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Relations of lipid concentrations to heart failure incidence: the Framingham Heart Study
Raghava S Velagaleti1, Joseph Massaro, Ramachandran S Vasan
1Framingham Heart Study, Center for Population Studies, National Heart, Lung, and Blood Institute, 73 Mt Wayte Avenue, Framingham, MA 01702, USA.
Insights
High non-high-density lipoprotein cholesterol (HDL-C) and low HDL-C increase heart failure (HF) risk independently of myocardial infarction. Lipid modification may reduce HF incidence.
Area of Science:
- Cardiology
- Preventive Medicine
- Lipid Metabolism
Background:
- The relationship between lipid levels and heart failure (HF) risk requires comprehensive elucidation.
- Understanding these associations is crucial for developing effective prevention strategies.
Purpose of the Study:
- To investigate the independent associations of high-density lipoprotein cholesterol (HDL-C) and non-high-density lipoprotein cholesterol (non-HDL-C) with heart failure (HF) incidence.
- To evaluate the population-attributable risk of dyslipidemia for HF.
Main Methods:
- Analysis of 6860 participants from the Framingham Heart Study, free of coronary heart disease at baseline.
- Long-term follow-up to assess HF incidence, with lipid concentrations updated periodically.
- Multivariable regression models were used to adjust for clinical covariates and myocardial infarction.
Main Results:
- Higher non-HDL-C and lower HDL-C levels were significantly associated with increased HF risk, independent of myocardial infarction.
- A 1-SD increase in non-HDL-C raised HF hazard by 19-23%, while a 1-SD decrease in HDL-C raised HF hazard by 18-23%.
- High non-HDL-C and low HDL-C accounted for 7.5% and 15% of HF cases in the population, respectively.
Conclusions:
- Dyslipidemia contributes to HF risk independently of myocardial infarction.
- Targeting lipid modification could be a viable strategy for reducing heart failure incidence.
Background:
The relations of lipid concentrations to heart failure (HF) risk have not been elucidated comprehensively.
Methods And Results:
In 6860 Framingham Heart Study participants (mean age, 44 years; 54% women) free of baseline coronary heart disease, we related high-density lipoprotein cholesterol (HDL-C) and non-HDL-C to HF incidence during long-term follow-up, adjusting for clinical covariates and myocardial infarction at baseline and updating these at follow-up examinations. We evaluated dyslipidemia-specific population burden of HF by calculating population attributable risks. During follow-up (mean of 26 years), 680 participants (49% women) developed HF. Unadjusted HF incidence in the low (<160 mg/dL) versus high (> or =190 mg/dL) non-HDL-C groups was 7.9% and 13.8%, respectively, whereas incidence in the high (> or =55 [men], > or =65 [women] mg/dL) versus low (<40 [men], <50 [women] mg/dL) HDL-C groups was 6.1% and 12.8%, respectively. In multivariable models, baseline non-HDL-C and HDL-C, modeled as continuous measures, carried HF hazards (confidence intervals) of 1.19 (1.11 to 1.27) and 0.82 (0.75 to 0.90), respectively, per SD increment. In models updating lipid concentrations every 8 years, the corresponding hazards (confidence intervals) were 1.23 (1.16 to 1.31) and 0.77 (0.70 to 0.85). Participants with high baseline non-HDL-C and those with low HDL-C experienced a 29% and 40% higher HF risk, respectively, compared with those in the desirable categories; the population attributable risks for high non-HDL-C and low HDL-C were 7.5% and 15%, respectively. Hazards associated with non-HDL-C and HDL-C remained statistically significant after additional adjustment for interim myocardial infarction.
Conclusions:
Dyslipidemia carries HF risk independent of its association with myocardial infarction, suggesting that lipid modification may be a means for reducing HF risk.
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