射血分数保留的心力衰竭研究进展

射血分数保留的心力衰竭拥有较为独特的发病因素、病理生理变化及预后,缺乏有效的诊断治疗方法.本文总结近年相关领域的研究结果,从流行病学、病因、病理生理、诊断及治疗等方面讨论射血分数保留的心力衰竭目前的研究进展.     

左室射血分数保留的心力衰竭研究进展

心力衰竭是各种临床心血管疾病发展的终末阶段,高发生率及高病死率使其受到越来越多的关注。在美国,其总体发生率约为1.5%～2.0%,而在年龄≥65岁的人群当中,则高达6%～10%[1]。中国的一项随机调查研究选取了15518位成年人(年龄     

射血分数中间值心力衰竭新进展

心力衰竭（心衰）是心脏疾病发展的终末阶段。既往研究通过左心室射血分数对心力衰竭进行分类,分为射血分数降低性心力衰竭与射血分数保留性心力衰竭。近年研究发现介于上述两种心衰的灰色区域,2016年欧洲心脏病学会（ESC）慢性心衰指南首次提出,并将这个灰色区域命名为射血分数中间值心衰。本文对射血分数中间值心衰近年的研究进行综述。     

射血分数保留型心力衰竭的药物治疗进展

射血分数保留型心力衰竭(HFpEF)是心力衰竭的一种特殊类型,尚缺乏确切有效的特异性治疗药物或方法,目前主要采用经验性治疗.该文主要介绍HFpEF的药物治疗新进展.     

左心室重量指数对老年左室射血分数正常心力衰竭的诊断价值

目的评价左心室重量指数(LVMI)对老年左心室射血分数(LVEF)正常心力衰竭(HFNEF)患者的诊断价值。方法选择2014年1~12月于该院心内科诊断为心功能不全的患者,年龄≥60岁,心功能分级Ⅱ~Ⅳ级,入院24 h内行超声心动图检查共232例,根据心脏超声结果中的LVEF分为HFNEF组158例(LVEF≥45%)和LVEF降低的心衰(HFREF)组74例(LVEF≤40%),并选取同期健康对照组100例。对入选对象进一步搜集超声心动图中收缩末期左房内径(LAD)、舒张末期左室内径(LVEDd)、室间隔厚度(IVST)、左室后壁厚度(LVPWT),血液常规检查,在常规超声心动图的基础上计算出LVMI。结果 1与健康对照组相比,心力衰竭组LVEDd、IVST和LVPWT均升高(P0.05);与HFREF组相比,HFNEF组IVST和LVPWT增大(P0.05);LVEDd、E/A较HFREF组减小(P0.05);2以LVMI122 g/m~2(女性),LVMI149 g/m~2(男性)为临界值,诊断HFNEF的灵敏度(男性18.7%,女性47.9%)、特异度(男性96%,女性99%);HFNEF患者中,LVMI随NYHA心功能分级的恶化而升高,在各级心功能分级之间差异显著(P0.05)。结论 LVMI检测可作为诊断心衰的方法之一,可提高对老年HFNEF患者诊断。     

射血分数保留和降低的慢性心力衰竭临床研究

【摘要】 目的 探讨射血分数保留的心力衰竭 (heart failure with preserved ejection fraction, HF-PEF) 与射血分数降低的心力衰竭 (heart failure with reduced ejection fraction, HF-REF) 临床特征差异。方法 选取慢性心衰患者202例作为研究对象,其中HF-PEF 151例,HF-REF 51例。每位患者均接受心脏超声、12导同步体表心电图、血生化及超敏C反应蛋白检测,比较HF-PEF与HF-REF患者的临床特征。结果 HF-PEF以心功能Ⅱ级为主,女性和高血压所占比例、房颤发生率,体重指数均高于HF-REF(P＜0.05);HF-REF以心功能Ⅳ级为主,男性和冠心病所占比例较高(P＜0.05)。 HF-REF患者的肺动脉内径、LVEDD 、LVESD均较HF-PEF大(P＜0.05);而HF-PEF患者的室间隔厚度较HF-REF大(P＜0.05);HF-PEF患者的E/A比值、左房内径均小于HF-REF(P＜0.05)。HF-PEF患者与HF-REF相比较,心率较慢、QRS间期较短(P＜0.05);HF-PEF房颤多见(P＜0.05),而室性心律失常多见于HF-REF(P＜0.05)。HF-PEF患者的血肌酐、血尿素氮、血尿酸及超敏C反应蛋白均较HF-REF患者低(P＜0.05);HF-PEF患者的总胆固醇及甘油三酯均较HF-REF患者高(P＜0.05)。结论 HF-PEF女性所占比例较HF-REF女性所占比例高,其主要病因为高血压,房颤发生率高,以向心性肥厚为主,有明显的舒张功能不全;而HF-REF多为男性,其主要病因为冠心病,室性心律失常多见,以离心性肥厚为主,或许常合并舒张功能不全。     

