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  • 1.
    Aboyans, Victor
    et al.
    Dupuytren University Hospital.
    Criqui, Michael
    University of California, USA.
    Abraham, Pierre
    University Hospital of Angers, France.
    Allison, Matthew
    University of California, USA.
    Creager, Mark
    Brigham and Women’s Hospital, USA.
    Diehm, Curt
    Karlsbad Clinic/University of Heidelberg, Germany.
    Fowkes, Gerry
    University of Edinburgh, UK.
    Hiatt, William
    University of Colorado, USA.
    Jönsson, Björn
    Linköping University, Department of Medical and Health Sciences, Thoracic Surgery. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Thoracic and Vascular Surgery.
    Lacroix, Philippe
    Limoges University, France.
    Marin, Benoit
    Limoges Teaching Hospital, France.
    McDermott, Mary
    Northwestern University,USA.
    Norgren, Lars
    University Hospital, Örebro, Sweden.
    Pande, Reena
    Brigham and Women’s Hospital, USA.
    Preux, Pierre-Marie
    University of Limoges, France.
    Stoffers, H.E.
    Maastricht University, Netherlands.
    Treat-Jacobsson, Diane
    University of Minnesota, USA.
    Measurement and interpretation of the ankle-brachial index: a scientific statement from the Ammerican Heart Association2012In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539Article in journal (Refereed)
  • 2.
    Alfredsson, Joakim
    et al.
    Region Östergötland, Heart and Medicine Center, Department of Cardiology in Linköping. Linköping University, Faculty of Medicine and Health Sciences. Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Duke Clin Research Institute, NC 27705 USA.
    Stebbins, Amanda
    Duke Clin Research Institute, NC 27705 USA.
    Brennan, J. Matthew
    Duke University, NC USA.
    Matsouaka, Roland
    Duke University, NC USA.
    Afilalo, Jonathan
    McGill University, Canada.
    Peterson, Eric D.
    Duke Clin Research Institute, NC 27705 USA; Duke University, NC USA.
    Vemulapalli, Sreekanth
    Duke University, NC USA.
    Rumsfeld, John S.
    University of Colorado, CO USA.
    Shahian, David
    Massachusetts Gen Hospital, MA 02114 USA.
    Mack, Michael J.
    Baylor Scott and White Heatlh, TX USA.
    Alexander, Karen P.
    Duke Clin Research Institute, NC 27705 USA; Duke University, NC USA.
    Gait Speed Predicts 30-Day Mortality After Transcatheter Aortic Valve Replacement Results From the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Therapy Registry2016In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 133, no 14, p. 1351-1359Article in journal (Refereed)
    Abstract [en]

    Background Surgical risk scores do not include frailty assessments (eg, gait speed), which are of particular importance for patients with severe aortic stenosis considering transcatheter aortic valve replacement. Methods and Results We assessed the association of 5-m gait speed with outcomes in a cohort of 8039 patients who underwent transcatheter aortic valve replacement (November 2011-June 2014) and were included in the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Therapy Registry. We evaluated the association between continuous and categorical gait speed and 30-day all-cause mortality before and after adjustment for Society of Thoracic Surgeons-predicted risk of mortality score and key variables. Secondary outcomes included in-hospital mortality, bleeding, acute kidney injury, and stroke. The overall median gait speed was 0.63 m/s (25th-75th percentile, 0.47-0.79 m/s), with the slowest walkers (<0.5 m/s) constituting 28%, slow walkers (0.5-0.83 m/s) making up 48%, and normal walkers (>0.83 m/s) constituting 24% of the population. Thirty-day all-cause mortality rates were 8.4%, 6.6%, and 5.4% for the slowest, slow, and normal walkers, respectively (P<0.001). Each 0.2-m/s decrease in gait speed corresponded to an 11% increase in 30-day mortality (adjusted odds ratio, 1.11; 95% confidence interval, 1.01-1.22). The slowest walkers had 35% higher 30-day mortality than normal walkers (adjusted odds ratio, 1.35; 95% confidence interval, 1.01-1.80), significantly longer hospital stays, and a lower probability of being discharged to home. Conclusions Gait speed is independently associated with 30-day mortality after transcatheter aortic valve replacement. Identification of frail patients with the slowest gait speeds facilitates preprocedural evaluation and anticipation of a higher level of postprocedural care. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT01737528.

  • 3.
    Altimiras, Jordi
    et al.
    Linköping University, Department of Physics, Chemistry and Biology, Zoology . Linköping University, The Institute of Technology.
    Milberg, Per
    Linköping University, The Institute of Technology. Linköping University, Department of Physics, Chemistry and Biology, Ecology .
    Letter regarding article by Kahn et al. "Predictive adaptive responses to maternal high-fat diet prevent endothelial dysfunction but not hypertension in adult rat offspring" (Adaption is not predictive)2005In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 111, p. 166-166Article in journal (Other academic)
  • 4.
    Ballantyne, Christie M.
    et al.
    Baylor Coll Med, Dept Med, Houston, TX 77030 USA Linkoping Univ Hosp, Dept Internal Med, S-58185 Linkoping, Sweden Merck Res Labs, Rahway, NJ USA Aker Hosp, Med Clin, Oslo, Norway Natl Hosp Norway, Dept Med, Oslo, Norway.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medical and Health Sciences, Internal Medicine. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Cook, Thomas J.
    Baylor Coll Med, Dept Med, Houston, TX 77030 USA Linköping Univ Hosp, Dept Internal Med, S-58185 Linkoping, Sweden Merck Res Labs, Rahway, NJ USA Aker Hosp, Med Clin, Oslo, Norway Natl Hosp Norway, Dept Med, Oslo, Norway.
    Mercuri, Michele F.
    Baylor Coll Med, Dept Med, Houston, TX 77030 USA Linkoping Univ Hosp, Dept Internal Med, S-58185 Linkoping, Sweden Merck Res Labs, Rahway, NJ USA Aker Hosp, Med Clin, Oslo, Norway Natl Hosp Norway, Dept Med, Oslo, Norway.
    Pedersen, Terje R.
    Baylor Coll Med, Dept Med, Houston, TX 77030 USA Linkoping Univ Hosp, Dept Internal Med, S-58185 Linkoping, Sweden Merck Res Labs, Rahway, NJ USA Aker Hosp, Med Clin, Oslo, Norway Natl Hosp Norway, Dept Med, Oslo, Norway.
    Kjekshus, John
    Baylor Coll Med, Dept Med, Houston, TX 77030 USA Linkoping Univ Hosp, Dept Internal Med, S-58185 Linkoping, Sweden Merck Res Labs, Rahway, NJ USA Aker Hosp, Med Clin, Oslo, Norway Natl Hosp Norway, Dept Med, Oslo, Norway.
    Low high-density lipoprotein cholesterol and response to simvastatin therapy in Scandinavian Simvastatin Survival Study (4S) - Response2002In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 106, no 2, p. E8-E8article id e8Article in journal (Other academic)
  • 5. Ballantyne, CM
    et al.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Cook, TJ
    Mercuri, MF
    Pedersen, TR
    Kjekshus, J
    Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S2001In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 104, no 25, p. 3046-3051Article in journal (Refereed)
    Abstract [en]

    Background - Patients with low HDL cholesterol (HDL-C) and elevated triglyceride had an increased risk for coronary heart disease (CHD) events and received the greatest benefit with fibrate therapy in substudy analyses of the Helsinki Heart Study and the Bezafibrate Infarction Prevention Study. Methods and Results - In this post hoc analysis of the Scandinavian Simvastatin Survival Study, which enrolled patients with elevated LDL cholesterol (LDL-C) and CHD, subgroups defined by HDL-C and triglyceride quartiles were compared to examine the influence of HDL-C and triglyceride on CHD events and response to therapy. Patients in the lowest HDL-C (<1.00 mmol/L [39 mg/dL]) and highest triglyceride (>1.80 mmol/L [159 mg/dL]) quartiles (lipid triad, n=458) had increased proportions of other features of the metabolic syndrome (increased body mass index, hypertension, diabetes), men, prior myocardial infarction, prior revascularization, and ▀-blocker use than patients in the highest HDL-C (>1.34 mmol/L [52 mg/dL]) and lowest triglyceride (<1.11 mmol/L [98 mg/dL]) quartiles (isolated LDL-C elevation, n=545). The major coronary event rate was highest in lipid triad patients on placebo (35.9%), and this subgroup had the greatest event reduction (relative risk 0.48, 95% CI 0.33 to 0.69), a significant treatment-by-subgroup interaction (P=0.03) indicated a greater treatment effect in the lipid triad subgroup than the isolated LDL-C elevation subgroup. Conclusions - Patients with elevated LDL-C, low HDL-C, and elevated triglycerides were more likely than patients with isolated LDL-C elevation to have other characteristics of the metabolic syndrome, had increased risk for CHD events on placebo, and received greater benefit with simvastatin therapy.

  • 6. Belonje, Anne M S
    et al.
    Voors, Adriaan A
    van der Meer, Peter
    van Gilst, Wiek H
    Jaarsma, Tiny
    van Veldhuisen, Dirk J
    Endogenous erythropoietin and outcome in heart failure.2010In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 121, no 2, p. 245-51Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Endogenous erythropoietin is increased in patients with heart failure (HF). Previous small-scale data suggest that these erythropoietin levels are related to prognosis. This study aims to analyze the clinical and prognostic value of erythropoietin levels in relation to hemoglobin in a large cohort of HF patients. METHODS AND RESULTS: In patients hospitalized for HF, endogenous erythropoietin levels were measured at discharge and after 6 months. In anemic patients, the relation between erythropoietin and hemoglobin levels was determined by calculating the observed/predicted ratio of erythropoietin levels. We studied data from 605 patients with HF. Mean age was 71+/-11 years; 62% were male; and mean left ventricular ejection fraction was 0.33+/-0.14. Median erythropoietin levels were 9.6 U/L at baseline and 10.5 U/L at 6 months. Higher erythropoietin levels at baseline were independently related to an increased mortality at 18 months (hazard ratio, 2.06; 95% confidence interval, 1.40 to 3.04; P<0.01). In addition, persistently elevated erythropoietin levels (higher than median at baseline and at 6 months) were related to an increased mortality risk (hazard ratio, 2.24; 95% confidence interval, 1.02 to 4.90; P=0.044). The observed/predicted ratio was determined in a subset of anemic patients, 79% of whom had erythropoietin levels lower than expected and 9% had levels higher than expected on the basis of their hemoglobin. Multivariate Cox regression analysis revealed that a higher observed/predicted ratio was related to an increased mortality risk (hazard ratio, 3.52; 95% confidence interval, 1.53 to 8.12; P=0.003). CONCLUSIONS: Erythropoietin levels predict mortality in HF patients, and persistently elevated levels have an independent prognostic value. In anemic HF patients, the majority had a low observed/predicted ratio. However, a higher observed/predicted ratio may be related to an independent increased mortality risk.

