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  • 1.
    Aspelin, P
    et al.
    Huddinge Univ Hosp, Stockholm, Sweden Hop Bichat, F-75877 Paris, France Linkoping Univ Hosp, S-58185 Linkoping, Sweden Dresden Univ Technol, D-8027 Dresden, Germany FranzVolhard Klin, Berlin, Germany Natl Hosp Norway, Oslo, Norway.
    Aubry, P
    Huddinge Univ Hosp, Stockholm, Sweden Hop Bichat, F-75877 Paris, France Linkoping Univ Hosp, S-58185 Linkoping, Sweden Dresden Univ Technol, D-8027 Dresden, Germany FranzVolhard Klin, Berlin, Germany Natl Hosp Norway, Oslo, Norway.
    Fransson, Sven Göran
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care. Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Strasser, R
    Huddinge Univ Hosp, Stockholm, Sweden Hop Bichat, F-75877 Paris, France Linkoping Univ Hosp, S-58185 Linkoping, Sweden Dresden Univ Technol, D-8027 Dresden, Germany FranzVolhard Klin, Berlin, Germany Natl Hosp Norway, Oslo, Norway.
    Willenbrock, R
    Huddinge Univ Hosp, Stockholm, Sweden Hop Bichat, F-75877 Paris, France Linkoping Univ Hosp, S-58185 Linkoping, Sweden Dresden Univ Technol, D-8027 Dresden, Germany FranzVolhard Klin, Berlin, Germany Natl Hosp Norway, Oslo, Norway.
    Berg, KJ
    Nephrotoxicity in high-risk patients. A double-blind, randomized multicenter study of iso-osmolar and low-osmolar nonionic contrast media: The nephrotoxicity, high risk, iso-osmolar, contrast media (NEPHRIC) study.2002In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 90, no 6A, p. TCT367-Conference paper (Other academic)
  • 2.
    Carlhäll, Carljohan
    et al.
    Linköping University, Department of Medicine and Care, Clinical Physiology. Linköping University, Faculty of Health Sciences.
    Wranne, Bengt
    Linköping University, Department of Medicine and Care, Clinical Physiology. Linköping University, Faculty of Health Sciences.
    Jurkevicius, R.
    Institute of Cardiology of Kaunas Medical University, Kaunas, Lithuania.
    Is left ventricular postsystolic long-axis shortening a marker for severity of hypertensive heart disease?2003In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 91, no 12, p. 1490-1493Article in journal (Refereed)
    Abstract [en]

    No abstract available.

  • 3.
    Gotto, AM
    et al.
    Care Of Jou J, Cornell Univ, Weill Med Coll, New York, NY 10021 USA Linkoping Univ Hosp, Clin Res Ctr, 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.
    A symposium: In Search of the Ideal Lipid-Lowering Agent - Introduction2001In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 87, no 5A, p. 1B-1BOther (Other academic)
  • 4. Jonasson, L
    et al.
    Linderfalk, C
    Olsson, J
    Wikby, A
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Systemic T-cell activation in stable angina pectoris2002In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 89, no 6, p. 754-756Article in journal (Refereed)
  • 5.
    Liuba, Ioan
    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.
    Jönsson, Anna
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery.
    Safstrom, K.
    Säfström, K., Department of Cardiology, University Hospital Linköping, Linköping, Sweden.
    Walfridsson, Håkan
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Cardiology . Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Gender-related differences in patients with atrioventricular nodal reentry tachycardia2006In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 97, no 3, p. 384-388Article in journal (Refereed)
    Abstract [en]

    The present study sought to assess the extent of gender differences in electrophysiologic parameters in patients with atrioventricular nodal reentrant tachycardia (AVNRT). The study population consisted of 203 patients (women/men ratio 2:1) who underwent slow pathway ablation. Patients with associated heart disease experienced the first episode of tachycardia at a significantly older age than patients with lone AVNRT (women 50 ± 18 vs 29 ± 15 years, p <0.0001, men 45 ± 20 vs 31 ± 17 years, p = 0.01). Sinus cycle length (797 ± 142 vs 870 ± 161 ms, p = 0.0001), HV interval (41 ± 7 vs 45 ± 8 ms, p = 0.0001), atrioventricular (AV) block cycle length (348 ± 53 vs 371 ± 75 ms, p = 0.01), slow pathway effective refractory period (ERP) (258 ± 46 vs 287 ± 62 ms, p = 0.006), and tachycardia cycle length (354 ± 58 vs 383 ± 60 ms, p = 0.001) were shorter in women. No gender differences were noted in fast pathway ERP and ventriculoatrial (VA) block cycle length. In women, an AV block cycle length <350 ms along with a VA block cycle length <400 ms predicted tachycardia induction without the need for autonomic intervention, with a positive predictive value of 93% (sensitivity 71%, specificity 82%). No such cut-off values could be found in men. The acute success rate (100% vs 98%) and the recurrence rate (3% vs 6%) were similar for the 2 genders. In conclusion, in patients with lone AVNRT, the onset of symptoms occurred at a younger age than in patients with concomitant heart disease. Women had shorter slow pathway refractory periods, AV block cycle lengths, and tachycardia cycle lengths. No gender differences were noted in the fast pathway ERP. Therefore, women have a wider "tachycardia window" (i.e., the difference between the fast and slow pathway refractory periods), a finding that may explain their greater incidence of AVNRT. © 2006 Elsevier Inc. All rights reserved.

