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|dc.identifier.citation||Arteriosclerosis, Thrombosis, and Vascular Biology, 2016; 36(11):2220-2228||en|
|dc.description.abstract||Objectives: Non–high-density lipoprotein cholesterol (non-HDLC) levels reflect the full burden of cholesterol transported in atherogenic lipoproteins. Genetic studies suggest a causal association between elevated triglycerides (TGs)-rich lipoproteins and atherosclerosis. We evaluated associations between achieved non-HDLC and TG levels on changes in coronary atheroma volume. Approach and Results: Data were analyzed from 9 clinical trials involving 4957 patients with coronary disease undergoing serial intravascular ultrasonography to assess changes in percent atheroma volume (ΔPAV) and were evaluated against on-treatment non-HDLC and TG levels. The effects of lower (<100 mg/dL) versus higher (≥100 mg/dL) achieved non-HDLC levels and lower (<200 mg/dL) versus higher (≥200 mg/dL) achieved TG levels were evaluated in populations with variable on-treatment low-density lipoprotein cholesterol (LDLC) </≥70 mg/dL and C-reactive protein </≥2 mg/L and in patients with or without diabetes mellitus. On-treatment non-HDLC levels linearly associated with ΔPAV. Overt PAV progression (ΔPAV>0) was associated with achieved TG levels >200 mg/dL, respectively. Lower on-treatment non-HDLC and TG levels associated with significant PAV regression compared with higher non-HDLC and TG levels across all levels of LDLC and C-reactive protein and irrespective of diabetic status (P<0.001 across all comparisons). ΔPAV were more strongly influenced by changes in non-HDLC (β=0.62; P<0.001) compared with changes in LDLC (β=0.51; P<0.001). Kaplan–Meier sensitivity analyses demonstrated significantly greater major adverse cardiovascular event rates in those with higher versus lower non-HDLC and TG levels, with an earlier separation of the non-HDLC compared with the LDLC curve. Conclusions: Achieved non-HDLC levels seem more closely associated with coronary atheroma progression than LDLC. Plaque progression associates with achieved TGs, but only above levels of 200 mg/dL. These observations support a more prominent role for non-HDLC (and possibly TG) lowering in combating residual cardiovascular risk.||en|
|dc.description.statementofresponsibility||Rishi Puri, Steven E. Nissen, Mingyuan Shao, Mohamed B. Elshazly, Yu Kataoka, Samir R. Kapadia, E. Murat Tuzcu, Stephen J. Nicholls||en|
|dc.publisher||Lippincott Williams & Wilkins||en|
|dc.rights||© 2016 American Heart Association, Inc.||en|
|dc.subject||Atherosclerosis; low-density lipoprotein; non-HDL; residual risk; triglycerides||en|
|dc.title||Non-HDL cholesterol and triglycerides: implications for coronary atheroma progression and clinical events||en|
|dc.identifier.orcid||Nicholls, S. [0000-0002-9668-4368]||en|
|Appears in Collections:||Medicine publications|
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