  • 7.
    Bergström, Anders
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Cardiology . Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Andersson, B
    Edner, M
    Dept Cardiol, Linkoping, Sweden Gothenburg Univ, S-41124 Gothenburg, Sweden Linkoping Univ, S-58183 Linkoping, Sweden Danderyd Hosp, Stockholm, Sweden.
    Nylander, E
    Persson, H
    Dept Cardiol, Linkoping, Sweden Gothenburg Univ, S-41124 Gothenburg, Sweden Linkoping Univ, S-58183 Linkoping, Sweden Danderyd Hosp, Stockholm, Sweden.
    Dahlström, Ulf
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Cardiology . Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Carvedilol improves diastolic function in patients with diastolic heart failure.2001In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 104, no 17, p. 3388-Conference paper (Other academic)
  • 8.
    Bolger, Ann F
    et al.
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Clinical Physiology in Linköping.
    Eidenvall, Lars
    Ask, Per
    Linköping University, Department of Biomedical Engineering, Physiological Measurements. Linköping University, The Institute of Technology.
    Loyd, Dan
    Linköping University, Department of Management and Engineering, Applied Thermodynamics and Fluid Mechanics. Linköping University, The Institute of Technology.
    Wranne, Bengt
    Linköping University, Department of Medicine and Care, Clinical Physiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Clinical Physiology in Linköping.
    THE MULTIPLE DETERMINANTS OF CONTINUOUS WAVE SIGNAL INTENSITY1992In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 86, no 4, SArticle in journal (Refereed)
  • 9.
    Bothe, Wolfgang
    et al.
    Stanford University School of Medicine, USA.
    Kuhl, Elllen
    Stanford University School of Medicine, USA.
    Kvitting, John-Peder Escobar
    Stanford University School of Medicine, USA.
    Rausch, Manuel K.
    Stanford University School of Medicine, USA.
    Göktepe, Serdar
    Stanford University School of Medicine, USA.
    Swanson, Julia C.
    Stanford University School of Medicine, USA.
    Farahmandnia, Saideh
    Stanford University School of Medicine, USA.
    Ingels, Neil B.
    Research Institute, Palo Alto Medical Foundation, USA.
    Miller, D. Craig
    Stanford University School of Medicine, USA.
    Rigid, complete annuloplasty rings increase anterior mitral leaflet strain in normal beating ovine heart2011In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 124, p. S81-S96Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    Annuloplasty ring or band implantation during surgical mitral valve repair perturbs mitral annular dimensions, dynamics, and shape, which have been associated with changes in anterior mitral leaflet (AML) strain patterns and suboptimal long-term repair durability. We hypothesized that rigid rings with nonphysiological three-dimensional shapes, but not saddle-shaped rigid rings or flexible bands, increase AML strains.

    METHODS AND RESULTS:

    Sheep had 23 radiopaque markers inserted: 7 along the anterior mitral annulus and 16 equally spaced on the AML. True-sized Cosgrove-Edwards flexible, partial band (n=12), rigid, complete St Jude Medical rigid saddle-shaped (n=12), Carpentier-Edwards Physio (n=12), Edwards IMR ETlogix (n=11), and Edwards GeoForm (n=12) annuloplasty rings were implanted in a releasable fashion. Under acute open-chest conditions, 4-dimensional marker coordinates were obtained using biplane videofluoroscopy along with hemodynamic parameters with the ring inserted and after release. Marker coordinates were triangulated, and the largest maximum principal AML strains were determined during isovolumetric relaxation. No relevant changes in hemodynamics occurred. Compared with the respective control state, strains increased significantly with rigid saddle-shaped annuloplasty ring, Carpentier-Edwards Physio, Edwards IMR ETlogix, and Edwards GeoForm (0.14 ± 0.05 versus 0.16 ± 0.05, P=0.024, 0.15 ± 0.03 versus 0.18 ± 0.04, P=0.020, 0.11 ± 0.05 versus 0.14 ± 0.05, P=0.042, and 0.13 ± 0.05 versus 0.16 ± 0.05, P=0.009), but not with Cosgrove-Edwards band (0.15 ± 0.05 versus 0.15 ± 0.04, P=0.973).

    CONCLUSIONS:

    Regardless of three-dimensional shape, rigid, complete annuloplasty rings, but not a flexible, partial band, increased AML strains in the normal beating ovine heart. Clinical studies are needed to determine whether annuloplasty rings affect AML strains in patients, and, if so, whether ring-induced perturbations in leaflet strain states are linked to repair failure.

  • 10. Brodszki, J
    et al.
    Länne, Toste
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Clinical Physiology. Östergötlands Läns Landsting, Heart Centre, Department of Thoracic and Vascular Surgery.
    Marsal, K
    Ley, D
    Impaired vascular growth in late adolescence after intrauterine growth restriction2005In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 111, no 20, p. 2623-2628Article in journal (Refereed)
    Abstract [en]

    Background - Abnormal blood flow in a fetus small for gestational age indicates true fetal intrauterine growth restriction (IUGR). We tested the hypothesis that IUGR with abnormal fetal blood flow is associated with long-term abnormal vascular morphology and function in adolescence. Methods and Results - In a prospective study, vascular mechanical properties of the common carotid artery (CCA), abdominal aorta , and popliteal artery (PA) were assessed by echo-tracking sonography in 21 adolescents with IUGR and abnormal fetal aortic blood flow and in 23 adolescents with normal fetal growth and normal fetal aortic blood flow. Endothelium-dependent and -independent vasodilatation of the brachial artery was measured by high-resolution ultrasound. After adjustment for body surface area and sex, the IUGR group had significantly smaller end-diastolic vessel diameters than the referents in the abdominal aorta and PA (mean difference, 1.7 mm [95% CI, 0.62 to 2.74] and 0.6 mm [95% CI, 0.25 to 1.02], respectively) (P=0.003 and P=0.002, respectively), with a similar trend in the CCA (P=0.09). A higher resting heart rate was observed in the IUGR group (P=0.01). No differences were found in stiffness or in endothelium-dependent and -independent vasodilatation between the 2 groups. Conclusions - IUGR caused by placental insufficiency appears to be associated with impaired vascular growth persisting into young adulthood in both men and women. The smaller aortic dimensions and the higher resting heart rate seen in adolescents with previous IUGR may be of importance for future cardiovascular health. © 2005 American Heart Association, Inc.

  • 11.
    Carlhäll, Carljohan
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Clinical Physiology . Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Nguyen, Tom C.
    Itoh, Akinobu
    Ennis, Daniel B.
    Bothe, Wolfgang
    Liang, David
    Stanford Univ, Sch Med, Div Cardiovasc Med, Stanford, CA 94305 USA.
    Ingels, Neil B.
    Palo Alto Med Fdn, Res Inst, Palo Alto, CA 94301 USA.
    Miller, D. Craig
    Stanford Univ, Sch Med, Falk Cardiovasc Res Ctr, Dept Cardiothorac Surg, Stanford, CA 94305 USA.
    Alterations in transmural myocardial strain - An early marker of left ventricular dysfunction in mitral regurgitation?2008In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 118, no 14, p. S256-S262Article in journal (Refereed)
    Abstract [en]

    Background-In asymptomatic patients with severe isolated mitral regurgitation (MR), identifying the onset of early left ventricular (LV) dysfunction can guide the timing of surgical intervention. We hypothesized that changes in LV transmural myocardial strain represent an early marker of LV dysfunction in an ovine chronic MR model. Methods and Results-Sheep were randomized to control (CTRL, n = 8) or experimental (EXP, n = 12) groups. In EXP, a 3.5-or 4.8-mm hole was created in the posterior mitral leaflet to generate "pure" MR. Transmural beadsets were inserted into the lateral and anterior LV wall to radiographically measure 3-dimensional transmural strains during systole and diastolic filling, at 1 and 12 weeks postoperatively. MR grade was higher in EXP than CTRL at 1 and 12 weeks (3.0 [2-4] versus 0.5 [0-2], 3.0 [1-4] versus 0.5 [0-1], respectively, both P < 0.001). At 12 weeks, LV mass index was greater in EXP than CTRL (201 +/- 18 versus 173 +/- 17 g/m(2), P < 0.01). LVEDVI increased in EXP from 1 to 12 weeks (P = 0.015). Between the 1 and 12 week values, the change in BNP (-4.5 +/- 4.4 versus-3.0 +/- 3.6 pmol/L), PRSW (9 +/- 13 versus 23 +/- 18 mm Hg), tau (-3 +/- 11 versus-4 +/- 7 ms), and systolic strains was similar between EXP and CTRL. The changes in longitudinal diastolic filling strains between 1 and 12 weeks, however, were greater in EXP versus CTRL in the subendocardium (lateral:-0.08 +/- 0.05 versus 0.02 +/- 0.14, anterior:-0.10 +/- 0.05 versus-0.02 +/- 0.07, both P < 0.01). Conclusions-Twelve weeks of ovine "pure" MR caused LV remodeling with early changes in LV function detected by alterations in transmural myocardial strain, but not by changes in BNP, PRSW, or tau.

