Fernández-Fúnez Angel, Cabrera Solé Ricardo, Hernández Antonio, Martínez Victoria, Solera Javier
Servicios de Medicina Interna, Complejo Hospitalario Universitario de Albacete, Spain.
Med Clin (Barc). 2002 Mar 16;118(9):321-6. doi: 10.1016/s0025-7753(02)72374-9.
Diabetic cardiomyopathy (DMC) is a complication of diabetes mellitus (DM)that is more frequently observed in those patients with microalbuminuria. Left ventricular diastolic dysfunction (LVDD) in patients with diabetes, in absence of another etiology that justifies it, is an early marker of DMC. We carried out a prospective study on young diabetic type 1 patients with microalbuminuria, aimed at knowing the effect of captopril on LVDD.
We included 30 patients (18 males and 12 females) diagnosed with type 1 DM,aged 40 years old, who had been recently found to have microalbuminuria and thus they were candidates to receive captopril. We excluded patients having factors different from DM that could modify the diastolic function. All patients underwent a complete biochemical and echocardiographic study before starting the treatment with captopril and six months later. A diagnosis of LVDD was made when at least one of the following parameters was present in the echocardiographic study: isovolumetric relaxing time (IRT) >100 ms, deceleration time (DT) > 220 ms or early filling rate peak/late filling rate peak ratio (E/A) < 1. According to the results of the second echocardiogram, patients were classified in two groups: improved group (when there was at least a 10% improvement of initial LVDD altered parameters) and non-improved group. A control group of 28 type 1 diabetic patients without microalbuminuria who were not given captopril was included (group C).
The initial echocardiographic study yielded 11 patients having a normal diastolic function (group FDN) and 19 patients having LVDD (group FDA). After 6 moths of captopril treatment, an improvement of the ratio E/A was observed in the group FDN: from 1.58 (0.36)in the beginning to 1,68 (0.29) six moths later (p < 0.05),and in the group FDA: from 1.09 (0.24) to 1.24 (0.28) (p <0.05). In the group FDA, an improvement of IRT was found: from 110 (16) ms to 99.9 (9.6) ms (p < 0.01). Moreover, in the group FDA, LVDD improved after sixth months in 15 (78.9%) patients but not in 4 (21,6%). This LVDD improvement was associated with a decrease of the diastolic blood pressure (DBP) and the systolic blood pressure (SBP) at the end of the study. A logistic regression analysis showed an independent association between the reduction of the mean SBP and the improvement of LVDD.
Our results suggest that captopril can improve LVDD in young patients with type 1 diabetes and microalbuminuria, possibly due to a decrease of blood pressure.
糖尿病性心肌病(DMC)是糖尿病(DM)的一种并发症,在微量白蛋白尿患者中更为常见。糖尿病患者若不存在其他可解释病因的情况下出现左心室舒张功能障碍(LVDD),则是DMC的早期标志。我们对患有微量白蛋白尿的年轻1型糖尿病患者进行了一项前瞻性研究,旨在了解卡托普利对LVDD的影响。
我们纳入了30例(18例男性和12例女性)诊断为1型糖尿病、年龄40岁、近期发现有微量白蛋白尿且因此适合接受卡托普利治疗的患者。我们排除了具有不同于DM且可能改变舒张功能的因素的患者。所有患者在开始卡托普利治疗前及6个月后均接受了完整的生化和超声心动图检查。当超声心动图检查中出现以下至少一项参数时,诊断为LVDD:等容舒张时间(IRT)>100毫秒、减速时间(DT)>220毫秒或早期充盈率峰值/晚期充盈率峰值比值(E/A)<1。根据第二次超声心动图的结果,将患者分为两组:改善组(初始LVDD异常参数至少改善10%)和未改善组。纳入了28例未接受卡托普利治疗的无微量白蛋白尿的1型糖尿病患者作为对照组(C组)。
初始超声心动图检查显示,11例患者舒张功能正常(FDN组),19例患者有LVDD(FDA组)。卡托普利治疗6个月后,FDN组的E/A比值有所改善:开始时为1.58(0.36),6个月后为1.68(0.29)(p<0.05);FDA组从1.09(0.24)改善至1.24(0.28)(p<0.05)。在FDA组中,IRT有所改善:从110(16)毫秒降至99.9(9.6)毫秒(p<0.01)。此外,在FDA组中,6个月后15例(78.9%)患者的LVDD有所改善,4例(21.6%)患者未改善。这种LVDD的改善与研究结束时舒张压(DBP)和收缩压(SBP)的降低有关。逻辑回归分析显示,平均SBP的降低与LVDD的改善之间存在独立关联。
我们的结果表明,卡托普利可改善患有1型糖尿病和微量白蛋白尿的年轻患者的LVDD,可能是由于血压降低所致。