A 38-year-old man presents with recurrent myocardial infarction despite atorvastatin 80 mg daily and normal LDL cholesterol of 95 mg/dL. Vital signs: BP 138/88 mmHg, HR 92 bpm, RR 16, temp 37°C, SpO2 98%. HDL cholesterol is markedly reduced at 28 mg/dL. Triglycerides are normal. Genetic testing reveals ABCA1 gene mutations. He denies smoking and alcohol use. Which mechanism best explains his accelerated atherosclerosis despite optimal LDL control?
- A)Reduced uptake of LDL particles by macrophage scavenger receptors
- B)Enhanced oxidation of apolipoprotein B-100 in LDL particles
- C)Decreased esterification of free cholesterol by LCAT
- D)Increased hepatic synthesis of apolipoprotein B-100
- E)Impaired efflux of cellular cholesterol to apolipoprotein A-I, reducing HDL formationGABARITO
Explicação
ABCA1 mediates ATP-dependent efflux of cholesterol from macrophages and other cells to apoA-I, the initial step in reverse cholesterol transport and HDL formation. ABCA1 mutations cause Tangier disease with severely reduced HDL and premature atherosclerosis. Ver explicação completa e trilha adaptativa →