  • 12.
    de Muinck, Ebo D.
    et al.
    Dartmouth-Hitchcock Medical Center, Lebanon, NH, USA.
    Simons, Michael
    Dartmouth-Hitchcock Medical Center, Lebanon, NH, USA.
    Calling on reserves: Granulocyte colony stimulating growth factor in cardiac repair2005In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 112, no 20, p. 3033-3035Article in journal (Other academic)
  • 13. EIDENVALL, L
    et al.
    Ask, Per
    Linköping University, Department of Biomedical Engineering, Physiological Measurements. Linköping University, The Institute of Technology.
    Loyd, Dan
    Linköping University, Department of Management and Engineering, Applied Thermodynamics and Fluid Mechanics. Linköping University, The Institute of Technology.
    Wranne, Bengt
    Linköping University, Department of Medicine and Care, Clinical Physiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Clinical Physiology in Linköping.
    DETERMINATION OF REGURGITANT FLOW IN A PULSATILE MODEL BY INTEGRATING VELOCITIES FROM THE ENTIRE 3D PROXIMAL VELOCITY-FIELD1993In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 88, no 4, 2Article in journal (Refereed)
  • 14.
    Ekerstad, Niklas
    et al.
    Linköping University, Department of Medical and Health Sciences, Health Technology Assessment and Health Economics. Linköping University, Faculty of Health Sciences.
    Swahn, Eva
    Linköping University, Department of Medical and Health Sciences, Cardiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Cardiology UHL.
    Janzon, Magnus
    Linköping University, Department of Medical and Health Sciences, Cardiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Cardiology UHL.
    Alfredsson, Joakim
    Linköping University, Department of Medical and Health Sciences, Cardiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Cardiology UHL.
    Löfmark, Rurik
    Department of Medical Ethics, LIME, Karolinska Institutet.
    Lindenberger, Marcus
    Department of Medicine, Ryhov County Hospital Jönköping.
    Carlsson, Per
    Linköping University, Department of Medical and Health Sciences, Health Technology Assessment and Health Economics. Linköping University, Faculty of Health Sciences.
    Frailty Is Independently Associated With Short-Term Outcomes for Elderly Patients With Non-ST-Segment Elevation Myocardial Infarction2011In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 124, no 22, p. 2397-2404Article in journal (Refereed)
    Abstract [en]

    Background: For the large and growing population of elderly patients with cardiovascular disease, it is important to identify clinically relevant measures of biological age and their contribution to risk. Frailty is an emerging concept in medicine denoting increased vulnerability and decreased physiological reserves. We analyzed the manner in which the variable frailty predicts short-term outcomes for elderly non-ST-segment elevation myocardial infarction patients.

    Methods and results: Patients aged ≥ 75 years, with diagnosed non-ST-segment elevation myocardial infarction were included at 3 centers, and clinical data including judgment of frailty were collected prospectively. Frailty was defined according to the Canadian Study of Health and Aging Clinical Frailty Scale. The impact of the comorbid conditions on risk was quantified by the coronary artery disease-specific index. Of 307 patients, 149 (48.5%) were considered frail. By multiple logistic regression, frailty was found to be strongly and independently associated with risk for the primary composite outcome (death from any cause, myocardial reinfarction, revascularization due to ischemia, hospitalization for any cause, major bleeding, stroke/transient ischemic attack, and need for dialysis up to 1 month after inclusion) (odds ratio, 2.2; 95% confidence interval, 1.3-3.7) in-hospital mortality (odds ratio, 4.6; 95% confidence interval, 1.3-16.8), and 1-month mortality (odds ratio, 4.7; 95% confidence interval, 1.7-13.0).

    Conclusions: Frailty is strongly and independently associated with in-hospital mortality, 1-month mortality, prolonged hospital care, and the primary composite outcome. The combined use of frailty and comorbidity may constitute an ultimate risk prediciton concept in regard to cardiovascular patients with complex needs.

  • 15.
    Freedman, Ben
    et al.
    University of Sydney, Australia; University of Sydney, Australia.
    Camm, John
    St George Hospital, England.
    Calkins, Hugh
    Johns Hopkins University, MD USA.
    Healey, Jeffrey S.
    McMaster University, Canada.
    Rosenqvist, Marten
    Karolinska Institute, Sweden.
    Wang, Jiguang
    Jiaotong University, Peoples R China.
    Albert, Christine M.
    Harvard Medical Sch, MA USA.
    Anderson, Craig S.
    George Institute Global Heatlh, Australia.
    Antoniou, Sotiris
    Barts Health NHS Trust, England.
    Benjamin, Emelia J.
    NHLBI, MA USA; Boston University, MA 02215 USA.
    Boriani, Giuseppe
    University of Modena and Reggio Emilia, Italy.
    Brachmann, Johannes
    Klinikum Coburg, Germany.
    Brandes, Axel
    Odense University Hospital, Denmark.
    Chao, Tze-Fan
    National Yang Ming University, Taiwan.
    Conen, David
    McMaster University, Canada; University Hospital, Switzerland.
    Engdahl, Johan
    Karolinska Institute, Sweden.
    Fauchier, Laurent
    Karolinska Institute, Sweden; University of Tours, France.
    Fitzmaurice, David A.
    University of Birmingham, England.
    Friberg, Leif
    Karolinska Institute, Sweden.
    Gersh, Bernard J.
    Mayo Clin, MN USA.
    Gladstone, David J.
    University of Toronto, Canada.
    Glotzer, Taya V.
    Hackensack University, NJ USA.
    Gwynne, Kylie
    University of Sydney, Australia.
    Hankey, Graeme J.
    University of Western Australia, Australia.
    Harbison, Joseph
    Trinity Coll Dublin, Ireland.
    Hillis, Graham S.
    University of Western Australia, Australia.
    Hills, Mellanie T.
    StopAfib Org, TX USA.
    Kamel, Hooman
    Weill Cornell Medical Coll, NY USA.
    Kirchhof, Paulus
    University of Birmingham, England; SWBH and UHB NHS trusts, England; AFNET, Germany.
    Kowey, Peter R.
    Lankenau Institute Medical Research, OK USA.
    Krieger, Derk
    University Hospital Zurich, Switzerland.
    Lee, Vivian W. Y.
    Chinese University of Hong Kong, Peoples R China.
    Levin, Lars-Åke
    Linköping University, Department of Medical and Health Sciences, Division of Health Care Analysis. Linköping University, Faculty of Medicine and Health Sciences.
    Lip, Gregory Y. H.
    University of Birmingham, England; Aalborg University, Denmark.
    Lobban, Trudie
    Arrhythmia Alliance, England.
    Lowres, Nicole
    University of Sydney, Australia.
    Mairesse, Georges H.
    Clin Sud Luxembourg, Belgium.
    Martinez, Carlos
    Institute Epidemiol Stat and Informat, Germany.
    Neubeck, Lis
    Edinburgh Napier University, Scotland.
    Orchard, Jessica
    University of Sydney, Australia.
    Piccini, Jonathan P.
    Duke University, NC USA.
    Poppe, Katrina
    University of Auckland, New Zealand.
    Potpara, Tatjana S.
    University of Belgrade, Serbia.
    Puererfellner, Helmut
    Ordensklinikum Linz, Austria.
    Rienstra, Michiel
    University of Groningen, Netherlands.
    Sandhu, Roopinder K.
    University of Alberta, Canada.
    Schnabel, Renate B.
    University of Heart Centre, Germany.
    Siu, Chung-Wah
    University of Hong Kong, Peoples R China.
    Steinhubl, Steven
    Scripps Translat Science Institute, CA USA.
    Svendsen, Jesper H.
    University of Copenhagen, Denmark.
    Svennberg, Emma
    Karolinska Institute, Sweden.
    Themistoclakis, Sakis
    Osped Angelo Venice Mestre, Italy.
    Tieleman, Robert G.
    Martini Hospital, Netherlands.
    Turakhia, Mintu P.
    Stanford University, CA 94305 USA; VA Palo Alto Health Care Syst, CA USA.
    Tveit, Arnljot
    Baerum Hospital, Norway.
    Uittenbogaart, Steven B.
    Academic Medical Centre, Netherlands.
    Van Gelder, Isabelle C.
    University of Groningen, Netherlands.
    Verma, Atul
    University of Toronto, Canada.
    Wachter, Rolf
    University of Gottingen, Germany.
    Yan, Bryan P.
    Chinese University of Hong Kong, Peoples R China.
    Screening for Atrial Fibrillation A Report of the AF-SCREEN International Collaboration2017In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 135, no 19, p. 1851-+Article in journal (Refereed)
    Abstract [en]

    Approximately 10% of ischemic strokes are associated with atrial fibrillation (AF) first diagnosed at the time of stroke. Detecting asymptomatic AF would provide an opportunity to prevent these strokes by instituting appropriate anticoagulation. The AF-SCREEN international collaboration was formed in September 2015 to promote discussion and research about AF screening as a strategy to reduce stroke and death and to provide advocacy for implementation of country-specific AF screening programs. During 2016, 60 expert members of AF-SCREEN, including physicians, nurses, allied health professionals, health economists, and patient advocates, were invited to prepare sections of a draft document. In August 2016, 51 members met in Rome to discuss the draft document and consider the key points arising from it using a Delphi process. These key points emphasize that screen-detected AF found at a single timepoint or by intermittent ECG recordings over 2 weeks is not a benign condition and, with additional stroke factors, carries sufficient risk of stroke to justify consideration of anticoagulation. With regard to the methods of mass screening, handheld ECG devices have the advantage of providing a verifiable ECG trace that guidelines require for AF diagnosis and would therefore be preferred as screening tools. Certain patient groups, such as those with recent embolic stroke of uncertain source (ESUS), require more intensive monitoring for AF. Settings for screening include various venues in both the community and the clinic, but they must be linked to a pathway for appropriate diagnosis and management for screening to be effective. It is recognized that health resources vary widely between countries and health systems, so the setting for AF screening should be both country-and health system-specific. Based on current knowledge, this white paper provides a strong case for AF screening now while recognizing that large randomized outcomes studies would be helpful to strengthen the evidence base.

  • 16. Haissaguerre, Michel
    et al.
    Hocini, Mélèze
    Sanders, Prashanthan
    Takahashi, Yoshihide
    Rotter, Martin
    Sacher, Frederic
    Rostock, Thomas
    Hsu, Li-Fern
    Jönsson, Anders
    Hôpital Cardiologique du Haut-Lévêque .
    ONeill, Mark D.
    Bordachar, Pierre
    Reuter, Sylvain
    Roudaut, Raymond
    Clémenty, Jacques
    Jais, Pierre
    Localized sources maintaining atrial fibrillation organized by prior ablation2006In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 113, p. 616-625Article in journal (Refereed)
    Abstract [en]

    Background— Endocardial mapping of localized sources drivingatrial fibrillation (AF) in humans has not been reported.

