Abstract：
The survival rate of adrenal Cushing syndrome patients has been greatly increased because of the availability of appropriate surgical and pharmacological treatments. Nevertheless, increased possibility of a heart attack induced by a cardiovascular event remains a major risk factor for the survival of affected patients. In experimental studies, hypercortisolemia has been found to cause cardiomyocyte hypertrophy via glucocorticoid receptor activation, including the possibility of cross talk among several hypertrophy signals related to cardiomyocytes and tissue-dependent regulation of 11β-hydroxysteroid dehydrogenase type 1. However, the factors are more complex in clinical cases, as both geometric and functional impairments leading to heart failure have been revealed, and their associations with a wide range of factors such as hypertension are crucial. In addition, knowledge regarding such alterations in autonomous cortisol secretion, which has a high risk of leading to heart attack as well as overt Cushing syndrome, is quite limited. When considering the effects of treatment, partial improvement of structural alterations is expected, while functional disorders are controversial. Therefore, whether the normalization of excess cortisol attenuates the risk related to cardiac hypertrophy has yet to be fully elucidated.
摘要：
由于有适当的手术和药物治疗，肾上腺库欣综合征患者的生存率大大提高。然而，心血管事件引起的心脏病发作的可能性增加仍然是影响患者生存的主要危险因素.在实验研究中,已经发现高皮质醇血症通过糖皮质激素受体激活引起心肌细胞肥大，包括与心肌细胞相关的几种肥大信号之间的串扰和11β-羟基类固醇脱氢酶1型的组织依赖性调节的可能性。然而,这些因素在临床病例中更为复杂，因为已经揭示了导致心力衰竭的几何和功能损害，它们与高血压等多种因素的联系至关重要。此外,关于这种自主皮质醇分泌变化的知识，导致心脏病发作和明显库欣综合征的风险很高，是相当有限的。在考虑治疗效果时，预计结构改造会有部分改进，而功能障碍是有争议的。因此,过量皮质醇的正常化是否会降低与心脏肥大相关的风险尚未完全阐明.
