Journal
LANCET
Volume 371, Issue 9626, Pages 1800-1809Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S0140-6736(08)60768-0
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Funding
- NHLBI NIH HHS [P01 HL018645, P01 HL030086, P01 HL048743, HL071745, R01 HL039653-17, R01 HL071745, P01 HL030086-250013, HL48743, HL39653, R01 HL039653, P01 HL048743-160013, P01 HL018645-340022, R01 HL071745-04, HL19645, HL30086] Funding Source: Medline
- NIDDK NIH HHS [R56 DK071711, R01 DK071711-03, DK71711, R01 DK071711] Funding Source: Medline
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Individuals with type 2 diabetes mellitus have increased cardiovascular disease risk compared with those without diabetes. Treatment of the residual risk, other than blood pressure and LDL-cholesterol control, remains important as the rate of diabetes increases worldwide. The accelerated atherosclerosis and cardiovascular disease in diabetes is likely to be multifactorial and therefore several therapeutic approaches can be considered. Results of mechanistic studies done in vitro and in vivo-animals and people-can provide important insights with the potential to improve clinical management decisions and outcomes. in this Review, we focus on three areas in which pathophysiological. considerations could be particularly informative ie, the roles of hyperglycaemia, diabetic dyslipidaemia (other than the control of LDL-cholesterol concentrations), and inflammation (including that in adipose tissue) in the acceleration of vascular injury.
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