Influence Of Hypoglycaemic Agents On The Level Of Circulating EPCs In CHD And DM Patients

ObjectiveThe decreased level as well as insufficient functions of endothelial cells is believed to involve in the initiation and progression of coronary heart disease(CHD). Endothelial progenitor cells (EPCs) have the potential to differentiate into mature endothelial cells, improving impairment of damaged endothelium. A variety of characteristic parameters of EPCs(including the numbers and functions)have an inverse relationship with the conventional cardiovascular risk factors, including DM, which is popular found in CHD patients. By means of measuring serum concentration of CD34~+/VEGFR~+ EPCs with fluorescence activated cell sorter in patients who are suffering from stable CHD together with diabetes mellitus (DM) .Simultaneously, we can observe the contribution of DM for the impairment of endothelial cells in vascular by choosing CHD patients without DM in comparison with CHD with DM patients. We do not only investigate the effect of EPCs on the genesis and development of such type of disease, but also evaluate the improvement effect of oral hypoglycaemic agents /insulin on the levels of CD34~+/VEGFR-2~+EPCs.This can be acomplished by a following-up period of four weeks ensueing such condition that the level of FPG is beteewn 5-7.2mmol/L, together with the level of 2hPG is under 10mmol/L.MethodsTaken from oct.2010 to Apr.2011,patients after admission of CHD by having undergone coronary angiography (CAG)were involved in this study. Blood samples were obtained from venous at the next morning for the lipoprotein and glucose. And those who were suspicious of abnormal glucose were singled out to take part in standard glucose intolerance test. Those cases who had been diagnosed DM but with badly-controlled blood glucose also could enroll in. Finally, 44cases of CHD and DM patients were recruited (GHbA1c were tested in this group),41cases of CHD patients without DM were engaged. 2ml of heparinized blood samples were immediately disposed for direct immunofluor- escence.The levels of CD34~+/VEGFR-2~+ EPCs were evaluated by FACS to analyze the levels in the whole blood. At last,we performed a follow-up period of 4 weeks ensuing a stable level of blood glucose by adopting feasible hypoglycaemic agents for CHD and DM patients to observe the changes of items above,and affirmed the conclusion that OHAs/insulin have regulation effect on the functional endolithial cells.Results:(1) There were no significant differences in age, gender, blood lipid, blood pressure, frequency of smoking, or body weight index between CHD patients and CHD with DM patients.(2) The severity was classified in terms of the morbid branch numbers of coronary arteries. It demonstrated that the decreased levels of CD34~+/VEGFR-2~+EPCs were in accordance with the severity of coronary artery disease. Patients with multivessel CHD, had significantly lower EPC counts as compared to those without.(3) The severity of coronary artery disease positively correlate with GHbA1c(P<0.05). the decreasing levels of EPCs was followed by the increasing levels of GHbA1c.That is to say, EPCs is negatively with GHbA1c(P<0.05).(4) Compaired on the same branch number of morbid coronary artery, CD34~+/ VEGF- R-2~+EPCs in CHD and DM patients are lower than that in CHD patients (P<0.05).(5) Hypoglycaemic agents contribute to ascending the serum level of CD34~+/VEGFR- 2~+ EPCs(P<0.05).ConclusionsThe maintenance of endothelial integrity is of crucial importance for preventing the triggering of these processes. CHD combination with DM patents have a more possibility to suffer form multivessel impairement, which bring about the result that the mobilization of EPCs is much more. EPCs has the potential to different into endothelium. GHbA1c act as the criteria of the levels of blood glucose, maybe envolve in the process of EPCs impairment.The hypoglycemic agents can promote the levels of EPCs by decreasing the leves of blood glucose. This can ameliorate the the loss of endothelium, and is in favor of retarding the processs of atherosclerosis(AS).However, it still can't revert to the level of EPCs in CHD.