TY - JOUR
T1 - Relation of high-density lipoprotein cholesterol:apolipoprotein a-i ratio to progression of coronary atherosclerosis in statin-treated patients
AU - Mani, Preethi
AU - Uno, Kiyoko
AU - St. John, Julie
AU - Tuzcu, E. Murat
AU - Nissen, Steven E.
AU - Nicholls, Stephen J.
N1 - Funding Information:
Dr. Nicholls reports receiving research support from AstraZeneca, Novartis, Eli Lilly, Anthera, LipoScience, Roche and Resverlogix and has received honoraria or been a consultant for AstraZeneca, Roche, Esperion, Sanofi-Aventis, Atheronova, Anthera, CSL Behring and Boehringer. Dr. Nissen has received research support from AstraZeneca, Abbott, Pfizer, Merck, Takeda, LipoScience, Omthera, Novo-Nordisk, Eli Lilly, Pfizer, Takeda, Sankyo, and Sanofi-Aventis. He has consulted for a number of pharmaceutical companies without financial compensation. All honoraria, consulting fees or any other payments from any for-profit entity are paid directly to charity, so that neither income nor any tax deduction is received. Drs. Mani, Uno and Tuzcu and Ms St. John have no disclosures to report.
PY - 2014/9/1
Y1 - 2014/9/1
N2 - High-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I (apoA-I) levels are inversely associated with adverse cardiovascular outcomes. Associations between these HDL-C-related measurements and coronary plaque progression have not been studied. We performed a retrospective analysis of 2,566 statin-treated patients with angiographic coronary artery disease who underwent serial evaluation of atheroma burden with intravascular ultrasound. Relations between achieved levels of HDL-related measurements with clinical characteristics and changes in plaque burden were determined. A strong correlation between HDL-C and apoA-I (r = 0.80, p <0.001) was observed. HDL-C, apoA-I, and the HDL-C:apoA-I ratio demonstrated negative correlations with the change in percent atheroma volume and total atheroma volume (all p ≤0.001). Increasing levels of achieved HDL-C:apoA-I (p = 0.04), but not HDL-C (p = 0.18) or apoA-I (p = 0.67), were associated with less progression of percent atheroma volume. Similar results were seen for change in total atheroma volume, with less progression seen with increased HDL-C:apoA-I (p = 0.002) but not with increases in HDL-C (p = 0.09) or apoA-I (p = 0.19). In conclusion, increasing levels of HDL-C:apoA-I associated with less progression of coronary atherosclerosis. This suggests that interventions increasing the cholesterol content of HDL particles may be of cardiovascular benefit.
AB - High-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I (apoA-I) levels are inversely associated with adverse cardiovascular outcomes. Associations between these HDL-C-related measurements and coronary plaque progression have not been studied. We performed a retrospective analysis of 2,566 statin-treated patients with angiographic coronary artery disease who underwent serial evaluation of atheroma burden with intravascular ultrasound. Relations between achieved levels of HDL-related measurements with clinical characteristics and changes in plaque burden were determined. A strong correlation between HDL-C and apoA-I (r = 0.80, p <0.001) was observed. HDL-C, apoA-I, and the HDL-C:apoA-I ratio demonstrated negative correlations with the change in percent atheroma volume and total atheroma volume (all p ≤0.001). Increasing levels of achieved HDL-C:apoA-I (p = 0.04), but not HDL-C (p = 0.18) or apoA-I (p = 0.67), were associated with less progression of percent atheroma volume. Similar results were seen for change in total atheroma volume, with less progression seen with increased HDL-C:apoA-I (p = 0.002) but not with increases in HDL-C (p = 0.09) or apoA-I (p = 0.19). In conclusion, increasing levels of HDL-C:apoA-I associated with less progression of coronary atherosclerosis. This suggests that interventions increasing the cholesterol content of HDL particles may be of cardiovascular benefit.
UR - http://www.scopus.com/inward/record.url?scp=84908363311&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84908363311&partnerID=8YFLogxK
U2 - 10.1016/j.amjcard.2014.06.001
DO - 10.1016/j.amjcard.2014.06.001
M3 - Article
C2 - 25030535
AN - SCOPUS:84908363311
SN - 0002-9149
VL - 114
SP - 681
EP - 685
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 5
ER -