  • 6.
    Loyd, Dan
    et al.
    Linköping University, Department of Management and Engineering, Applied Thermodynamics and Fluid Mechanics. Linköping University, The Institute of Technology.
    Ask, Per
    Linköping University, Department of Biomedical Engineering, Physiological Measurements. 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.
    Doppler prediction of transvalvular gradient and stenotic orifice area.1988In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 61, no 11, p. 958-959Article in journal (Refereed)
  • 7.
    Maccubbin, Darbie L
    et al.
    Merck Sharp and Dohme Corp, NJ USA .
    Chen, Fabian
    Merck Sharp and Dohme Corp, NJ USA .
    Weimer Anderson, Jennifer
    Merck Sharp and Dohme Corp, NJ USA .
    Sirah, Waheeda
    Merck Sharp and Dohme Corp, NJ USA .
    McCrary Sisk, Christine
    Merck Sharp and Dohme Corp, NJ USA .
    Kher, Uma
    Merck Sharp and Dohme Corp, NJ USA .
    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.
    Bays, Harold E
    Louisville Metab and Atherosclerosis Research Centre, KY USA .
    Mitchel, Yale B
    Merck Sharp and Dohme Corp, NJ USA .
    Effectiveness and Safety of Laropiprant on Niacin-Induced Flushing2012In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 110, no 6, p. 817-822Article in journal (Refereed)
    Abstract [en]

    Extended-release niacin (ERN) improves multiple lipid parameters but is underused owing to niacin-induced flushing (NIF). Laropiprant (LRPT) reduces NIF; however, its effects on chronic flushing (andgt;6 months) have not been studied. We examined whether after 20 weeks of treatment with ERN/LRPT, patients who continued ERN/LRPT would experience less NIF than patients who stopped LRPT and continued ERN alone. A total of 1,152 dyslipidemic patients were randomized 2:2:1 to group 1, ERN/LRPT 1 g/20 mg/day from 0 to 4 weeks and then ERN/LRPT 2 g/40 mg/day from 5 to 32 weeks; group 2, ERN/LRPT 1 g/20 mg/day from 0 to 4 weeks, ERN/LRPT 2 g/40 mg/day from 5 to 20 weeks, and then ERN 2 g/day without LRPT from 21 to 32 weeks; or group 3, placebo for the entire study. The end points included the number of days each week with a moderate or greater Global Flushing Severity Score (GFSS) andgt;= 4 (primary end point) and the percentage of patients with a maximum GFSS of andgt;= 4 (secondary end point) during the postwithdrawal period (weeks 21 to 32). ERN/LRPT produced significantly less NIF than ERN alone during the postwithdrawal period, as measured by the number of days each week with a GFSS of andgt;= 4 (p andlt; 0.001) and the percentage of patients with a maximum GFSS of andgt;= 4 (p andlt; 0.001; ERN/LRPT 19.6%; ERN 48.9%; placebo 9.2%). Compared with ERN alone, ERN/LRPT produced fewer drug-related adverse experiences during the postwithdrawal period. After 20 weeks of stable maintenance therapy, dyslipidemic patients treated continuously with ERN/LRPT experienced less NIF than did patients who had had LRPT withdrawn and had continued with ERN alone. In conclusion, the results of our study support the long-term efficacy of ERN/LRPT in reducing NIF symptoms.

  • 8.
    Maisel, Alan
    et al.
    University of Calif San Diego, CA 92103 USA.
    Xue, Yang
    University of Calif San Diego, CA 92103 USA.
    van Veldhuisen, Dirk J.
    University of Groningen, Netherlands.
    Voors, Adriaan A.
    University of Groningen, Netherlands.
    Jaarsma, Tiny
    Linköping University, Department of Social and Welfare Studies, Division of Health, Activity and Care. Linköping University, Faculty of Health Sciences.
    Pang, Peter S.
    Northwestern University, IL 60611 USA.
    Butler, Javed
    Emory University, GA 30322 USA.
    Pitt, Bertram
    University of Michigan, MI 48109 USA.
    Clopton, Paul
    University of Calif San Diego, CA 92103 USA.
    de Boer, Rudolf A.
    University of Groningen, Netherlands.
    Effect of Spironolactone on 30-Day Death and Heart Failure Rehospitalization (from the COACH Study)2014In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 114, no 5, p. 737-742Article in journal (Refereed)
    Abstract [en]

    The aim of our study is to investigate the effect of spironolactone on 30-day outcomes in patients with acute heart failure (AHF) and the association between treatment and outcomes stratified by biomarkers. We conducted a secondary analysis of the biomarker substudy of the multicenter COACH (Co-ordinating Study Evaluating Outcomes of Advising and Counseling in Heart Failure) trial involving 534 AHF patients for 30-day mortality and HF rehospitalizations. Spironolactone therapy was initiated and terminated at the discretion of the treating physician; 30-day outcomes were compared between patients who were treated with spironolactone and those who were not. Outcomes with spironolactone therapy. were explored based on N-terminal pro-B-type natriuretic peptide, ST2, galectin-3, and creatinine levels. Spironolactone was prescribed to 297 (55.6%) patients at discharge (158 new and 139 continued). There were 19 deaths and 30 HF rehospitalizations among 46 patients by 30 days. Patients discharged on spironolactone had significantly less 30-day event (hazard ratio 0.538, p = 0.039) after adjustment for multiple risk factors. Initiation of spironolactone in patients who were not on spironolactone before admission was associated with a significant reduction in event rate (hazard ratio 0.362, p = 0.027). The survival benefit of spironolactone was more prominent in patient groups with elevations of creatinine, N-terminal pro B-type natriuretic peptide, ST2, or galectin-3. In conclusion, AHF patients who received spironolactone during hospitalization had significantly fewer 30-day mortality and HF rehospitalizations, especially in high-risk patients.

