[Glyco-lipid changes in hypertensive diabetic patients undergoing treatment with nifedipine and captopril]

Atherosclerosis in diabetic subjects is improved by the reduced repair capacity of endothelial damage and by the increased platelet aggregation, peculiar to diabetic pathology. The contemporary presence of high blood pressure, diabetes and lipoidoproteinosis, increasing the possibility of cardiovascular damage, also under well-controlled blood pressure values, certainly increases the risk of atherosclerosis. However we have valued the presence of lipoidoproteinosis in 52 of our diabetic-hypertensive patients in a follow-up of 40 months. The patients have been split in to two groups of 26 patients each, one being treated with nifedipine, the other to with captopril. The data obtained have been compared with the data for the two control groups (non diabetic patients). The selection has been carried out according to established criteria. We have investigated: glycaemia, total cholesterol, HDL-C, LDL-C, triglycerides, tot. Chol./HDL-C, LDL-C/HDL-C. During follow-up the blood pressure values were significantly reduced (p < 0.01) (captopril: delta SBP = -13.88, delta DBP = -12.38, nifedipine: delta SBP = -22.03, delta DBP = -21.35). In the nifedipine group lipoidoproteinosis has been more marked: delta% glicaemia = +17.69, delta% cholesterolemia = +20.11; delta% CFR = +18.57; LDL-C = +35.11; delta% VRF = +34.61, while in the patients treated with captopril we have had the following results: delta% glycaemia = +15.43; delta% cholesterolemia = +16.36; delta% LDL-C = +26.68. The control group with nifedipine treatment have shown only increased values of cholesterolemia: delta% = +4.80, moreover in the control group treated with captopril we have observed a reduction of VRF: delta% = -15. A significant relationship between total cholesterolemia and glycaemia in the group with nifedipine treatment (p < 0.01) and captopril (p < 0.01) has been reported. This study could appear to underline the autonomic nervous system activation by nifedipine which does not affect lipoidoproteinosis in diabetic hypertensive subjects. This would seem to confirm on the contrary, the utility of captopril in the treatment of atherosclerotic subjects, as diabetic hypertensive patients.