Approach to Risk Assessment and Management of ASCVD

A 38-year-old white man is referred to the lipid clinic for optimization of his cardiovascular (CV) health. He has history of obesity and hypertension (HTN). He has no known history of CV disease. His family history is significant for premature coronary artery disease (CAD) in multiple family members: his father had a myocardial infarction (MI) at 47 years of age, his paternal grandfather had an MI and revascularization with coronary artery bypass grafting at 50 years of age, and his uncle had an MI in his 40s. Most recently, his older brother had an MI at 45 years of age. In this setting, he was diagnosed with heterozygous familial hypercholesterolemia (HeFH) approximately 6 months earlier. His current medications include lisinopril 10 mg daily and atorvastatin 40 mg daily.

His lipid profile at the time of his HeFH diagnosis was significant for elevated cholesterol levels, with low-density lipoprotein (LDL) level 220 mg/dL. He also underwent noncontrast cardiac computed tomography, which revealed coronary artery calcium (CAC) score 88 (>99th percentile for age and sex).

His physical examination findings are notable for body mass index (BMI) 34 kg/m2 but are otherwise unremarkable, without tendon xanthomas or arcus cornealis. His blood pressure is 120/80 mm Hg.

A recent fasting lipid panel on his current therapy showed total cholesterol level 242 mg/dL, triglyceride level 100 mg/dL, high-density lipoprotein cholesterol (HDL-C) level 42 mg/dL, and low-density lipoprotein cholesterol (LDL-C) level 170 mg/dL. His creatinine, liver enzyme, lipoprotein(a) (Lp[a]), thyroid-stimulating hormone, and vitamin D levels are within the reference ranges. Genetic testing confirms a mutation in the LDL receptor.

He is working on a regular exercise regimen with 50 min of moderate aerobic exercise daily, and has been referred to a weight-loss counselor. He has good exercise capacity at baseline and denies any chest pain, shortness of breath, palpitations, leg swelling, dizziness, or syncope. He notes that he was alerted about elevated LDL-C (or "bad cholesterol") levels in the 250s mg/dL range 10 years earlier, but at that time had decided to focus on modifying his diet and exercise pattern rather than starting medications. He was lost to follow-up until 6 months earlier; after his brother's heart attack, he re-engaged with medical care and started atorvastatin. He would like to keep his risk of future adverse CV events as low as possible.

What are the next steps to consider in optimal management of atherosclerotic cardiovascular disease (ASCVD) risk in this patient?

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