  • 9. Muhr, T
    et al.
    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.
    Markers for myocardial injury during percutaneous coronary intervention2003In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 92, no 6A, p. 145L-145LConference paper (Other academic)
  • 10.
    Mölgaard, J
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Wärjestam-Elf, S
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Cardiology.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Efficacy and safety of simvastatin for highrisk hypercholseterolemia.1999In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 83, p. 1043-1048Article in journal (Refereed)
  • 11.
    Nieuwenhuis, Maurice M W
    et al.
    University of Groningen, Netherlands .
    Jaarsma, Tiny
    Linköping University, Department of Social and Welfare Studies, Health, Activity, Care. Linköping University, Faculty of Health Sciences.
    van Veldhuisen, Dirk J
    University of Groningen, Netherlands .
    Postmus, Douwe
    University of Groningen, Netherlands .
    van der Wal, Martje H L
    University of Groningen, Netherlands .
    Long-Term Compliance With Nonpharmacologic Treatment of Patients With Heart Failure2012In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 110, no 3, p. 392-397Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to examine long-term compliance with nonpharmacologic treatment of patients with heart failure (HF) and its associated variables. Data from 648 hospitalized patients with HF (mean age 69 +/- 12 years, 38% women, mean left ventricular ejection fraction 33 +/- 14%) were analyzed. Compliance was assessed by means of self-report at baseline and 1, 6, 12, and 18 months after discharge. Patients completed questionnaires on depressive symptoms, HF knowledge, and physical functioning at baseline. Logistic regression analyses were performed to examine independent associations with low long-term compliance. From baseline to 18-month follow-up, long-term compliance with diet and fluid restriction ranged from 77% to 91% and from 72% to 89%, respectively. In contrast, compliance with daily weighing (34% to 85%) and exercise (48% to 64%) was lower. Patients who were in New York Heart Association functional class II were more often noncompliant with fluid restriction (odds ratio [OR] 1.97, 95% confidence interval [CI] 1.25 to 3.08). A lower level of knowledge on HF was independently associated with low compliance with fluid restriction (OR 0.78, 95% CI 0.71 to 0.86) and daily weighing (OR 0.86, 95% CI 0.79 to 0.94). Educational support improved compliance with these recommendations. Female gender (OR 1.91, 95% CI 1.26 to 2.90), left ventricular ejection fraction andgt;= 40% (OR 1.55, 95% CI 1.03 to 2.34), a history of stroke (OR 3.55, 95% CI 1.54 to 8.16), and less physical functioning (OR 0.99, 95% CI 0.98 to 0.99) were associated with low compliance with exercise. In conclusion, long-term compliance with exercise and daily weighing was lower than long-term compliance with advice on diet and fluid restriction. Although knowledge on HF and being offered educational support positively affected compliance with weighing and fluid restriction, these variables were not related to compliance with exercise. Therefore, new approaches to help patients with HF stay physically active are needed. (C) 2012 Elsevier Inc. All rights reserved. (Am J Cardiol 2012;110:392-397)

  • 12.
    Nijm, Johnny
    et al.
    Linköping University, Department of Medicine and Health Sciences. Linköping University, Faculty of Health Sciences.
    Wikby, Anders
    Tompa, Andrea
    Research Center of Cardiovascular Disease, Högland Hospital, Eksjö, Sweden.
    Olsson, Anders G
    Linköping University, Department of Medicine and Care. Linköping University, Faculty of Health Sciences.
    Jonasson, Lena
    Linköping University, Department of Medicine and Care. Linköping University, Faculty of Health Sciences.
    Circulating levels of proinflammatory cytokines and neutrophil-platelet aggregates in patients with coronary artery disease2005In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 95, no 4, p. 452-456Article in journal (Refereed)
    Abstract [en]

    Several lines of evidence indicate that increased inflammatory activity in peripheral blood is associated with the acute coronary syndrome. Systemic inflammation in clinically stable conditions of coronary artery disease has been less studied. We examined cytokine profiles in 20 patients who had acute coronary syndrome, 45 who had angiographically verified coronary artery disease and stable angina pectoris, and 45 healthy controls. Circulating levels of C-reactive protein, interleukin-1 receptor antagonist, interleukin-2 receptor, interleukin-6, interleukin-10, and interleukin-18 were determined. Subpopulations of peripheral immune cells, including neutrophil-platelet aggregates, were analyzed by 3-color flow cytometry using a panel of monoclonal antibodies. Patients who had acute coronary syndrome and stable angina pectoris had significantly higher levels of C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist than did controls, whereas levels of interleukin-2 receptor, interleukin-10, and interleukin-18 were similar across groups. Patients had significantly more neutrophils, and the numbers of neutrophil-platelet aggregates were particularly large in patients who had stable angina pectoris. High levels of C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist in patients were significantly related to numbers of neutrophils and neutrophil-platelet aggregates but not to other immune cell subpopulations. The data suggest that the interaction between neutrophils and platelets is an important component of proinflammatory activity seen in peripheral blood of stable and unstable forms of coronary artery disease.

  • 13.
    Nilsson, Göran
    et al.
    Dept Cadriology Västerås sjukhus.
    Åhlfeldt, Hans
    Linköping University, The Institute of Technology. Linköping University, Department of Biomedical Engineering, Medical Informatics.
    Ahrén, Tom
    Dept Cardiology Västerås Hospital.
    Jonasson, Tommy
    Dept Cardiology Västerås Hospital.
    Distribution patterns of ventricular premature complexes in long-term electrocardographic recordings and their usefulness in disclosing modulated parasystole1991In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 68, p. 1045-1048Article in journal (Refereed)
  • 14.
    Nous, Fay M. A.
    et al.
    Erasmus MC, Netherlands; Erasmus MC, Netherlands.
    Coenen, Adriaan
    Erasmus MC, Netherlands; Erasmus MC, Netherlands.
    Boersma, Eric
    Erasmus MC, Netherlands.
    Kim, Young-Hak
    Univ Ulsan, South Korea.
    Kruk, Mariusz B. P.
    Inst Cardiol, Poland.
    Tesche, Christian
    Med Univ South Carolina, SC 29425 USA.
    de Geer, Jakob
    Linköping University, Department of Medical and Health Sciences, Division of Radiological Sciences. Linköping University, Faculty of Medicine and Health Sciences. Linköping University, Center for Medical Image Science and Visualization (CMIV).
    Yang, Dong Hyun
    Univ Ulsan, South Korea; Univ Ulsan, South Korea.
    Kepka, Cezary
    Inst Cardiol, Poland.
    Schoepf, U. Joseph
    Univ Ulsan, South Korea.
    Persson, Anders
    Linköping University, Department of Medical and Health Sciences, Division of Radiological Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Radiology in Linköping. Linköping University, Center for Medical Image Science and Visualization (CMIV).
    Kurata, Akira
    Erasmus MC, Netherlands; Ehime Univ, Japan.
    Budde, Ricardo P. J.
    Erasmus MC, Netherlands; Erasmus MC, Netherlands.
    Nieman, Koen
    Erasmus MC, Netherlands; Erasmus MC, Netherlands; Stanford Univ, CA 94305 USA.
    Comparison of the Diagnostic Performance of Coronary Computed Tomography Angiography-Derived Fractional Flow Reserve in Patients With Versus Without Diabetes Mellitus (from the MACHINE Consortium)2019In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 123, no 4, p. 537-543Article in journal (Refereed)
    Abstract [en]

