Abstract 17807: Rapid Progression of CAD After Stopping Statin and Starting a Ketogenic Diet in a Phenotypic Lean Mass Hyper-Responder

Abstract

Introduction: Ketogenic diet (KD) has been a popular diet method for weight loss and described as an alternative to pharmacotherapy on social media. KD is thought to improve some risk factors of ASCVD, such as type 2 DM, obesity, and decrease LDL. Recent studies have described lean mass hyper-responders (LMHR), a specific phenotype with lower BMI, total cholesterol >200 mg/dL, HDL >80, and TG <70. LMHR is thought to be protective against ASCVD. While on carbohydrate restricted diet, LMHR may have significant rise in LDL. We present a patient with known CAD and similar phenotype to LMHR that developed rapid progression of CAD after stopping statin and initiating strict KD. Hypothesis: KD may accelerate disease in those with known CAD, despite being LMHR phenotype. Methods: 51-year-old male with BMI 23, CAD with previous PCI to proximal LAD, HTN, HLD, family history of early CAD, presented with inferior STEMI. He underwent emergent catheterization revealing 95% stenosis of the mid RCA and 99% occlusion of the distal RCA treated with two drug eluting stents. Previous catheterization showed only moderate disease of the distal RCA. He had discontinued atorvastatin about 2 years after his first coronary intervention due to myalgias. Prior to starting it, his total cholesterol was 207, LDL 131, HDL 43, and TG 67 with a normal BMI- similar traits to LMHR phenotype. Atorvastatin 80 mg was started, and his LDL decreased to 44. After he discontinued the statin, he started a KD to try to manage his cholesterol and CAD. Results: When he presented with STEMI, his total cholesterol was 388, LDL 301, HDL 73, TG 71, and Lp(a) 155 nmol/L. He resumed atorvastatin 80 mg and started alirocumab at discharge with subsequent LDL of 14. Conclusions: Social media has influenced many to try ketogenic diet to manage metabolic health. Some influencers have questioned high-LDL association with ASCVD and have recommended avoiding pharmacotherapy. Despite popular opinion that high-LDL in this phenotype does not have clinical implication, our patient with a similar profile had rapid progression of CAD while on a KD and was untreated for HLD. Patients with known CAD and LMHR should be very cautious when starting popular diets and should discuss the possible implications with their provider.