Article Text
Abstract
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.
Footnotes
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.
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