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Sökning: WFRF:(Dahlof Bjorn)

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  • Lampl, Yair, et al. (författare)
  • Infrared laser therapy for ischemic stroke : a new treatment strategy
  • 2007
  • Ingår i: Stroke. - 0039-2499 .- 1524-4628. ; 38:6, s. 1843-9
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND AND PURPOSE: The NeuroThera Effectiveness and Safety Trial-1 (NEST-1) study evaluated the safety and preliminary effectiveness of the NeuroThera Laser System in the ability to improve 90-day outcomes in ischemic stroke patients treated within 24 hours from stroke onset. The NeuroThera Laser System therapeutic approach involves use of infrared laser technology and has shown significant and sustained beneficial effects in animal models of ischemic stroke.METHODS: This was a prospective, intention-to-treat, multicenter, international, double-blind, trial involving 120 ischemic stroke patients treated, randomized 2:1 ratio, with 79 patients in the active treatment group and 41 in the sham (placebo) control group. Only patients with baseline stroke severity measured by National Institutes of Health Stroke Scale (NIHSS) scores of 7 to 22 were included. Patients who received tissue plasminogen activator were excluded. Outcome measures were the patients' scores on the NIHSS, modified Rankin Scale (mRS), Barthel Index, and Glasgow Outcome Scale at 90 days after treatment. The primary outcome measure, prospectively identified, was successful treatment, documented by NIHSS. This was defined as a complete recovery at day 90 (NIHSS 0 to 1), or a decrease in NIHSS score of at least 9 points (day 90 versus baseline), and was tested as a binary measure (bNIH). Secondary outcome measures included mRS, Barthel Index, and Glasgow Outcome Scale. Primary statistical analyses were performed with the Cochran-Mantel-Haenszel rank test, stratified by baseline NIHSS score or by time to treatment for the bNIH and mRS. Logistic regression analyses were conducted to confirm the results.RESULTS: Mean time to treatment was >16 hours (median time to treatment 18 hours for active and 17 hours for control). Time to treatment ranged from 2 to 24 hours. More patients (70%) in the active treatment group had successful outcomes than did controls (51%), as measured prospectively on the bNIH (P=0.035 stratified by severity and time to treatment; P=0.048 stratified only by severity). Similarly, more patients (59%) had successful outcomes than did controls (44%) as measured at 90 days as a binary mRS score of 0 to 2 (P=0.034 stratified by severity and time to treatment; P=0.043 stratified only by severity). Also, more patients in the active treatment group had successful outcomes than controls as measured by the change in mean NIHSS score from baseline to 90 days (P=0.021 stratified by time to treatment) and the full mRS ("shift in Rankin") score (P=0.020 stratified by severity and time to treatment; P=0.026 stratified only by severity). The prevalence odds ratio for bNIH was 1.40 (95% CI, 1.01 to 1.93) and for binary mRS was 1.38 (95% CI, 1.03 to 1.83), controlling for baseline severity. Similar results held for the Barthel Index and Glasgow Outcome Scale. Mortality rates and serious adverse events (SAEs) did not differ significantly (8.9% and 25.3% for active 9.8% and 36.6% for control, respectively, for mortality and SAEs).CONCLUSIONS: The NEST-1 study indicates that infrared laser therapy has shown initial safety and effectiveness for the treatment of ischemic stroke in humans when initiated within 24 hours of stroke onset. A larger confirmatory trial to demonstrate safety and effectiveness is warranted.
