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COQ10 does not improve statin myalgia–A randomized controlled trial
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Abstracts / Atherosclerosis 241 (2015) e149ee229
ultrasound, Russian Cardiology Research and Production Complex, Moscow, Russia
* Corresponding author. Aim: Detection of carotid plaque on an ultrasound scan could improve CHD risk prediction, allowing early appropriate management. Aim of the study was to assess the effect of a 1-year treatment with atorvastatin on progression of carotid atherosclerosis in intermediate risk patients. Methods: A total of 84 asymptomatic, intermediate-risk patients who underwent duplex ultrasound investigations of the extracranial carotid arteries, and who had carotid plaque with a degree of stenosis <50% were randomly assigned to lipid-lowering therapy with atorvastatin to target LDL-C <1.8 mmol/l (group 1; n¼42), or <2.6 mmol/l (group 2, n¼42). Patients underwent repeat carotid ultrasound examination after a period of 12 months to compare carotid atherosclerosis progression in both groups. Results: The clinical characteristics were similar for both groups at baseline. In patients with <1.8 mmol/l of achieved LDL-C levels there was no significant change in the mean number of plaques, in the average plaque score, and in the cumulative carotid stenosis score after 1-year treatment. In patients with <2.6 mmol/l of achieved LDL-C levels there was increase in the mean number of plaques (2.4±1.6 to 2.9±1.5, p<0.001), in the average plaque score (6.2±4.5 ?? to 7.1±4.9 ??, p<0.001), and in the mean cumulative carotid stenosis score (70.4±54.2% to 83.4±55.3%, p¼0.002). Conclusions: Patients with nonobstructive asymptomatic carotid stenosis and who aren’t cardiovascular high-risk patients would benefit from intensive statin therapy.
EAS-0801. THE PROPROTEIN CONVERTASE SUBTILISIN/KEXIN TYPE 9 (PCSK9) R46L GENE POLYMORPHISM AND STATIN RESPONSE IN A TUNISIAN CORONARY ATERY DISEASE POPULATION A. Kallel 1, S. Omar 1, *, W. Ben Achour 1, M. Sbaï 1, R. Mechmeche 2, R. Jemaa 1, N. Kaabachi 1. 1 Biochemistry, La Rabta Hospital, Tunis, Tunisia; 2 Cardiology, La Rabta Hospital, Tunis, Tunisia
* Corresponding author. Aim: The proprotein convertase subtilisin/kexin type 9 (PCSK9) gene encodes a proprotein convertase which is a member of the subtilase family. It is involved in cholesterol metabolism through the degradation of the LDL receptors (LDLRs). Mutations in the PCSK9 gene that disrupt the normal function of PCSK9 could therefore result in increased number of LDLRs and hypocholesterolemia. The missense mutation R46L (rs11591147)of the PCSK9 gene was described to beassociated with increased response to statin therapy. The aim of our study was to determine the alleles and genotypes frequencies of the polymorphism R46L in patients treated with statins and see the impact of this treatment on lipid parameters and to study the response to statin therapy according the R46L polymorphism genotypes. Methods: Our study population consists of 107 subjects recruited from patients hospitalized in the Intensive Care Unit at the Cardiology Department of la Rabta Hospital for myocardial infarction, receiving treatment statins (atorvastatin) during 2 months. Genotyping of R46L Polymorphism was done by PCR-RFLP. Results: The mean level of TG, TC, LDL were significantly lowered after statin treatment, whereas concentrations of HDL-C are not. The T and C alleles were identified with respective frequencies (0.92, 0.07) and three genotypes CC, CT and TT with respective frequencies (87.9%, 9.3%, 2.8%).There was no significant variation in lipid parameters according to genotypes. Conclusion: Our results showed that the polymorphism R46L of PCSK9 gene is not associated with lipid-lowering statin response.
