FRI102 A Case Of Subclavian Artery Stenosis: Utility Of Lipoprotein (a) In Secondary Prevention Of Atherosclerotic Vascular Disease

Disclosure: F. Iqbal: None. R.A. Haas: None. Introduction: Atherosclerosis is the most common cause of upper extremity peripheral arterial disease (PAD). Prevalence of subclavian artery stenosis in the general population is approximately 2% with one study reporting a prevalence of 6.8% in those with diabetes mellitus (DM). We present a case of symptomatic upper extremity PAD in a patient with well controlled Type 1 DM and LDL-cholesterol at goal, but significantly elevated Lp(a). Clinical Case: 57-year-old Caucasian female with Type 1 DM (on CSII), hypothyroidism, obesity (BMI:43), hypertension and hyperlipidemia presented with several month history of left arm pain and cramping worsened by activity. At presentation, HbA1c was 6.1% and TSH 1.036 uIU/mL. She had been on atorvastatin, 40 mg once daily for several years with the addition of ezetimibe two years prior following an elevated coronary calcium score of 63. She underwent a left upper arm arterial duplex which showed 50-99% left subclavian and left axillary artery stenosis along with bilateral ICA stenosis. Lipid profile showed Total-C 112 mg/dL, LDL-C 59 mg/dL and HDL-C 34 mg/dL. She denied any symptoms of TIA or CVA. Vascular surgery recommended medical management with aspirin and risk factor modification. Cardiology advised CT chest-angiogram which showed moderate left subclavian stenosis and mild wall thickening of the great vessels and descending thoracic aorta. Work-up for arteritis was negative. A stress Echocardiogram showed inducible apical wall ischemia however no significant coronary artery disease was seen on angiogram. Her atorvastatin dose was increased to 80 mg once daily but as her diffuse atherosclerosis was out of proportion to her risk factors an Lp(a) level was checked and came back elevated at 356 nmol/L (desirable <75). She was continued on statin therapy, ezetimibe discontinued and Evolocumab (PCSK-9 inhibitor) was commenced. At follow-up (after 6 months of evolucamab treatment), she reported improvement in symptoms and repeat lipid profile was notable for Total-C 90, LDL-C 33, HDL38 and a 41% reduction in Lp(a) to 209. Conclusion: Lipoprotein (a) is an atherogenic, pro-inflammatory LDL-cholesterol like particle, the concentration of which is largely genetically determined. While the association between elevated Lp(a) and coronary artery disease has been well studied, there are few studies describing its relevance in peripheral artery disease. In our patient with symptomatic subclavian stenosis, the high Lp(a) served as marker of her diffuse atherosclerosis and elevated ASCVD risk. Although targeted Lp(a) lowering therapies are currently under investigation with promising initial results, currently the focus of management remains LDL-cholesterol lowering. PCSK9 inhibitors lower Lp(a) by 25%-40% and are a valuable treatment option. Presentation: Friday, June 16, 2023