  • Bang, Casper N., et al. (författare)
  • Four-Group Classification of Left Ventricular Hypertrophy Based on Ventricular Concentricity and Dilatation Identifies a Low-Risk Subset of Eccentric Hypertrophy in Hypertensive Patients
  • 2014
  • Ingår i: Circulation Cardiovascular Imaging. - 1941-9651 .- 1942-0080. ; 7:3, s. 422-429
  • Tidskriftsartikel (refereegranskat)abstract
    • Background-Left ventricular hypertrophy (LVH; high LV mass [LVM]) is traditionally classified as concentric or eccentric based on LV relative wall thickness. We evaluated the prediction of subsequent adverse events in a new 4-group LVH classification based on LV dilatation (high LV end-diastolic volume [EDV] index) and concentricity (mass/end-diastolic volume [M/EDV](2/3)) in hypertensive patients. Methods and Results-In the Losartan Intervention for Endpoint Reduction (LIFE) echocardiography substudy, 939 hypertensive patients with measurable LVM at baseline were randomized to a mean of 4.8 years of losartan- or atenolol-based treatment. Patients with LVH (LVM/body surface area >= 116 and >= 96 g/m(2) in men and woman, respectively) were divided into 4 groups-concentric nondilated (increased M/EDV, normal EDV), eccentric dilated (increased EDV, normal M/EDV), concentric dilated (increased M/EDV and EDV), and eccentric nondilated (normal M/EDV and EDV)-and compared with patients with normal LVM. Time-varying LVH classes were tested for association with all-cause and cardiovascular mortality and a composite end point of myocardial infarction, stroke, heart failure, and cardiovascular death in multivariable Cox analyses. At baseline, the LVs were categorized as eccentric nondilated in 12%, eccentric dilated in 20%, concentric nondilated in 29%, concentric dilated in 14%, and normal LVM in 25%. Treatment changed the prevalence of 4 LVH groups to 23%, 4%, 5%, and 7%; 62% had normal LVM after 4 years. In time-varying Cox analyses, compared with normal LVM, those with eccentric dilated and both concentric nondilated and dilated LVH had increased risks of all-cause or cardiovascular mortality or the composite end point, whereas the eccentric nondilated group did not. Conclusions-Hypertensive patients with relatively mild LVH without either increased LV volume or concentricity have similar risk of all-cause mortality or cardiovascular events because hypertensive patients with normal LVM seem to be a low-risk group.
  • Bhatt, Deepak L., et al. (författare)
  • Rationale, design and baseline characteristics of the effect of ticagrelor on health outcomes in diabetes mellitus patients Intervention study
  • 2019
  • Ingår i: Clinical Cardiology. - : Wiley. - 0160-9289 .- 1932-8737. ; 42:5, s. 498-505
  • Tidskriftsartikel (refereegranskat)abstract
    • In the setting of prior myocardial infarction, the oral antiplatelet ticagrelor added to aspirin reduced the risk of recurrent ischemic events, especially, in those with diabetes mellitus. Patients with stable coronary disease and diabetes are also at elevated risk and might benefit from dual antiplatelet therapy. The Effect of Ticagrelor on Health Outcomes in diabEtes Mellitus patients Intervention Study (THEMIS, NCT01991795) is a Phase 3b randomized, double-blinded, placebo-controlled trial of ticagrelor vs placebo, on top of low dose aspirin. Patients >= 50 years with type 2 diabetes receiving anti-diabetic medications for at least 6 months with stable coronary artery disease as determined by a history of previous percutaneous coronary intervention, bypass grafting, or angiographic stenosis of >= 50% of at least one coronary artery were enrolled. Patients with known prior myocardial infarction (MI) or stroke were excluded. The primary efficacy endpoint is a composite of cardiovascular death, myocardial infarction, or stroke. The primary safety endpoint is Thrombolysis in Myocardial Infarction major bleeding. A total of 19 220 patients worldwide have been randomized and at least 1385 adjudicated primary efficacy endpoint events are expected to be available for analysis, with an expected average follow-up of 40 months (maximum 58 months). Most of the exposure is on a 60 mg twice daily dose, as the dose was lowered from 90 mg twice daily partway into the study. The results may revise the boundaries of efficacy for dual antiplatelet therapy and whether it has a role outside acute coronary syndromes, prior myocardial infarction, or percutaneous coronary intervention.
