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Träfflista för sökning "L773:0167 5273 OR L773:1874 1754 ;pers:(Fu Michael 1963)"

Sökning: L773:0167 5273 OR L773:1874 1754 > Fu Michael 1963

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  • Basic, Carmen, 1975, et al. (författare)
  • Sex-related differences among young adults with heart failure in Sweden
  • 2022
  • Ingår i: International Journal of Cardiology. - : Elsevier BV. - 0167-5273 .- 1874-1754. ; 362, s. 97-103
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Differences between the sexes among the non-elderly with heart failure (HF) have been insufficiently evaluated. This study aims to investigate sex-related differences in early-onset HF. Methods: Patients aged 18 to 54 years who were registered from 2003 to 2014 in the Swedish Heart Failure Register were included. Each patient was matched with two controls from the Swedish Total Population Register. Data on comorbidities and outcomes were obtained through the National Patient Register and Cause of Death Register. Results: We identified 3752 patients and 7425 controls. Of the patients, 971 (25.9%) were women and 2781 (74.1%) were men with a mean (standard deviation) age of 44.9 (8.4) and 46.4 (7.3) years, respectively. Men had more hypertension and ischemic heart disease, whereas women had more congenital heart disease and obesity. During the median follow-up of 4.87 years, 26.5 and 24.7 per 1000 person-years male and female patients died, compared with 3.61 and 2.01 per 1000 person-years male and female controls, respectively. The adjusted hazard ratios for all-cause mortality, compared with controls, were 4.77 (3.78-6.01) in men and 7.84 (4.85-12.7) in women (p for sex difference = 0.11). When HF was diagnosed at 30, 35, 40, and 45 years, women and men lost up to 24.6 and 24.2, 24.4 and 20.9, 20.5 and 18.3, and 20.7 and 16.5 years of life, respectively. Conclusion: Long-term mortality was similar between the sexes. Women lost more years of life than men.
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3.
  • Cui, X., et al. (författare)
  • Prevalence and correlates of left ventricular diastolic dysfunction and heart failure with preserved ejection fraction in elderly community residents
  • 2017
  • Ingår i: International journal of cardiology. - : Elsevier BV. - 0167-5273 .- 1874-1754. ; 227, s. 820-825
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Left ventricular diastolic dysfunction (LVDD) is closely related to heart failure with preserved ejection fraction (HFpEF), while the prevalence and correlates of either LVDD or HFpEF in elderly population remain largely unknown. METHODS: The study was performed in 1274 community residents (769 women, aged >/=65years) who participated in the Shanghai Heart Health Study. Demographic, laboratory and echocardiographic data were obtained to analyze correlates of LVDD and HFpEF using univariate and multivariate Logistic analysis. RESULTS: LVDD was detected in 31.9% (406/1274) residents and it was significantly higher in women than in men (34.2% vs. 28.3%, P=0.027). HFpEF prevalence was 2.8% (35/1274), and increased with aging in the whole cohort. For residents with left ventricular ejection fraction >/=50% and normal-sized ventricular cavity, female sex (odds ratio [OR] 1.69, 95% confidence interval [CI] 1.24-2.29), heart rate (OR 0.76, 95% CI 0.68-0.86), atrial fibrillation (OR 7.37, 95% CI 3.13-17.36), hypertension (OR 1.32, 95% CI 1.00-1.75), N-terminal pro-B type natriuretic peptide (OR 2.33, 95% CI 1.50-3.61) and high-sensitivity troponin T (hs-TnT) (OR 1.90, 95% CI 1.12-3.23) were independent correlates of asymptomatic LVDD. While age (OR 1.44, 95% CI 1.01-2.06), heart rate (OR 0.66, 95% CI 0.47-0.93) and hs-TnT (OR 4.37, 95% CI 1.46-13.12) were independently related to HFpEF. CONCLUSIONS: LVDD is common in this community elderly population, and HFpEF is also not rare. Different factors played roles in different stages of HFpEF. Future studies are warranted to explore the predictors of LVDD and HFpEF in the community elderly.
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4.
