Prevention of Cardiac and Vascular Events in Patients With NGT/IGT.
Status:
Completed
Trial end date:
2006-11-01
Target enrollment:
Participant gender:
Summary
Impaired glucose tolerance or mild glucose elevations in the non-diabetic range are
associated with increased cardiovascular disease and recent studies suggested the need to
detect these glucose abnormalities early in the post-infarction period. Although in the last
ten years procedures of coronary revascularisation have dramatically improved the outcome of
non diabetic patients affected by ischemic heart disease, these procedures are less effective
in patients with type 2 diabetes mellitus and IGT. Possible causes of worse prognosis in
these patients could be related to the presence of hyperinsulinemia and insulin resistance
due to the well known effect of insulin to increase neointimal tissue proliferation and
in-stent restenosis, by stimulating vascular smooth muscle cell growth factors and migration.
In addition, it is well known that endothelial dysfunction is an early functional disturbance
in the development of atherosclerotic lesions. The impairment of eNOS action might change the
turnover rate of eNOS or nitric oxide production and action influencing nitric oxide
signalling, apoptosis cascade and angiogenesis. All these factors can contribute to
endothelial dysfunction to a certain extent, and accelerate atherosclerosis with increased
risk for cardiovascular disease.
The constitutively expressed eNOS, is likely to be the major contributors to whole-body
nitric oxide production. It is interesting to note that a region of chromosome 7q seems to
influence both insulin resistance and blood pressure, suggesting that this locus may broadly
influence traits associated with insulin resistance.
L-arginine is an essential amino acid and its availability is important for the normal
endothelial cell function and its intracellular reduction may contribute to the dysfunctional
endothelial state. It is well known that L-arginine is as a precursor for nitric oxide and
both in vitro and in vivo studies have demonstrated that L-arginine can augment vascular
dilation under certain conditions.
Our hypothesis is to evaluate the modulating effect of L-arginine on metabolic, endothelial
variables and on myocardial function in patients with cardiovascular disease.