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Original Articles

Lipoprotein-Associated Phospholipase A₂ and Risk of Congestive Heart Failure in Older Adults

The Cardiovascular Health Study

Takeki Suzuki, MD, MPH; Cam Solomon, PhD; Nancy Swords Jenny, PhD; Russell Tracy, PhD; Jeanenne J. Nelson, PhD; Bruce M. Psaty, MD, PhD; Curt Furberg, MD, PhD and Mary Cushman, MD, MSc

From the Department of Medicine (T.S., M.C.), University of Vermont College of Medicine, Burlington, Vt; Department of Biostatistics (C.S.), University of Washington, Seattle, Wash; Department of Pathology (N.S.J., R.T., M.C.), University of Vermont College of Medicine, Burlington, Vt; Department of Epidemiology (J.J.N.), GlaxoSmithKline, Research Triangle Park, NC; Cardiovascular Health Research Unit, Departments of Medicine (B.M.P.), Epidemiology and Health Services, University of Washington and Center for Health Studies, Group Health, Seattle, Wash; and Division of Public Health Sciences (C.F.), Wake Forest University School of Medicine, Winston-Salem, NC.

Correspondence to Mary Cushman, MD, MSc, Department of Medicine, University of Vermont, 208 South Park Dr, Colchester, VT 05446. E-mail mary.cushman{at}uvm.edu

Received December 2, 2008; accepted May 20, 2009.

Background— Inflammation may be a causative factor in congestive heart failure (CHF). Lipoprotein-associated phospholipase A₂ (Lp-PLA₂) is an inflammation marker associated with vascular risk. One previous study showed an association of Lp-PLA₂ activity with CHF risk, but there were only 94 CHF cases and Lp-PLA₂ antigen, which is available clinically in the United States, was not measured.

Methods and Results— We measured baseline Lp-PLA₂ antigen and activity in 3991 men and women without baseline CHF or cardiovascular disease who were participating in the Cardiovascular Health Study, a prospective observational study of adults 65 years or older. Cox proportional hazards models adjusted for age, sex, clinic site, race, low-density and high-density lipoprotein cholesterol, body mass index, systolic and diastolic blood pressure, hypertension, smoking status, pack-years, and diabetes were used to calculate hazard ratios and 95% CIs for incident CHF. Further models adjusted for coronary disease events during follow-up and C-reactive protein. Eight hundred twenty-nine participants developed CHF during 12.1 years. Adjusted hazard ratios for CHF with Lp-PLA₂ in the fourth compared with the first quartile were 1.44 (95% CI, 1.16 to 1.79) for Lp-PLA₂ antigen and 1.06 (95% CI, 0.84 to 1.32) for activity. Adjustment for incident coronary disease attenuated the hazard ratio for Lp-PLA₂ antigen to 1.26 (95% CI, 1.02 to 1.57), adjustment for C-reactive protein had minimal impact.

Conclusions— Lp-PLA₂ antigen was associated with risk of future CHF in older people, independent of CHF and coronary risk factors, and partly mediated by coronary disease events. Further clinical and basic research is needed to better understand the role of Lp-PLA₂ in CHF.

Key Words: epidemiology • heart failure

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