    Methods and Results— Fifty patients with AF organizedby prior pulmonary vein and linear ablation were studied. AFwas considered organized if mapping during AF showed irregularbut discrete atrial complexes exhibiting consistent activationsequences for >75% of the time using a 20-pole catheter with5 radiating spines covering 3.5-cm diameter or sequential conventionalmapping. A site or region centrifugally activating the remainingatrial tissue defined a source. During AF with a cycle lengthof 211±32 ms, activation mapping identified 1 to 3 sourcesat the origin of atrial wavefronts in 38 patients (76%) predominantlyin the left atrium, including the coronary sinus region. Electrogramsat the earliest area varied from discrete centrifugal activationto an activity spanning 75% to 100% of the cycle length in 42%of cases, the latter indicating complex local conduction ora reentrant circuit. A gradient of cycle length (>20 ms)to the surrounding atrium was observed in 28%. Local radiofrequencyablation prolonged AF cycle length by 28±22 ms and eitherterminated AF or changed activation sequence to another organizedrhythm. In 4 patients, the driving source was isolated, surroundedby the atrium in sinus rhythm, and still firing at high frequency(228±31 ms) either permanently or in bursts.

    Conclusions— AF associated with consistent atrial activationsequences after prior ablation emanates mostly from localizedsources that can be mapped and ablated. Some sources harborelectrograms suggesting the presence of localized reentry.

  • 17.
    Hope, Michael D.
    et al.
    University of Calif San Francisco, CA 94143 USA.
    Sigovan, Monica
    University of Lyon, France.
    Dyverfeldt, Petter
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Health Sciences. Linköping University, Center for Medical Image Science and Visualization (CMIV).
    Letter by Hope et al Regarding Article, "Bicuspid Aortic Cusp Fusion Morphology Alters Aortic Three-Dimensional Outflow Patterns, Wall Shear Stress, and Expression of Aortopathy"2014In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 130, no 19, p. E170-E170Article in journal (Other academic)
    Abstract [en]

    n/a

  • 18. Jonasson, L
    et al.
    Linderfalk, C
    Hoeglandssjukhuset, Eksjoe, Sweden Univ Coll Hlth Sci, Jonkoping, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Wikby, A
    Hoeglandssjukhuset, Eksjoe, Sweden Univ Coll Hlth Sci, Jonkoping, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    T lymphocyte activation in stable angina pectoris: The influence of statin treatment.2000In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 102, no 18, p. 1990-Conference paper (Other academic)
  • 19.
    Jonkman, Nini H.
    et al.
    University of Medical Centre Utrecht, Netherlands.
    Westland, Heleen
    University of Medical Centre Utrecht, Netherlands.
    Groenwold, Rolf H. H.
    University of Medical Centre Utrecht, Netherlands.
    Ågren, Susanna
    Linköping University, Department of Medical and Health Sciences, Division of Nursing Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Thoracic and Vascular Surgery.
    Atienza, Felipe
    Hospital Gen University of Gregorio Maranon, Spain.
    Blue, Lynda
    British Heart Fdn, Scotland.
    Bruggink-Andre de la Porte, Pieta W. F.
    Deventer Hospital, Netherlands.
    DeWalt, Darren A.
    University of N Carolina, NC USA.
    Hebert, Paul L.
    Heisler, Michele
    University of Washington, WA 98195 USA.
    Jaarsma, Tiny
    Linköping University, Department of Social and Welfare Studies, Division of Nursing Science. Linköping University, Faculty of Medicine and Health Sciences.
    Kempen, Gertrudis I. J. M.
    Maastricht University, Netherlands.
    Leventhal, Marcia E.
    University of Basel, Switzerland.
    Lok, Dirk J. A.
    Deventer Hospital, Netherlands.
    Martensson, Jan
    Jonköping University, Sweden.
    Muniz, Javier
    University of A Coruna, Spain; INIBIC, Spain.
    Otsu, Haruka
    Hirosaki University, Japan.
    Peters-Klimm, Frank
    University of Heidelberg Hospital, Germany.
    Rich, Michael W.
    Washington University, MO 63110 USA.
    Riegel, Barbara
    University of Penn, PA 19104 USA.
    Strömberg, Anna
    Linköping University, Department of Medical and Health Sciences, Division of Nursing Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Cardiology in Linköping.
    Tsuyuki, Ross T.
    University of Alberta, Canada.
    van Veldhuisen, Dirk J.
    University of Medical Centre Groningen, Netherlands.
    Trappenburg, Jaap C. A.
    University of Medical Centre Utrecht, Netherlands.
    Schuurmans, Marieke J.
    University of Medical Centre Utrecht, Netherlands.
    Hoes, Arno W.
    University of Medical Centre Utrecht, Netherlands.
    Do Self-Management Interventions Work in Patients With Heart Failure? An Individual Patient Data Meta-Analysis2016In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 133, no 12, p. 1189-1198Article in journal (Refereed)
    Abstract [en]

    Background- Self-management interventions are widely implemented in the care for patients with heart failure (HF). However, trials show inconsistent results, and whether specific patient groups respond differently is unknown. This individual patient data meta-analysis assessed the effectiveness of self-management interventions in patients with HF and whether subgroups of patients respond differently. Methods and Results- A systematic literature search identified randomized trials of self-management interventions. Data from 20 studies, representing 5624 patients, were included and analyzed with the use of mixed-effects models and Cox proportional-hazard models, including interaction terms. Self-management interventions reduced the risk of time to the combined end point of HF-related hospitalization or all-cause death (hazard ratio, 0.80; 95% confidence interval [CI], 0.71-0.89), time to HF-related hospitalization (hazard ratio, 0.80; 95% CI, 0.69-0.92), and improved 12-month HF-related quality of life (standardized mean difference, 0.15; 95% CI, 0.00-0.30). Subgroup analysis revealed a protective effect of self-management on the number of HF-related hospital days in patients &lt; 65 years of age (mean, 0.70 versus 5.35 days; interaction P=0.03). Patients without depression did not show an effect of self-management on survival (hazard ratio for all-cause mortality, 0.86; 95% CI, 0.69-1.06), whereas in patients with moderate/severe depression, self-management reduced survival (hazard ratio, 1.39; 95% CI, 1.06-1.83, interaction P=0.01). Conclusions- This study shows that self-management interventions had a beneficial effect on time to HF-related hospitalization or all-cause death and HF-related hospitalization alone and elicited a small increase in HF-related quality of life. The findings do not endorse limiting self-management interventions to subgroups of patients with HF, but increased mortality in depressed patients warrants caution in applying self-management strategies in these patients.

  • 20.
    Kastelein, John J. P.
    et al.
    Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1100 DD Amsterdam, Netherlands.
    van der Steeg, Wim A.
    Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1100 DD Amsterdam, Netherlands.
    Holme, Ingar
    Ullevaal Univ Hosp, Ctr Prevent Med, Oslo, Norway.
    Gaffney, Michael
    Pfizer Inc, New York, NY USA.
    Cater, Nilo B.
    Pfizer Inc, New York, NY USA.
    Barter, Philip
    Heart Res Inst, Sydney, NSW, Australia.
    Deedwania, Prakash
    Vet Affairs Cent Calif Healthcare Syst, San Francisco, CA USA.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Boekholdt, S. Matthijs
    Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1100 DD Amsterdam, Netherlands.
    Demicco, David A.
    Pfizer Inc, New York, NY USA.
    Szarek, Michael
    Pfizer Inc, New York, NY USA.
    LaRosa, John C.
    SUNY Hlth Sci Ctr, Brooklyn, NY 11203 USA.
    Pedersen, Terje R.
    Ullevaal Univ Hosp, Ctr Prevent Med, Oslo, Norway.
    Grundy, S
    Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
    Lipids, apolipoproteins, and their ratios in relation to cardiovascular events with statin treatment2008In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 117, no 23, p. 3002-3009Article in journal (Refereed)
    Abstract [en]

    Background - Low-density lipoprotein (LDL)cholesterol is the principal target of lipid-lowering therapy, but recent evidence has suggested more appropriate targets. We compared the relationships of on-treatment levels of LDL cholesterol, non-high-density lipoprotein (HDL) cholesterol, and apolipoprotein B, as well as ratios of total/HDL cholesterol, LDL/HDL cholesterol, and apolipoprotein B/A-I, with the occurrence of cardiovascular events in patients receiving statin therapy. Methods and Results - A post hoc analysis was performed that combined data from 2 prospective, randomized clinical trials in which 10 001 ("Treating to New Targets") and 8888 ("Incremental Decrease in End Points through Aggressive Lipid Lowering") patients with established coronary heart disease were assigned to usual-dose or high-dose statin treatment. In models with LDL cholesterol, non-HDL cholesterol and apolipoprotein B were positively associated with cardiovascular outcome, whereas a positive relationship with LDL cholesterol was lost. In a model that contained non-HDL cholesterol and apolipoprotein B, neither was significant owing to collinearity. Total/HDL cholesterol ratio and the apolipoprotein B/A-I ratio in particular were each more closely associated with outcome than any of the individual proatherogenic lipoprotein parameters. Conclusions - In patients receiving statin therapy, on-treatment levels of non-HDL cholesterol and apolipoprotein B were more closely associated with cardiovascular outcome than levels of LDL cholesterol. Inclusion of measurements of the antiatherogenic lipoprotein fraction further strengthened the relationships. These data support the use of non-HDL cholesterol or apolipoprotein B as novel treatment targets for statin therapy. Given the absence of interventions that have been proven to consistently reduce cardiovascular disease risk through raising plasma levels of HDL cholesterol or apolipoprotein A-I, it seems premature to consider the ratio variables as clinically useful.