    Coronary computed tomography angiography-derived fractional flow reserve (CT-FFR) is a noninvasive application to evaluate the hemodynamic impact of coronary artery disease by simulating invasively measured FFR based on CT data. CT-FFR is based on the assumption of a normal coronary microvascular response. We assessed the diagnostic performance of a machine-learning based application for on-site computation of CT-FFR in patients with and without diabetes mellitus with suspected coronary artery disease. The study population included 75 diabetic and 276 nondiabetic patients who were enrolled in the MACHINE consortium. The overall diagnostic performance of coronary CT angiography alone and in combination with CT-FFR were analyzed with direct invasive FFR comparison in 110 coronary vessels of the diabetic group and in 415 coronary vessels of the nondiabetic group. Per-vessel discrimination of lesion-specific ischemia by CT-FFR was assessed by the area under the receiver operating characteristic curves. The overall diagnostic accuracy of CT-FFR in diabetic patients was 83% and in nondiabetic patients 75% (p = 0.088), showing improvement over the diagnostic accuracy of coronary CT angiography, which was 58% and 65% (p = 0.223), respectively. In addition, the diagnostic accuracy of CT-FFR was similar between diabetic and nondiabetic patients per stratified CT-FFR group (CT-FFR amp;lt; 0.6, 0.6 to 0.69, 0.7 to 0.79, 0.8 to 0.89, amp;gt;= 0.9). The area under the curves for diabetic and nondiabetic patients were also comparable, 0.88 and 0.82 (p = 0.113), respectively. In conclusion, on-site machine-learning CT-FFR analysis improved the diagnostic performance of coronary CT angiography and accurately discriminated lesion-specific ischemia in both diabetic and nondiabetic patients suspected of coronary artery disease. (C) 2018 Elsevier Inc. All rights reserved.

  • 15.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Statin therapy and reductions in low-density lipoprotein cholesterol: Initial clinical data on the potent new statin rosuvastatin2001In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 87, no 5 SUPPL. 1Article in journal (Refereed)
    Abstract [en]

    The utility of statins with increased potency in reducing low-density lipoprotein cholesterol (LDL-C) is indicated by evidence that aggressive LDL-C lowering is associated with increased reduction in coronary artery disease risk, and the need for such agents is illustrated by the fact that many patients currently fail to achieve LDL-C target levels during treatment with available drugs. In dose-ranging studies of patients with hypercholesterolemia, the new synthetic statin rosuvastatin (formerly ZD4522) produced significant, dose-dependent reductions in LDL-C compared with placebo across a range of doses. Reductions ranged from 34% at 1 mg per day to 65% at 80 mg per day, with linear regression analysis indicating an additional 4.5% reduction in LDL-C with each doubling of the rosuvastatin dose. Rosuvastatin treatment was well tolerated. Phase 3 clinical trials of this agent are under way.

  • 16.
    Olsson, Anders
    et al.
    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.
    Pears, J.
    AstraZeneca, Alderley Park, Cheshire, United Kingdom.
    McKellar, J.
    AstraZeneca, Alderley Park, Cheshire, United Kingdom.
    Mizan, J.
    AstraZeneca, Alderley Park, Cheshire, United Kingdom.
    Raza, A.
    AstraZeneca, Alderley Park, Cheshire, United Kingdom.
    Effect of rosuvastatin on low-density lipoprotein cholesterol in patients with hypercholesterolemia2001In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 88, no 5, p. 504-508Article in journal (Refereed)
    Abstract [en]

    Rosuvastatin is a new, synthetic, orally active statin, with marked low-density lipoprotein (LDL) cholesterol-lowering activity. We conducted 2 dose-ranging studies. In the first study, after a 6-week dietary run-in, 142 moderately hypercholesterolemic patients were randomized equally to receive double-blind placebo or rosuvastatin 1, 2.5, 5, 10, 20, or 40 mg or open-label atorvastatin 10 or 80 mg once daily for 6 weeks, in the second study, conducted to extend the rosuvastatin dose range, 64 patients were randomized to double-blind, once-daily placebo or rosuvastatin 40 or 80 mg (1:1:2 ratio) for 6 weeks. Data from both studies were combined for analysis of lipid effects. No statistical comparison of atorvastatin arms with placebo or rosuvastatin was performed. Rosuvastatin was associated with highly significant dose-dependent reductions in LDL cholesterol compared with placebo (p <0.001), decreases ranged from 34% (1 mg) to 65% (80 mg). Linear regression analysis indicated an additional 4.5% LDL cholesterol reduction for each doubling of the rosuvastatin dose. Across the dose range, approximately 90% of LDL cholesterol reduction occurred within the first 2 weeks of treatment. Significant, dose-dependent reductions in total cholesterol and apolipoprotein B with rosuvastatin were also observed (p <0.001). High-density lipoprotein cholesterol increases and triglyceride reductions were consistently observed and statistically significant at some dose levels. All lipid ratios were significantly reduced at all rosuvastatin dose levels (p <0.001). Adverse events were similar across placebo and active treatments. No significant increases in alanine aminotransferase or creatine kinase were seen in any patient. Over 6 weeks, rosuvastatin produced large, rapid, dose-dependent LDL cholesterol reductions and was well tolerated in hypercholesterolemic patients. © 2001 by Excerpta Medica, Inc.

