Effect of Rosuvastatin on Bovine Pericardial Aortic Tissue Valve Calcification in a Rat Subdermal Implantation Model

BACKGROUND AND OBJECTIVES: There are pathophysiologic similarities between calcification and atherosclerosis because both are the product of an active inflammatory process. The aim of this study was to examine the effects of statin treatment on calcification in bovine pericardial tissue valves. MATERIALS AND METHODS: Forty Sprague-Dawley rats were randomly divided into 4 groups according to hypercholesterolemia induction and statin intake (Group 1, n=10: normal diet without statin treatment, Group 2, n=10: normal diet with statin treatment, Group 3, n=10: high fat diet without statin treatment, Group 4, n=10: high fat diet with statin treatment). Serum lipid levels were measured just before the experiment and after 4 and 12 weeks. Bovine pericardial tissue valve cusps were surgically implanted in rat dorsal subcutis at 4 weeks. After the surgery, statin was administered daily to Groups 2 and 4. Serum interleukin-6 (IL-6) level was measured at 5 weeks. Cusps were explanted at 12 weeks and calcium levels were determined by atomic absorption spectroscopy. RESULTS: Mean IL-6 was significantly higher in Group 3 at 5 weeks (7.14, 2.03, 31.70, and 6.90 pg/dL for each group, respectively). Mean calcium level in Group 3 was significantly higher among groups but Group 4 was significantly lower compared to Group 3 and was similar to Group 1, 2 (1.86, 1.92, 2.55, and 1.80 mg/g for each group, respectively, p<0.01). CONCLUSION: Hypercholesterolemia may be a significant risk factor for bovine pericardial valve calcification. Statin treatment significantly attenuated calcification of bovine pericardial valve tissue in a rat subdermal implantation model and might prolong the durability of bioprostheses.

The Effects of Rosuvastatin on Plaque Regression in Patients Who Have a Mild to Moderate Degree of Coronary Stenosis With Vulnerable Plaque

BACKGROUND AND OBJECTIVES: Intensive lipid-lowering therapy with statins improves the clinical outcomes and patient survival and it reduces the progression of atherosclerosis. Intravascular ultrasound (IVUS) has been used for calculating the plaque volumes to evaluate the mechanisms that may be involved in the progression or regression of coronary artery disease. We used serial IVUS exams to assess the efficacy of rosuvastatin on plaque regression in angina patients who had a mild to moderate degree of vulnerable plaque burden. SUBJECTS AND METHODS: This study was a prospective, randomized, comparative study for lipid lowering therapy with using rosuvastatin 20 mg or atorvastatin 40 mg. IVUS was performed during the baseline coronary angiography and it was repeated after 12 months of treatment. The efficacy parameters included the changes in the atheroma volume and the lipid pool size as determined by IVUS. A total of 45 lesions in 30 patients were analyzed (rosuvastatin: 24 lesions in 16 patients vs. atorvastatin: 21 lesions in 14 patients). RESULTS: The low density lipoprotein (LDL)-cholesterol level was reduced from 121+/-45 mg/dL to 65+/-25 mg/dL in the rosuvastatin group (a 46% decrease, p<0.001), and from 127+/-37 mg/dL to 72+/-26 mg/dL in the atorvastatin group (a 43% decrease, p<0.001). The total atheroma and vessel volumes were significantly decreased, whereas the lumen volume was significantly increased from baseline to follow-up in both groups (for the rosuvastatin group: the total atheroma volume, 252+/-80 to 246+/-79 mm3, p<0.001; the vessel volume, 555+/-158 to 553+/-130 mm3, p<0.001; the lumen volume, 303+/-91 to 307+/-92 mm3, p<0.001, and for the atorvastatin group: the total atheroma volume, 288+/-98 to 283+/-98 mm3, p<0.001; the vessel volume, 607+/-165 to 604+/-166 mm3, p<0.001; the lumen volume, 319+/-71 to 321+/-73 mm3, p<0.001). The follow-up LDL-cholesterol level was correlated with the change in the total atheroma volume (r=0.577, p<0.001), the change in the percent atheroma volume (r=0.558, p<0.001) and the change in the lipid pool size (r=0.470, p=0.001). CONCLUSION: Both rosuvastatin 20 mg and atorvastatin 40 mg could contribute to the regression of lipid-rich plaque. The follow-up LDL-cholesterol level is related to the regression and stabilization of vulnerable coronary plaque.