Cicco G, Pirrelli A
Università degli Studi, Policlinico Consorziale, Bari.
Minerva Med. 1993 Mar;84(3):119-24.
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.
糖尿病患者的动脉粥样硬化因内皮损伤修复能力降低以及血小板聚集增加(这是糖尿病病理的特有现象)而加重。高血压、糖尿病和脂蛋白血症同时存在,增加了心血管损伤的可能性,即便血压值控制良好,也无疑会增加动脉粥样硬化的风险。然而,我们在40个月的随访中评估了52例糖尿病高血压患者中脂蛋白血症的情况。患者被分为两组,每组26例,一组用硝苯地平治疗,另一组用卡托普利治疗。将所得数据与两个对照组(非糖尿病患者)的数据进行了比较。选择是根据既定标准进行的。我们调查了:血糖、总胆固醇、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、甘油三酯、总胆固醇/高密度脂蛋白胆固醇、低密度脂蛋白胆固醇/高密度脂蛋白胆固醇。在随访期间,血压值显著降低(p<0.01)(卡托普利:收缩压变化量= -13.88,舒张压变化量= -12.38;硝苯地平:收缩压变化量= -22.03,舒张压变化量= -21.35)。在硝苯地平组中,脂蛋白血症更为明显:血糖变化百分比= +17.69,胆固醇血症变化百分比= +20.11;高密度脂蛋白胆固醇变化百分比= +18.57;低密度脂蛋白胆固醇= +35.11;极低密度脂蛋白变化百分比= +34.61,而在接受卡托普利治疗的患者中,我们得到了以下结果:血糖变化百分比= +15.43;胆固醇血症变化百分比= +16.36;低密度脂蛋白胆固醇变化百分比= +26.68。接受硝苯地平治疗的对照组仅显示胆固醇血症值升高:变化百分比= +4.80,此外,在接受卡托普利治疗的对照组中,我们观察到极低密度脂蛋白降低:变化百分比= -15。据报道,硝苯地平治疗组(p<0.01)和卡托普利治疗组(p<0.01)中总胆固醇血症与血糖之间存在显著关系。这项研究似乎强调了硝苯地平对糖尿病高血压患者自主神经系统的激活作用,而这并不影响脂蛋白血症。相反,这似乎证实了卡托普利在治疗动脉粥样硬化患者(如糖尿病高血压患者)中的效用。