  • 17.
    Olsson, Andes G.
    et al.
    Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Schwartz, G.G.
    VA Medical Center, University of Colorado Health Sciences, Denver, CO, United States.
    Szarek, M.
    Pfizer, Inc., New York, NY, United States.
    Luo, D.
    Pfizer, Inc., New York, NY, United States.
    Jamieson, M.J.
    Pfizer, Inc., New York, NY, United States.
    Effects of High-Dose Atorvastatin in Patients =65 Years of Age With Acute Coronary Syndrome (from the Myocardial Ischemia Reduction With Aggressive Cholesterol Lowering [MIRACL] Study)2007In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 99, no 5, p. 632-635Article in journal (Refereed)
    Abstract [en]

    After acute coronary syndromes (ACSs), older patients are particularly susceptible to early complications, including death and recurrent ACS. Lipid management guidelines do not differentiate elderly from younger patients, and lack of evidence for statin benefits in older patients has led to underutilization of statins in the elderly. The MIRACL study randomized 3,086 patients to 16 weeks of 80 mg/day of atorvastatin or placebo 24 to 96 hours after ACS and demonstrated significant decreases in the combined primary end point (nonfatal acute myocardial infarction, resuscitated cardiac arrest, recurrent symptomatic myocardial ischemia). This post hoc analysis compared benefits of 80 mg of atorvastatin in older (=65 years) versus younger (<65 years) patients. Event rates were approximately two- to threefold higher in older than in younger patients. Treatment-by-age heterogeneity testing indicated no difference in treatment effect by age for any of the primary or secondary end points, and relative risk decreases in the primary end point with atorvastatin versus placebo were similar in younger and older patients (22% vs 14%, respectively). The safety profile of atorvastatin was similar between the 2 age groups. In conclusion, these results and a greater immediate cardiovascular risk in older patients argue for early, intensive atorvastatin therapy as routine practice after ACS. © 2007 Elsevier Inc. All rights reserved.

  • 18.
    Pedersen, T.R.
    et al.
    Center for Preventive Medicine, Ullevål University Hospital, Oslo, Norway, Center for Preventive Medicine, Building K, Ulleval Univ. Hosp., N-0407 Oslo, N..
    Faergeman, O.
    Department of Medicine-Cardiology A, Århus University Hospital, Århus, Denmark.
    Kastelein, J.J.P.
    Academic Hospital Amsterdam, Amsterdam, The Netherlands.
    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.
    Tikkanen, M.J.
    Medical Clinic, Helsinki University Hospital, Helsinki, Finland.
    Holme, I.
    Center for Preventive Medicine, Ullevål University Hospital, Oslo, Norway.
    Larsen, M.L.
    Department of Medicine-Cardiology A, Århus University Hospital, Århus, Denmark.
    Bendiksen, F.S.
    Hamar, Lysaker, Norway.
    Lindahl, C.
    Pfizer Sweden, Täby, Sweden.
    Palmer, G.
    Pfizer Inc., New York, New York, USA.
    Design and baseline characteristics of the Incremental Decrease in End Points through Aggressive Lipid Lowering study2004In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 94, no 6, p. 720-724Article in journal (Refereed)
    Abstract [en]

    The Incremental Decrease in End Points through Aggressive Lipid Lowering (IDEAL) study is an investigator-initiated trial designed to determine whether additional clinical benefit might be gained through a strategy that decreases levels of low-density lipoprotein cholesterol levels better than those currently achieved with established statin therapy in patients who have coronary heart disease. IDEAL is a multicenter prospective, randomized, open-label, blinded, end point classification study. Patients who had myocardial infarction were randomized to prescription treatment with 80 mg/day of atorvastatin or 20 mg/day of simvastatin (the dose was increased to 40 mg/day at week 24 in those patients whose plasma total cholesterol remained >5.0 mmol/L, or 190 mg/dl, or whose low-density lipoprotein cholesterol remained >3.0 mmol/L, or 115 mg/dl). The primary clinical outcome variable is the time to initial occurrence of a major coronary event, which is defined as nonfatal acute myocardial infarction, coronary death, or resuscitated cardiac arrest. The study is designed to have a power of 90% to detect a relative decrease of 20% in the atorvastatin-group compared with the simvastatin-group in the number of major events caused by coronary heart disease over ~5.5 years. The 8,888 randomized patients had the following characteristics: mean age 61.7 ± 9.5 years, 19.1% women (mean age 64.0 ± 9.5 years), baseline total cholesterol 5.1 ± 1.0 mmol/L (197 mg/dl), low-density lipoprotein cholesterol 3.2 ± 0.9 mmol/L (124 mg/dl), and high-density lipoprotein cholesterol 1.2 ± 0.3 mmol/L (46 mg/dl). Drug treatment before randomization consisted of statins in 77% of patients, aspirin in 78.9%, ß blockers in 75.1%, and angiotensin-converting enzyme inhibitors in 30%. © 2004 by Excerpta Medica, Inc.

