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Premature Coronary Artery Disease in a Young Female Patient With High Lipoprotein(a)
Yahya Bawahab1, Vlad C Vasile2
1Department of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Insights
High lipoprotein(a) [Lp(a)] drives premature coronary artery disease (CAD) progression, even with optimal cholesterol control. Early Lp(a) testing is crucial for young patients with unexplained or familial CAD.
Area of Science:
- Cardiology
- Genetics
- Lipidology
Background:
- Premature coronary artery disease (CAD) presents diagnostic challenges, especially in individuals with few traditional risk factors.
- High lipoprotein(a) [Lp(a)] is a significant, genetically determined risk factor for atherosclerotic cardiovascular disease, contributing to early and advanced CAD.
Background:
Premature coronary artery disease (CAD) poses diagnostic challenges, particularly in patients with minimal traditional risk factors. High lipoprotein(a) [Lp(a)] is an independent, genetically determined risk factor for atherosclerotic cardiovascular disease, and it contributes to early and progressive CAD.
Case Summary:
We report the case of a 35-year-old African American woman with recurrent chest pain who was diagnosed with severe multivessel CAD despite minimal traditional cardiovascular risk factors. Further evaluation revealed markedly high Lp(a) levels. She underwent successful percutaneous coronary intervention and achieved optimal low-density lipoprotein cholesterol (LDL-C) control with high-intensity statin therapy and a PCSK9 inhibitor. Despite aggressive lipid-lowering therapy, she developed recurrent angina within 6 months, and repeat coronary angiography demonstrated disease progression.
Discussion:
This case highlights the role of high Lp(a) in driving premature and progressive CAD independent of LDL-C levels. Early identification of high Lp(a) may improve risk stratification and inform management strategies.
Take-Home Message:
High Lp(a) may contribute to premature and progressive CAD even with optimal LDL-C control, supporting consideration of Lp(a) testing in young patients with unexplained or familial CAD.
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