Zhu Shuzhen, Li Hualing, Xu Xiaoyan, Luo Yuqi, Deng Bin, Guo Xingfang, Guo Yang, Yang Wucheng, Wei Xiaobo, Wang Qing
Department of Neurology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Aging Dis. 2021 Oct 1;12(7):1675-1692. doi: 10.14336/AD.2021.0214. eCollection 2021 Oct.
Cardiovascular autonomic dysfunctions (CAD) are prevalent in Parkinson's disease (PD). It contributes to the development of cognitive dysfunction, falls and even mortality. Significant progress has been achieved in the last decade. However, the underlying mechanisms and effective treatments for CAD have not been established yet. This review aims to help clinicians to better understand the pathogenesis and therapeutic strategies. The literatures about CAD in patients with PD were reviewed. References for this review were identified by searches of PubMed between 1972 and March 2021, with the search term "cardiovascular autonomic dysfunctions, postural hypotension, orthostatic hypotension (OH), supine hypertension (SH), postprandial hypotension, and nondipping". The pathogenesis, including the neurogenic and non-neurogenic mechanisms, and the current pharmaceutical and non-pharmaceutical treatment for CAD, were analyzed. CAD mainly includes four aspects, which are OH, SH, postprandial hypotension and nondipping, among them, OH is the main component. Both non-neurogenic and neurogenic mechanisms are involved in CAD. Failure of the baroreflex circulate, which includes the lesions at the afferent, efferent or central components, is an important pathogenesis of CAD. Both non-pharmacological and pharmacological treatment alleviate CAD-related symptoms by acting on the baroreflex reflex circulate. However, pharmacological strategy has the limitation of failing to enhance baroreflex sensitivity and life quality. Novel OH treatment drugs, such as pyridostigmine and atomoxetine, can effectively improve OH-related symptoms via enhancing residual sympathetic tone, without adverse reactions of supine hypertension. Baroreflex impairment is a crucial pathological mechanism associated with CAD in PD. Currently, non-pharmacological strategy was the preferred option for its advantage of enhancing baroreflex sensitivity. Pharmacological treatment is a second-line option. Therefore, to find drugs that can enhance baroreflex sensitivity, especially via acting on its central components, is urgently needed in the scientific research and clinical practice.
心血管自主神经功能障碍(CAD)在帕金森病(PD)中普遍存在。它会导致认知功能障碍、跌倒甚至死亡。在过去十年中已经取得了重大进展。然而,CAD的潜在机制和有效治疗方法尚未确立。本综述旨在帮助临床医生更好地理解其发病机制和治疗策略。对有关PD患者CAD的文献进行了综述。通过检索1972年至2021年3月期间的PubMed确定了本综述的参考文献,检索词为“心血管自主神经功能障碍、体位性低血压、直立性低血压(OH)、卧位高血压(SH)、餐后低血压和非勺型血压”。分析了其发病机制,包括神经源性和非神经源性机制,以及目前针对CAD的药物和非药物治疗。CAD主要包括四个方面,即OH、SH、餐后低血压和非勺型血压,其中OH是主要组成部分。非神经源性和神经源性机制均参与CAD。压力反射循环功能衰竭,包括传入、传出或中枢成分的病变,是CAD的重要发病机制。非药物和药物治疗均通过作用于压力反射循环来缓解CAD相关症状。然而,药物治疗策略存在无法提高压力反射敏感性和生活质量的局限性。新型OH治疗药物,如吡啶斯的明和托莫西汀,可通过增强残余交感神经张力有效改善OH相关症状,且无卧位高血压不良反应。压力反射损害是PD中与CAD相关的关键病理机制。目前,非药物治疗策略因其增强压力反射敏感性的优势而成为首选。药物治疗是二线选择。因此,在科研和临床实践中迫切需要找到能够提高压力反射敏感性的药物,尤其是通过作用于其中心成分的药物。