  • 19.
    Pedersen, T.R.
    et al.
    Aker Hospital, University of Oslo, Oslo, Norway.
    Wilhelmsen, L.
    Sahlgrenska Hospital, University of Gothenburg, Gothenburg, Sweden.
    Faergeman, O.
    Færgeman, O., Århus University Hospital, Århus, Denmark.
    Strandberg, T.E.
    Helsinki University Hospital, Helsinki, Finland.
    Thorgeirsson, G.
    Landspitalinn University Hospital, Reykjavik, Iceland.
    Troedsson, L.
    MSD Scandinavia, Stockholm, Sweden.
    Kristianson, J.
    MSD Scandinavia, Stockholm, Sweden.
    Berg, K.
    Ullevål Hospital, University of, Oslo, Norway.
    Cook, T.J.
    Merck Research Laboratories, Rahway, NJ, United States.
    Haghfelt, T.
    Odense University Hospital, Odense, Denmark.
    Kjekshus, J.
    National Hospital, University of Oslo, Oslo, Norway.
    Miettinen, T.
    Helsinki University Hospital, Helsinki, Finland.
    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.
    Pyorala, K.
    Pyörälä, K., Kuopio University Hospital, Kuopio, Finland, Nordic Sch. Pub. H., Gothenburg, Sweden.
    Wedel, H.
    Aker Hospital, University of Oslo, Oslo, Norway.
    Follow-up study of patients randomized in The Scandinavian Simvastatin Survival Study (4S) of cholesterol lowering2000In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 86, no 3, p. 257-262Article in journal (Refereed)
    Abstract [en]

    The Scandinavian Simvastatin Survival Study (4S) and other randomized clinical trials have demonstrated that cholesterol-lowering treatment with statins improves prognosis in patients with coronary atherosclerosis compared with placebo. The effect of therapy with statins beyond the typical 5 to 6 years' duration of the trials, in particular regarding the risk of cancer, has not been investigated. This study examines the long-term effects of simvastatin for up to 8 years on cause-specific mortality in patients with coronary heart disease (CHD). We performed an observational, government registry-based study of mortality in the groups originally randomized to simvastatin or placebo in the 4S over an additional 2-year follow-up period, so that the median total follow-up period was 7.4 years (range 6.9 to 8.3 in surviving patients). Randomization took place at outpatient clinics at 94 clinical centers in Denmark, Finland, Iceland, Norway, and Sweden from 1988 to 1989. Of 4,444 patients with CHD, 2,223 and 2,221 were randomized to treatment with placebo or simvastatin therapy, respectively. Patients received treatment with simvastatin, starting at 20 mg/day, with titration to 40 mg/day at 12 or 24 weeks if total cholesterol was >5.2 mmol/L (200 mg/dl), or placebo. After the double-blind period, most patients in both treatment groups received simvastatin as open-label prescription. Of the 1,967 patients originally treated with placebo and surviving the double-blind period, 97 (4.9%) died during the following 2 years. In the group randomized to simvastatin the corresponding number was 74 of the 2,039 survivors (3.6%). Adding these deaths to those occurring during the original trial, the total was 353 (15.9%) and 256 (11.5%) deaths in the groups originally randomized to placebo and simvastatin, respectively. The relative risk was 0.70 (95% confidence interval 0.60 to 0.82, p = 0.00002). The total number of cancer deaths was 68 (3.1%) in the placebo group and 52 (2.3%) in the simvastatin group (relative risk 0.73, 95% confidence interval 0.51 to 0.05, p = 0.087), and the numbers of noncardiovascular and other deaths were similar in both groups. We therefore conclude that treatment with simvastatin for up to 8 years in patients with CHD is safe and yields continued survival benefit. Copyright (C) 2000 Excerpta Medica Inc.

  • 20.
    Platonov, Pyotr G.
    et al.
    Lund Univ, Sweden.
    Haugaa, Kristina H.
    Oslo Univ Hosp, Norway; Univ Oslo, Norway.
    Bundgaard, Henning
    Univ Copenhagen, Denmark; Univ Copenhagen, Denmark.
    Svensson, Anneli
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Cardiology in Linköping.
    Gilljam, Thomas
    Sahlgrens Univ Hosp, Sweden.
    Hansen, Jim
    Univ Copenhagen, Denmark.
    Madsen, Trine
    Aalborg Univ Hosp, Denmark.
    Host, Anders Gaarsdal
    Univ Copenhagen, Denmark.
    Carlson, Jonas
    Lund Univ, Sweden.
    Lie, Oyvind H.
    Oslo Univ Hosp, Norway; Univ Oslo, Norway.
    Jensen, Morten Kvistholm
    Aarhus Univ Hosp, Denmark.
    Edvardsen, Thor
    Oslo Univ Hosp, Norway; Univ Oslo, Norway.
    Jensen, Henrik K.
    Aarhus Univ Hosp, Denmark; Aarhus Univ, Denmark.
    Svendsen, Jesper H.
    Univ Copenhagen, Denmark.
    Primary Prevention of Sudden Cardiac Death With Implantable Cardioverter-Defibrillator Therapy in Patients With Arrhythmogenic Right Ventricular Cardiomyopathy2019In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 123, no 7, p. 1156-1162Article in journal (Refereed)
    Abstract [en]

    Implantable cardioverter-defibrillator (ICD) therapy remains a corner stone of sudden cardiac death (SCD) prevention in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). We aimed to assess predictors of appropriate ICD therapies in the Scandinavian cohort of ARVC patients who received ICD for primary prevention of SCD. Study group comprised of 79 definite ARVC patients by 2010 Task Force criteria (60% male, age at ICD implant 39 +/- 14 years) who were enrolled in the Nordic ARVC Registry and received an ICD for primary SCD prevention. The primary end point of appropriate ICD shock or death from any cause was assessed and compared with 137 definite ARVC patients who received ICD for secondary SCD prevention (74% male, age at ICD implant 42 +/- 15 years). In the study group, 38% were amp;lt;= 35 years of age at baseline, 25% had non-sustained ventricular tachycardia, and 29% had syncope at baseline. Major repolarization abnormality (hazard ratio = 4.00, 95% confidence interval 1.30 to 12.30, p = 0.015) and age amp;lt;= 35 years (hazard ratio = 4.21, 95% confidence interval 1.49 to 11.85, p = 0.001) independently predicted the primary end point. The outcome did not differ between the primary prevention patients with either of these risk factors and the secondary prevention cohort (2% to 4% annual event rate) whereas patients without risk factors did not have any appropriate ICD shocks during follow-up. In conclusion, young age at ARVC diagnosis and major repolarization abnormality independently predict ICD shocks or death in the primary prevention ICD recipients and associated with the event rate similar to the one observed in the secondary prevention cohort. Our data indicate the benefit of ICD for primary prevention in patients with any of these risk factors. (C) 2019 Elsevier Inc. All rights reserved.

