Silent myocardial ischaemia episodes in non-insulin dependent diabetes mellitus: relationship with haemostatic alterations

Abstract A hypercoagulable state possibly associated with metabolic alterations may contribute to the development of vascular damage in diabetes mellitus. The aim of this study was to evaluate the coagulation-fibrinolysis system in patients with non-insulin dependent diabetes mellitus (NIDDM), silent myocardial ischaemia (SMI). Fifty NIDDM patients were studied (24 men and 26 women) age 58.3±0.9 (mean ± M.S.E.) years and diabetes duration 9.2±0.8 (mean ± M.S.E.) years. None of the patients showed basal ECG alterations and all were under continuous ambulatory electrocardiographic monitoring for 48 h. A SMI episode was defined as an asymptomatic downslope of ST segment ⩾ 0.1 mV with a duration 0.08 s after J point of QRS complex, remaining at least for 1 min. Peripheral vasculopathy was evaluated from clinical data and physical examination. Pre and post venous occlusion blood samples were collected, measuring tissue-type plasminogen activator (t-PA) levels, tissue plasminogen activator fast acting inhibitor (PAI) activity, antithrombin III (AT-III) and glycosylated haemoglobin (Hb A 1c ). Ninety-eight control persons matched by age and sex were studied. Twenty-nine patients showed SMI, 7 had peripheral vasculopathy; none of the patients without SMI had peripheral vasculopathy (p 1c levels were higher in patients with SMI than those without it (p The increase of PAI levels in patients with SMI in comparison to controls may indicate an inhibition in fibrinolytic activity. The increase of AT-III may be considered as a reaction to hypercoagulability. Fibrinolytic response to stimulous was decreased in patients with peripheral vasculopathy and normal in the ones with SMI, which suggest that there are different stages in the evolution of vascular damage.