  • Devereux, Richard B., et al. (författare)
  • Left Ventricular Wall Stress-Mass-Heart Rate Product and Cardiovascular Events in Treated Hypertensive Patients LIFE Study
  • 2015
  • Ingår i: Hypertension. - 0194-911X .- 1524-4563. ; 66:5, s. 945-953
  • Tidskriftsartikel (refereegranskat)abstract
    • In the Losartan Intervention for End Point Reduction in Hypertension (LIFE) study, 4.8 years' losartan- versus atenolol-based antihypertensive treatment reduced left ventricular hypertrophy and cardiovascular end points, including cardiovascular death and stroke. However, there was no difference in myocardial infarction (MI), possibly related to greater reduction in myocardial oxygen demand by atenolol-based treatment. Myocardial oxygen demand was assessed indirectly by the left ventricular massxwall stressxheart rate (triple product) in 905 LIFE participants. The triple product was included as time-varying covariate in Cox models assessing predictors of the LIFE primary composite end point (cardiovascular death, MI, or stroke), its individual components, and all-cause mortality. At baseline, the triple product in both treatment groups was, compared with normal adults, elevated in 70% of patients. During randomized treatment, the triple product was reduced more by atenolol, with prevalences of elevated triple product of 39% versus 51% on losartan (both P0.001). In Cox regression analyses adjusting for age, smoking, diabetes mellitus, and prior stroke, MI, and heart failure, 1 SD lower triple product was associated with 23% (95% confidence interval 13%-32%) fewer composite end points, 31% (18%-41%) less cardiovascular mortality, 30% (15%-41%) lower MI, and 22% (11%-33%) lower all-cause mortality (all P0.001), without association with stroke (P=0.34). Although losartan-based therapy reduced ventricular mass more, greater heart rate reduction with atenolol resulted in larger reduction of the triple product. Lower triple product during antihypertensive treatment was strongly, independently associated with lower rates of the LIFE primary composite end point, cardiovascular death, and MI, but not stroke.
  • Greve, Anders M., et al. (författare)
  • Contrasting Hemodynamic Mechanisms of Losartan- vs. Atenolol-Based Antihypertensive Treatment : A LIFE Study
  • 2012
  • Ingår i: American Journal of Hypertension. - : Oxford University Press (OUP). - 0895-7061 .- 1941-7225. ; 25:9, s. 1017-1023
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND Pharmaceutical differences in central hemodynamics might influence cardiac response to antihypertensive treatment despite similar lowering of brachial blood pressure (BP). METHODS Data from all patients with at least two echocardiographic examinations in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) echocardiographic substudy (n = 801); high-risk patients on losartan- vs. atenolol-based antihypertensive therapy. Echocardiography was performed annually for 4 years to measure stroke index (SI), heart rate, cardiac index (CI), conduit artery stiffness assessed as pulse pressure/stroke index (PP/SI) and total peripheral resistance index (TPRI). RESULTS Atenolol- and losartan-based therapy reduced BP similarly (cumulative difference in mean brachial blood pressure 0.3 mm Hg, P = 0.65). After 4 years the cumulative means of SI and heart rate were 1.8 ml/m(2) higher and 5.7 beats/min lower on atenolol-based treatment, respectively (both P < 0.001). This kept CI below baseline in atenolol-treated patients, whereas in the losartan group CI was unchanged from baseline throughout the study. TPRI was decreased more and remained lower in the losartan group (cumulative difference in mean TPRI 287 dynes/sec(-5)/cm/m(2), P < 0.001). These findings partly explained univariate differences in systolic- and diastolic function indices between the two treatments; fully adjusted losartan was only associated with a smaller left atrial diameter (cumulative mean difference 0.07 cm; 95% confidence intervals, -0.13 to -0.01, P = 0.03). CONCLUSIONS Contrasting hemodynamics impacted cardiac response to similar reductions in brachial BP on losartan- vs. atenolol-based therapy. The similar reduction of PP/SI suggests that the antihypertensive regimens used in the LIFE study had comparable effects on arterial stiffness (LIFE study; NCT00338260)
  • Magnusson, Martin, et al. (författare)
  • Natriuretic peptides as indicators of cardiac remodeling in hypertensive patients.