  • 21.
    Kee Ryu, Sung
    et al.
    Eulji University.
    Mallat, Ziad
    University of Cambridge.
    Benessiano, Joelle
    Paris Descartes University.
    Tedgui, Alain
    Paris Descartes University.
    Olsson, Anders
    Linköping University, Department of Medical and Health Sciences, Internal Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Endocrinology and Gastroenterology UHL.
    Bao, Weihang
    Pfizer Inc.
    Schwartz, Gregory G
    University of Colorado.
    Tsimikas, Sotirios
    University of Calif San Diego.
    Phospholipase A(2) Enzymes, High-Dose Atorvastatin, and Prediction of Ischemic Events After Acute Coronary Syndromes2012In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 125, no 6, p. 757-U71Article in journal (Refereed)
    Abstract [en]

    Background-Secretory phospholipase A2 (sPLA(2)) and lipoprotein-associated phospholipase A2 (Lp-PLA(2)) are enzyme biomarkers of increased cardiovascular risk and targets of emerging therapeutic agents. Their relationship to cardiovascular events in the setting of high-dose statin therapy compared with placebo in patients with acute coronary syndrome is not known. less thanbrgreater than less thanbrgreater thanMethods and Results-sPLA(2) and Lp-PLA(2) mass and activity were measured in 2587 patients in the Myocardial Ischemia Reduction With Acute Cholesterol Lowering (MIRACL) trial at baseline and after 16 weeks of treatment with atorvastatin 80 mg/d or placebo. Baseline levels of sPLA(2) and Lp-PLA(2) mass and activity were not associated with the primary efficacy measure of the trial of death, myocardial infarction, or unstable angina. However, in the overall cohort, baseline sPLA(2) mass predicted risk of death after multivariable adjustment (hazard ratio for 2-fold increase, 1.30; 95% confidence interval, 1.09 -1.56; P = 0.004). This association remained significant when examined separately in the placebo group but not in the atorvastatin group. Compared with placebo, atorvastatin reduced median sPLA(2) mass (-32.1% versus -23.1%), sPLA(2) activity (-29.5% versus -19.2%), Lp-PLA(2) mass (-35.8% versus -6.2%), and Lp-PLA(2) activity (-24.3% versus 5.4%; P andlt; 0.001 for all). Atorvastatin reduced the hazard of death associated with elevated sPLA(2) mass and activity by approximate to 50%. less thanbrgreater than less thanbrgreater thanConclusions-sPLA(2) mass independently predicts death during a 16-week period after acute coronary syndrome. High-dose atorvastatin significantly reduces sPLA(2) and Lp-PLA(2) mass and activity after acute coronary syndrome and mitigates the risk of death associated with sPLA(2) mass. Atorvastatin may exert antiinflammatory effects on phospholipases that contribute to its therapeutic benefit after acute coronary syndrome.

  • 22. Kinlay, S
    et al.
    Libby, P
    Ganz, P
    Schwartz, GG
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Leslie, SJ
    Sasiela, WJ
    Szarek, M
    Early intervention with atorvastatin modulates Th1/Th2 imbalance in patients with acute coronary syndrome: From bedside to bench - Response2004In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 109, no 18, p. E213-E214Other (Other academic)
  • 23. Kinlay, S
    et al.
    Schwartz, G
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MC - Medicincentrum, EMT-endo.
    Rifai, N
    Leslie, S
    Sasiela, WJ
    Szarek, M
    Libby, P
    Ganz, P
    High-dose atorvastatin enhances the decline in inflammatory markers in patients with acute coronary syndromes in the MIRACL study2003In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 108, no 13, p. 1560-1566Article in journal (Refereed)
    Abstract [en]

    Background - Inflammation promotes acute coronary syndromes and ensuing clinical complications. Although statins reduce inflammatory markers in asymptomatic adults or in patients with stable angina, the effect of statins on the markedly heightened inflammation in patients with acute coronary syndromes is unknown. Methods and Results - We measured C-reactive protein (CRP), serum amyloid A (SAA), and interleukin 6 (IL-6) in 2402 subjects enrolled the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study. Subjects with unstable angina or non-Q-wave myocardial infarction were randomized to atorvastatin 80 mg/d or placebo within 24 to 96 hours of hospital admission and treated for 16 weeks. The effect of treatment on inflammatory markers was assessed by ANCOVA after adjustment for presenting syndrome, country, and initial level of marker. All 3 markers were markedly elevated at randomization and declined over the 16 weeks in both treatment groups. Compared with placebo, atorvastatin significantly reduced CRP, -83% (95% CI, -84%, -81%) versus -74% (95% CI, -75%, -71%) (P<0.0001) and SAA, -80% (95% CI, -82%, -78%) versus -77% (-79%, -75%) (P=0.0006) but not IL-6, -55% (95% CI, -57%, -53%) versus -53% (95% CI, -55%, -51%) (P=0.3). Reductions in CRP and SAA were observed in patients with unstable angina and non-Q-wave myocardial infarction, with initial LDL cholesterol <3.2 of =3.2 mmol/L (125 mg/dL), age =65 or <65 years, and in men and women. By 16 weeks, CRP was 34% lower with atorvastatin than with placebo. Conclusions - High-dose atorvastatin potentiated the decline in inflammation in patients with acute coronary syndromes. This supports the value of early statin therapy in these patients.

  • 24. Kinlay, S
    et al.
    Schwartz, G
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Rifai, N
    Sasiela, W
    Szarek, M
    Ganz, P
    Libby, P
    Effect of atorvastatin on risk of recurrent cardiovascular events after an acute coronary syndrome associated with high soluble CD40 ligand in the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study2004In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 110, no 4, p. 386-391Article in journal (Refereed)
    Abstract [en]

    Background - Patients with acute coronary syndromes have elevated plasma levels of the proinflammatory, prothrombotic cytokine CD40 ligand (sCD40L). Statins inhibit CD40L signaling in vitro, but there are no prospective studies of statins and sCD40L in acute coronary syndromes. Methods and Results - We measured sCD40L in subjects with an acute coronary syndrome enrolled in the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study. Subjects were randomized in this double-blind trial to atorvastatin 80 mg/d or placebo for 16 weeks. Plasma CD40L was measured from 2908 (94%) of 3086 subjects at baseline and 2352 (76%) at 16 weeks. Odds ratios (Ors) and 95% Cis from logistic regression models assessed the risk of recurrent cardiovascular events over 16 weeks (death, nonfatal myocardial infarction, cardiac arrest, and worsening angina requiring rehospitalization) in the placebo group from baseline sCD40L and the effect of atorvastatin on the risk associated with CD40L in all subjects. The effects of atorvastatin on plasma concentrations of CD40L were assessed by Wilcoxon tests. There was a threshold effect, with only high sCD40L (>90th centile) being a risk factor for a recurrent cardiovascular event (OR 1.86, 95% CI 1.25 to 2.77). This risk was abolished by atorvastatin (OR 1.09, 95% CI 0.69 to 1.76), which reduced the risk by 48%. Atorvastatin had only a modest effect on sCD40L (P=0-08). Conclusions - In patients with acute coronary syndromes, atorvastatin abrogated the risk of recurrent cardiovascular events associated with high sCD40L. Early statin therapy after acute coronary syndromes counters the risk associated with elevated sCD40L.

