高血压在射血分数保留的心力衰竭发展中的作用

射血分数保留的心力衰竭目前依然有很多问题尚未解决,例如未能形成公认的定义和治疗方法等。大多数射血分数保留的心力衰竭患者存在动脉性高血压,目前尚不清楚其是否是导致射血分数保留的心力衰竭发展的必要条件。高血压和射血分数保留的心力衰竭的潜在发病机制涉及相同的生物系统:肾素-血管紧张素-醛固酮系统、交感神经系统和氧化应激反应。并非所有高血压患者都有射血分数保留的心力衰竭,但其中一些高血压患者具有发展为射血分数保留的心力衰竭的倾向性。对于射血分数保留的心力衰竭患者大型随机对照试验未证实肾素-血管紧张素-醛固酮系统抑制剂、利尿剂、钙通道阻滞剂和β受体阻滞剂的治疗有效性,即大多数研究未能证明射血分数保留的心力衰竭患者用药后全因死亡率降低,这些研究的主要局限性之一是射血分数保留的心力衰竭定义的不一致性,指在不同研究中左心室射血分数截断值介于40%～50%。这篇综述文章提供了关于高血压和射血分数保留的心力衰竭之间的病理生理学和机制,以及在这两种情况下调查和治疗的有价值数据。     

射血分数保留性心力衰竭:从机制到治疗

射血分数保留性心力衰竭是一个全球性的重大公共卫生问题.它是一种异质性综合征,由于复杂的病理机制和缺乏单一的诊断标准,其诊断及治疗具有挑战性.目前还无公认的能改变射血分数保留性心力衰竭临床进程的治疗方法.现阐述射血分数保留性心力衰竭潜在的发病机制及治疗靶点,以期为该病的基础及临床治疗提供研究思路.     

射血分数中间值心力衰竭的研究进展

射血分数中间值心力衰竭是区别于射血分数保留的心力衰竭和射血分数降低的心力衰竭的新亚组,其在人口学、病因学、合并症、生物标志物、超声心动图及预后方面均具有介于射血分数保留的心力衰竭和射血分数降低的心力衰竭之间的独特临床特征,而在治疗方面,射血分数中间值心力衰竭患者似乎受益于能够改善射血分数降低的心力衰竭预后的药物治疗,但其获益情况有待进一步证实。现从临床特点、治疗和预后方面对射血分数中间值心力衰竭的研究进展做一综述。     

他汀类药物在射血分数保留的心力衰竭中的治疗进展

对于治疗射血分数保留的心衰,他汀类药物除了具有各种潜在的益处之外,可能直接影响舒张性心力衰竭的预后,本文将对其作用机制及治疗进展进行综述。     

心房颤动合并射血分数保留的心力衰竭的研究进展

心房颤动和射血分数保留的心力衰竭是两种常见的心血管疾病,两者经常共存,导致该类疾病患者预后不佳,加重了社会的经济和医疗负担。两者的发病机制和治疗策略仍存在争议,现主要针对目前心房颤动合并射血分数保留的心力衰竭的研究及治疗进展进行综述。     

射血分数保留性心力衰竭的病理生理机制和治疗进展

射血分数保留性心力衰竭(HFp EF)是左心室射血分数(LVEF)正常或接近正常的心力衰竭,其发生率与射血分数降低性心力衰竭(HFr EF)相当,预后并不优于HFr EF。HFp EF有着复杂的病理生理机制。心肌主动松弛功能障碍和心室僵硬度增加导致的左心室舒张功能不全仍被认为是HFp EF的核心,但其他器官系统也参与疾病的发生发展。HFp EF患者具有高度的异质性,对疾病的分型治疗可能对改善预后有帮助。     

射血分数保留的心力衰竭的药物治疗新进展

射血分数保留的心力衰竭(HFpEF)具有较高的发病率与死亡率，在心力衰竭中的占比日益增加，成为现在研究的重点。目前HFpEF的治疗尚无公认有效的方法，许多能改善射血分数降低的心力衰竭患者预后的药物却未能使HFpEF患者获益。HFpEF具有复杂的病理生理学机制，近期研究表明，针对炎症反应、心肌纤维化、NO-sGC-cGMP通路、能量代谢以及心肌收缩力等治疗靶点的药物已取得了一定进展，现对此进行综述，以期为HFpEF患者的治疗提供更多策略。     

影响射血分数保留的心力衰竭相关疾病及心功能障碍的机制研究进展

射血分数保留的心力衰竭（HFpEF）是一种严重威胁人类健康且机制复杂的临床综合征,约占全部心力衰竭总数的一半。其发病率伴随着人口老龄化的发展而逐年上升,病死率与射血分数减少的心力衰竭（HFrEF）相当,传统的药物治疗虽能降低HFrEF患者的再住院率及死亡率,却不能有效的改善HFpEF患者的预后。目前,对HFpEF的发病机制、诊断、治疗等许多方面尚无统一的认识,加之临床医师对HFpEF的认识存在局限性,均使得HFpEF成为心血管防治领域的社会公共难题及主要挑战。为了解国内外射血分数保留的心力衰竭的病理机制及诊疗情况,现从其影响其的相关疾病、病理机制、诊断治疗等方面进行综述。     