  • 21. Schwartz, Gregory G
    et al.
    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.
    The case for intensive statin therapy after acute coronary syndromes2005In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 96, no 5 SUPPL.Article in journal (Refereed)
    Abstract [en]

    Acute coronary syndromes (ACS) consist of unstable angina or acute myocardial infarction and are associated with a high risk of early recurrent ischemic events. Revascularization procedures do not modify underlying pathophysiology and only modestly reduce early ischemic events after an index episode of ACS. Although statins improve dyslipidemia and cardiovascular risk over the long term, efforts to identify new ACS treatments are focusing on the ability of statins to modify the arterial wall-blood interface and reduce the risk of early recurrent ischemic events. Statins have been shown to reduce circulating markers of inflammation within days of an acute ischemic event. Short-term statin therapy also has been associated with improved coronary endothelial function, reversal of prothrombotic states, and reduction in atherosclerotic plaque volume. Findings from 6 randomized, controlled intervention trials were evaluated to determine if risk reduction is associated with the intensity of statin therapy. In addition, the predictive ability of baseline lipid levels and inflammatory markers were examined. High-intensity statin therapy (atorvastatin 80 mg) reduced early recurrent ischemic events after ACS compared with moderate-intensity treatment (eg, pravastatin 40 mg) or placebo. Moderate-intensity regimens (simvastatin 40 mg, pravastatin 20 to 40 mg, fluvastatin 80 mg, cerivastatin 0.4 mg) provided minimal benefit compared with placebo. Although there was no apparent relation between low-density lipoprotein (LDL) cholesterol levels before or during randomized treatment and short-term (4-month) risk of recurrent events, the degree of LDL cholesterol reduction with statin treatment after ACS may be related to longer-term event reduction. Moreover, evidence suggests that anti-inflammatory effects of high-intensity statin treatment are associated with clinical benefit. © 2005 Elsevier Inc. All rights reserved.

  • 22.
    Sherman, Jonathan A.
    et al.
    Dartmouth Medical School, Lebanon, New Hampshire, USA.
    Hall, Amy
    Dartmouth Medical School, Lebanon, New Hampshire, USA.
    Malenka, David J.
    Dartmouth Medical School, Lebanon, New Hampshire, USA.
    De Muinck, Ebo D.
    Dartmouth Medical School, Lebanon, New Hampshire, USA.
    Simons, Michael
    Dartmouth Medical School, Lebanon, New Hampshire, USA.
    Humoral and cellular factors responsible for coronary collateral formation2006In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 98, no 9, p. 1194-1197Article in journal (Refereed)
    Abstract [en]

    Clinical observations suggest that patients with coronary artery disease (CAD) display a marked heterogenerty in collateral formation despite similar degrees of coronary obstruction. The development of coronary collaterals helps protect the myocardium from ischemic damage, yet the factors responsible for collateral formation are poorly understood. To better understand the biochemical and cellular mechanisms of collateral artery formation, monocyte function and circulating levels of pro- and antiangiogenic factors were measured in 101 patients with angiographically assessed CAD and extensively developed (score 2, n = 33) or absent (score 0, n = 68) collateral circulations. Compared with patients with score 0, those with score 2 were slightly older and had more advanced CAD. The score 2 group, was also more likely to have had a previous myocardial infarction or coronary artery bypass grafting and a family history of CAD. At the same time, there were no significant differences between groups with regard to circulating levels of vascular endothelial growth factor-A(165), platelet-derived growth factor-beta beta, fibroblast growth factor-2, fibroblast growth factor-4, hepatocyte growth factor, tumor necrosis factor-alpha, interleukin-1 beta, endostatin, matrix metalloproteinase-9, promatrix metalloproteinase-1, and CD40 ligand. Monocytes isolated from patients with score 2 and 0 collateral circulations demonstrated no differences in migration assays. However, adhesion to fibrinogen and collagen was significantly higher for monocytes from patients with score 0 (p = 0.05 and 0.04, respectively). In conclusion, these data suggest that the degree of coronary collateral formation is not determined by differences in systemically measurable levels of pro- or antiangiogenic factors assessed in this study. Rather, cellular properties, such as cell adhesion, or genetic differences between patients may be the driving force for collateral development. (c) 2006 Elsevier Inc. All rights reserved.

  • 23.
    Sutherland, George
    et al.
    Department of Cardiology, University Hospital, Gasthuisberg Leuven, Belgium.
    Kukulsi, Tomasz
    Department of Cardiology, University Hospital, Gasthuisberg Leuven, Belgium.
    Escobar Kvitting, John-Peder
    Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    D'hooge, Jan
    Department of Cardiology, University Hospital, Gasthuisberg Leuven, Belgium.
    Arnold, Martina
    Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Brandt, Einar
    Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Hatle, Liv
    Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Wranne, Bengt
    Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Quantitation of left-ventricular asynergy by cardiac ultrasound2000In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 86, no 4, p. 4-9Article in journal (Refereed)
    Abstract [en]

