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Atheroma progression in hyporesponders to statin therapy.
Arterioscler Thromb Vasc Biol. 2015 Apr; 35(4):990-5.AT

Abstract

OBJECTIVE

Lowering low-density lipoprotein cholesterol (LDL-C) with statins has been demonstrated to slow plaque progression. This antiatherosclerotic effect in patients with minimal LDL-C lowering has not been investigated.

APPROACH AND RESULTS

Six hundred forty-seven patients with angiographic coronary artery disease who were commenced on statin therapy underwent serial imaging with intravascular ultrasound. Responders were defined as a percentage reduction in LDL-C of <15%. Disease progression was compared in responders (n=517) and hyporesponders (n=130) to statin therapy. Twenty percentage of patients demonstrated minimal changes in LDL-C, despite commencement of statin therapy. Statin hyporesponders were younger (55 versus 57 years; P=0.01), more likely to be male (79% versus 66%; P=0.005), and obese (body mass index, 31.5 ± 6.1 versus 30.3 ± 5.9 kg/m(2); P=0.04) and less likely to have a history of dyslipidemia (50% versus 66%; P<0.001). Baseline levels of systolic blood pressure (127 ± 15 versus 132 ± 17 mm Hg; P=0.01) and LDL-C (2.5 ± 0.6 versus 3.4 ± 0.8 mmol/L; P<0.001) were lower in statin hyporesponders. Baseline percent atheroma volume was similar between statin hyporesponders and responders (36.9 ± 9.8% versus 38.3 ± 9.2%; P=0.13). On serial evaluation, greater progression of percent atheroma volume (1.19 ± 0.48% versus 0.09 ± 0.43%; P=0.003) was observed in statin hyporesponders. After adjusting for baseline clinical characteristics and measures of plaque burden, statin hyporesponders still exhibited greater atheroma progression (+0.83 ± 0.58% versus -0.21 ± 0.52%; P=0.006).

CONCLUSIONS

A substantial proportion of patients with coronary artery disease fail to achieve effective reductions in LDL-C, despite prescription of statin therapy. Greater progression of atherosclerosis is observed in these patients. Our current study underscores monitoring LDL-C level after the commencement of statin to ensure adequate response to statin therapy.

Links

Publisher Full Text (DOI)

Authors+Show Affiliations

Kataoka Y
From the South Australian Health and Medical Research Institute, Heart Health Theme, University of Adelaide, Adelaide, Australia (Y.K., S.J.N.); and C5 Research (J.S.J., K.W., K.U., R.P., S.E.N.) and Department of Cardiovascular Medicine, Heart and Vascular Institute (R.P., E.M.T., S.E.N.), Cleveland Clinic, OH.
St John J
From the South Australian Health and Medical Research Institute, Heart Health Theme, University of Adelaide, Adelaide, Australia (Y.K., S.J.N.); and C5 Research (J.S.J., K.W., K.U., R.P., S.E.N.) and Department of Cardiovascular Medicine, Heart and Vascular Institute (R.P., E.M.T., S.E.N.), Cleveland Clinic, OH.
Wolski K
From the South Australian Health and Medical Research Institute, Heart Health Theme, University of Adelaide, Adelaide, Australia (Y.K., S.J.N.); and C5 Research (J.S.J., K.W., K.U., R.P., S.E.N.) and Department of Cardiovascular Medicine, Heart and Vascular Institute (R.P., E.M.T., S.E.N.), Cleveland Clinic, OH.
Uno K
From the South Australian Health and Medical Research Institute, Heart Health Theme, University of Adelaide, Adelaide, Australia (Y.K., S.J.N.); and C5 Research (J.S.J., K.W., K.U., R.P., S.E.N.) and Department of Cardiovascular Medicine, Heart and Vascular Institute (R.P., E.M.T., S.E.N.), Cleveland Clinic, OH.
Puri R
From the South Australian Health and Medical Research Institute, Heart Health Theme, University of Adelaide, Adelaide, Australia (Y.K., S.J.N.); and C5 Research (J.S.J., K.W., K.U., R.P., S.E.N.) and Department of Cardiovascular Medicine, Heart and Vascular Institute (R.P., E.M.T., S.E.N.), Cleveland Clinic, OH.
Tuzcu EM
From the South Australian Health and Medical Research Institute, Heart Health Theme, University of Adelaide, Adelaide, Australia (Y.K., S.J.N.); and C5 Research (J.S.J., K.W., K.U., R.P., S.E.N.) and Department of Cardiovascular Medicine, Heart and Vascular Institute (R.P., E.M.T., S.E.N.), Cleveland Clinic, OH.
Nissen SE
From the South Australian Health and Medical Research Institute, Heart Health Theme, University of Adelaide, Adelaide, Australia (Y.K., S.J.N.); and C5 Research (J.S.J., K.W., K.U., R.P., S.E.N.) and Department of Cardiovascular Medicine, Heart and Vascular Institute (R.P., E.M.T., S.E.N.), Cleveland Clinic, OH.
Nicholls SJ
From the South Australian Health and Medical Research Institute, Heart Health Theme, University of Adelaide, Adelaide, Australia (Y.K., S.J.N.); and C5 Research (J.S.J., K.W., K.U., R.P., S.E.N.) and Department of Cardiovascular Medicine, Heart and Vascular Institute (R.P., E.M.T., S.E.N.), Cleveland Clinic, OH. stephen.nicholls@sahmri.com.

