6533b826fe1ef96bd1283d5c

RESEARCH PRODUCT

Effects of fluvastatin slow-release (XL 80 mg) versus simvastatin (20 mg) on the lipid triad in patients with type 2 diabetes.

Enrica ChebatTarcisio VagoVelella RighiniMaurizio BevilacquaMassimo BarrellaLigia J. Dominguez

subject

Malemedicine.medical_specialtySimvastatinIndolesHDLApolipoprotein BSmall dense LDLType 2 diabetesTriglycerideLDLFatty Acids MonounsaturatedFluvastatin XLInternal medicineDiabetes mellitusType 2 diabetes mellitusmedicineHumansPharmacology (medical)Prospective StudiesFluvastatinAgedHypertriglyceridemiabiologybusiness.industryAnticholesteremic AgentsApoA-IHypertriglyceridemianutritional and metabolic diseasesType 2 Diabetes MellitusGeneral MedicineMiddle Agedmedicine.diseaseLipoproteins LDLEndocrinologyDiabetes Mellitus Type 2SimvastatinDelayed-Action Preparationsbiology.proteinlipids (amino acids peptides and proteins)FemaleApoBbusinessLipoproteins HDLFluvastatinmedicine.drugLipoprotein

description

The lipid triad is the association of small, dense (sd) low-density lipoprotein (LDL), low high-density lipoprotein (HDL), and hypertriglyceridemia, all of which play a role in coronary artery disease in patients with type 2 diabetes. Although statins have demonstrated clear positive effects on cardiovascular morbidity/mortality in patients with diabetes and on single components of the lipid triad, it remains controversial whether they affect all components of the triad in these patients. Therefore, we performed a single-center, parallel-group, prospective, randomized, open-label, blinded-endpoint (PROBE)-type comparison of fluvastatin extended-release (XL) 80 mg (n=48) and simvastatin 20 mg (n=46), each given once daily for 2 months to patients with type 2 diabetes with the lipid triad, who were enrolled after a 1-month lifestyle modification and dietary intervention program. After fluvastatin therapy, LDL (-51%; P > .01), apolipoprotein B (ApoB;-33%; P > .01, intermediate-density LDL (idLDL) (-14.3%; P > .05), sdLDL (-45%; P > .01), and triglycerides (-38%; P > .01) were significantly decreased, and HDL (+14.3%; P > .05) and apolipoprotein A-I (ApoA-I; +7%; P > .05) were increased; large buoyant (lb) LDL did not change (P=NS). Simvastatin therapy decreased LDL (-55.1 %; P > .01), ApoB (-46%; P > .01), lbLDL (-33.3%; P > .05), idLDL (-22.7%; P > .05), sdLDL (-33.3%; P > .05), and triglycerides (-47.9%; P > .01); HDL was not changed (P=NS) after simvastatin, but ApoA-I was increased (+11.3%; P > .01). HDL increases (P > .01) and sdLDL decreases (P > .01) were significantly greater after fluvastatin compared with simvastatin therapy; LDL, triglycerides, ApoB, and idLDL changes were similar after both therapies (P=NS), and lbLDL decreases were greater with simvastatin therapy (P > .05). With both treatments, classic mean LDL and ApoB target levels were achieved in most patients. We conclude that the lipid triad can be controlled with fluvastatin XL 80 mg in patients with type 2 diabetes.

10.1007/bf02849947https://pubmed.ncbi.nlm.nih.gov/16510370