Anandita Agarwala1, Yashashwi Pokharel2, Anum Saeed3, Wensheng Sun3, Salim S Virani4, Vijay Nambi4, Chiadi Ndumele5, Eyal Shahar6, Gerardo Heiss7, Eric Boerwinkle8, Suma Konety9, Ron C Hoogeveen3, Christie M Ballantyne10. 1. Department of Medicine, Baylor College of Medicine, Houston, TX, USA. 2. Mid-America Heart Institute, University of Missouri-Kansas City, Kansas City, MO, USA. 3. Center for Cardiovascular Disease Prevention, Houston Methodist DeBakey Heart and Vascular Center, Houston, TX, USA; Section of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, TX, USA. 4. Center for Cardiovascular Disease Prevention, Houston Methodist DeBakey Heart and Vascular Center, Houston, TX, USA; Section of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, TX, USA; Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, USA. 5. Johns Hopkins University School of Medicine, Baltimore, MD, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. 6. Department of Epidemiology and Biostatistics, Mel and Enid Zuckerman College of Public Health, University of Arizona, Tucson, AZ, USA. 7. Gillings School of Global Public Health, The University of North Carolina, Chapel Hill, NC, USA. 8. The University of Texas Health Science Center at Houston, Houston, TX, USA; Human Genome Sequencing Center, Baylor College of Medicine, Houston, TX, USA. 9. Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, MN, USA. 10. Center for Cardiovascular Disease Prevention, Houston Methodist DeBakey Heart and Vascular Center, Houston, TX, USA; Section of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, TX, USA. Electronic address: cmb@bcm.edu.
Abstract
BACKGROUND AND AIMS: Lipoprotein(a) [Lp(a)] is a proatherogenic lipoprotein associated with coronary heart disease, ischemic stroke, and more recently aortic stenosis and heart failure (HF). We examined the association of Lp(a) levels with incident HF hospitalization in the Atherosclerosis Risk in Communities (ARIC) study. We also assessed the relationship between Lp(a) levels and arterial stiffness as a potential mechanism for development of HF. METHODS: Lp(a) was measured in 14,154 ARIC participants without prevalent HF at ARIC visit 1 (1987-1989). The association of Lp(a) quintiles with incident HF hospitalization was assessed using Cox proportional-hazards models. Arterial stiffness parameters were stratified based on Lp(a) quintiles, and p-trend was calculated across ordered groups. RESULTS: At a median follow-up of 23.4 years, there were 2605 incident HF hospitalizations. Lp(a) levels were directly associated with incident HF hospitalization in models adjusted for age, race, gender, systolic blood pressure, history of hypertension, diabetes, smoking status, body mass index, heart rate, and high-density lipoprotein cholesterol (quintile 5 vs. quintile 1: hazard ratio [HR] 1.24, 95% confidence interval [CI] 1.09-1.41; p-trend across increasing quintiles <0.01), but not after excluding prevalent and incident myocardial infarction cases (HR 1.07, 95% CI 0.91-1.27; p-trend = 0.70). When adjusted for age, gender, and race, Lp(a) quintiles were not significantly associated with arterial stiffness parameters. CONCLUSIONS: Increased Lp(a) levels were associated with increased risk of incident HF hospitalization. After excluding prevalent and incident myocardial infarction, the association was no longer significant. Lp(a) levels were not associated with arterial stiffness parameters.
BACKGROUND AND AIMS: Lipoprotein(a) [Lp(a)] is a proatherogenic lipoprotein associated with coronary heart disease, ischemic stroke, and more recently aortic stenosis and heart failure (HF). We examined the association of Lp(a) levels with incident HF hospitalization in the Atherosclerosis Risk in Communities (ARIC) study. We also assessed the relationship between Lp(a) levels and arterial stiffness as a potential mechanism for development of HF. METHODS:Lp(a) was measured in 14,154 ARIC participants without prevalent HF at ARIC visit 1 (1987-1989). The association of Lp(a) quintiles with incident HF hospitalization was assessed using Cox proportional-hazards models. Arterial stiffness parameters were stratified based on Lp(a) quintiles, and p-trend was calculated across ordered groups. RESULTS: At a median follow-up of 23.4 years, there were 2605 incident HF hospitalizations. Lp(a) levels were directly associated with incident HF hospitalization in models adjusted for age, race, gender, systolic blood pressure, history of hypertension, diabetes, smoking status, body mass index, heart rate, and high-density lipoprotein cholesterol (quintile 5 vs. quintile 1: hazard ratio [HR] 1.24, 95% confidence interval [CI] 1.09-1.41; p-trend across increasing quintiles <0.01), but not after excluding prevalent and incident myocardial infarction cases (HR 1.07, 95% CI 0.91-1.27; p-trend = 0.70). When adjusted for age, gender, and race, Lp(a) quintiles were not significantly associated with arterial stiffness parameters. CONCLUSIONS: Increased Lp(a) levels were associated with increased risk of incident HF hospitalization. After excluding prevalent and incident myocardial infarction, the association was no longer significant. Lp(a) levels were not associated with arterial stiffness parameters.
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