Pathophysiology-based novel pharmacotherapy for heart failure with preserved ejection fraction

被引:12
|
作者
Konstantinou, Dimitrios M. [1 ,2 ]
Chatzizisis, Yiannis S. [1 ,3 ]
Giannoglou, George D. [1 ]
机构
[1] Aristotle Univ Thessaloniki, AHEPA Univ Hosp, Sch Med, Dept Cardiol 1, Thessaloniki, Greece
[2] Royal Brompton Hosp, London Imperial Coll, Heart Failure Care Grp, London SW3 6LY, England
[3] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Cardiovasc, Boston, MA 02115 USA
关键词
Heart failure; Diastolic dysfunction; Pathophysiology; Pharmacotherapy; LEFT-VENTRICULAR FUNCTION; NITRIC-OXIDE SYNTHASE; TROPONIN-I PHOSPHORYLATION; DIRECT RENIN INHIBITION; LATE SODIUM CURRENT; DIASTOLIC DYSFUNCTION; NATRIURETIC-PEPTIDE; RYANODINE RECEPTOR; EXERCISE CAPACITY; PHOSPHODIESTERASE-5; INHIBITION;
D O I
10.1016/j.pharmthera.2013.05.012
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Heart failure has become increasingly prevalent and poses a significant socioeconomic burden in the developed world. Approximately half of heart failure patients have preserved ejection fraction (HFpEF) and experience an increased morbidity and mortality attributed to the lack of effective therapies and to the presence of comorbidities. Suppression of neurohormonal activation by beta-blockers and renin-angiotensin-aldosterone system inhibitors is the cornerstone in the pharmacotherapy of heart failure with reduced ejection fraction (HFrEF). However, these medications are not associated with significant clinical benefit in HFpEF. In this review, we provide an in-depth pathophysiology-based update on novel pharmacotherapies of HFpEF. A deeper insight into the pathophysiologic mechanisms of HFpEF may create opportunities for novel pharmacological interventions. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:156 / 166
页数:11
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