射血分数保留的心力衰竭新进展

射血分数保留的心力衰竭是临床中常见的一组症候群,在所有心力衰竭患者中占有接近50%的比例,其发病率、病死率以及住院率与射血分数减低的心力衰竭相当。过去20年,射血分数减低的心力衰竭的生存率明显改善,射血分数保留的心力衰竭却驻足不前,并且发病率不断上升。目前尚缺乏对射血分数保留的心力衰竭的诊断标准,药物治疗循证医学证据尚不充分,一般实施经验性个体化治疗,其预后仍然较差,近年来在射血分数保留的心力衰竭诊治上取得了一些新进展,现对此进行阐述。     

射血分数保留的心力衰竭的研究进展

射血分数保留的心力衰竭是一个重大的全球公共健康问题,其发生率为1.1%～5.5%,占心力衰竭人数的40%～71%,严重影响了患者的生活质量,同时造成了社会的医疗支出沉重的负担。基于其发病率的持续增长,射血分数保留的心力衰竭在不久将来会成为心力衰竭最常见的表现形式。虽然近10年射血分数保留的心力衰竭的治疗有了发展,但射血分数保留的心力衰竭患者的预后却并没有得到明显改善。现将国内外有关射血分数保留的心力衰竭的诊断及治疗进行简要综述,旨在了解国内外射血分数保留的心力衰竭的诊断及治疗情况,探讨这些研究带来的启示。     

心血管疾病中认知衰弱的研究进展

认知衰弱是无痴呆的患者同时存在衰弱和轻度认知障碍的状态。认知衰弱直接影响心血管疾病患者的健康,增加失能、降低生活质量。现对老年心血管疾病患者认知衰弱的概念、评估、流行病学、预后、机制和干预措施进行综述。     

老年肺癌患者合并衰弱的研究进展

肺癌是我国发病率和死亡率最高的癌症,给医疗保健系统带来了巨大压力。老年人是肺癌的高发人群,老年肺癌患者易发生衰弱,衰弱会增加其术后并发症、放化疗不良反应、全因死亡风险、住院时长及再入院率,严重影响预后。而衰弱具有一定的可逆性,因此早期发现和采取相应的干预措施至关重要。本文对老年肺癌患者衰弱的危险因素、与不良健康结局的相关性及干预策略进行了综述,以便临床上尽早识别老年肺癌患者的衰弱状态,并进行早期干预,从而改善患者预后。     

Frailty and multiple comorbidities in the elderly patient with heart failure: implications for management

Heart failure (HF) in the elderly is a major public health problem, and its prevalence is rising. Outcomes of HF in the elderly have not changed in the past 2 decades despite the introduction of novel HF therapies. This may be due to the combined impact of multiple comorbidities and frailty. The majority of elderly patients with HF are frail with multiple comorbidities. These comorbidities, along with frailty, contribute to the poor outcome of HF in the elderly and pose independent management challenges. More research is needed to better understand the interaction between frailty and multiple comorbidities and the mechanisms by which they impact HF and its management; develop prognostic tools that incorporate frailty and multiple comorbidities and provide more accurate prediction of outcomes; test available treatments in typical elderly patients; and develop and test novel interventions that directly address the adverse impact of multiple comorbidities and frailty.     

射血分数保留型心力衰竭合并肾功能不全的研究进展

射血分数保留型心力衰竭（HFpEF）是发病率及死亡率均较高的一种常见疾病,肾功能不全是HFpEF患者常见的伴随疾病。HFpEF-肾功能不全共病的发病机制尚未完全阐明,HFpEF与肾功能损伤常相互影响、交互促进疾病的进展。与单纯HFpEF患者相比,HFpEF合并肾功能不全患者预后较差,且随肾损伤程度的加重患者死亡风险增加。HFpEF合并肾功能不全目前无公认有效治疗方法,亟需研究新型治疗策略以改善患者预后。     

Lower Extremity Function Is Independently Associated With Hospitalization Burden in Heart Failure With Preserved Ejection Fraction

Background

Frailty reflects decreased resilience to physiological stressors; its prevalence and prognosis are not fully defined in heart failure with preserved ejection fraction (HFpEF).