  • 25.
    Kurland, L
    et al.
    Univ Uppsala, S-75105 Uppsala, Sweden Karolinska Inst, S-10401 Stockholm, Sweden Linkoping Univ, S-58183 Linkoping, Sweden.
    Melhus, H
    Univ Uppsala, S-75105 Uppsala, Sweden Karolinska Inst, S-10401 Stockholm, Sweden Linkoping Univ, S-58183 Linkoping, Sweden.
    Karlsson, J
    Kahan, T
    Univ Uppsala, S-75105 Uppsala, Sweden Karolinska Inst, S-10401 Stockholm, Sweden Linkoping Univ, S-58183 Linkoping, Sweden.
    Malmqvist, K
    Univ Uppsala, S-75105 Uppsala, Sweden Karolinska Inst, S-10401 Stockholm, Sweden Linkoping Univ, S-58183 Linkoping, Sweden.
    Ohman, P
    Univ Uppsala, S-75105 Uppsala, Sweden Karolinska Inst, S-10401 Stockholm, Sweden Linkoping Univ, S-58183 Linkoping, Sweden.
    Nystrom, F
    Hagg, A
    Univ Uppsala, S-75105 Uppsala, Sweden Karolinska Inst, S-10401 Stockholm, Sweden Linkoping Univ, S-58183 Linkoping, Sweden.
    Lind, L
    Angiotensinogen and AT1-receptor gene polymorphisms are related to regression of left ventricular mass during AT1-receptor antagonist treatment in hypertensives2001In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 104, no 17, p. 1465-Conference paper (Other academic)
  • 26.
    Lagerqvist, B
    et al.
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Diderholm, E
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Lindahl, B
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Husted, S
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Kontny, F
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Stahle, E
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Swahn, Eva
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Cardiology . Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Venge, P
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Wallentin, L
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Coronary angiography in relation to troponin T level in patients with unstable coronary artery disease a FRISC-II substudy.2000In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 102, no 18, p. 2860-Conference paper (Other academic)
  • 27.
    Lagerqvist, B
    et al.
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Husted, S
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Kontny, F
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Stahle, E
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Swahn, Eva
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Cardiology . Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Wallentin, L
    Univ Uppsala Hosp, Uppsala, Sweden Aarhus Univ Hosp, DK-8000 Aarhus, Denmark Univ Hosp, Oslo, Norway Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Better outcome after 2 years with an early invasive strategy in unstable coronary artery disease (UCAD) - FRISCII 2 year follow-up.2001In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 104, no 17, p. 2589-Conference paper (Other academic)
  • 28. Levine, Glenn N
    et al.
    Steinke, Elaine E
    Bakaeen, Faisal G
    Bozkurt, Biykem
    Cheitlin, Melvin D
    Conti, Jamie Beth
    Foster, Elyse
    Jaarsma, Tiny
    Linköping University, Department of Social and Welfare Studies, Health, Activity, Care. Linköping University, Faculty of Health Sciences.
    Kloner, Robert A
    Lange, Richard A
    Lindau, Stacy Tessler
    Maron, Barry J
    Moser, Debra K
    Ohman, E Magnus
    Seftel, Allen D
    Stewart, William J
    Sexual activity and cardiovascular disease: a scientific statement from the American Heart Association2012In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 125, no 8, p. 1058-1072Article in journal (Refereed)
  • 29.
    Madler, CF
    et al.
    Wales Heart Res Inst, Cardiff, S Glam, Wales Hop Charles Nicolle, Rouen, France Univ Hosp Liege, Liege, Belgium Linkoping Univ, Linkoping, Sweden Univ Hosp Gasthuisberg, B-3000 Louvain, Belgium Huddinge Univ Hosp, Stockholm, Sweden.
    Payne, N
    Wales Heart Res Inst, Cardiff, S Glam, Wales Hop Charles Nicolle, Rouen, France Univ Hosp Liege, Liege, Belgium Linkoping Univ, Linkoping, Sweden Univ Hosp Gasthuisberg, B-3000 Louvain, Belgium Huddinge Univ Hosp, Stockholm, Sweden.
    Newcombe, RG
    Wales Heart Res Inst, Cardiff, S Glam, Wales Hop Charles Nicolle, Rouen, France Univ Hosp Liege, Liege, Belgium Linkoping Univ, Linkoping, Sweden Univ Hosp Gasthuisberg, B-3000 Louvain, Belgium Huddinge Univ Hosp, Stockholm, Sweden.
    Derumeaux, G
    Wales Heart Res Inst, Cardiff, S Glam, Wales Hop Charles Nicolle, Rouen, France Univ Hosp Liege, Liege, Belgium Linkoping Univ, Linkoping, Sweden Univ Hosp Gasthuisberg, B-3000 Louvain, Belgium Huddinge Univ Hosp, Stockholm, Sweden.
    Pierard, L
    Wales Heart Res Inst, Cardiff, S Glam, Wales Hop Charles Nicolle, Rouen, France Univ Hosp Liege, Liege, Belgium Linkoping Univ, Linkoping, Sweden Univ Hosp Gasthuisberg, B-3000 Louvain, Belgium Huddinge Univ Hosp, Stockholm, Sweden.
    Engvall, J
    Sutherland, GR
    Wales Heart Res Inst, Cardiff, S Glam, Wales Hop Charles Nicolle, Rouen, France Univ Hosp Liege, Liege, Belgium Linkoping Univ, Linkoping, Sweden Univ Hosp Gasthuisberg, B-3000 Louvain, Belgium Huddinge Univ Hosp, Stockholm, Sweden.
    Brodin, LA
    Fraser, AG
    Wales Heart Res Inst, Cardiff, S Glam, Wales Hop Charles Nicolle, Rouen, France Univ Hosp Liege, Liege, Belgium Linkoping Univ, Linkoping, Sweden Univ Hosp Gasthuisberg, B-3000 Louvain, Belgium Huddinge Univ Hosp, Stockholm, Sweden.
    Diagnostic accuracy of quantitative stress echocardiography using tissue Doppler. Final results of the MYDISE study.2001In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 104, no 17, p. 3177-Conference paper (Other academic)
  • 30.
    Norhammar, A
    et al.
    Karolinska Hosp, S-10401 Stockholm, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Univ Uppsala Hosp, Uppsala, Sweden.
    Malmberg, K
    Karolinska Hosp, S-10401 Stockholm, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Univ Uppsala Hosp, Uppsala, Sweden.
    Ryden, L
    Karolinska Hosp, S-10401 Stockholm, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Univ Uppsala Hosp, Uppsala, Sweden.
    Tornvall, P
    Karolinska Hosp, S-10401 Stockholm, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Univ Uppsala Hosp, Uppsala, Sweden.
    Stenestrand, Ulf
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Cardiology . Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Wallentin, L
    Karolinska Hosp, S-10401 Stockholm, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Univ Uppsala Hosp, Uppsala, Sweden.
    Under-utilisation of evidence-based treatment a partial explanation to the unfavourable prognosis in diabetic patients with acute myocardial infarction2001In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 104, no 17, p. 2962-Conference paper (Other academic)
  • 31.
    Nygard, O
    et al.
    Haukeland Univ Hosp, N-5021 Bergen, Norway Univ Bergen, N-5020 Bergen, Norway Univ Oslo, Natl Hosp, Oslo, Norway Locus Homocysteine, Bergen, Norway Univ Oslo, Inst Med Genet, Oslo 3, Norway Inst Internal Med, Linkoping, Sweden Merck Res Lab, Rahway, NJ USA Aker Hosp, Oslo, Norway.
    Refsum, H
    Haukeland Univ Hosp, N-5021 Bergen, Norway Univ Bergen, N-5020 Bergen, Norway Univ Oslo, Natl Hosp, Oslo, Norway Locus Homocysteine, Bergen, Norway Univ Oslo, Inst Med Genet, Oslo 3, Norway Inst Internal Med, Linkoping, Sweden Merck Res Lab, Rahway, NJ USA Aker Hosp, Oslo, Norway.
    Kjekshus, J
    Haukeland Univ Hosp, N-5021 Bergen, Norway Univ Bergen, N-5020 Bergen, Norway Univ Oslo, Natl Hosp, Oslo, Norway Locus Homocysteine, Bergen, Norway Univ Oslo, Inst Med Genet, Oslo 3, Norway Inst Internal Med, Linkoping, Sweden Merck Res Lab, Rahway, NJ USA Aker Hosp, Oslo, Norway.
    Ueland, PM
    Haukeland Univ Hosp, N-5021 Bergen, Norway Univ Bergen, N-5020 Bergen, Norway Univ Oslo, Natl Hosp, Oslo, Norway Locus Homocysteine, Bergen, Norway Univ Oslo, Inst Med Genet, Oslo 3, Norway Inst Internal Med, Linkoping, Sweden Merck Res Lab, Rahway, NJ USA Aker Hosp, Oslo, Norway.
    Vollset, SE
    Haukeland Univ Hosp, N-5021 Bergen, Norway Univ Bergen, N-5020 Bergen, Norway Univ Oslo, Natl Hosp, Oslo, Norway Locus Homocysteine, Bergen, Norway Univ Oslo, Inst Med Genet, Oslo 3, Norway Inst Internal Med, Linkoping, Sweden Merck Res Lab, Rahway, NJ USA Aker Hosp, Oslo, Norway.
    Berg, K
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Cook, TJ
    Haukeland Univ Hosp, N-5021 Bergen, Norway Univ Bergen, N-5020 Bergen, Norway Univ Oslo, Natl Hosp, Oslo, Norway Locus Homocysteine, Bergen, Norway Univ Oslo, Inst Med Genet, Oslo 3, Norway Inst Internal Med, Linkoping, Sweden Merck Res Lab, Rahway, NJ USA Aker Hosp, Oslo, Norway.
    Pedersen, TR
    Haukeland Univ Hosp, N-5021 Bergen, Norway Univ Bergen, N-5020 Bergen, Norway Univ Oslo, Natl Hosp, Oslo, Norway Locus Homocysteine, Bergen, Norway Univ Oslo, Inst Med Genet, Oslo 3, Norway Inst Internal Med, Linkoping, Sweden Merck Res Lab, Rahway, NJ USA Aker Hosp, Oslo, Norway.
    Total homocysteine levels predicts major coronary events and mortality in simvastatin treated patients of 4S2001In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 104, no 17, p. 2601-Conference paper (Other academic)
  • 32.
    Olofsson, Peder S.
    et al.
    Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Söderström, Leif Å.
    Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Wågsäter, Dick
    University of Örebro, Sweden .
    Sheikine, Yuri
    Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden .
    Ocaya, Pauline
    University of Örebro, Sweden .
    Lang, Francois
    INSERM U601, Nantes, France.
    Rabu, Catherine
    INSERM U601, Nantes, France.
    Chen, Lieping
    Johns Hopkins University School of Medicine, Baltimore, USA.
    Rudling, Mats
    Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Aukrust, Pål
    University of Oslo, Norway .
    Hedin, Ulf
    Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Paulsson-Berne, Gabrielle
    Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Sirsjö, Allan
    University of Örebro, Sweden .
    Hansson, Göran K.
    Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    CD137 is expressed in human atherosclerosis and promotes development of plaque inflammation in hypercholesterolemic mice2008In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 117, no 10, p. 1292-1301Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    Atherosclerosis is a multifactorial disease in which inflammatory processes play an important role. Inflammation underlies lesion evolution at all stages, from establishment to plaque rupture and thrombosis. Costimulatory molecules of the tumor necrosis factor superfamily such as CD40/CD40L and OX40/OX40L have been implicated in atherosclerosis.

    METHODS AND RESULTS:

    This study shows that the tumor necrosis factor superfamily members CD137 and CD137 ligand (CD137L), which play a major role in several autoimmune diseases, may constitute a pathogenic pair in atherogenesis. We detected CD137 protein in human atherosclerotic lesions not only on T cells but also on endothelial cells and showed that CD137 in cultured endothelial cells and smooth muscle cells was induced by proinflammatory cytokines implicated in atherosclerosis. Activation of CD137 by CD137L induced adhesion molecule expression on endothelial cells and reduced smooth muscle cell proliferation. In addition, treatment of atherosclerosis-prone apolipoprotein E-deficient mice with a CD137 agonist caused increased inflammation. T-cell infiltration, mainly of CD8(+) cells, and expression of the murine major histocompatibility complex class II molecule I-A(b) increased significantly in atherosclerotic lesions, as did the aortic expression of proinflammatory cytokines.

    CONCLUSIONS:

    Taken together, these observations suggest that CD137-CD137L interactions in the vasculature may contribute to the progression of atherosclerosis via augmented leukocyte recruitment, increased inflammation, and development of a more disease-prone phenotype.

  • 33. ONeill, Mark D
    et al.
    Jönsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Cardiology. Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Takahasi, Yoshihide
    Hocini, Mélèze
    Jais, Pierre
    Haissaguerre, Michel
    Epicardial tachycardia originating from a persistent left superior vena cava2006In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 114, p. 569-570Article in journal (Other academic)
    Abstract [en]

      

  • 34.
    Polak, Monika
    Linköping University, Center for Medical Image Science and Visualization (CMIV). Linköping University, Department of Medical and Health Sciences. Linköping University, Faculty of Health Sciences.
    Pioneer in Cardiology: Anders Persson MD, PhD2011In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 123, no 17, p. F100-F102Article in journal (Other academic)
  • 35.
    Powell, J.T.
    et al.
    Vascular Surgery Research Group, Imperial College at Charing Cross, London, United Kingdom, Vascular Surgery Research Group, Imperial College at Charing Cross, St Dunstan's Rd, London W6 8RP, United Kingdom.
    Lanne, T.
    Länne, T., Department of Physiology and Cardiovascular Surgery, University Hospital, Linköping University, Linköping, Sweden.
    Through thick and thin collagen fibrils, stress, and aortic rupture: Another piece in the jigsaw2007In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 115, no 21, p. 2687-2688Other (Other academic)
    Abstract [en]

    [No abstract available]

