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Visit-to-visit lipid variability, coronary artery calcification, inflammation, and mortality in the Multi-Ethnic
Jeffrey Shi Kai Chan1,2, Danish Iltaf Satti3, Raymond Ngai Chiu Chan1,4
1Cardiovascular Analytics Group, China-UK Collaboration, Hong Kong SAR, China.
Insights
High variability in high-density lipoprotein cholesterol (HDL-C) is linked to increased coronary artery calcification (CAC) and higher risks of cardiovascular and all-cause mortality. This association may extend beyond atherosclerosis.
Area of Science:
- Cardiovascular Medicine
- Lipid Metabolism
- Atherosclerosis Research
Background:
- Visit-to-visit variability in lipid levels, such as high-density lipoprotein cholesterol (HDL-C), is an emerging area of research.
- Understanding the prognostic relevance of lipid variability is crucial for cardiovascular risk assessment.
Purpose of the Study:
- To investigate the association between visit-to-visit lipid variability (HDL-C, LDL-C, TC, triglycerides) and coronary artery calcification (CAC).
- To explore the relationship between lipid variability and long-term risks of cardiovascular mortality, all-cause mortality, and inflammation (hsCRP).
Main Methods:
- Prospective cohort study utilizing data from the Multi-Ethnic Study of Atherosclerosis.
- Calculated visit-to-visit variability (coefficient of variation) for lipids from three initial exams.
- Assessed CAC using computed tomography and tracked mortality outcomes over a median follow-up of 15.1 years.
Main Results:
- Higher HDL-C variability correlated with greater CAC burden (Agatston score).
- Increased HDL-C and TC variability were associated with higher cardiovascular mortality risk, independent of CAC.
- HDL-C variability also predicted higher all-cause mortality risk and correlated with hsCRP levels.
Conclusions:
- Elevated HDL-C variability is a significant predictor of increased CAC and long-term mortality.
- The observed mortality associations suggest mechanisms potentially beyond established atherosclerosis.
- Lipid variability, particularly in HDL-C, warrants consideration in cardiovascular risk stratification.
Aims:
This study aimed to explore relationships between visit-to-visit lipid variability, coronary artery calcification (CAC), inflammation, and long-term mortality, which may be prognostically relevant.
Methods And Results:
This prospective cohort study included participants from the Multi-Ethnic Study of Atherosclerosis with available plasma LDL cholesterol (LDL-C), HDL cholesterol (HDL-C), total cholesterol (TC), and triglycerides from all three initial exams who underwent computed tomography CAC quantification at the third (index) exam. Visit-to-visit variability (coefficient of variation) was calculated from all three initial exams. Outcomes included the index Agatston score, cardiovascular mortality, all-cause mortality, and high-sensitivity C-reactive protein. Altogether, 1515 participants were analysed. Higher HDL-C variability was associated with higher index Agatston score [Quartile 4 (Q4; vs. Q1) adjusted marginal effects 0.25 0.02-0.48)], but not LDL-C, TC, and triglyceride variability. Over a 15.1-year median follow-up, higher HDL-C [Q4 vs. Q1: adjusted sub-hazard ratio 2.68 (1.61-4.48)] and TC [Q4 vs. Q1: adjusted sub-hazard ratio 2.13 (1.17-3.89)] variability, but not LDL-C and triglyceride variability, was associated with higher risk of cardiovascular mortality, which remained significant after adjusting for the index Agatston score. Additionally, higher HDL-C variability was associated with higher risk of all-cause mortality [Q4 vs. Q1: adjusted hazard ratio 1.46 (1.00-2.11)], but LDL-C, TC, and triglyceride variability were not. HDL-C [Q4 vs. Q1: adjusted β: 0.132 (0.034-0.230)] and TC [Q4 vs. Q1: adjusted β: 0.210 (0.064-0.357)] variability, but not LDL-C and triglyceride variability, may be correlated with high-sensitivity C-reactive protein.
Conclusion:
Elevated HDL-C variability was associated with greater CAC burden and long-term risks of cardiovascular and all-cause mortality. These mortality-related associations were probably not completely explainable by atherosclerosis.
Registration:
ClinicalTrials.gov: NCT00005487.
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