  • 2009
  • Ingår i: Blood Pressure. - : Taylor & Francis. - 0803-7051 .- 1651-1999. ; 18, s. 196-203
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims. This study was performed to evaluate the relationship between three different natriuretic peptides and left ventricular mass, function and diameter, and kidney function in patients with hypertension. Methods. One hundred and thirty-nine patients with moderate hypertension were consecutively included. N-terminal brain natriuretic peptide (Nt-BNP), brain natriuretic peptide (BNP) and N-terminal pro-atrial natriuretic peptide (Nt-ANP) were analyzed. Cardiac remodeling was assessed by echocardiography (UCG) and glomerular filtration was estimated by cystatin C. Results. Patients were stratified into four groups with regard to the extent of cardiac remodeling: (1) no remodeling; (2) one of left ventricular hypertrophy, left ventricular dysfunction or left ventricular dilatation; (3) two of above and (4) all three parameters. All peptides differed significantly between the groups (all p<0.001), with a continuous stepwise increase from groups 1 through 4. Receiver operating characteristic analysis showed equal diagnostic performances for the detection of any cardiac abnormalities for Nt-BNP [area under curve, AUC= 0.63 (0.52-0.75), p= 0.026] and BNP [AUC= 0.64 (0.53-0.76), p= 0.019], both, however superior to Nt-ANP [AUC=0.59 (0.47-0.70), p= 0.139]. In multivariable linear regression analysis, all three indicators of cardiac remodeling were independently correlated with ln Nt-BNP and ln BNP, whereas only left ventricular diameter was independently correlated with ln Nt-ANP. Conclusions. Natriuretic peptide levels increased with increasing number of markers of cardiac remodeling. Nt-BNP and BNP are useful to discriminate between patients with regard to cardiac remodeling and might be considered a screening tool in order select patients eligible for further examination with UCG examination.
  • Okin, Peter M., et al. (författare)
  • The relationship of electrocardiographic left ventricular hypertrophy to decreased serum potassium
  • 2012
  • Ingår i: Blood Pressure. - : Informa UK Limited. - 0803-7051 .- 1651-1999. ; 21:3, s. 146-152
  • Tidskriftsartikel (refereegranskat)abstract
    • Background. Low serum potassium (K) is associated with increased blood pressure, impaired cardiac function and renal dysfunction. Although lower serum K is associated with cardiac hypertrophy in animal models, the relationship of low serum K to the presence and severity of electrocardiographic left ventricular hypertrophy (LVH) is unclear. Methods. Baseline and yearly Cornell product LVH levels were examined in relation to low serum K (serum K <= 3.90 mEq/l, the lowest quartile of baseline K levels) in 8586 patients with baseline K levels. Patients were randomized to losartan-vs atenolol-based treatment and additional hydrochlorothiazide (HCTZ) therapy as needed. Results. After adjusting for age, sex, race, prior antihypertensive treatment, losartan vs atenolol therapy, HCTZ use, baseline diastolic and systolic pressure, body mass index, serum creatinine and urine albumin/creatinine ratio, baseline serum K <= 3.90 was associated with significantly higher mean baseline Cornell product LVH (2898 vs 2801 mm.ms, p = 0.001) and a 24% higher risk of Cornell product LVH > 2440 mm.ms at baseline (OR 1.24, 95% CI 1.11-1.38, p < 0.001). After also adjusting for baseline Cornell product and changes in diastolic and systolic pressure between baseline and each year of measurement, in-treatment serum K <= 3.90 determined yearly was associated with significantly higher mean Cornell product LVH at years 1-3 and with statistically signifi cant 16-32% increased risks of LVH by Cornell product at years 1-4. Conclusions. A low serum K is independently associated with a greater likelihood and severity of Cornell product LVH during antihypertensive therapy.