  • 36. Powell, JT
    et al.
    Länne, Toste
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Physiology. Östergötlands Läns Landsting, Heart Centre, Department of Thoracic and Vascular Surgery.
    Through thick and thin collagen fibrils, stress and aortic rupture: another piece in the jigsaw.2007In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 115, p. 2687-2688Article in journal (Other academic)
  • 37. Steinke, Elaine E
    et al.
    Jaarsma, Tiny
    Linköping University, Department of Social and Welfare Studies, Division of Health, Activity and Care. Linköping University, Faculty of Health Sciences.
    Barnason, Susan A
    Byrne, Molly
    Doherty, Sally
    Dougherty, Cynthia M
    Fridlund, Bengt
    Kautz, Donald D
    Mårtensson, Jan
    Mosack, Victoria
    Moser, Debra K
    Sexual counseling for individuals with cardiovascular disease and their partners: a consensus document from the American Heart Association and the ESC Council on Cardiovascular Nursing and Allied Professions (CCNAP).2013In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 128, no 18, p. 2075-2096Article in journal (Refereed)
    Abstract [en]

    After a cardiovascular event, patients and their families often cope with numerous changes in their lives, including dealing with consequences of the disease or its treatment on their daily lives and functioning. Coping poorly with both physical and  psychological challenges may lead to impaired quality of life. Sexuality is one aspect of quality of life that is important  for many patients and partners that may be adversely affected by a cardiac event. The World Health Organization defines sexual health as “… a state of physical, emotional, mental and social well-being in relation to sexuality; it is not merely the absence  of disease, dysfunction or infirmity. Sexual health requires a positive and respectful approach to sexuality and sexual relationships,   as well as the possibility of having pleasurable and safe sexual experiences….”1(p4) The safety and timing of return to sexual activity after a cardiac event have been well addressed in an American Heart Association  scientific statement, and decreased sexual activity among cardiac patients is frequently reported.2 Rates of erectile dysfunction (ED) among men with cardiovascular disease (CVD) are twice as high as those in the general  population, with similar rates of sexual dysfunction in females with CVD.3 ED and vaginal dryness may also be presenting signs of heart disease and may appear 1 to 3 years before the onset of angina pectoris. Estimates reflect that only a small percentage of those with sexual dysfunction seek medical care4; therefore, routine assessment of sexual problems and sexual counseling

  • 38.
    Stenestrand, Ulf
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Cardiology. Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Lindbäck, Johan
    Wallentin, Lars
    Anticoagulation therapy in atrial fibrillation in combination with acute myocardial infarction influences long-term outcome: A prospective cohort study from the Register of Information and Knowledge about Swedish Heart Intensive Care Admissions (RIKS-HIA)2005In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 112, no 21, p. 3225-3231Article in journal (Refereed)
    Abstract [en]

    Background - The American and European guidelines do not agree with regard to antithrombotic treatment in patients with atrial fibrillation (AF) and acute myocardial infarction (AMI), thus causing uncertainty among physicians. We investigated the prescription of oral anticoagulation (OAC) in patients discharged alive with AF after an AMI and the influence of OAC treatment on 1-year mortality. Methods and Results - This was a prospective cohort study using data from the Register of Information and Knowledge about Swedish Heart Intensive care Admissions (RIKS-HIA) on patients admitted to the coronary care units of 72 Swedish hospitals from 1995 to 2002. A total of 6182 patients discharged alive with first registry-recorded AMI and AF on discharge ECG were included. One-year mortality data were obtained from the Swedish National Cause of Death Register. Only 30% (n=1848) of the 6182 patients with AF were prescribed OAC. At 1 year, the unadjusted mortality was 31% (1183 deaths) in the platelet-inhibitors only group and 22% (414 deaths) in the OAC-treated group. In Cox regression analysis with adjustment for confounding factors, OAC treatment was associated with a reduction in 1-year mortality (relative risk 0.73, 95% CI 0.62 to 0.86, P<0.001) in hospital survivors of AMI with AF. The reduction in mortality appeared to be caused primarily by a lower rate of ischemic heart death (55.6% versus 62.0%) and fatal stroke (5.7% versus 7.5%) in the OAC group. This reduction of mortality was similar among most subgroups based on age, sex, baseline characteristics, previous disease manifestations, and medications. Conclusions - In daily clinical practice, OAC was only given to a minority (30%) of AMI patients with AF, despite the fact that OAC was associated with a 29% relative and 7% absolute reduction in 1-year mortality after adjustment for confounding variables. The results emphasize the importance of OAC treatment for AF after AMI. © 2005 American Heart Association, Inc.

  • 39.
    Stenestrand, Ulf
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Cardiology. Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Tabrizi, F
    Lindbäck, J
    Englund, A
    Rosenqvist, M
    Wallentin, L
    Comorbidity and myocardial dysfunction are the main explanations for the higher 1-year mortality in acute myocardial infarction with left bundle-branch block2004In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 110, no 14, p. 1896-1902Article in journal (Refereed)
    Abstract [en]

    Background - The purpose of this study was to assess the independent contribution of left bundle-branch block (LBBB) on cause-specific 1-year mortality in a large cohort with acute myocardial infarction (MI). Methods and Results - We studied a prospective cohort of 88 026 cases of MI from the Register of Information and Knowledge about Swedish Heart Intensive care Admissions in 72 hospitals in 1995 to 2001. Long-term mortality was calculated by Cox regression analysis, adjusted for multiple covariates that affect mortality by calculation of a propensity score. LBBB was present in 9% (8041 of 88 026) of the MI admissions. Patients with LBBB were older and had a higher prevalence of comorbid conditions than patients with no LBBB. The unadjusted relative risk of death within 1 year was 2.16 (95% CI, 2.08 to 2.24, P<0.001) for LBBB (42%, 3350 of 8041) compared with those with no LBBB (22%, 17 044 of 79 011). After adjustment for a propensity score that takes into account differences in risk factors and acute intervention, LBBB was associated with a relative risk of death of 1.19 (95% CI, 1.14 to 1.24, P<0.001). In a subgroup of 11 812 patients for whom left ventricular ejection fraction was available and could be added to the analysis, the contributing relative risk of LBBB for death was only 1.08 (95% CI, 0.93 to 1.25, P=0.33). The most common cause of death in both groups was ischemic heart disease. Conclusions - MI patients with LBBB have more comorbid conditions and an increased unadjusted 1-year mortality. When adjusted for age, baseline characteristics, concomitant diseases, and left ventricular ejection fraction, LBBB does not appear to be an important independent predictor of 1-year mortality in MI.

  • 40.
    Stenestrand, Ulf
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Cardiology . Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Wallentin, L
    Linkoping Univ Hosp, S-58185 Linkoping, Sweden Univ Uppsala Hosp, Uppsala, Sweden.
    Improvement of long term outcome in ST-elevation, acute myocardial infarction (AMI) - Experiences from the Swedish Registry of Cardiac Intensive Care.2000In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 102, no 18, p. 2979-Conference paper (Other academic)
  • 41. Stromberg, A
    et al.
    Martensson, J
    Fridlund, B
    Dahlström, Ulf
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Cardiology . Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Delay time and factors causing hospitalization due to heart failure2002In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 106, no 19, p. 2963-Conference paper (Other academic)
  • 42. Stromberg, A
    et al.
    Martensson, J
    Fridlund, B
    Karlsson, JE
    Levin, Lars-Åke
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Health Technology Assessment and Health Economics.
    Dahlström, Ulf
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Cardiology . Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Follow up at a nurse-led heart failure clinic after hospitalization, effects on morbidity, mortality and self-care behavior. Results from a randomized study2002In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 106, no 19, p. 2413-Conference paper (Other academic)
  • 43.
    Sundström, Johan
    et al.
    Uppsala University, Sweden.
    Hedberg, Jakob
    Uppsala University, Sweden.
    Thuresson, Marcus
    Statisticon AB, Sweden.
    Aarskog, Pernilla
    AstraZeneca Nordic Balt, Sweden.
    Johannesen, Kasper
    Linköping University, Department of Medical and Health Sciences, Division of Health Care Analysis. Linköping University, Faculty of Medicine and Health Sciences.
    Oldgren, Jonas
    Uppsala University, Sweden.
    Low-Dose Aspirin Discontinuation and Risk of Cardiovascular Events A Swedish Nationwide, Population-Based Cohort Study2017In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 136, no 13, p. 1183-+Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: There are increasing concerns about risks associated with aspirin discontinuation in the absence of major surgery or bleeding. We investigated whether long-term low-dose aspirin discontinuation and treatment gaps increase the risk of cardiovascular events. METHODS: We performed a cohort study of 601 527 users of low-dose aspirin for primary or secondary prevention in the Swedish prescription register between 2005 and 2009 who were amp;gt;40 years of age, were free from previous cancer, and had amp;gt;= 80% adherence during the first observed year of treatment. Cardiovascular events were identified with the Swedish inpatient and cause-of-death registers. The first 3 months after a major bleeding or surgical procedure were excluded from the time at risk. RESULTS: During a median of 3.0 years of follow-up, 62 690 cardiovascular events occurred. Patients who discontinued aspirin had a higher rate of cardiovascular events than those who continued (multivariable-adjusted hazard ratio, 1.37; 95% confidence interval, 1.34-1.41), corresponding to an additional cardiovascular event observed per year in 1 of every 74 patients who discontinue aspirin. The risk increased shortly after discontinuation and did not appear to diminish over time. CONCLUSIONS: In long-term users, discontinuation of low-dose aspirin in the absence of major surgery or bleeding was associated with a amp;gt;30% increased risk of cardiovascular events. Adherence to low-dose aspirin treatment in the absence of major surgery or bleeding is likely an important treatment goal.

