High Non-HDL-C Levels in Adolescents tied to CAC in Mid-adulthood

Written By :  MD Bureau
Medically Reviewed By :  Dr. Kamal Kant Kohli
Published On 2021-02-17 01:15 GMT   |   Update On 2021-02-17 06:55 GMT

Biological processes underlying the causes of heart disease begin years before the emergence of clinical symptoms. In a recent study published in the JAMA Cardiology on January 27, 2021, researchers have reported that the elevated Non–high-density lipoprotein cholesterol (non-HDL-C) levels at all stages of life are associated with Coronary Atherosclerosis in mid-adulthood. They further...

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Biological processes underlying the causes of heart disease begin years before the emergence of clinical symptoms. In a recent study published in the JAMA Cardiology on January 27, 2021, researchers have reported that the elevated Non–high-density lipoprotein cholesterol (non-HDL-C) levels at all stages of life are associated with Coronary Atherosclerosis in mid-adulthood. They further reported that the elevated non-HDL-C levels in adolescents may indicate the presence of Coronary Artery Calcification (CAC) in mid-adulthood. They recommend greater awareness of the importance of elevated non–HDL-C among adolescence.

Low-density lipoprotein cholesterol (LDL-C) is an important risk factor for heart disease and is the primary target in the management of adult dyslipidemia. The non–HDL-C encompasses a greater number of atherogenic lipids and lipoproteins. It might provide a better marker of heart disease risk attributable to dyslipidemia. Elevated non–HDL-C is associated with the presence of coronary artery calcification (CAC), a marker of heart disease in adulthood. Yet, the relative importance of non–HDL-C levels at different life stages for predicting atherosclerotic disease in later life remains unclear. Therefore, Dr Matthew K. Armstrong and colleagues conducted a study, to identify the relative association of non-HDL-C measured at distinct life stages (adolescence, young adulthood, mid-adulthood) with the presence of CAC measured in mid-adulthood.

The Cardiovascular Risk in Young Finns Study was a multicenter, population-based cohort study that began in 1980 with subsequent follow-up in 1983, 1986, 1989, 1992, 2001, and 2007. Researchers analyzed the data of 589 participants from this 28 years study by February 2020. They noted the non-HDL-C levels at 3 life stages including adolescence (aged 12-18 years), young adulthood (aged 21-30 years), and mid-adulthood (aged 33-45 years). In 2008, CAC was determined using computed tomography. Researchers categorized the CAC as 0 (no CAC, Agatston score = 0) or 1 (presence of CAC, Agatston score ≥1) for the purpose of analysis. They used Bayesian relevant life course exposure model to determine the relative association between non–HDL-C at each life stage and the presence of CAC in mid-adulthood.

Key findings of the study were:

• Researchers adjusted the model for year of birth, sex, body mass index, systolic blood pressure, blood glucose level, smoking status, lipid-lowering and antihypertensive medication use, and family history of heart disease.

• They noted that the cumulative exposure to non–HDL-C across all life stages was associated with CAC (odds ratio [OR], 1.50).

• They found that the ORs of CAC presence due to elevated non–HDL-C exposure during young adulthood and mid-adulthood were 1.14 and 1.12, respectively.

• However, they noted that exposure to non–HDL-C during adolescence had the strongest association—with an OR of 1.16 (95%, 1.01-1.46).

The authors concluded, "These data suggest that elevated non–HDL-C levels at all life stages are associated with coronary atherosclerosis in mid-adulthood. However, adolescent non–HDL-C levels showed the strongest association with the presence of CAC in mid-adulthood".

They further added, "Altogether, early screening, identification, and management of elevated non–HDL-C levels may represent an important goal toward reducing the burden of heart disease in adulthood".

For further information:

https://jamanetwork.com/journals/jamacardiology/fullarticle/2775672


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Article Source :  JAMA Cardiology

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