EAS-0814. COQ10 DOES NOT IMPROVE STATIN MYALGIAeA RANDOMIZED CONTROLLED TRIAL C. Buettner 1, *, R.B. Davis 1, R.S. Phillips 1, M.A. Mittleman 2. 1 Medicine, BIDMC/Harvard Medical School, Boston, USA; 2 Cardiology, BIDMC/Harvard Medical School, Boston, USA
* Corresponding author. Aim: Most past studies evaluating CoQ10 for statin myalgia have not confirmed statin myalgia in patients studied and show varied results. We aimed to test if CoQ10 supplementation improves confirmed statin myalgia. Methods: Patients with suspected statin myalgia were confirmed to have statin myalgia if myalgia improved on statin cessation and returned on observed rechallenge of simvastatin 20mg/day. Those who had a return of myalga within 3 months were randomized to CoQ10 300mg or placebo twice/day with continued use of simvastatin 20mg/day. Improvement was defined, a priori, as a reduction >1.5 points on the Brief Pain InventorySeverity Scale (“BPI-SS”, 0-10). Results: Of 68 enrolled, 39 had confirmed statin myalgia. Of 39 randomized, 19 received CoQ10þsimvastatin and 20 received placeboþsimvastatin. Pain was reduced by >1.5 points in 10 participants (53%) who received CoQ10 and in 13 participants (65%) who received placebo (pvalue¼0.43, Wilcoxin rank sum test). The smallest change in myalgia pain that patients identified as important was a reduction of least 2 points. There were no differences in adherence to statin use; the majority (90%) in each group used >85% of statin doses. CoQ10 levels increased significantly in the treatment, but not the placebo, group and did not correlate with improvements in symptoms. Conclusion: Among individuals with confirmed statin myalgia, supplemental CoQ10 did not improve statin myalgia compared to placebo. The majority of participants with statin myalgia had improvement in pain (>1.5 points on the BPI-SS) over 4 weeks. Adherence to statin use did not differ by randomization group.
EAS-0871. EFFECTS OF DIFFERENT DOSES OF ROSUVASTATIN ON BLOOD LIPIDS, ENDOTHELIAL FUNCTION, AND CEREBRAL BLOOD FLOW IN PATIENTS WITH HYPERLIPIDEMIA AND CEREBRAL ISCHEMIC STROKE M. Bubnova*, D. Aronov, E. Semenova. Prevention Atherosclerosis and Trombosis, National Research Center for Preventive medicine, Moscow, Russia
* Corresponding author. Objective: to study the dose-dependent effect of rosuvastatin (R) on blood LP, endothelial functional activity, cerebral blood flow in patients (pts) with hyperlipidemia (HLP) and hypertension after ischemic stroke (IS). Subjects and method: The trial included 34 pts (mean age 59,4±7,4 years), who were randomized to R 10 mg and R 20 mg for 12 weeks. The R effects on the blood concentration of LP, fibrinogen, end-metabolites of nitric oxide (NO?), endothelin-1 (ET-1), angiotensin (AT) II, cerebral blood flow (CBF) by great cerebral artery Doppler ultrasound data. Results: After 12-wks there was a significant decrease in the level of LDLCh by 40% R 10 mg and 45% R 20 mg, and TG by 18 and 26%, respectively. R caused no changes in the high baseline level of fibrinogen and AT II. At the R 10 and 20 mg the concentrations of NOx increased by 14,3 and 12,4%, respectively (at R 20 mg after 6 wks). ET-1 levels decreased at R 10 mg (by 9,5%, p<0<05). In the pts who had an ET-1 level of >0,51 fmol/ml, its drop was 22,5% (p<0,05). The improvement of CBF in the internal carotid artery and in the V2/V3-segments of the vertebral artery might be expected in post-CIS patients taking R 20 mg. Conclusion: The pleiotropic activity of R was manifested on the starting (10 mg) and average (20 mg) doses. At the same time, RS showed dosedepended effects in lowering LDL cholesterol levels, enhancing NO bioavailability, and improving cerebral blood flow velocities.