    The clinical evaluation of regional delays in myocardial motion (myocardial asynchrony) has proved problematic, yet it remains an important functional parameter to evaluate. Prior attempts to quantify regional asynergy have met with limited success, often thwarted by the low temporal resolution of imaging-system data acquisition. If a delay in onset of motion of 30–40 msec is clinically important to measure, then data acquisition at frame rates of 50–100 per second is required. This is out of the current temporal resolution of angiographic, nuclear, or magnetic resonance studies. Only cardiac ultrasound can currently achieve the necessary frame rates. Furthermore, quantitative studies into the accuracy with which a trained observer can identify computed regional myocardial asynchrony in a left-ventricular 2-dimensional (2-D) image have shown that regional delays of <80 msec are not normally recognized in a moving image. This may be improved to 60 msec when either training is undertaken or comparative image review is used. However, this is still out of the temporal resolution required in clinical practice. Thus, visual interpretation of asynchrony is not sufficiently accurate. Two ultrasound data sets based on either integrated backscatter or Doppler myocardial imaging data may provide the solution. Doppler myocardial imaging is a new ultrasound technique which, in either its pulsed or color Doppler format, can achieve the required temporal resolution (with temporal resolutions of 8 msec and 16 msec, respectively). In contrast, color Doppler myocardial imaging, in its curved M-mode format, can display the timing of events during the cardiac cycle for all in-plane myocardial segments. This should allow the quantitation of regional delay for all systolic and diastolic events. Potentially, asynchrony due to regional ischemia, bundle branch block, ventricular premature beats, and ventricular preexcitation could all be identified and the degree of delay quantified. This overview will aim to establish the potential role of these new ultrasound methodologies in the recognition and quantitation of left-ventricular asynergy and how they might best be introduced into clinical practice.

  • 24.
    Tromp, Jasper
    et al.
    University of Groningen, Netherlands.
    ter Maaten, Jozine M.
    University of Groningen, Netherlands.
    Damman, Kevin
    University of Groningen, Netherlands.
    OConnor, Christopher M.
    Inova Heart and Vasc Institute, VA USA.
    Metra, Marco
    University of Brescia, Italy.
    Dittrich, Howard C.
    University of Iowa, IA USA.
    Ponikowski, Piot
    Medical University, Poland.
    Teerlink, John R.
    University of Calif San Francisco, CA 94143 USA; San Francisco VA Medical Centre, CA USA.
    Cotter, Gad
    Momentum Research, NC USA.
    Davison, Beth
    Momentum Research, NC USA.
    Cleland, John G. F.
    University of Hull, England.
    Givertz, Michael M.
    Harvard Medical Sch, MA USA.
    Bloomfield, Daniel M.
    Merck and Co Inc, NJ USA.
    van der Wal, Martje H. L.
    Linköping University, Department of Social and Welfare Studies, Division of Nursing Science. Linköping University, Faculty of Medicine and Health Sciences. University of Groningen, Netherlands.
    Jaarsma, Tiny
    Linköping University, Department of Social and Welfare Studies, Division of Nursing Science. Linköping University, Faculty of Medicine and Health Sciences.
    van Veldhuisen, Dirk J.
    University of Groningen, Netherlands.
    Hillege, Hans L.
    University of Groningen, Netherlands.
    Voors, Adriaan A.
    University of Groningen, Netherlands.
    van der Meer, Peter
    University of Groningen, Netherlands.
    Serum Potassium Levels and Outcome in Acute Heart Failure (Data from the PROTECT and COACH Trials)2017In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 119, no 2, p. 290-296Article in journal (Refereed)
    Abstract [en]

    Serum potassium is routinely measured at admission for acute heart failure (AHF), but information on association with clinical variables and prognosis is limited. Potassium measurements at admission were available in 1,867 patients with AHF in the original cohort of 2,033 patients included in the Patients Hospitalized with acute heart failure and Volume Overload to Assess Treatment Effect on Congestion and Renal FuncTion trial. Patients were grouped according to low potassium (amp;lt;3.5 mEq/l), normal potassium (3.5 to 5.0 mEq/l), and high potassium (amp;gt;5.0 mEq/l) levels. Results were verified in a validation cohort of 1,023 patients. Mean age of patients was 71 +/- 11 years, and 66% were men. Low potassium was present in 115 patients (6%), normal potassium in 1,576 (84%), and high potassium in 176 (9%). Potassium levels increased during hospitalization (0.18 +/- 0.69 mEq/l). Patients with high potassium more often used angiotensin-converting enzyme inhibitors and mineralocorticoid receptor antagonists before admission, had impaired baseline renal function and a better diuretic response (p = 0.005), independent of mineralocorticoid receptor antagonist usage. During 180-day follow-up, a total of 330 patients (18%) died. Potassium levels at admission showed a univariate linear association with mortality (hazard ratio [log] 2.36, 95% confidence interval 1.07 to 5.23; p = 0.034) but not after multivariate adjustment. Changes of potassium levels during hospitalization or potassium levels at discharge were not associated with outcome after multivariate analysis. Results in the validation cohort were similar to the index cohort. In conclusion, high potassium levels at admission are associated with an impaired renal function but a better diuretic response. Changes in potassium levels are common, and overall levels increase during hospitalization. In conclusion, potassium levels at admission or its change during hospitalization are not associated with mortality after multivariate adjustment. (C) 2016 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativeconunons.org/licenses/by/4.0/).

  • 25.
    Wranne, Bengt
    et al.
    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.
    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.
    Analysis of different methods of assessing the stenotic mitral valve area with emphasis on the pressure gradient half-time concept.1990In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 66, no 5, p. 614-620Article in journal (Refereed)
    Abstract [en]

    There are 2 different theoretical models that analyze factors influencing the transmitral pressure gradient half-time (T1/2), defined as the time needed for the pressure gradient to reach half its initial value. In this report the models and the assumptions inherent in them were summarized. One model includes left heart chamber compliance, the other does not. Although the models at a superficial glance seem to be contradictory, the conclusions drawn from them are similar: i.e., T1/2 is influenced not only by valve area, but also by initial maximal pressure gradient and by flow. Different clinical situations in which the T1/2 method for valve area estimation has been shown not to work are analyzed in the 2 models. It is concluded that these models have contributed to our understanding of the T1/2 concept and when it should not be used. We also advocate use of the continuity equation in these situations, since no assumptions then need be made.

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