2017 Taiwan lipid guidelines for high risk patients.

In Taiwan, the prevalence of hyperlipidemia increased due to lifestyle and dietary habit changes. Low density lipoprotein cholesterol (LDL-C) and non-high density lipoprotein cholesterol (non-HDL-C) are all significant predicting factors of coronary artery disease in Taiwan. We recognized that lipid control is especially important in patients with existed atherosclerotic cardiovascular diseases (ASCVD), including coronary artery disease (CAD), ischemic stroke and peripheral arterial disease (PAD). Because the risk of ASCVD is high in patients with diabetes mellitus (DM), chronic kidney disease (CKD) and familial hypercholesterolemia (FH), lipid control is also necessary in these patients. Lifestyle modification is the first step to control lipid. Weight reduction, regular physical exercise and limitation of alcohol intake all reduce triglyceride (TG) levels. Lipid-lowering drugs include HMG-CoA reductase inhibitors (statins), cholesterol absorption inhibitors (ezetimibe), proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, nicotinic acids (niacin), fibric acids derivatives (fibrates), and long-chain omega-3 fatty acids. Statin is usually the first line therapy. Combination therapy with statin and other lipid-lowering agents may be considered in some clinical settings. For patients with acute coronary syndrome (ACS) and stable CAD, LDL-C < 70 mg/dL is the major target. A lower target of LDL-C <55 mg/dL can be considered in ACS patients with DM. After treating LDL-C to target, non-HDL-C can be considered as a secondary target for patients with TG ≥ 200 mg/dL. The suggested non-HDL-C target is < 100 mg/dL in ACS and CAD patients. For patients with ischemic stroke or transient ischemic attack presumed to be of atherosclerotic origin, statin therapy is beneficial and LDL-C < 100 mg/dL is the suggested target. For patients with symptomatic carotid stenosis or intracranial arterial stenosis, in addition to antiplatelets and blood pressure control, LDL-C should be lowered to < 100 mg/dL. Statin is necessary for DM patients with CV disease and the LDL-C target is < 70 mg/dL. For diabetic patients who are ≥ 40 years of age, or who are < 40 years of age but have additional CV risk factors, the LDL-C target should be < 100 mg/dL. After achieving LDL-C target, combination of other lipid-lowering agents with statin is reasonable to attain TG < 150 mg/dL and HDL-C >40 in men and >50 mg/dL in women in DM. LDL-C increased CV risk in patients with CKD. In adults with glomerular filtration rate (GFR) < 60 mL/min/1.73m2 without chronic dialysis (CKD stage 3-5), statin therapy should be initiated if LDL-C ≥ 100 mg/dL. Ezetimibe can be added to statin to consolidate the CV protection in CKD patients. Mutations in LDL receptor, apolipoprotein B and PCSK9 genes are the common causes of FH. Diagnosis of FH usually depends on family history, clinical history of premature CAD, physical findings of xanthoma or corneal arcus and high levels of LDL-C. In addition to conventional lipid lowering therapies, adjunctive treatment with mipomersen, lomitapide, or PCSK9 inhibitors become necessary to further reduce LDL-C in patients with FH. Overall, these recommendations are to help the health care professionals in Taiwan to treat hyperlipidemia with current scientific evidences. We hope the prescription rate of lipid lowering drugs and control rate of hyperlipidemia in high risk patients could be increased by implementation of the clinical guidelines. The major purpose is to improve clinical outcomes of these high risk patients through the control of hyperlipidemia.

A novel inhibitory effect of Antrodia camphorata extract on vascular smooth muscle cell migration and neointima formation in mice.

Antrodia camphorata (AC) is a well-known traditional Chinese medicine that has been shown to inhibit proliferation and migration of cancer cells. We examined whether AC could inhibit rat aortic smooth muscle cell (RASMC) proliferation and migration and evaluated its effect on neointima formation in mouse carotid artery after injury. In Transwell migration assay and wound scratch assay, RASMCs were treated with AC or saline, and the number of migrated cells was counted or the distance was determined. Both assays showed that AC significantly inhibited platelet-derived growth factor (PDGF)-induced SMC migration. In 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) and 5-bromo-2' deoxyuridine (BrdU) proliferation assays, RASMCs were pretreated with AC or saline and stimulated with PDGF. Both assays showed that AC inhibited PDGF-induced SMC proliferation. The left common carotid arteries of C57BL/6 mice were ligated near the carotid bifurcation. The mice were given water or AC for 4 weeks. The severity of neointima formation was expressed as the neointima/media (N/M) ratio. The AC-treated mice had less neointima formation at 4 weeks after carotid ligation (N/M ratio, water versus 250 versus 1250 mg/kg AC; 1.33 +/- 0.87 versus 0.83 +/- 0.45 versus 0.63 +/- 0.32, P < 0.05).Our data indicate that AC is an effective inhibitor of PDGF-induced RASMC proliferation and migration. AC treatment reduced neointima formation in this mouse carotid ligation model.