"Evolocumab in the Management of Statin-Intolerant Familial Hyperlipoproteinemia with Elevated Lipoprotein(a) Post-TAVI: A Case Report"

Background

Lipoprotein(a) [Lp(a)] is a genetically inherited lipid marker associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD). Unlike LDL-C, Lp(a) is minimally responsive to lifestyle modification or statins. Management becomes especially challenging in patients with statin intolerance and co-existing cardiac conditions. PCSK9 inhibitors offer a therapeutic option by modestly lowering Lp(a) levels in addition to LDL-C. This case highlights the management of a patient with elevated Lp(a), statin intolerance, and a history of transcatheter aortic valve implantation (TAVI).

Case Presentation

A 65-year-old female with a history of chronic coronary syndrome and severe aortic valve stenosis underwent successful TAVI with a Sapien 3 bioprosthetic valve in November 2022. She was diagnosed with familial hyperlipoproteinemia and significantly elevated Lp(a) levels (801 mmol/L), alongside intolerance to high-dose statins. Due to her high cardiovascular risk, she was enrolled in the RDTL drug reimbursement program and initiated on evolocumab (a PCSK9 inhibitor) at 140 mg every 14 days.

At follow-up in December 2024, clinical assessment revealed stable cardiovascular status. Echocardiography showed preserved left ventricular ejection fraction (EF 60%) with good function of the implanted aortic valve. Blood pressure was 120/70 mmHg, ECG demonstrated sinus rhythm, and her Lp(a) level had decreased to 585 mmol/L, indicating a partial but significant response to therapy. Her medications included perindopril, metoprolol, rosuvastatin/ezetimibe (5/10 mg), metformin, clopidogrel, and evolocumab.

Conclusion

This case illustrates the long-term benefit of PCSK9 inhibitor therapy in a statin-intolerant patient with elevated Lp(a) and post-TAVI status. Partial biochemical response and clinical stability highlight the role of targeted lipid-lowering therapy and structured follow-up in managing genetically driven dyslipidemia in high-risk cardiac patients.