Burger A J, Aronson D
Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, West Campus Noninvasive Cardiology Laboratory, Baker-3 1 Deaconess Road, Boston, MA 02215, USA.
Int J Cardiol. 2001 Dec;81(2-3):243-9. doi: 10.1016/s0167-5273(01)00573-3.
The risk for congestive heart failure is strongly increased in diabetes, and the prognosis of diabetic patients with established heart failure is worse compared to nondiabetic patients. Heart failure entails complex alterations in autonomic and neurohormonal responses, which exert a direct deleterious effect on the heart and contribute to progressive circulatory failure. Altered neurohumoral physiology may underlie the poor prognosis of diabetic patients with heart failure.
We studied 88 patients (mean age 61+/-13 years) admitted for decompensated heart failure. Neurohormonal and cytokine profiles, including plasma renin activity, aldosterone, norepinephrine, endothelin-1, tumor necrosis factor-alpha, and interleukin-6, were obtained in all patients. In addition, a 24-h Holter recording was performed, and time and frequency domain heart rate variability indices were calculated.
Of 88 patients, 48 were classified as having diabetes based on history, diet therapy, or use of oral hypoglycemic agents or insulin. The only difference in the neurohormonal and cytokine profile between the diabetic and nondiabetic groups was a significantly lower norepinephrine level in diabetic patients (668+/-64 vs. 489+/-50 pg/ml, P=0.009). Heart rate variability analysis revealed that the low-frequency power in normalized units (an index of sympathetic modulation) was significantly lower in diabetic patients (4.7+/-1.4 vs. 5.9+/-0.9, P=0.04). No significant differences occurred in any of the time (the percentage of RR intervals with >50 ms variation and the square root of mean squared differences of successive RR intervals) or frequency domain (high frequency power) indices of parasympathetic modulation between the two groups.
Patients with diabetes mellitus exhibit a blunted sympathetic response during heart failure decompensation. Blunted sympathetic activation in the setting of symptomatic heart failure may impair the ability of the myocardium to compensate and contribute to the high incidence of symptomatic heart failure among diabetic patients.
糖尿病患者发生充血性心力衰竭的风险显著增加，与非糖尿病患者相比，已确诊心力衰竭的糖尿病患者预后更差。心力衰竭会导致自主神经和神经激素反应发生复杂改变，这些改变会对心脏产生直接有害影响，并促使循环衰竭进展。神经体液生理改变可能是糖尿病心力衰竭患者预后不良的原因。
我们研究了88例因失代偿性心力衰竭入院的患者（平均年龄61±13岁）。获取了所有患者的神经激素和细胞因子谱，包括血浆肾素活性、醛固酮、去甲肾上腺素、内皮素-1、肿瘤坏死因子-α和白细胞介素-6。此外，进行了24小时动态心电图记录，并计算了时域和频域心率变异性指标。
88例患者中，48例根据病史、饮食治疗或口服降糖药或胰岛素的使用情况被归类为患有糖尿病。糖尿病组和非糖尿病组在神经激素和细胞因子谱方面的唯一差异是糖尿病患者去甲肾上腺素水平显著较低（668±6 pg/ml对489±50 pg/ml，P=0.009）。心率变异性分析显示，糖尿病患者以标准化单位表示的低频功率（交感神经调节指标）显著较低（4.7±1.4对5.9±0.9，P=0.04）。两组之间在副交感神经调节的任何时域指标（RR间期变化>50 ms的百分比和连续RR间期均方差的平方根）或频域指标（高频功率）上均未出现显著差异。
糖尿病患者在心力衰竭失代偿期间表现出交感神经反应迟钝。在有症状心力衰竭的情况下，交感神经激活减弱可能会损害心肌的代偿能力，并导致糖尿病患者中有症状心力衰竭的发生率较高。