  • 44.
    Suuronen, Erik J.
    et al.
    Division of Cardiac Surgery, University of Ottawa, Ottawa, Ontario, Canada.
    Veinot, John P.
    Department of Pathology and Laboratory Medicine, University of Ottawa, Ottawa, Ontario, Canada.
    Wong, Serena
    Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada.
    Kapila, Varun
    Division of Cardiac Surgery, University of Ottawa, Ottawa, Ontario, Canada.
    Price, Joel
    Division of Cardiac Surgery, University of Ottawa, Ottawa, Ontario, Canada.
    Griffith, May
    Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada.
    Mesana, Thierry G.
    Division of Cardiac Surgery, University of Ottawa, Ottawa, Ontario, Canada.
    Ruel, Marc
    Division of Cardiac Surgery and Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, Canada.
    Tissue-engineered injectable collagen-based matrices for improved cell delivery and vascularization of ischemic tissue using CD133+progenitors expanded from the peripheral blood2006In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 114, p. I138-I144Article in journal (Refereed)
    Abstract [en]

    Background-The use of stem and/or progenitor cells to achieve potent vasculogenesis in humans has been hindered by low cell numbers, implant capacity, and survival. This study investigated the expansion of CD133(+) cells and the use of an injectable collagen-based tissue engineered matrix to support cell delivery and implantation within target ischemic tissue. Methods and Results-Adult human CD133(+) progenitor cells from the peripheral blood were generated and expanded by successive removal and culture of CD133(-) cell fractions, and delivered within an injectable collagen-based matrix into the ischemic hindlimb of athymic rats. Controls received injections of phosphate-buffered saline, matrix, or CD133(+) cells alone. Immunohistochemistry of hindlimb muscle 2 weeks after treatment revealed that the number of CD133(+) cells retained within the target site was greater than 2-fold greater when delivered by matrix than when delivered alone (P less than 0.01). The transplanted CD133(+) cells incorporated into vascular structures, and the matrix itself also was vascularized. Rats that received matrix and CD133(+) cells demonstrated greater intramuscular arteriole and capillary density than other treatment groups (P less than 0.05 and P less than 0.01, respectively). Conclusions-Compared with other experimental approaches, treatment of ischemic muscle tissue with generated CD133(+) progenitor cells delivered in an injectable collagen-based matrix significantly improved the restoration of a vascular network. This work demonstrates a novel approach for the expansion and delivery of blood CD133(+) cells with resultant improvement of their implantation and vasculogenic capacity.

  • 45.
    Svedjeholm, Rolf
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Thoracic Surgery. Östergötlands Läns Landsting, Heart Centre, Department of Thoracic and Vascular Surgery.
    Håkansson, E
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Anaesthesiology. Östergötlands Läns Landsting, Heart Centre, Department of Thoracic and Vascular Surgery.
    Szabo, Zoltán
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Anaesthesiology. Östergötlands Läns Landsting, Heart Centre, Department of Thoracic and Vascular Surgery.
    Optimal dosage of insulin and glucose in glucose-insulin-potassium treatment of acute myocardial infarction remains to be established.1999In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 100, p. 106-106Article in journal (Refereed)
  • 46.
    Swahn, Eva
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Cardiology . Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    A view from Sweden2006In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 113, no 4, p. F13-F14Other (Other academic)
  • 47. Tsimikas, S
    et al.
    Witztum, JL
    Miller, ER
    Sasiela, WJ
    Szarek, M
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Schwartz, GG
    High-dose atorvastatin reduces total plasma levels of oxidized phospholipids and immune complexes present on apolipoprotein B-100 in patients with acute coronary syndromes in the MIRACL trial2004In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 110, no 11, p. 1406-1412Article in journal (Refereed)
    Abstract [en]

    Background-Oxidized phospholipids (OxPL) are present within atherosclerotic plaques and bound by lipoprotein (a) [Lp(a)] in plasma. This study evaluated the impact of atorvastatin on oxidized LDL (OxLDL) in patients with acute coronary syndromes (ACS). Methods and Results-OxLDL-E06 (OxPL content on apolipoprotein B-100 [apoB] detected by antibody E06), apoB-100 immune complexes (apoB-IC), OxLDL autoantibodies, and Lp(a) levels were measured in 2341 patients at baseline and after 16 weeks of treatment with atorvastatin 80 mg/d or placebo. The OxLDL-E06 and apoB-IC data are reported per apoB-100 particle (OxPL/apoB, IC/apoB) and as total levels on all apoB-100 particles (total apoB-OxPL and total apoB-IC [eg, OxPL/apoB or IC/apoBXapoB-100 levels]). Compared with baseline values, atorvastatin reduced apoB-100 (-33%), total apoB-OxPL (-29.7%), total apoB-IC IgG (-29.5%), and IgM (-25.7%) (P<0.0001 for all), whereas no change or an increase was observed with placebo. When normalized per apoB-100, compared with placebo, atorvastatin increased OxPL/apoB (9.5% versus -3.9%, P<0.0001) and Lp(a) (8.8% versus -0.7%, (P<0.0001). A strong correlation was noted between OxPL/apoB and Lp(a) (R=0.85, P<0.0001), consistent with previous data that Lp(a) binds OxPL. Conclusions-After atorvastatin treatment, total OxPL on all apoB-100 particles was decreased. However, there was enrichment of OxPL on a smaller pool of apoB-100 particles, in parallel with similar increases in Lp(a), suggesting binding by Lp(a). These data support the hypothesis that atorvastatin promotes mobilization and clearance of proinflammatory OxPL, which may contribute to a reduction in ischemic events after ACS.

  • 48.
    Waters, D
    et al.
    Univ Calif San Francisco, San Francisco Gen Hosp, San Francisco, CA 94143 USA Univ Colorado, Hlth Sci Ctr, Denver, CO USA Linkoping Univ, S-58183 Linkoping, Sweden Natl Heart & Lung Inst, Imperial Coll, London, England Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA Med Coll Penn & Hahnemann Univ, Philadelphia, PA USA Pfizer, New York, NY USA Pfizer, Ann Arbor, MI USA.
    Schwartz, GG
    Univ Calif San Francisco, San Francisco Gen Hosp, San Francisco, CA 94143 USA Univ Colorado, Hlth Sci Ctr, Denver, CO USA Linkoping Univ, S-58183 Linkoping, Sweden Natl Heart & Lung Inst, Imperial Coll, London, England Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA Med Coll Penn & Hahnemann Univ, Philadelphia, PA USA Pfizer, New York, NY USA Pfizer, Ann Arbor, MI USA.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Oliver, MF
    Univ Calif San Francisco, San Francisco Gen Hosp, San Francisco, CA 94143 USA Univ Colorado, Hlth Sci Ctr, Denver, CO USA Linkoping Univ, S-58183 Linkoping, Sweden Natl Heart & Lung Inst, Imperial Coll, London, England Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA Med Coll Penn & Hahnemann Univ, Philadelphia, PA USA Pfizer, New York, NY USA Pfizer, Ann Arbor, MI USA.
    Ganz, P
    Univ Calif San Francisco, San Francisco Gen Hosp, San Francisco, CA 94143 USA Univ Colorado, Hlth Sci Ctr, Denver, CO USA Linkoping Univ, S-58183 Linkoping, Sweden Natl Heart & Lung Inst, Imperial Coll, London, England Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA Med Coll Penn & Hahnemann Univ, Philadelphia, PA USA Pfizer, New York, NY USA Pfizer, Ann Arbor, MI USA.
    Ezekowitz, MD
    Univ Calif San Francisco, San Francisco Gen Hosp, San Francisco, CA 94143 USA Univ Colorado, Hlth Sci Ctr, Denver, CO USA Linkoping Univ, S-58183 Linkoping, Sweden Natl Heart & Lung Inst, Imperial Coll, London, England Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA Med Coll Penn & Hahnemann Univ, Philadelphia, PA USA Pfizer, New York, NY USA Pfizer, Ann Arbor, MI USA.
    Leslie, S
    Univ Calif San Francisco, San Francisco Gen Hosp, San Francisco, CA 94143 USA Univ Colorado, Hlth Sci Ctr, Denver, CO USA Linkoping Univ, S-58183 Linkoping, Sweden Natl Heart & Lung Inst, Imperial Coll, London, England Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA Med Coll Penn & Hahnemann Univ, Philadelphia, PA USA Pfizer, New York, NY USA Pfizer, Ann Arbor, MI USA.
    Stern, T
    Univ Calif San Francisco, San Francisco Gen Hosp, San Francisco, CA 94143 USA Univ Colorado, Hlth Sci Ctr, Denver, CO USA Linkoping Univ, S-58183 Linkoping, Sweden Natl Heart & Lung Inst, Imperial Coll, London, England Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA Med Coll Penn & Hahnemann Univ, Philadelphia, PA USA Pfizer, New York, NY USA Pfizer, Ann Arbor, MI USA.
    Stroke reduction with atorvastatin in acute coronary syndromes: Results of the myocardial ischemia reduction with aggressive cholesterol lowering (MIRACL) trial2001In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 104, no 17, p. 2503-Conference paper (Other academic)
  • 49. Waters, DD
    et al.
    Schwartz, GG
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Zeiher, A
    Oliver, MF
    Ganz, P
    Ezekowitz, M
    Chaitman, BR
    Leslie, SJ
    Stern, T
    Effects of atorvastatin on stroke in patients with unstable angina or non-Q-wave myocardial infarction: A myocardial ischemia reduction with aggressive cholesterol lowering (MIRACL) substudy2002In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 106, no 13, p. 1690-1695Article in journal (Refereed)
    Abstract [en]

    Background - This report describes the effect of intensive cholesterol lowering with atorvastatin on the incidence of nonfatal stroke, a secondary end point, in a randomized, placebo-controlled trial of patients with unstable angina or non-Q-wave myocardial infarction. The primary end point, a composite of death, nonfatal myocardial infarction, resuscitated cardiac arrest, or recurrent symptomatic myocardial ischemia with objective evidence requiring emergency rehospitalization, was reduced from 17.4% in the placebo group to 14.8% in the atorvastatin group over the 16 weeks of the trial (P=0.048). Methods and Results - Strokes were adjudicated by a blinded end-point committee using standard clinical and imaging criteria. The outcomes of nonfatal stroke and fatal plus nonfatal stroke were analyzed by time to first occurrence during the 16-week trial. Of 38 events (in 36 patients) adjudicated as fatal or nonfatal strokes, 3 were classified as hemorrhagic, one as embolic, and 29 as thrombotic or embolic, 5 could not be categorized. Nonfatal stroke occurred in 9 patients in the atorvastatin group and 22 in the placebo group (relative risk, 0.40, 95% confidence intervals, 0.19 to 0.88, P=0.02). Fatal or nonfatal stroke occurred in 12 atorvastatin patients and 24 placebo patients (relative risk, 0.49, 95% confidence intervals, 0.24 to 0.98, P=0.04). All 3 hemorrhagic strokes occurred in the placebo group. Conclusion - Intensive cholesterol lowering with atorvastatin over 16 weeks in patients with acute coronary syndromes reduced the overall stroke rate by half and did not cause hemorrhagic stroke. These findings need to be confirmed in future trials.

  • 50. Zeng, G
    et al.
    Nyström, Fredrik
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Ravichandran, L V
    Cong, L
    Kirby, M
    Mostowski, H
    Quon, M J
    Roles for Inuslin receptor, PI3-kinase, and AKT in insulin-signaling pathways related to production of nitric oxide in human vascular endothelial cells.2000In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 101, p. 1539-1545Article in journal (Refereed)
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