MeSH

AgedBiomarkersBlood PressureCholesterol, LDLClinical Trials as TopicCoronary Artery DiseaseDisease ProgressionDrug ResistanceDyslipidemiasFemaleHumansHydroxymethylglutaryl-CoA Reductase InhibitorsMaleMiddle AgedPrevalenceRisk FactorsTime FactorsTomography, X-Ray ComputedTreatment OutcomeUltrasonography, Interventional

Pub Type(s)

Journal Article

Language

eng

PubMed ID

25722430

Clinical Trial Links

Safety and Efficacy of Propionate for Reduction of LDL Cholesterol

Citation

Kataoka, Yu, et al. "Atheroma Progression in Hyporesponders to Statin Therapy." Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 35, no. 4, 2015, pp. 990-5.
Kataoka Y, St John J, Wolski K, et al. Atheroma progression in hyporesponders to statin therapy. Arterioscler Thromb Vasc Biol. 2015;35(4):990-5.
Kataoka, Y., St John, J., Wolski, K., Uno, K., Puri, R., Tuzcu, E. M., Nissen, S. E., & Nicholls, S. J. (2015). Atheroma progression in hyporesponders to statin therapy. Arteriosclerosis, Thrombosis, and Vascular Biology, 35(4), 990-5. https://doi.org/10.1161/ATVBAHA.114.304477
Kataoka Y, et al. Atheroma Progression in Hyporesponders to Statin Therapy. Arterioscler Thromb Vasc Biol. 2015;35(4):990-5. PubMed PMID: 25722430.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Atheroma progression in hyporesponders to statin therapy. AU - Kataoka,Yu, AU - St John,Julie, AU - Wolski,Kathy, AU - Uno,Kiyoko, AU - Puri,Rishi, AU - Tuzcu,E Murat, AU - Nissen,Steven E, AU - Nicholls,Stephen J, Y1 - 2015/02/26/ PY - 2015/2/28/entrez PY - 2015/2/28/pubmed PY - 2015/6/3/medline KW - LDL cholesterol KW - coronary artery disease KW - disease progression KW - statins, HMG-CoA SP - 990 EP - 5 JF - Arteriosclerosis, thrombosis, and vascular biology JO - Arterioscler Thromb Vasc Biol VL - 35 IS - 4 N2 - OBJECTIVE: Lowering low-density lipoprotein cholesterol (LDL-C) with statins has been demonstrated to slow plaque progression. This antiatherosclerotic effect in patients with minimal LDL-C lowering has not been investigated. APPROACH AND RESULTS: Six hundred forty-seven patients with angiographic coronary artery disease who were commenced on statin therapy underwent serial imaging with intravascular ultrasound. Responders were defined as a percentage reduction in LDL-C of <15%. Disease progression was compared in responders (n=517) and hyporesponders (n=130) to statin therapy. Twenty percentage of patients demonstrated minimal changes in LDL-C, despite commencement of statin therapy. Statin hyporesponders were younger (55 versus 57 years; P=0.01), more likely to be male (79% versus 66%; P=0.005), and obese (body mass index, 31.5 ± 6.1 versus 30.3 ± 5.9 kg/m(2); P=0.04) and less likely to have a history of dyslipidemia (50% versus 66%; P<0.001). Baseline levels of systolic blood pressure (127 ± 15 versus 132 ± 17 mm Hg; P=0.01) and LDL-C (2.5 ± 0.6 versus 3.4 ± 0.8 mmol/L; P<0.001) were lower in statin hyporesponders. Baseline percent atheroma volume was similar between statin hyporesponders and responders (36.9 ± 9.8% versus 38.3 ± 9.2%; P=0.13). On serial evaluation, greater progression of percent atheroma volume (1.19 ± 0.48% versus 0.09 ± 0.43%; P=0.003) was observed in statin hyporesponders. After adjusting for baseline clinical characteristics and measures of plaque burden, statin hyporesponders still exhibited greater atheroma progression (+0.83 ± 0.58% versus -0.21 ± 0.52%; P=0.006). CONCLUSIONS: A substantial proportion of patients with coronary artery disease fail to achieve effective reductions in LDL-C, despite prescription of statin therapy. Greater progression of atherosclerosis is observed in these patients. Our current study underscores monitoring LDL-C level after the commencement of statin to ensure adequate response to statin therapy. SN - 1524-4636 UR - https://www.unboundmedicine.com/medline/citation/25722430/Atheroma_progression_in_hyporesponders_to_statin_therapy_ DB - PRIME DP - Unbound Medicine ER -