Inspiratory Muscle Training and Functional Electrical Stimulation for Treatment of Heart Failure With Preserved Ejection Fraction: Rationale and Study Design of a Prospective Randomized Controlled Trial

Heart failure with preserved ejection fraction (HFpEF) has become the most prevalent form of heart failure in developed countries. Regrettably, there is no evidence‐based effective therapy for HFpEF. We seek to evaluate whether inspiratory muscle training, functional electrical stimulation, or a combination of both can improve exercise capacity as well as left ventricular diastolic function, biomarker profile, quality of life (QoL), and prognosis in patients with HFpEF. A total of 60 stable symptomatic patients with HFpEF (New York Heart Association class II–III/IV) will be randomized (1:1:1:1) to receive a 12‐week program of inspiratory muscle training, functional electrical stimulation, a combination of both, or standard care alone. The primary endpoint of the study is change in peak exercise oxygen uptake; secondary endpoints are changes in QoL, echocardiogram parameters, and prognostic biomarkers. As of March 21, 2016, thirty patients have been enrolled. Searching for novel therapies that improve QoL and autonomy in the elderly with HFpEF has become a health care priority. We believe that this study will add important knowledge about the potential utility of 2 simple and feasible physical interventions for the treatment of advanced HFpEF.     

Role of Physical Training in Heart Failure with Preserved Ejection Fraction

About 50 % or more of heart failure (HF) patients living in the community have preserved left ventricular ejection fraction (HFpEF), and the proportion is higher among women and the very elderly. A cardinal feature of HFpEF is reduced aerobic capacity, measured objectively as peak exercise pulmonary oxygen uptake (peak VO₂), that results in decreased quality of life. Specifically, peak VO₂ of HFpEF patients is 30–70 % lower than age-, sex-, and comorbidity-matched control patients without HF. The mechanisms for the reduced peak VO₂ are due to cardiovascular and skeletal muscle dysfunction that results in reduced oxygen delivery to and/or utilization by the active muscles. Currently, four randomized controlled exercise intervention trials have been performed in HFpEF patients. These studies have consistently demonstrated that 3–6 months of aerobic training performed alone or in combination with strength training is a safe and effective therapy to increase aerobic capacity and endurance and quality of life in HFpEF patients. Despite these benefits, the physiologic mechanisms underpinning the improvement in peak exercise performance have not been studied; therefore, future studies are required to determine the role of physical training to reverse the impaired cardiovascular and skeletal muscle function in HFpEF patients.     

Caveat medicus! Pulmonary hypertension in the elderly: a word of caution

Heart failure with preserved ejection fraction (HFpEF) is a common but under‐recognized cause of pulmonary hypertension (PH), particularly among the elderly. While elevated pulmonary artery pressures are clearly associated with increased mortality in HFpEF, it remains unknown whether or how pulmonary vascular disease in HFpEF should be treated. This case emphasizes the importance of maintaining a high index of suspicion for HFpEF in elderly patients presenting with PH and illustrates potential hazards associated with selective pulmonary vasodilation in this growing population.     

Heart failure with preserved ejection fraction: New approaches to diagnosis and management

The majority of older patients who develop heart failure (HF), particularly older women, have a preserved left ventricular ejection fraction (HFpEF). Patients with HFpEF have severe symptoms of exercise intolerance, poor quality-of-life, frequent hospitalizations, and increased mortality. The prevalence of HFpEF is increasing and its prognosis is worsening. However, despite its importance, our understanding of the pathophysiology of HFpEF is incomplete, and drug development has proved immensely challenging. Currently, there are no universally accepted therapies that alter the clinical course of HFpEF. Originally viewed as a disorder due solely to abnormalities in left ventricular (LV) diastolic function, our understanding has evolved such that HFpEF is now understood as a systemic syndrome, involving multiple organ systems, likely triggered by inflammation and with an important contribution of aging, lifestyle factors, genetic predisposition, and multiple-comorbidities, features that are typical of a geriatric syndrome. HFpEF is usually progressive due to complex mechanisms of systemic and cardiac adaptation that vary over time, particularly with aging. In this review, we examine evolving data regarding HFpEF that may help explain past challenges and provide future directions to care patients with this highly prevalent, heterogeneous clinical syndrome.     

Exercise intolerance in heart failure with preserved ejection fraction: more than a heart problem

Heart failure (HF) with preserved ejection fraction (HFpEF) is the most common form of HF in older adults, and is increasing in prevalence as the population ages. Furthermore, HFpEF is increasing out of proportion to HF with reduced EF (HFrEF), and its prognosis is worsening while that of HFrEF is improving. Despite the importance of HFpEF, our understanding of its pathophysiology is incomplete, and optimal treatment remains largely undefined. A cardinal feature of HFpEF is reduced exercise tolerance, which correlates with symptoms as well as reduced quality of life. The traditional concepts of exercise limitations have focused on central dysfunction related to poor cardiac pump function. However, the mechanisms are not exclusive to the heart and lungs, and the understanding of the pathophysiology of this disease has evolved. Substantial attention has focused on defining the central versus peripheral mechanisms underlying the reduced functional capacity and exercise tolerance among patients with HF. In fact, physical training can improve exercise tolerance via peripheral adaptive mechanisms even in the absence of favorable central hemodynamic function. In addition, the drug trials performed to date in HFpEF that have focused on influencing cardiovascular function have not improved exercise capacity. This suggests that peripheral limitations may play a significant role in HF limiting exercise tolerance, a hallmark feature of HFpEF.