Introduction
Type 2 diabetes mellitus (T2DM) is an important independent risk factor
for cardiovascular and cerebrovascular diseases.1Insulin has been widely used in the treatment of T2DM patients, and it
has made obvious effect on improving blood glucose level. But, according
to several research conclusions published recently, both insulin treated
DM and non-insulin treated DM patients have greater risk of major
adverse cardiovascular events (MACE) and mortality compared with
non-DM patients, and insulin treated DM suffered greater risk than
non-insulin treated DM,2-7 including short-term and
long-term risks.3, 7, 8 Nevertheless, it is unclear
about any causality suggestion between insulin treatment and outcomes.
As well known, Insulin has antiplatelet effect as well as hypoglycemic
effect,9, 10 normally, it should reduce the occurrence
of MACE, but the fact is opposite. Therefore, the relationship between
insulin therapy and platelet function has gradually become an important
research direction. In a randomized trial, Vivas et al thought that
intensive glucose control with insulin in patients with an acute
coronary syndrome reduced platelet reactivity during hospitalization.11 Nevertheless, after 12 months of follow-up,
platelet aggregation following adenosine diphosphate stimulation showed
no differences between optimized glucose control with insulin and
conventional control groups.12 Westerbacka et al found
that platelet-inhibitory actions of insulin under conditions mimicking
thrombus formation are blunted or absent in obese or insulin resistance
subjects.13 In order to further explore the
relationship between insulin therapy and platelet function, this study
was carried out.