Verloop Willemien L, Beeftink Martine M A, Santema Bernadet T, Bots Michiel L, Blankestijn Peter J, Cramer Maarten J, Doevendans Pieter A, Voskuil Michiel
Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.
The Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands.
PLoS One. 2015 Feb 6;10(2):e0117332. doi: 10.1371/journal.pone.0117332. eCollection 2015.
Heart failure with preserved left ventricular ejection fraction (HFPEF) affects about half of all patients diagnosed with heart failure. The pathophysiological aspect of this complex disease state has been extensively explored, yet it is still not fully understood. Since the sympathetic nervous system is related to the development of systolic HF, we hypothesized that an increased sympathetic nerve activation (SNA) is also related to the development of HFPEF. This review summarizes the available literature regarding the relation between HFPEF and SNA.
Electronic databases and reference lists through April 2014 were searched resulting in 7722 unique articles. Three authors independently evaluated citation titles and abstracts, resulting in 77 articles reporting about the role of the sympathetic nervous system and HFPEF. Of these 77 articles, 15 were included for critical appraisal: 6 animal and 9 human studies. Based on the critical appraisal, we selected 9 articles (3 animal, 6 human) for further analysis. In all the animal studies, isoproterenol was administered to mimic an increased sympathetic activity. In human studies, different modalities for assessment of sympathetic activity were used. The studies selected for further evaluation reported a clear relation between HFPEF and SNA.
Current literature confirms a relation between increased SNA and HFPEF. However, current literature is not able to distinguish whether enhanced SNA results in HFPEF, or HFPEF results in enhanced SNA. The most likely setting is a vicious circle in which HFPEF and SNA sustain each other.
左心室射血分数保留的心力衰竭(HFpEF)影响着约一半被诊断为心力衰竭的患者。这种复杂疾病状态的病理生理学方面已得到广泛探索,但仍未被完全理解。由于交感神经系统与收缩性心力衰竭的发展有关,我们假设交感神经激活增加(SNA)也与HFpEF的发展有关。本综述总结了关于HFpEF与SNA之间关系的现有文献。
检索截至2014年4月的电子数据库和参考文献列表,共获得7722篇独特文章。三位作者独立评估文章标题和摘要,最终有77篇文章报道了交感神经系统与HFpEF的作用。在这77篇文章中,15篇被纳入严格评价:6篇动物研究和9篇人体研究。基于严格评价,我们选择了9篇文章(3篇动物研究,6篇人体研究)进行进一步分析。在所有动物研究中,使用异丙肾上腺素来模拟交感活性增加。在人体研究中,采用了不同的交感活性评估方式。被选作进一步评估的研究报道了HFpEF与SNA之间存在明确关系。
当前文献证实了SNA增加与HFpEF之间的关系。然而,当前文献无法区分是增强的SNA导致HFpEF,还是HFpEF导致增强的SNA。最可能的情况是一个恶性循环,即HFpEF和SNA相互维持。