A 64-year-old man with prior myocardial infarction presents with hypertension (BP 152/88 mmHg), heart rate 82 bpm, and denies chest pain. He takes atorvastatin 80 mg daily with LDL-cholesterol of 110 mg/dL and triglycerides of 95 mg/dL. Laboratory analysis reveals elevated lipoprotein(a) of 120 nmol/L (reference <50 nmol/L). Which of the following best explains his persistent cardiovascular risk despite adequate LDL-cholesterol control?
- A)Statins increase hepatic synthesis of lipoprotein(a) through SREBP-2 activation
- B)Lp(a) inhibits the activity of tissue plasminogen activator, impairing fibrinolysis
- C)Lp(a) directly inhibits the expression of apolipoprotein A-I in HDL particles
- D)Lp(a) competes with LDL for hepatic receptors, preventing cholesterol feedback regulation
- E)Lp(a) is oxidized and taken up by macrophages, promoting foam cell formation and atherosclerosis independent of LDLGABARITO
Explicação
Lipoprotein(a), consisting of apoB-100 covalently linked to apolipoprotein(a), acts as an independent atherogenic factor. Elevated Lp(a) confers additional cardiovascular risk beyond LDL-C. Oxidized Lp(a) is taken up by macrophages via scavenger receptors (par... Ver explicação completa e trilha adaptativa →