ERYTHROCYTE NA+ H+ EXCHANGE AND PRECLINICAL ABNORMALITIES OF THE LEFT-VENTRICULAR DIASTOLIC FUNCTION IN NORMOTENSIVE TYPE-1 (INSULIN-DEPENDENT) DIABETIC-PATIENTS/

We assessed the relationship between erythrocyte Na+/H+ antiport activ ity and myocardial anatomical-functional parameters (by Doppler echoca rdiography) in normotensive IDDM patients, with and without microalbum inuria. We studied 33 normotensive IDDM subjects and 14 matched health y controls (group 4). Based on urinary albumin excretion rate (UAER), 23 diabetics were normoalbuminuric, 10 microalbuminuric (group 3). Nor moalbuminurics were divided up for normal (group 1, n = 13) or high (g roup 2, n = 10) antiport activity. We evaluated fasting glycaemia and 24-h urine glucose output, HbAlc, plasma lipids, urea, creatinine and electrolyte clearances, UAER, erythrocyte Na+/H+ countertransport, M-M ode and 2D echocardiograms with Doppler analysis. Antiport, which was higher in diabetics than controls, was significantly overactive in gro ups 2 and 3 vs group 4, independently from UAER. Diabetics showed left ventricular volume, cardiac mass and systolic function within the con trol range. In left ventricular diastolic filling, while peak E was si milar in diabetic and healthy people, the late peak transmitral flow v elocity (peak A) was significantly higher in diabetics than controls, and this was also true in groups 2 and 3 vs group 4. Antiport activity was positively related to peak A (p < 0.03). These observations sugge st that (a) the Na+/H+ antiport may be overactive in diabetes, apart f rom microalbuminuria; (b) increased Na+/H+ antiport activity, in normo tensive IDDM people, may be associated with preclinical diastolic myoc ardial dysfunction (''incipient diabetic cardiomyopathy''?).