Abstracts / Atherosclerosis 241 (2015) e149ee229
ultrasound, Russian Cardiology Research and Production Complex, Moscow, Russia
* Corresponding author. Aim: Detection of carotid plaque on an ultrasound scan could improve CHD risk prediction, allowing early appropriate management. Aim of the study was to assess the effect of a 1-year treatment with atorvastatin on progression of carotid atherosclerosis in intermediate risk patients. Methods: A total of 84 asymptomatic, intermediate-risk patients who underwent duplex ultrasound investigations of the extracranial carotid arteries, and who had carotid plaque with a degree of stenosis <50% were randomly assigned to lipid-lowering therapy with atorvastatin to target LDL-C <1.8 mmol/l (group 1; n¼42), or <2.6 mmol/l (group 2, n¼42). Patients underwent repeat carotid ultrasound examination after a period of 12 months to compare carotid atherosclerosis progression in both groups. Results: The clinical characteristics were similar for both groups at baseline. In patients with <1.8 mmol/l of achieved LDL-C levels there was no significant change in the mean number of plaques, in the average plaque score, and in the cumulative carotid stenosis score after 1-year treatment. In patients with <2.6 mmol/l of achieved LDL-C levels there was increase in the mean number of plaques (2.4±1.6 to 2.9±1.5, p<0.001), in the average plaque score (6.2±4.5 ?? to 7.1±4.9 ??, p<0.001), and in the mean cumulative carotid stenosis score (70.4±54.2% to 83.4±55.3%, p¼0.002). Conclusions: Patients with nonobstructive asymptomatic carotid stenosis and who aren’t cardiovascular high-risk patients would benefit from intensive statin therapy.
EAS-0801. THE PROPROTEIN CONVERTASE SUBTILISIN/KEXIN TYPE 9 (PCSK9) R46L GENE POLYMORPHISM AND STATIN RESPONSE IN A TUNISIAN CORONARY ATERY DISEASE POPULATION A. Kallel 1, S. Omar 1, *, W. Ben Achour 1, M. Sbaï 1, R. Mechmeche 2, R. Jemaa 1, N. Kaabachi 1. 1 Biochemistry, La Rabta Hospital, Tunis, Tunisia; 2 Cardiology, La Rabta Hospital, Tunis, Tunisia
* Corresponding author. Aim: The proprotein convertase subtilisin/kexin type 9 (PCSK9) gene encodes a proprotein convertase which is a member of the subtilase family. It is involved in cholesterol metabolism through the degradation of the LDL receptors (LDLRs). Mutations in the PCSK9 gene that disrupt the normal function of PCSK9 could therefore result in increased number of LDLRs and hypocholesterolemia. The missense mutation R46L (rs11591147)of the PCSK9 gene was described to beassociated with increased response to statin therapy. The aim of our study was to determine the alleles and genotypes frequencies of the polymorphism R46L in patients treated with statins and see the impact of this treatment on lipid parameters and to study the response to statin therapy according the R46L polymorphism genotypes. Methods: Our study population consists of 107 subjects recruited from patients hospitalized in the Intensive Care Unit at the Cardiology Department of la Rabta Hospital for myocardial infarction, receiving treatment statins (atorvastatin) during 2 months. Genotyping of R46L Polymorphism was done by PCR-RFLP. Results: The mean level of TG, TC, LDL were significantly lowered after statin treatment, whereas concentrations of HDL-C are not. The T and C alleles were identified with respective frequencies (0.92, 0.07) and three genotypes CC, CT and TT with respective frequencies (87.9%, 9.3%, 2.8%).There was no significant variation in lipid parameters according to genotypes. Conclusion: Our results showed that the polymorphism R46L of PCSK9 gene is not associated with lipid-lowering statin response.
