Atheroma progression in hyporesponders to statin therapy

• Published in: Arteriosclerosis, thrombosis, and vascular biology Vol. 35; no. 4; pp. 990 - 995
• Main Authors: Kataoka, Yu, St John, Julie, Wolski, Kathy, Uno, Kiyoko, Puri, Rishi, Tuzcu, E Murat, Nissen, Steven E, Nicholls, Stephen J
• Format: Journal Article
• Language: English
• Published: United States 01.04.2015
• Subjects: Aged; Biomarkers - blood; Blood Pressure; Cholesterol, LDL - blood; Clinical Trials as Topic; Coronary Artery Disease - blood; Coronary Artery Disease - diagnosis; Coronary Artery Disease - drug therapy; Coronary Artery Disease - epidemiology; Coronary Artery Disease - physiopathology; Disease Progression; Drug Resistance; Dyslipidemias - blood; Dyslipidemias - diagnosis; Dyslipidemias - drug therapy; Dyslipidemias - epidemiology; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use; Male; Middle Aged; Prevalence; Risk Factors; Time Factors; Tomography, X-Ray Computed; Treatment Outcome; Ultrasonography, Interventional; coronary artery disease; disease progression; statins, HMG-CoA; LDL cholesterol
• ISSN: 1079-5642; 1524-4636
• DOI: 10.1161/atvbaha.114.304477

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. 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). 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.