1.
High-Sensitivity C-Reactive Protein Combined with Low-Density Lipoprotein Cholesterol as the Targets of Statin Therapy in Patients with Acute Coronary Syndrome.
Fang, M, Qian, Q, Zhao, Z, Zhu, L, Su, J, Li, X
International heart journal. 2018;(2):300-306
Abstract
To investigate the combination of high-sensitivity C-reactive protein (hs-CRP) and Low-density lipoprotein (LDL)-C as the targets for statin treatment in patients with acute coronary syndrome (ACS). This single-center, prospective, randomized study was performed in 400 patients treated with atorvastatin 40 mg/day for 1 month and then with atorvastatin 20 mg/day as maintenance. The patients were randomized to the LDL group (LDL-C target of < 2.07 mmol/L according to the Chinese dyslipidemia guidelines) and to the LDL-CRP group (LDL-C target of < 2.07 mmol/L and hs-CRP target of < 3 mg/L). The patients were followed up for major adverse cardiac events (MACE) at 6, 12, and 18 months. The two groups had similar baseline characteristics and 391 patients completed the follow-up. No differences were found in LDL-C between the two groups, but a difference was found in hs-CRP at 12 and 18 months. There was a significant difference in revascularization (8.7% versus 3.6%, P = 0.04) and MACE (16.8% versus 9.7%; P = 0.04) between the LDL and LDL-CRP groups at 18 months. Compared to LDL-C as the single target, targeting both LDL-C and hs-CRP by statin therapy in patients with ACS could further reduce the incidence of MACE and the residual cardiovascular risk.
2.
Effects of combination of statin and calcium channel blocker in patients with cardiac syndrome X.
Zhang, X, Li, Q, Zhao, J, Li, X, Sun, X, Yang, H, Wu, Z, Yang, J
Coronary artery disease. 2014;(1):40-4
Abstract
OBJECTIVES Statins and calcium channel blockers have been proven beneficial toward improvement of endothelial function. The aim of this study was to compare the effect of combination therapy of statin and calcium channel blocker with solo treatment in patients with cardiac syndrome X. METHODS AND RESULTS Sixty-eight patients with cardiac syndrome X were divided randomly into three groups: fluvastatin (40 mg/day, n=23), diltiazem (90 mg/day, n=22), and combination of fluvastatin (40 mg/day) and diltiazem (90 mg/day, n=23). At the end of 90 days, the coronary flow reserve was improved in the three groups (fluvastatin-treated group: 23.2%; diltiazem-treated group: 12.4%; fluvastatin+diltiazem-treated group: 29.1%, all P<0.05). The time to 1 mm ST segment depression increased significantly in the fluvastatin-treated group (from 241±97 to 410±140 s, P<0.05), the diltiazem-treated group (from 258±91 to 392±124 s, P<0.05), and the fluvastatin+diltiazem-treated group (from 250±104 to 446±164 s, P<0.05). The improvement in coronary flow reserve and prolonged time to 1 mm ST segment depression in the combination treatment group were more remarkable than in those who received monotherapy. Combination therapy also induced a significant increase (35.6%, P<0.05) in nitric oxide and an apparent reduction (48.7%, P<0.05) in endothelin-1. CONCLUSION Combination treatment with fluvastatin and diltiazem is more effective on endothelial function and exercise tolerance than solo treatment in patients with cardiac syndrome X. The benefits of these drugs may be related to the elevation of nitric oxide and reduction of endothelin-1.
3.
Lipid and apolipoprotein levels and distribution in patients with hypertriglyceridemia: effect of triglyceride reductions with atorvastatin.
Le, NA, Innis-Whitehouse, W, Li, X, Bakker-Arkema, R, Black, D, Brown, WV
Metabolism: clinical and experimental. 2000;(2):167-77
Abstract
Atorvastatin is a new hepatic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibitor that has been demonstrated to be efficacious in reducing both triglyceride (TG) and cholesterol (CHOL) levels in humans. Twenty-seven (N = 27) patients with primary hypertriglyceridemia (TG > 350 mg/dL) were studied before and after 4 weeks on atorvastatin treatment at a dosage of either 20 (n = 16) or 80 (n = 11) mg/d. The present report examines changes in the plasma levels of several apolipoproteins, including apolipoprotein C-II (apoC-II), apoC-III, and apoE, after atorvastatin. Dose-dependent reductions in both CHOL (20.3% v 43.1%) and TG (26.5% v 45.8%) for the low and high dose, respectively, have been reported in these individuals. In addition to the reductions in apoB commonly associated with the use of HMG-CoA reductase inhibitors, significant reductions in apoE (37% and 49%), apoC-II (28% and 42%), and apoC-III (18% and 30%) were observed with this agent at the 20- and 80-mg/d dosage, respectively. Using fast protein liquid chromatography (FPLC) to fractionate whole plasma according to particle size, the effect of atorvastatin on lipid and apolipoprotein distribution in 20 lipoprotein fractions was also determined. Our results indicate that after 4 weeks on atorvastatin, (1) there was a 2-fold increase in the CHOL content as assessed by the CHOL/apoB ratio for 13 subfractions from very-low-density lipoprotein (VLDL) to small low-density lipoprotein (LDL); (2) there was a statistically significant reduction in the percentage of plasma apoB associated with VLDL-sized particles (30.5% v 26.8%); (3) there was a preferential reduction in plasma apoE from non-apoB-containing lipoproteins with treatment; (4) the losses of apoC-II and apoC-III, on the other hand, were comparable for all lipoprotein fractions; and (5) the fraction of plasma TG associated with HDL was increased after treatment. These changes in lipids and apolipoproteins did not depend on the dose of atorvastatin. There was, on the other hand, a dose-dependent reduction in cholesteryl ester transfer protein (CETP) activity, defined as the percentage of 3H-cholesteryl oleate transferred from high-density lipoprotein (HDL) to LDL. CETP activity was reduced by 10.3% and 26.4% with the low and high dose of atorvastatin. Together, these composition data would be consistent with a net reduction in the number of TG-rich lipoproteins that may be explained by (1) a reduction in VLDL synthesis, (2) a preferential removal of VLDL without conversion to LDL, and (3) a preferential accelerated removal of a subpopulation of LDL.