  • Olsen, Michael H., et al. (författare)
  • Changes in subclinical organ damage vs. in Framingham risk score for assessing cardiovascular risk reduction during continued antihypertensive treatment : a LIFE substudy
  • 2011
  • Ingår i: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 29:5, s. 997-1004
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: To investigate whether in-treatment measurements of subclinical organ damage (SOD) assessed by elevated urine albumin/creatinine ratio (UACR) or electrocardiographic left ventricular hypertrophy improved the prediction of the composite cardiovascular endpoint of cardiovascular death, nonfatal myocardial infarction and stroke beyond in-treatment Framingham risk score (FRS).Methods: Excluding patients with a composite cardiovascular endpoint within the first year of treatment, 598 endpoints occurred in 6460 patients from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study with baseline and 1 year values for UACR, left ventricular hypertrophy by electrocardiography and FRS available.Results: Using Cox-regression analyses, FRS1year [hazard ratio = 1.006 (0.98-1.04)] did not predict the endpoint independently of history of cardiovascular disease [hazard ratio = 1.76 (1.49-2.08)], FRSbaseline [hazard ratio = 1.07 (1.04-1.11)], UACR(baseline) [hazard ratio = 1.15 (1.07-1.23), all three P < 0.001], Sokolow-Lyon(baseline) [hazard ratio = 1.01 (1.006-1.02), P < 0.01] and treatment allocation, whereas Cornell product(1yea)r [hazard ratio = 1.01 (1.006-1.02), P < 0.001] and to some degree UACR(1year) [hazard ratio = 1.05 (0.99-1.10), P = 0.09] predicted the endpoint independently of history of cardiovascular disease [hazard ratio = 1.71 (1.44-2.02)], FRSbaseline [hazard ratio = 1.08 (1.06-1.10)], Sokolow-Lyon(baseline) [hazard ratio = 1.01 (1.007-1.02), both P < 0.001], UACR(baseline) [hazard ratio = 1.11 (1.03-1.20), P < 0.01] and treatment allocation decreasing -2 Log likelihood significantly (P < 0.01).Presence of left ventricular hypertrophy by Cornell product1year or UACR(1year) at least 1 mmol/l [hazard ratio = 1.40 (1.15-1.70), P = 0.001] but not FRS1year above the median baseline value of 20 [hazard ratio = 1.22 (0.94-1.57), not significant] was associated with higher risk of subsequent endpoint after adjustment for history of cardiovascular disease [hazard ratio = 1.82 (1.54-2.15)], FRSbaseline at least 20 [hazard ratio = 1.67 (1.30-2.16)], left ventricular hypertrophy by Sokolow-Lyonbaseline or UACR(baseline) at least 1 mmol/l [hazard ratio = 1.61 (1.33-1.94), all P < 0.001] and treatment allocation [hazard ratio = 0.93 (0.79-1.09), not significant]. In contrast to FRS1year at least 20 decreased, SOD1year decreased -2Log likelihood significantly (P < 0.01).Conclusion: Cornell product(1year) and UACR(1year) improved in contrast to FRS1year risk prediction based on FRSbaseline, Sokolow-Lyon(baseline) and UACR(baseline) significantly in LIFE patients during antihypertensive treatment.
  • Ruwald, Anne Christine H., et al. (författare)
  • Losartan versus atenolol-based antihypertensive treatment reduces cardiovascular events especially well in elderly patients : the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study
  • 2012
  • Ingår i: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 30:6, s. 1252-1259
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study has previously demonstrated a beneficial effect of losartan compared to atenolol-based antihypertensive treatment in patients with essential hypertension and left-ventricular hypertrophy (LVH). However, patient age often influences the choice of antihypertensive drugs. Therefore, we investigated the influence of age on the effects of losartan versus atenolol-based antihypertensive treatment. Methods: A total of 9193 hypertensive patients with LVH aged 45-83 years were followed for a mean of 4.8 years. Blood pressure, high-density lipoprotein cholesterol (HDL-C), Sokolow-Lyon voltage, Cornell voltage-duration product and urine albumin-creatinine ratio (UACR) were measured yearly throughout the study. Patients were divided into two age groups according to the median age of 67 years and the effects of losartan versus atenolol-based antihypertensive treatment on the primary composite endpoint (CEP) consisting of cardiovascular death, nonfatal stroke or nonfatal myocardial infarction were investigated. Results: The beneficial effect of losartan versus atenolol-based treatment was greater in the group of patients older than 67 years [hazard ratio 0.79 (0.69-0.91), P=0.001] compared to the group of patients younger than 67 years [hazard ratio 1.03 (0.82-1.28), P=0809], P=0.045 for interaction. The beneficial effects of losartan versus atenolol-based antihypertensive treatment on pulse pressure, HDL-C, UACR, and Cornell and Sokolow-Lyon voltage were not more pronounced in patients older than 67 years compared to patients younger than 67 years. All five risk factors considered as time-varying covariates predicted CEP independently (P<0.01) with the exception of pulse pressure (P=0.37) and the interaction between age and treatment on outcome remained significant (P=0.042). Conclusions: We showed a greater beneficial effect of losartan versus atenolol-based antihypertensive treatment in the group of patients older than 67 years compared to the group of patients younger than 67 years. This difference was not explained by a more pronounced effect of losartan-based treatment on any of the cardiovascular risk factors demonstrated to have independent prognostic importance.
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