Fazio S, Sabatini D, Capaldo B, Vigorito C, Giordano A, Guida R, Pardo F, Biondi B, Saccà L
Department of Internal Medicine, University Federico II, Naples, Italy.
N Engl J Med. 1996 Mar 28;334(13):809-14. doi: 10.1056/NEJM199603283341301.
Cardiac hypertrophy is a physiologic response that allows the heart to adapt to an excess hemodynamic load. We hypothesized that inducing cardiac hypertrophy with recombinant human growth hormone might be an effective approach to the treatment of idiopathic dilated cardiomyopathy, a condition in which compensatory cardiac hypertrophy is believed to be deficient.
Seven patients with idiopathic dilated cardiomyopathy and moderate-to-severe heart failure were studied at base line, after three months of therapy with human growth hormone, and three months after the discontinuation of growth hormone. Standard therapy for heart failure was continued throughout the study. Cardiac function was evaluated with Doppler echocardiography, right-heart catheterization, and exercise testing.
When administered at a dose of 14 IU per week, growth hormone doubled the serum concentrations of insulin-like growth factor I. Growth hormone increased left-ventricular-wall thickness and reduced chamber size significantly. Consequently, end-systolic wall stress (a function of both wall thickness and chamber size) fell markedly (from a mean [+/-SE] of 144+/-11 to 85+/-8 dyn per square centimeter, P<0.001). Growth hormone improved cardiac output, particularly during exercise (from 7.4+/-0.7 to 9.7+/-0.9 liters per minute, P=0.003), and enhanced ventricular work, despite reductions in myocardial oxygen consumption (from 56+/-6 to 39+/-5 ml per minute, P=0.005) and energy production (from 1014+/-100 to 701+/-80 J per minute, P=0.002). Thus, ventricular mechanical efficiency rose from 9+/-2 to 21+/-5 percent (P=0.006). Growth hormone also improved clinical symptoms, exercise capacity, and the patients' quality of life. The changes in cardiac size and shape, systolic function, and exercise tolerance were partially reversed three months after growth hormone was discontinued.
Recombinant human growth hormone administered for three months to patients with idiopathic dilated cardiomyopathy increased myocardial mass and reduced the size of the left ventricular chamber, resulting in improvement in hemodynamics, myocardial energy metabolism, and clinical status.
心脏肥大是一种生理反应，可使心脏适应过高的血流动力学负荷。我们推测，用重组人生长激素诱导心脏肥大可能是治疗特发性扩张型心肌病的一种有效方法，这种疾病被认为存在代偿性心脏肥大不足的情况。
对7例特发性扩张型心肌病合并中重度心力衰竭患者进行了研究，分别在基线、接受生长激素治疗3个月后以及停用生长激素3个月后进行观察。在整个研究过程中持续进行心力衰竭的标准治疗。采用多普勒超声心动图、右心导管检查和运动试验评估心脏功能。
当以每周14 IU的剂量给药时，生长激素使胰岛素样生长因子I的血清浓度增加了一倍。生长激素显著增加了左心室壁厚度并减小了腔室大小。因此，收缩末期壁应力（壁厚度和腔室大小的函数）显著下降（从平均[±标准误]144±11降至85±8达因每平方厘米），P<0.001。生长激素改善了心输出量，尤其是在运动期间（从7.4±0.7升至9.7±0.9升每分钟），P=0.003，并增强了心室作功，尽管心肌氧耗量（从56±6降至39±5毫升每分钟），P=0.005和能量产生（从1014±100降至701±80焦耳每分钟），P=0.002有所降低。因此，心室机械效率从9±2升至21±5%，P=0.006。生长激素还改善了临床症状、运动能力和患者的生活质量。在停用生长激素3个月后，心脏大小和形状、收缩功能以及运动耐量的变化部分得到逆转。
对特发性扩张型心肌病患者给予重组人生长激素治疗3个月可增加心肌质量并减小左心室腔室大小，从而改善血流动力学、心肌能量代谢和临床状况。
