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Träfflista för sökning "LAR1:gu ;pers:(Dahlöf Björn 1953)"

Sökning: LAR1:gu > Dahlöf Björn 1953

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51.
  • Gerdts, E., et al. (författare)
  • Left atrial size and risk of major cardiovascular events during antihypertensive treatment: losartan intervention for endpoint reduction in hypertension trial
  • 2007
  • Ingår i: Hypertension. - 1524-4563. ; 49:2, s. 311-6
  • Tidskriftsartikel (refereegranskat)abstract
    • The influence of left atrial size on cardiovascular events during antihypertensive treatment has not been reported previously from a long-term, prospective, randomized hypertension treatment trial. We recorded left atrial diameter by annual echocardiography and cardiovascular events in 881 hypertensive patients (41% women) with electrocardiographic left ventricular hypertrophy aged 55 to 80 (mean: 66) years during a mean of 4.8 years of randomized losartan- or atenolol-based treatment in the Losartan Intervention for Endpoint Reduction in Hypertension Study. During follow-up, a total of 88 primary end points (combined cardiovascular death, myocardial infarction, or stroke) occurred. In Cox regression, baseline left atrial diameter/height predicted incidence of cardiovascular events (hazard ratio: 1.98 per cm/m [95% CI: 1.02 to 3.83 per cm/m]; P=0.042) adjusted for significant effects of Framingham risk score and history of atrial fibrillation. Greater left atrial diameter reduction during follow-up was associated with greater reduction in left ventricular hypertrophy, absence of new-onset atrial fibrillation or mitral regurgitation during follow-up, and losartan-based treatment (B=-0.13+/-0.03 cm/m; P<0.001) in multiple linear regression, adjusting for baseline left atrial diameter/height. However, in time-varying Cox regression analysis, left atrial diameter reduction was not independent of left ventricular hypertrophy regression in predicting cardiovascular events during follow-up. In conclusion, left atrial diameter/height predicts risk of cardiovascular events independent of other clinical risk factors in hypertensive patients with left ventricular hypertrophy and may be useful in pretreatment clinical assessment of cardiovascular risk in these patients.
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52.
  • Gerdts, E., et al. (författare)
  • Pulse pressure, left ventricular function and cardiovascular events during antihypertensive treatment (the LIFE study)
  • 2009
  • Ingår i: Blood Press. - 1651-1999. ; 18:4, s. 180-186
  • Tidskriftsartikel (refereegranskat)abstract
    • Background. Pulse pressure (PP) has been related to risk of cardiovascular events in hypertension. However, less is known about modification of this risk marker during antihypertensive treatment in patients with left ventricular (LV) hypertrophy. Methods. Associations of in-treatment PP with LV systolic function and cardiovascular events was assessed in 883 patients with electrocardiographic LV hypertrophy during 4.8 years of randomized losartan- or atenolol-based treatment within the echocardiographic substudy of the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. Results. PP was similarly reduced by both treatments. In different multiple regression models, lower in-treatment PP was independently associated with lower in-treatment LV ejection fraction (beta = 0.16), stress-corrected midwall shortening (beta = 0.20), stroke volume (beta = 0.11) and cardiac index (beta = 0.07, all p<0.05). In time-varying Cox regression models, 10mmHg lower in-treatment PP was associated with a 28% higher rate of cardiovascular events [hazard ratio, HR = 1.28 (1.09 - 1.52), p <0.01] independent of in-treatment LV mass and ejection fraction, history of ischemic heart disease, Framingham risk score and study treatment allocation. Conclusion. During systematic antihypertensive treatment in hypertensive patients with electrocardiographic LV hypertrophy, lower in-treatment PP was associated with lower in-treatment LV function and cardiac output as well as higher rate of cardiovascular events.
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53.
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54.