  • Cui, Xiaotong, et al. (författare)
  • Temporal trends in cause-specific readmissions and their risk factors in heart failure patients in Sweden
  • 2020
  • Ingår i: International Journal of Cardiology. - : ELSEVIER IRELAND LTD. - 0167-5273 .- 1874-1754. ; 306, s. 116-122
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: It remains unclear whether readmissions of patients with heart failure (HF) have decreased over time in an era of improved therapy and management of HF. This study aimed to determine the temporal short- and long-term trends of cause-specific rehospitalization and their risk factors in a Swedish context. Methods: HF patients in the Swedish Heart Failure Registry (SwedeHF) were investigated. Maximum follow-up time was 1 year. Outcomes included the first occurrence of all-cause, cardiovascular (CV) and HF rehospitalizations. Cox proportional hazards models were performed to determine the impact of increasing years on risk for rehospitalization and its known risk factors. Results: Totally, 25,644 index-hospitalized HF patients in SwedeHF from 2004 to 2011 were enrolled in the study. For 8 years, the incidence risk of 1-year all-cause rehospitalization remained unchanged, whereas the incidence risk of CV (P = 0.038) or HF (P = 0.0038) rehospitalization decreased. After adjustment for age and sex, a 3% decrease per every second year was observed for 1-year CV and HF rehospitalizations (P < 0.05). However, time to the first occurring all-cause, CV and HF rehospitalization did not change significantly from 2004 to 2011 (P-values 0.13-0.87). When two study periods (2004-2005 vs. 2010-2011) were compared, the risk factor profile for rehospitalization was found to change. Conclusions: Throughout the 8-year study period, CV- and HF-related rehospitalizations decreased, whereas all-cause rehospitalization remained unchanged, indicating a parallel increase in non-CV rehospitalization in the HF patients. (c) 2020 Elsevier B.V. All rights reserved.
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5.
  • Fu, Michael, 1963 (författare)
  • Beta-blocker therapy in heart failure in the elderly.
  • 2008
  • Ingår i: International journal of cardiology. - : Elsevier BV. - 1874-1754 .- 0167-5273. ; 125:2, s. 149-53
  • Forskningsöversikt (refereegranskat)abstract
    • Chronic heart failure (CHF) is a common and disabling condition with morbidity and mortality that increase dramatically with advancing age. There is some evidence available about beta-blocker therapy in the elderly. The Study of the Effects of Nebivolol Intervention on Outcomes and Rehospitalisation in Seniors with Heart Failure (SENIORS) and retrospective subgroup (elderly) analyses of landmark clinical trials in stable systolic heart failure have provided data supporting the use of beta-blocker as baseline therapy in heart failure in the elderly. However, beta-blocker is still less frequently used in elderly compared to younger patients. There are many reasons, one of which is that available data on elderly patients are not as convincing as those pertaining to their younger counterparts. There is uncertainty or disagreement about whether beta-blockers are equally beneficial and well tolerated in elderly heart failure patients as in younger ones. In other words, the level of evidence regarding beta-blocker therapy in the elderly is not regarded as high as that in younger patients. Indeed, the senior heart failure population, which in fact comprises the majority of all heart failure patients, is in general less well studied, both experimentally and clinically, than younger populations. Both clinical studies and experience indicate good tolerability in the use of beta-blocker in the elderly. Although beta-blockers are well tolerated by the elderly, target doses (based on previous clinical trials) may be difficult to achieve. The question is whether we should use the same target dose in the elderly as that in younger patients. Theoretically, the most effective dose is the highest dose tolerated, which may differ across different age groups. Is it time to abandon the "target dose" for the "highest dose tolerated"? The time has come to carry out active research to achieve better documentation of evidence based heart failure management in the elderly for the benefit of a large number of elderly patients with heart failure. We need clinical trial data that show definite improvement in outcomes as well as a clear-cut, favourable benefit-risk analysis involving beta-blockers in typical older heart failure patients irrespective of comorbidity and polypharmacy. Until the above is available, it may be wiser to adhere to beta-blocker therapy, which at present is better documented than other heart failure therapies in the elderly.
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8.
  • Haugen, Espen, 1973, et al. (författare)
  • Increased adiponectin level in parallel with increased NT-pro BNP in patients with severe heart failure in the elderly: A hospital cohort study.
