A 46-year man is taken to the emergency department with complaints of chest pressure, dyspnea and diaphoresis that developed shortly after he arrived home. His blood pressure is low at 146/54 mm Hg even though he reports treatment for hypertension. His pulse was 88/min. Pertinent findings on the physical examination include corneal arcus and xanthelasmas. His heart sounds are dynamic and there is a crescendo-decrescendo early-peaking murmur grade 2/6 at the left sternal border. The carotid upstrokes and peripheral pulses are normal. He has central obesity and the liver span is normal. The ECG revealed a rightward axis and anterolateral wall ST segment depressions. He was admitted with an acute non-ST segment myocardial infarction (NSTEMI).

He states that his LDL cholesterol level was elevated but they were reduced by simvastatin 40 mg nightly, but his HDL cholesterol (HDL-C) levels have been persistently between 28 mg/dL to 32 mg/dL. His blood pressure is usually high normal and his glucose has been mildly elevated at 102 mg/dL. He was advised to lose weight and start exercising, but the workload at the hospital has been extensive and he tries to spend as much time with his two young children when he is home. He is aware that his cardiac risk is high as his father has had four myocardial infarction with the first event occurring at the age at 47 years. He reports that his father has a low HDL-C as well.

He is hydrated, placed on aspirin, metoprololol succinate, nitrates for continued chest pain, and scheduled for a coronary arteriogram. He is found to have a proximal LAD stenosis of 85%, and receives a PCI. Later that night, the simvastatin was changed to atorvastatin 80 mg daily.

At six weeks post-discharge his lipid and lipoprotein values reveal:

• Total cholsterol: 152 mg/dL
• LDL-C: 92 mg/dL
• Triglycerides: 160 mg/dL
HDL-C: 28 mg/dL
• ApoB: 126 mg/dL
• Total LDL-P: 1910 nmol/L (high risk)
• Small LDL-P: 1746 nmol/L (high risk)
• Total HDL-P: 22.6 μmol/L (high risk)