  • Gupta, A., et al. (författare)
  • Adverse events associated with unblinded, but not with blinded, statin therapy in the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid-Lowering Arm (ASCOT-LLA): a randomised double-blind placebo-controlled trial and its non-randomised non-blind extension phase
  • 2017
  • Ingår i: Lancet. - : Elsevier BV. - 0140-6736. ; 389:10088, s. 2473-2481
  • Tidskriftsartikel (refereegranskat)abstract
    • Background In blinded randomised controlled trials, statin therapy has been associated with few adverse events (AEs). By contrast, in observational studies, larger increases in many different AEs have been reported than in blinded trials. Methods In the Lipid-Lowering Arm of the Anglo-Scandinavian Cardiac Outcomes Trial, patients aged 40-79 years with hypertension, at least three other cardiovascular risk factors, and fasting total cholesterol concentrations of 6.5 mmol/L or lower, and who were not taking a statin or fibrate, had no history of myocardial infarction, and were not being treated for angina were randomly assigned to atorvastatin 10 mg daily or matching placebo in a randomised double-blind placebo-controlled phase. In a subsequent non-randomised non-blind extension phase (initiated because of early termination of the trial because efficacy of atorvastatin was shown), all patients were offered atorvastatin 10 mg daily open label. We classified AEs using the Medical Dictionary for Regulatory Activities. We blindly adjudicated all reports of four prespecified AEs of interest-muscle-related, erectile dysfunction, sleep disturbance, and cognitive impairment-and analysed all remaining AEs grouped by system organ class. Rates of AEs are given as percentages per annum. Results The blinded randomised phase was done between February, 1998, and December, 2002; we included 101 80 patients in this analysis (5101 [50%] in the atorvastatin group and 5079 [50%] in the placebo group), with a median follow-up of 3.3 years (IQR 2.7-3.7). The non-blinded non-randomised phase was done between December, 2002, and June, 2005; we included 9899 patients in this analysis (6409 [65%] atorvastatin users and 3490 [35%] nonusers), with a median follow-up of 2.3 years (2.2-2.4). During the blinded phase, muscle-related AEs (298 [2.03% per annum] vs 283 [2.00% per annum]; hazard ratio 1.03 [95% CI 0.88-1.21]; p= 0.72) and erectile dysfunction (272 [1.86% per annum] vs 302 [2.14% per annum]; 0.88 [0.75-1.04]; p= 0.13) were reported at a similar rate by participants randomly assigned to atorvastatin or placebo. The rate of reports of sleep disturbance was significantly lower among participants assigned atorvastatin than assigned placebo (149 [1.00% per annum] vs 210 [1.46% per annum]; 0.69 [0.56-0.85]; p= 0.0005). Too few cases of cognitive impairment were reported for a statistically reliable analysis (31 [0.20% per annum] vs 32 [0.22% per annum]; 0.94 [057-1.54]; p= 0.81). We observed no significant differences in the rates of all other reported AEs, with the exception of an excess of renal and urinary AEs among patients assigned atorvastatin (481 [1.87%] per annum vs 392 [1.51%] per annum; 1.23 [1.08-1.41]; p= 0.002). By contrast, during the non-blinded non-randomised phase, muscle-related AEs were reported at a significantly higher rate by participants taking statins than by those who were not (161 [1.26% per annum] vs 124 [1.00% per annum]; 1.41 [1.10-1.79]; p= 0.006). We noted no significant differences between statin users and non-users in the rates of other AEs, with the exception of musculoskeletal and connective tissue disorders (992 [8.69% per annum] vs 831 [7.45% per annum]; 1.17 [1.06-1.29]; p= 0.001) and blood and lymphatic system disorders (114 [0.88% per annum] vs 80 [0.64% per annum]; 1.40 [1.04-1.88]; p= 0.03), which were reported more commonly by statin users than by non-users. Interpretation These analyses illustrate the so-called nocebo effect, with an excess rate of muscle-related AE reports only when patients and their doctors were aware that statin therapy was being used and not when its use was blinded. These results will help assure both physicians and patients that most AEs associated with statins are not causally related to use of the drug and should help counter the adverse effect on public health of exaggerated claims about statin-related side-effects. C1, 2013, Heart of the matter part 2-cholesterol drug war
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55.
