The increased risk for CAD from diabetes is due to factors that may be specific for diabetes. The blood in diabetic patients have been found to have increased platelet aggregation, decreased red cell deformability and reduced fibrinolytic activity. The glycation of lipoproteins may lead to decreased clearance by the liver and increased atherosclerosis.
There are a lot of possible mechanisms but determining causality is difficult. Diabetes often present with 'diabetic dyslipidemia' or low HDL-c and high LDL-c. Increased LDL-c alone is enough to increase CVD risk. How LDL-c becomes elevated with diabetes probably stems from hepatic insulin resistance and/or steatosis, resulting in overproduction of apoB100-containing lipoproteins (VLDL).
LDL-c independent effects of hyperglycemia could be through promoting inflammation (a major component of atherosclerosis) or through increasing endothelial cell dysfunction, making the vessel walls themselves more inflamed and susceptible to lipoprotein infiltration and retention.
A recent study shed some light on an outstanding question which was whether lowering glucose (HBa1c) on its own could reduce CVD risk. The Veterans Affairs Diabetes Trial (VADT) had previously showed that after 5 years there was a non-significant decrease in CVD risk with intensive glucose management therapy . Recently published in NEJM was an extended follow-up of VADT (after 10 years) and it in fact did show a significant reduction in CVD events with strict glucose managagement therapy. http://www.nejm.org/doi/full/10.1056/NEJMoa1414266#t=article
Also, empagliflozin has recently been shown to be the first anti-diabetic drug to lower mortality in a CVOT. http://www.nejm.org/doi/full/10.1056/NEJMoa1504720#t=article
Some of various mechanisms are cited propely above. We know that +/- 70% of diabetics dye of cardiovascular complications. There's no consensus about the links and development of cardiovascular patology in diabetics. I offer to you and all of us a reviiew paper by Roever at all with a good vision over this issue:
Roever at all, J. Diabetic Metabolics 2014, 5:8 - omicsonline.org
I agree with all commentaries. Many consider daibetes itself a disease entity that is a precursor to macrovascular disease which accelerated atherosclerosis.
Insulin regulates the cardiovascular system apart from its effect on glucose. Insulin regulates eNOS and NO (capillary recruitment, tissue recruitment etc.). Insulin deficiency/insulin resistance decreases NO and capillary function.
The cause of Macrovascular complications such as cardiac diseases in T2DM is due to associated Dyslipidemia & hypertension which cause Atherosclerotic cardiovascular disease . This is probably due to polygenic inheritance of DM / Dyslipidemia & hypertension . Control of DM does not prevent coronary artery disease & there is need for statins to treat dyslipidemia & ACEI/ARB to treat hypertension to prevent CAD . In T1DM it is microvascular complications ( CKD) which is the cause of morbidity & mortality than CAD .