ABSTRACT
Diabetes mellitus is a risk factor for cardiovascular and cerebrovascular events independently of other factors such as age, sex, BMI and blood pressure. Diabetes plays an important role in the pathogenesis of atrial fibrillation because it causes alterations to the autonomic nervous system. It may also be associated with an increased prevalence of asymptomatic episodes of atrial fibrillation, which cause cerebrovascular disease more often than chronic atrial fibrillation. The presence of silent cerebral ischemia doubles the risk of stroke in the general population independently of other cardiovascular risk factors; therefore, early detection of these episodes is important to determine preventive measures against the first cerebrovascular disease.
Subject(s)
Atrial Fibrillation/complications , Cerebrovascular Disorders/complications , Diabetes Complications/complications , Diabetes Mellitus/diagnosis , Stroke/complications , Animals , Atrial Fibrillation/diagnosis , Atrial Fibrillation/etiology , Cerebrovascular Disorders/etiology , Diabetes Complications/diagnosis , Humans , Risk Factors , Stroke/diagnosis , Stroke/etiologyABSTRACT
BACKGROUND: We examined the effects of peri-procedural intensive glycemic control during early percutaneous coronary intervention (PCI) on the number and differentiation of endothelial progenitor cells (EPCs) and myocardial salvage (MS) in hyperglycemic patients with first ST-elevation myocardial infarction (STEMI). METHODS AND RESULTS: We conducted a randomized, prospective, open label study on 194 patients with STEMI undergoing PCI: 88 normoglycemic patients (glucose < 140 mg/dl) served as the control group. Hyperglycemic patients (glucose ≥140 mg/dl) were randomized to intensive glycemic control (IGC) for almost 24 h after PCI (n = 54; 80-140 mg/dl) or conventional glycemic control (CGC, n = 52; 180-200 mg/dl). EPC number, differentiation, and SIRT1expression were assessed immediately before, 24 h, 7, 30 and 180 days after PCI. The primary end point of the study was salvage index, measured as the proportion of initial perfusion defect (acute technetium-99m sestamibi scintigraphy, performed 5 to 7 days after STEMI) and myocardium salvaged by therapy (6 months after STEMI). Hyperglycemic patients had lower EPC number and differentiation and lower SIRT1 levels than normoglycemic patients (P < 0.01). After the insulin infusion, mean plasma glucose during peri-procedural period was greater in CGC group than in IGC group (P < 0.001). The EPC number, their capability to differentiate, and SIRT1 levels were significantly higher in IGC group than in CGC, peaking after 24 h (P < 0.01). In the IGC group, the salvage index was greater than in patients treated with CGC (P < 0.001). CONCLUSIONS: Optimal peri-procedural glycemic control, by increasing EPC number and their capability to differentiate, may improve the myocardial salvage.
