Healthy Lifestyle

What Lp(a) level is equivalent to cardiovascular risk in familial hypercholesterolemia? JACC Danish research gives you answers

The 2019 ESC/EAS guidelines for the management of dyslipidemia suggest that every adult should consider at least one Lipoprotein(a) [Lp(a)] measurement to identify patients with very high genetic Lp(a) levels (>180 mg/dL [>430 nmol/L]) who may have higher atherosclerosis Lifetime risk of atherosclerotic cardiovascular disease (ASCVD) comparable to heterozygous familial hypercholesterolemia (HeFH). Elevated plasma Lp(a) and familial hypercholesterolemia (FH) can both lead to an increased risk of early ASCVD, but at what level does Lp(a) increase to a similar cardiovascular risk to FH remains unclear.

Recently, Journal of the American College of Cardiology published a Results showed that for MI risk, plasma Lp(a) 67-402 mg/dL was comparable to clinical FH, and Lp(a) 180 mg/dL was comparable to genetic FH; for ASCVD risk, Lp(a) 130-391 mg /dL is comparable to clinical FH, and Lp(a) 175 mg/dL is comparable to genetic FH.

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Introduction to Research

In the study, blood lipid levels were measured using blood samples collected in the non-fasted state; indicators were defined using multiple indicators Blood lipid levels of MI and ASCVD risk, including American MEDPED criteria, Simon Broome criteria and Dutch Lipid Clinic Network (DLCN) criteria.

The researchers used data from the Copenhagen General Population Study, including a total of 69,644 patients, who performed Lp(a) Detection and clinical or genetic diagnosis of FH. We also determined the combined effect of elevated Lp(a) levels, clinical and genetic HeFH, or a family history of premature MI on MI and ASCVD risk. During 42 years of follow-up, a total of 4166 patients developed MI and 11464 patients developed ASCVD.

The study found that for MI risk, the plasma Lp(a) level was 67-402 mg/dL large difference) comparable to clinical FH, Lp(a) 180 mg/dL comparable to genetic FH; for ASCVD risk, Lp(a) levels 130-391 mg/dL comparable to clinical FH, Lp(a) 175 mg/dL dL is comparable to hereditary FH. Compared with patients with only one genetic risk factor, patients with elevated Lp(a) and FH or a family history of early-onset MI had a higher risk of MI and ASCVD, with the highest HR for MI being 14.0 (95% CI, 9.15-21.3), the highest HR for ASCVD was 5.05 (95%CI, 3.41-7.48).

An additional study also found that the risk of MI and ASCVD was highest in individuals with elevated FH and Lp(a) , emphasizing the importance of detecting Lp(a) in FH patients and evaluating elevated Lp(a) in FH patients.

< strong data-brushtype="text">Expert Discussion

Pamela B. Morris, MD, Chief of Preventive Cardiology and Co-Director of Women’s Cardiac Care at the Medical University of South Carolina, discusses the use of Lp(a) and periodic lipid testing to assess cardiovascular risk , regardless of the clinical diagnosis, the most reliable test for FH is probably the actual LDL-C level. In understanding the relative risk of FH and Lp(a), a more reliable analysis may be to compare risks by similar changes in LDL-C and Lp(a).

Substantial and strong evidence suggests that inherited lipid metabolism disorders, elevated Lp(a) levels, and FH are There is a causal relationship between the increased risk of developing ASCVD. In addition to regular lipid assessments according to evidence-based guidelines, for ASCVD risk assessment, everyone should have Lp(a) levels measured at least once in their lifetime. Continuing to increase clinician and patient awareness of these high-risk inherited lipid disorders is critical. Our understanding of these two diseases is advancing, and promising new therapies may in the future offer hope for the prevention of CVD in patients with elevated Lp(a) levels。

Performance Features:

1 In FH, Lp(a) levels comparable to LDL in risk for premature poor outcomes. Healio. November 14, 2022.

2 Pamela B. Morris, Jagat Narula, Sotirios Linguists. Lipoprotein(a) and LDL-C: The Relevance of Equivalence. J Am Coll Cardiol. 2022 Nov, 80(21) 2011-2013