左心室射血分数正常的心力衰竭

<正>近年来,左心室射血分数(left ventricularej ection fraction,LVEF)正常的心力衰竭(心衰)得到了心血管专业医生越来越多的重视,特别是近来研究发现其高发病率及和收缩性心衰相比毫不逊色的住院率、病死率使其成为了临床工作的重点之一。各家对此认知不同。     

左心室射血分数保存的心力衰竭研究进展

左心室射血分数(left ventricular ejection fraction,LVEF)保存的心力衰竭(心衰)(heart failure with preserved ejection fraction,HFpEF)是一近年来逐渐受到重视的心衰类型,发病率逐年升高,致死率和致残率居高不下,目前在发病机制、诊断、治疗方面仍然存在很多不确定之处,为当下心衰领域的研究热点。概念20世纪70年代末期开始有报道在肥厚型心肌病、主动脉狭窄、高血压性心脏病导致的心衰中     

射血分数保留心力衰竭患者与高尿酸血症的相关研究

目的探讨射血分数保留心力衰竭患者与高尿酸血症的相关性。方法选取射血分数保留心力衰竭患者285例,非心力衰竭组218例,观察各组血液指标及超声心动图指标。结果分别按照N-末端B型脑钠肽前体(NT-pro BNP)值及血尿酸(UA)值分组后,比较差异具有统计学意义(χ2=6.59,P0.05)。Pearson相关分析结果显示:NT-pro BNP与血尿素氮(BUN)(r=0.25,P0.01)、肌酐(Scr)(r=0.24,P0.01)、UA(r=0.11,P0.05)等指标呈正相关。二元Logistic回归检验结果显示:尿酸对射血分数保留心力衰竭的OR为1.93(95%CI:1.16~3.21,P0.05)。结论心力衰竭组患者高尿酸血症比例高于非心力衰竭组,UA水平与NT-pro BNP呈正相关,高尿酸血症是射血分数保留心力衰竭患者的独立危险因素。     

Treatment of heart failure with preserved ejection fraction

Opinion statement  Heart failure with preserved ejection fraction (HFpEF) is a major public health problem in the United States. However, in contrast to systolic heart failure, there are little data to guide treatment decisions in HFpEF, and no therapies have been shown to improve outcome in these patients. This review explores what is currently known about the pathophysiologic mechanisms causing HFpEF in order to frame appropriate therapeutic targets and better understand the clinical responses commonly observed in patients with HFpEF. Data from published clinical trials are reviewed, and the roles for each class of drug commonly used in practice are examined. Finally, novel therapies and future directions for basic investigation and clinical trials are discussed.     

白细胞介素-6和前白蛋白与左心室射血分数保留心力衰竭的相关性

目的探讨白细胞介素-6(IL-6)和前白蛋白(PA)与左心室射血分数保留心力衰竭(HF-PEF)的相关性。方法回顾性分析2017年6月至2019年5月中国医科大学附属第一医院老年心血管内科HF-PEF患者126例,根据彩色多普勒超声心动图结果将患者分为左心室舒张功能减低组和左心室舒张功能正常组,每组63例,比较2组患者的IL-6、PA和脑钠肽(BNP)等生化指标水平。多因素logistic回归分析HF-PEF的影响因素。采用SPSS 22.0统计软件对数据进行分析。结果左心室舒张功能减低组相比左心室舒张功能正常组年龄[(78.2±9.3)和(70.3±8.9)岁]、体质量指数[(25.2±3.4)和(23.8±2.8)kg/m~2]、BNP[(115.0±128.9)和(46.7±59.5)pg/ml]、E/e′[(13.4±5.5)和(9.2±1.8)]、IL-6[(5.3±5.2)和(3.3±3.4)pg/ml]水平高,白蛋白[(38.9±3.8)和(40.7±3.8)g/L]、PA[(21.5±4.6)和(24.7±5.2)mg/dl]水平低,差异均有统计学意义(P0.05)。Logistic回归分析结果表明年龄(OR=1.062,95%CI 1.007～1.119;P=0.026)及E/e′(OR=1.365,95%CI 1.127～1.653;P=0.002)与HF-PEF正相关,PA与HF-PEF负相关(OR=0.916,95%CI 0.842～0.997;P=0.043)。结论 HF-PEF与年龄及PA水平相关,检测PA可能有助于HF-PEF的早期诊断。     

Predictive value of serum galectin-3 levels in patients with acute heart failure with preserved ejection fraction

Aims

This study was conducted to determine whether galectin-3 (Gal3), a β-galactoside-binding lectin, has usefulness to predict outcomes in patients with heart failure (HF) and preserved left ventricular ejection fraction (LVEF).

Methods and results

We measured Gal3, urea, creatinine and natriuretic peptides on admission in 419 selected patients with HF and LVEF over 45%. The primary endpoint was all-cause mortality and/or readmission at one-year follow-up. Multivariable Cox proportional hazards models were generated for Gal3 and classical risk factors. We also evaluated the reclassification of patients on the basis of the different score category after adding Gal3 levels.A total of 219 patients had combined adverse events, and 129 patients died during the follow-up. Kaplan–Meir survival curve showed significantly increased primary endpoint and all-cause mortality according to quartiles of Gal3 (log rank, P < 0.001). Serum Gal3 levels above median (13.8 ng/ml) was a significant predictor of primary endpoint risk after adjustment for age, estimated glomerular filtration rate, anemia, diabetes, serum sodium, brain natriuretic peptide levels, NYHA class and urea, respectively (hazard ratio 1.43, 95% CI 1.07–1.91 P = 0.015). The reclassification index increased significantly after addition of Gal3 (9.5%, P < 0.001) and the integrated discrimination index was 0.022, (P = 0.001). The clinical prediction model with Gal3 increased the c-statistic from 0.711 to 0.731 (difference of 0.020, P = 0.001).

Conclusions

Serum Gal3 is a strong and independent predictor of unfavorable outcomes in patients with HF and preserved LVEF. We also demonstrated the improvement of adding the new biomarker to the model.     

Current understanding of heart failure with preserved ejection fraction

PURPOSE OF REVIEW: A substantial proportion of patients with heart failure have preserved ejection fraction. Though patients with preserved ejection fraction experience a substantial burden of morbidity and mortality, the understanding of heart failure pathophysiology in this group remains incomplete and evidence-based therapeutic options are limited. RECENT FINDINGS: The prevalence of heart failure in patients with preserved ejection fraction is increasing and prognosis in this population remains poor despite modern medical therapy. Though diastolic dysfunction is typically present, increasing evidence suggests that extracardiac factors such as renal dysfunction and enhanced central aortic stiffness may play an important role in the development and progression of heart failure symptoms. Results of the first randomized, controlled clinical trials in this population suggest a possible therapeutic role for renin-angiotensin system blockade in reducing heart failure-associated morbidity, but there is still no evidence-supported strategy for reducing mortality in this population. SUMMARY: Though the epidemiology and impact of heart failure with preserved ejection fraction are increasingly clear, consensus regarding pathophysiology and the optimal therapeutic approach is still lacking. Pending completion of additional therapeutic trials in this population, treatment remains largely empiric and focused on optimizing myocardial performance in diastole by control of blood pressure, restoration or maintenance of sinus rhythm, and relief of volume overload.     

Cardiac mechanics in heart failure with preserved ejection fraction

Heart failure with preserved ejection fraction (HFpEF) is a complex clinical entity associated with significant morbidity and mortality. Common comorbidities including hypertension, coronary artery disease, diabetes, chronic kidney disease, obesity, and increasing age predispose to preclinical diastolic dysfunction that often progresses to frank HFpEF. Clinical HFpEF is typically associated with some degree of diastolic dysfunction, but can occur in the absence of many conventional diastolic dysfunction indices. The exact biologic links between risk factors, structural changes, and clinical manifestations are not clearly apparent. Innovative approaches including deformation imaging have enabled deeper understanding of HFpEF cardiac mechanics beyond conventional metrics. Furthermore, predictive analytics through data-driven platforms have allowed for a deeper understanding of HFpEF phenotypes. This review focuses on the changes in cardiac mechanics that occur through preclinical myocardial dysfunction to clinically apparent HFpEF.