EAS-0814. COQ10 DOES NOT IMPROVE STATIN MYALGIAeA RANDOMIZED CONTROLLED TRIAL C. Buettner 1, *, R.B. Davis 1, R.S. Phillips 1, M.A. Mittleman 2. 1 Medicine, BIDMC/Harvard Medical School, Boston, USA; 2 Cardiology, BIDMC/Harvard Medical School, Boston, USA
* Corresponding author. Aim: Most past studies evaluating CoQ10 for statin myalgia have not confirmed statin myalgia in patients studied and show varied results. We aimed to test if CoQ10 supplementation improves confirmed statin myalgia. Methods: Patients with suspected statin myalgia were confirmed to have statin myalgia if myalgia improved on statin cessation and returned on observed rechallenge of simvastatin 20mg/day. Those who had a return of myalga within 3 months were randomized to CoQ10 300mg or placebo twice/day with continued use of simvastatin 20mg/day. Improvement was defined, a priori, as a reduction >1.5 points on the Brief Pain InventorySeverity Scale (“BPI-SS”, 0-10). Results: Of 68 enrolled, 39 had confirmed statin myalgia. Of 39 randomized, 19 received CoQ10þsimvastatin and 20 received placeboþsimvastatin. Pain was reduced by >1.5 points in 10 participants (53%) who received CoQ10 and in 13 participants (65%) who received placebo (pvalue¼0.43, Wilcoxin rank sum test). The smallest change in myalgia pain that patients identified as important was a reduction of least 2 points. There were no differences in adherence to statin use; the majority (90%) in each group used >85% of statin doses. CoQ10 levels increased significantly in the treatment, but not the placebo, group and did not correlate with improvements in symptoms. Conclusion: Among individuals with confirmed statin myalgia, supplemental CoQ10 did not improve statin myalgia compared to placebo. The majority of participants with statin myalgia had improvement in pain (>1.5 points on the BPI-SS) over 4 weeks. Adherence to statin use did not differ by randomization group.
EAS-0871. EFFECTS OF DIFFERENT DOSES OF ROSUVASTATIN ON BLOOD LIPIDS, ENDOTHELIAL FUNCTION, AND CEREBRAL BLOOD FLOW IN PATIENTS WITH HYPERLIPIDEMIA AND CEREBRAL ISCHEMIC STROKE M. Bubnova*, D. Aronov, E. Semenova. Prevention Atherosclerosis and Trombosis, National Research Center for Preventive medicine, Moscow, Russia
* Corresponding author. Objective: to study the dose-dependent effect of rosuvastatin (R) on blood LP, endothelial functional activity, cerebral blood flow in patients (pts) with hyperlipidemia (HLP) and hypertension after ischemic stroke (IS). Subjects and method: The trial included 34 pts (mean age 59,4±7,4 years), who were randomized to R 10 mg and R 20 mg for 12 weeks. The R effects on the blood concentration of LP, fibrinogen, end-metabolites of nitric oxide (NO?), endothelin-1 (ET-1), angiotensin (AT) II, cerebral blood flow (CBF) by great cerebral artery Doppler ultrasound data. Results: After 12-wks there was a significant decrease in the level of LDLCh by 40% R 10 mg and 45% R 20 mg, and TG by 18 and 26%, respectively. R caused no changes in the high baseline level of fibrinogen and AT II. At the R 10 and 20 mg the concentrations of NOx increased by 14,3 and 12,4%, respectively (at R 20 mg after 6 wks). ET-1 levels decreased at R 10 mg (by 9,5%, p<0<05). In the pts who had an ET-1 level of >0,51 fmol/ml, its drop was 22,5% (p<0,05). The improvement of CBF in the internal carotid artery and in the V2/V3-segments of the vertebral artery might be expected in post-CIS patients taking R 20 mg. Conclusion: The pleiotropic activity of R was manifested on the starting (10 mg) and average (20 mg) doses. At the same time, RS showed dosedepended effects in lowering LDL cholesterol levels, enhancing NO bioavailability, and improving cerebral blood flow velocities.