticagrelor 180 mg loading dose on day 1, then 90 mg twice daily on days 2–30, or matching placebo. All patients will also receive open-label aspirin 300–325 mg on day 1, then 75–100 mg once daily on days 2–30.Study outcomesThe primary efficacy outcome is time to the composite endpoint of stroke or death through 30-day follow-up. The primary safety outcome is time to first severe bleeding event.DiscussionThe THALES trial will provide important information about the benefits and risks of dual antiplatelet therapy with ticagrelor and aspirin in patients with acute cerebral ischemia in a global setting (funding: AstraZeneca)
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- Sandholm, Niina, et al.
(författare)
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The genetic landscape of renal complications in type 1 diabetes
- 2017
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Ingår i: Journal of the American Society of Nephrology. - 1046-6673. ; 28:2, s. 557-574
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Tidskriftsartikel (refereegranskat)abstract
- Diabetes is the leading cause of ESRD. Despite evidence for a substantial heritability of diabetic kidney disease, efforts to identify genetic susceptibility variants have had limited success. We extended previous efforts in three dimensions, examining a more comprehensive set of genetic variants in larger numbers of subjects with type 1 diabetes characterized for a wider range of cross-sectional diabetic kidney disease phenotypes. In 2843 subjects, we estimated that the heritability of diabetic kidney disease was 35% (P=6.4310-3). Genome-wide association analysis and replication in 12,540 individuals identified no single variants reaching stringent levels of significance and, despite excellent power, provided little independent confirmation of previously published associatedvariants.Whole-exome sequencing in 997 subjects failed to identify any large-effect coding alleles of lower frequency influencing the risk of diabetic kidney disease. However, sets of alleles increasing body mass index (P=2.2310-5) and the risk of type 2 diabetes (P=6.1310-4) associated with the risk of diabetic kidney disease.Wealso found genome-wide genetic correlation between diabetic kidney disease and failure at smoking cessation (P=1.1310-4). Pathway analysis implicated ascorbate and aldarate metabolism (P=9.0310-6), and pentose and glucuronate interconversions (P=3.0310-6) in pathogenesis of diabetic kidney disease. These data provide further evidence for the role of genetic factors influencing diabetic kidney disease in those with type 1 diabetes and highlight some key pathways that may be responsible. Altogether these results reveal important biology behind the major cause of kidney disease.
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