Key result
Elevated Lp(a) is linked to ~10-fold higher aortic stenosis risk in heterozygous familial hypercholesterolemia.
Why the study?
Factors influencing the development of aortic stenosis in patients with heterozygous familial hypercholesterolemia needed to be analyzed.
Observational (n=114)
Effect estimate: OR 10.5 (95% CI 5.0-21.9)
p-value: p=0.0017
In patients with heterozygous familial hypercholesterolemia, the development of aortic stenosis is strongly associated with cumulative lipid burden, Lp(a) levels, and tendon xanthomas.
May warrant AS monitoring in HeFH with high Lp(a) or xanthomas; leaves open causal effects and intervention benefits.
Aim . To analyze factors influencing the development of aortic stenosis (AS) in patients with heterozygous familial hypercholesterolemia (heFH). Material and methods . A total of 114 patients with heFH were examined (mean age 54,3±2,7 years, 85 men (69,1%)), of whom 10 (8,8%) had AS. FH was diagnosed according to the Dutch Lipid Clinic Network criteria. Lipid profile parameters, lipoprotein(a) (Lp(a)) level, age, family history of cardiovascular disease, smoking, hypertension (AH), hyperglycemia were analyzed. The history of coronary artery disease (CAD), myocardial infarction (MI), and ischemic stroke was taken into account. Cumulative levels of low-density lipoprotein (LDL) and non-HDL cholesterol were calculated as the total LDL-C over the patient's life, taking into account the levels achieved during lipid-lowering therapy. Results . AS development was influenced by age (odds ratio (OR) 1,1 [1,02; 1,15], p=0,009), HTN (OR 8,15 [1,50; 44,08], p=0,017), lipid profile parameters: total cholesterol (OR 2,09 [1,38; 3,10], p=0,0006; LDL-C (OR 2,8 [1,59; 4,79], p=0,0004), non-HDL-C (OR 1,012 [1,005; 1,019], p=0,003), triglycerides (OR 1,97 [1,33; 2,87], p=0,0007). Cumulative indicators also influenced the risk of AS: cumulative LDL accumulated over the years of life (OR 2,13 [1,31; 3,54], p=0,003), cumulative non-HDL-C level accumulated over life (OR 1,56 [1,01; 2,18], p=0,013), Lp(a) level (AS risk increases by 10,6 times with an increase in Lp(a) by 1 unit of measurement (1 g/l) (OR 10,5 [5,0; 21,9], p=0,0017). The presence of CAD and MI in FH increases the risk of AS (for CAD, OR 8,62 [1,07; 69,113], p=0,044; for MI, OR 3,93 [1,08; 14,36], p=0,034). The combination of MI and cerebrovascular accident increases the risk of AS by 4,94 (OR 4,94 [1,23; 19,62], p=0,021). Tendon xanthomas significantly affects the AS (OR 50,2 [6,03; 413,00], p<0,001). Conclusion . AS detected at a young age can be a manifestation of FH. The development of AS in FH is influenced by age and HTN, and following lipid factors: total cholesterol, LDL, triglycerides, as well as Lp(a) levels and cumulative indicators.
No takes yet. Share an insight, caveat, or question.
Kuznetsova et al. (2024) conducted an observational in heterozygous familial hypercholesterolemia (heFH) (n=114). Risk factors (including Lp(a), LDL-C, and tendon xanthomas) was evaluated on Development of aortic stenosis (AS) (OR 10.5, 95% CI 5.0-21.9, p=0.0017). Elevated Lp(a) (OR 10.5; 95% CI 5.0-21.9) and tendon xanthomas (OR 50.2) significantly increased the risk of aortic stenosis in patients with heterozygous familial hypercholesterolemia.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: