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Plasma viscosity, immunoglobulins and risk of cardiovascular disease and mortality: new data and meta-analyses
  1. Gordon D O Lowe1,
  2. Katie Harris2,
  3. Wolfgang Koenig3,4,
  4. Yoav Ben-Shlomo5,
  5. Barbara Thorand6,7,
  6. Annette Peters6,7,
  7. Christa Meisinger8,9,
  8. Armin Imhof10,
  9. Hugh Tunstall-Pedoe11,
  10. Sanne A E Peters2,12,13,
  11. Mark Woodward2,13
  1. 1 Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK
  2. 2 The George Institute for Global Health, University of New South Wales, Sydney, New South Wales, Australia
  3. 3 German Heart Center Munich, Technical University of Munich, Munchen, Germany
  4. 4 Partner Site Munich Heart Alliance, DZHK (German Centre for Cardiovascular Research), Munich, Germany
  5. 5 Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
  6. 6 Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany
  7. 7 Partner Munich-Neuherberg, German Center for Diabetes Research (DZD), Neuherberg, Germany
  8. 8 Chair of Epidemiology, University Hospital Augsburg, Augsburg, Germany
  9. 9 Independent Research Group Clinical Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany
  10. 10 Department of Internal Medicine II - Cardiology, University of Ulm Medical Centre, Ulm, Germany
  11. 11 Cardiovascular Epidemiology Unit, Institute of Cardiovascular Research, University of Dundee, Dundee, UK
  12. 12 Julius Centre for Health Sciences and Primary Care, University Medical Centre Utrecht, Utrecht, Netherlands
  13. 13 The George Institute for Global Health, Imperial College London, London, UK
  1. Correspondence to Dr Katie Harris, The George Institute for Global Health, University of New South Wales, Sydney, New South Wales, Australia; kharris{at}


Aims Associations of plasma viscosity and plasma Ig levels (a determinant of viscosity) with incident coronary heart disease (CHD) events; and with CHD, cardiovascular disease (CVD: CHD and stroke) and all-cause mortalities.

Methods Meta-analysis of plasma viscosity levels from the MONitoring of trends and determinants of CArdiovascular (MONICA)/Cooperative Health Research in the Region of Augsburg, MONICA Glasgow and Speedwell Studies; and five other published studies. Meta-analysis of IgA, IgG and IgM levels from the Augsburg, Glasgow and Speedwell studies; and one other published study.

Results Over median follow-up periods of 14–26 years, there were 2270 CHD events, and 4220 all cause deaths in 28 605 participants with baseline plasma viscosity measurements. After adjustment for major risk factors, (HRs; 95% CIs) for a 1 SD increase in viscosity were 1.14 (1.09 to 1.20) for CHD events; and 1.21 (1.17 to 1.25) for all-cause mortality. 821 CHD events and 2085 all-cause deaths occurred in 8218 participants with baseline Ig levels. For CHD events, adjusted HRs for 1 SD increases in IgA, IgG and IgM were, respectively, 0.97 (0.89 to 1.05); 0.95(0.76 to 1.17) and 0.90 (0.79 to 1.03). Corresponding adjusted HRs for all-cause mortality were 1.08 (95% CI 1.02 to 1.13), 1.03 (95% CI 0.94 to 1.14) and 1.01 (95% CI 0.96 to 1.06).

Conclusions After risk factor adjustment, plasma viscosity was significantly associated with risks of CHD events; and with CHD, CVD and all-cause mortalities. We found no significant association of IgA, IgG or IgM levels with incident CHD events or mortality, except for a borderline association of IgA with all-cause mortality.

  • Immunoglobulins
  • Blood Viscosity
  • Cardiovascular Diseases

Data availability statement

Data may be obtained from a third party and are not publicly available.

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Data availability statement

Data may be obtained from a third party and are not publicly available.

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  • Handling editor Tahir S Pillay.

  • Contributors GDOL conceived the study and wrote the first draft. MW designed the analysis plan and supervised the statistical analyses carried out by SAEP and KH. GDOL and WK directed the laboratories collecting the data. HT-P initiated and directed SHHEC and Glasgow MONICA. YB-S led the follow-up of the Speedwell cohort and acts as the data custodian. BT, AP and CM collected follow-up data for the MONICA/KORA Augsburg study. All authors contributed comments for redrafting the manuscript. GDOL is the guarantor of this work.

  • Funding The MONICA/KORA study was initiated and financed by the Helmholtz Zentrum München-German Research Centre for Environmental Health, which is funded by the German Federal Ministry of Education and Research (BMBF) and by the State of Bavaria. The MONICA Glasgow and SHHEC studies were funded by the Scottish Health Department Chief Scientist Office; British Heart Foundation; and the FP Fleming Trust. Measurements of immunoglobulins in MONICA/KORA Augsburg and MONICA Glasgow have been made possible through intramural funds from the University of Ulm.

  • Competing interests MW is a consultant to Amgen and Kirin. No other author declares conflicting interests.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.