  • Gupta, A. K., et al. (författare)
  • Metabolic syndrome, independent of its components, is a risk factor for stroke and death but not for coronary heart disease among hypertensive patients in the ASCOT-BPLA
  • 2010
  • Ingår i: Diabetes Care. - 0149-5992. ; 33:7, s. 1647-1651
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To evaluate whether in hypertensive patients the risk of cardiovascular disease is greater in association with the metabolic syndrome (MetS) or the sum of its individual components. RESEARCH DESIGN AND METHODS: Cox regression analysis models were developed to assess the influence of age, sex, ethnicity, and the individual components of MetS on risk associated with the MetS (using several definitions) of coronary outcomes, stroke, and all-cause mortality. RESULTS: MetS was significantly associated with coronary outcomes, stroke, and all-cause mortality after adjusting for age, sex, and ethnicity. However, when the model was further adjusted for the individual components, MetS was associated with significantly increased risk of stroke (hazard ratio 1.34 [95% CI 1.07-1.68]) and all-cause mortality (1.35 [1.16-1.58]) but not coronary outcomes (fatal coronary heart disease plus nonfatal myocardial infarction 1.16 [0.95-1.43] and total coronary events 1.06 [0.91-1.24]). CONCLUSIONS: MetS, independent of its individual components, is associated with increased risk of stroke and all-cause mortality but not coronary outcomes.
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56.
  • Hacke, W., et al. (författare)
  • Transcranial Laser Therapy in Acute Stroke Treatment Results of Neurothera Effectiveness and Safety Trial 3, a Phase III Clinical End Point Device Trial
  • 2014
  • Ingår i: Stroke. - : Ovid Technologies (Wolters Kluwer Health). - 0039-2499 .- 1524-4628. ; 45:11, s. 3187-3193
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and Purpose On the basis of phase II trials, we considered that transcranial laser therapy could have neuroprotective effects in patients with acute ischemic stroke. Methods We studied transcranial laser therapy in a double-blind, sham-controlled randomized clinical trial intended to enroll 1000 patients with acute ischemic stroke treated 24 hours after stroke onset and who did not undergo thrombolytic therapy. The primary efficacy measure was the 90-day functional outcome as assessed by the modified Rankin Scale, with hierarchical Bayesian analysis incorporating relevant previous data. Interim analyses were planned after 300 and 600 patients included. Results The study was terminated on recommendation by the Data Monitoring Committee after a futility analysis of 566 completed patients found no difference in the primary end point (transcranial laser therapy 140/282 [49.6%] versus sham 140/284 [49.3%] for good functional outcome; modified Rankin Scale, 0-2). The results remained stable after inclusion of all 630 randomized patients (adjusted odds ratio, 1.024; 95% confidence interval, 0.705-1.488). Conclusions Once the results of the interim futility analysis became available, all study support was immediately withdrawn by the capital firms behind PhotoThera, and the company was dissolved. Proper termination of the trial was difficult but was finally achieved through special efforts by former employees of PhotoThera, the CRO Parexel and members of the steering and the safety committees. We conclude that transcranial laser therapy does not have a measurable neuroprotective effect in patients with acute ischemic stroke when applied within 24 hours after stroke onset. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT01120301.
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57.
  • Haffner, S. M., et al. (författare)
  • Metabolic syndrome, new onset diabetes, and new end points in cardiovascular trials
  • 2006
  • Ingår i: J Cardiovasc Pharmacol. - 0160-2446. ; 47:3, s. 469-75
  • Tidskriftsartikel (refereegranskat)abstract
    • Metabolic syndrome affects approximately 44% of the US population over the age of 50 years. Although conflicting definitions exist, the syndrome is typically characterized by abdominal obesity, dyslipidemia, hypertension, and insulin resistance. Thus, it is a major risk factor for both coronary heart disease and type 2 diabetes. Furthermore, the risk of cardiovascular (CV) death is significantly increased in patients with diabetes and/or the metabolic syndrome. Although very few studies exist in patients with the metabolic syndrome, lifestyle changes and drug intervention targeted at the individual components have been shown to reduce the risk of developing diabetes and the incidence of CV disease in high-risk patients. Because many of the conventional antihypertensive drugs may affect the development of new onset diabetes, both positively and negatively, the choice of therapy is particularly important in this population. However, the long-term clinical trials to date have either not included new onset diabetes as a protocol end point or used various different criteria, making comparisons difficult. This review assesses the need for future research into metabolic syndrome and discusses whether clinical surrogates for CV end points, such as new onset diabetes, should be included in clinical trials of new drugs, new regimens, or new indications.
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58.