  • 2008
  • Ingår i: International journal of cardiology. - : Elsevier BV. - 1874-1754 .- 0167-5273. ; 125:2, s. 216-9
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Adiponectin, which is a collagen-like plasma protein produced by adipose tissue, has in general anti-atherogenic and anti-inflammatory effects. Recently it was shown to be elevated in chronic heart failure patients. However whether this holds true in the elderly heart failure patients who are often associated with malnutrition remains unknown. MATERIALS AND METHODS: Patients with severe heart failure (n=92, average age >70 years, NYHA III-IV) and age-matched healthy volunteers (n=70) as control were enrolled in the present study. Serum levels of adiponectin and NT-pro BNP were measured. RESULTS: Adiponectin levels were significantly increased in heart failure patients for those >70 years old as compared with control group. There were higher adiponectin levels in non-ischemic heart failure as compared with those with ischemic cause. Serum adiponectin levels were positively associated with serum NT-pro BNP levels. There was a strong trend of higher adiponectin levels in those who died as compared with those who survived. CONCLUSION: Serum adiponectin levels were increased in the very elderly heart failure patients, and particularly in those with underlying non-ischemic origin. Adiponectin levels appear to be associated with increased mortality.
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9.
  • Haugen, Espen, 1973, et al. (författare)
  • Parallel gene expressions of IL-6 and BNP during cardiac hypertrophy complicated with diastolic dysfunction in spontaneously hypertensive rats.
  • 2007
  • Ingår i: International journal of cardiology. - : Elsevier BV. - 1874-1754 .- 0167-5273. ; 115:1, s. 24-8
  • Tidskriftsartikel (refereegranskat)abstract
    • There is increasing evidence showing that inflammation is involved in heart failure. However, heart failure may differ greatly due to different aetiologies. The role of inflammation in hypertensive heart failure, particularly in the early stage of cardiac dysfunction, has not been studied completely. This study aims at finding out whether inflammation is involved in the early stage of heart dysfunction due to hypertension. METHODS: Ten spontaneously hypertensive rats (SHR) and ten age-matched Wistar rats were used. Cardiac morphology and function, as well as coronary flow reserve, were examined by echocardiography. mRNAs for cytokines and brain natriuretic peptide were determined by RT-PCR. RESULTS: The results demonstrate cardiac hypertrophy with increased heart/body weight ratio in SHR. Echocardiographic examination has shown that SHR developed diastolic heart dysfunction as determined by tissue Doppler without decrease in systolic function. In heart biopsies, there were increased mRNA levels for interleukin-6 and brain natriuretic peptide whereas decreased mRNA for interleukin-2, beta adrenergic receptor, interferon and NFkb in SHR as compared to WKY group. Coronary flow remained unchanged in both groups. CONCLUSION: SHR developed cardiac hypertrophy complicated with diastolic heart dysfunction with increased expression of brain natriuretic peptide, down-regulation of beta adrenergic receptors and simultaneous up-regulation of IL-6, which indicates active proinflammatory process as, at least partly, underlying mechanism during the early stage when cardiac hypertrophy associated with diastolic dysfunction occurs.
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10.
  • Haugen, Espen, 1973, et al. (författare)
  • TNFalpha antagonist upregulates interleukin-6 in rats with hypertensive heart failure.
  • 2008
  • Ingår i: International journal of cardiology. - : Elsevier BV. - 1874-1754 .- 0167-5273. ; 130:1, s. 64-8
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Tumor necrosis factor alpha (TNFalpha) has been shown to be a prognostic marker in heart failure, but recent clinical trials using TNFalpha antagonists in patients with severe heart failure have been disappointing. Hypertension is one of most common causes to chronic heart failure in humans. HYPOTHESIS: Suppression of a single cytokine in CHF is not an effective treatment strategy because it leads to the upregulation of other proinflammatory cytokines. OBJECTIVES: The aim of the present study was to investigate the effect of chronic treatment with a TNFalpha antagonist in a rat model of the early stage of heart failure due to hypertension. METHODS: Spontaneously hypertensive rats (SHR, n=30) and healthy Wistar Kyoto rats (WKY, n=30) were treated with either the TNFalpha antagonist etanercept or placebo for 12 weeks. At the end of the study, the rats were 26 weeks old and indices of cardiac structure, function and cytokines were analyzed. RESULTS: SHR displayed early stage of heart failure as shown by increased heart weight/body weight ratio and relative wall thickness by echocardiography, downregulated myocardial beta(1)-adrenoceptor, and upregulated myocardial brain natriuretic peptide and interleukin-6 (IL6). Chronic treatment with etanercept in SHR resulted in decreased relative wall thickness but also increased cardiac reserve and higher blood pressure. In addition, IL6 was further upregulated compared with placebo treatment. CONCLUSION: Chronic treatment with etanercept in SHR resulted in favorable cardiac remodeling, but also had a positive inotropic effect and was associated with an upregulation of IL6. These findings indicate that chronic treatment with TNFalpha antagonists is not an effective treatment strategy and may aggravate heart failure in the long term.
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