  • Hildebrandt, P., et al. (författare)
  • Impairment of cardiac function in hypertensive patients with Type 2 diabetes: a LIFE study
  • 2005
  • Ingår i: Diabet Med. - 0742-3071. ; 22:8, s. 1005-11
  • Tidskriftsartikel (refereegranskat)abstract
    • AIMS: Type 2 diabetic patients with hypertension have an increased left ventricular (LV) mass and impaired cardiac function compared to hypertensive patients without diabetes. However, it is unknown if the impaired cardiac function can be explained solely by LV hypertrophy, or is independently related to diabetes. The aim of the present study was to compare LV function between diabetic and non-diabetic hypertensive patients with electrocardiographic LV hypertrophy. METHODS: In 937 patients participating in the LIFE echocardiographic substudy, all echocardiograms were centrally evaluated by a core reading centre measuring LV mass, systolic and diastolic LV function. Known diabetes was present in 105 patients. RESULTS: Left ventricular mass was similar in diabetic and non-diabetic patients. Endocardial systolic LV function, estimated by LV ejection fraction, was reduced and indices of midwall systolic LV function were impaired in the diabetic patients. Diastolic LV filling pattern was impaired and arterial stiffness, measured by pulse pressure/stroke index, was increased in diabetic patients. CONCLUSIONS: Systolic and diastolic LV function in hypertensive patients with electrocardiographic LV hypertrophy and diabetes are impaired independent of LV mass, most likely reflecting the adverse effects of diabetes per se.
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59.
  • Hoieggen, A., et al. (författare)
  • The impact of serum uric acid on cardiovascular outcomes in the LIFE study
  • 2004
  • Ingår i: Kidney Int. - 0085-2538. ; 65:3, s. 1041-9
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study demonstrated the superiority of a losartan-based regimen over atenolol-based regimen for reduction of cardiovascular (CV) morbidity and mortality. It has been suggested that the LIFE study results may be related to the effects of losartan on serum uric acid (SUA). SUA has been proposed as an independent risk factor for CV morbidity and death. METHODS: Cox regression analysis was used to assess relationship of SUA and treatment regimens with the LIFE primary composite outcome (CV death, fatal or nonfatal myocardial infarction, fatal or nonfatal stroke). RESULTS: Baseline SUA was significantly associated with increased CV events [hazard ratio (HR) 1.024 (95% CI 1.017-1.032) per 10 micromol/L, P < 0.0001] in the entire study population. The association was significant in women [HR = 1.025 (1.013-1.037), P < 0.0001], but not in men [HR = 1.009 (0.998-1.019), P= 0.108]. After adjustment for Framingham risk score (FRS), SUA was no longer significant in the entire study population [HR = 1.006 (0.998-1.014), P= 0.122] or in men [HR = 1.006 (0.995-1.017), P= 0.291], but was significant in women [HR = 1.013 (1-1.025), P= 0.0457]. The baseline-to-end-of-study increase in SUA (standard deviation, SD) was greater (P < 0.0001) in atenolol-treated subjects (44.4 +/- 72.5 micromol/L) than in losartan-treated subjects (17.0 +/- 69.8 micromol/L). SUA as a time-varying covariate was strongly associated with events (P < 0.0001) in the entire population. The contribution of SUA to the treatment effect of losartan on the primary composite end point was 29% (14%-107%), P= 0.004. The association between time-varying SUA and increased CV risk tended to be stronger in women (P < 0.0001) than in men (P= 0.0658), although the gender-outcome interaction was not significant (P= 0.079). CONCLUSION: The increase in SUA over 4.8 years in the LIFE study was attenuated by losartan compared with atenolol treatment, appearing to explain 29% of the treatment effect on the primary composite end point. The association between SUA and events was stronger in women than in men with or without adjustment of FRS.
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60.
  • Ibsen, H., et al. (författare)
  • Albuminuria and cardiovascular risk in hypertensive patients with left ventricular hypertrophy: the LIFE Study
  • 2004
  • Ingår i: Kidney Int Suppl. - 0098-6577. ; :92, s. S56-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Studies have shown that albuminuria is associated with increased risk for cardiovascular events. We tested the relationship between albuminuria (UACR) and cardiovascular risk in 8206 hypertensive patients with left ventricular hypertrophy included in the LIFE Study. Follow-up was 39,122 patient years. The risk for the primary composite cardiovascular end point increases continuously from the lowest to the highest decile of baseline UACR. No specific threshold could be identified. In conclusion, albuminuria predicts the outcome in the LIFE Study. The risk for cardiovascular morbidity and mortality among hypertensive patients with left ventricular hypertrophy increases at much lower UACR than has been reported in diabetic patients.
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