期刊
JOURNAL OF THE AMERICAN HEART ASSOCIATION
卷 3, 期 6, 页码 -出版社
WILEY
DOI: 10.1161/JAHA.114.001293
关键词
exercise; heart failure; hemodynamics; myocardial oxygenation; preserved ejection fraction
资金
- Interuniversity Cardiology Institute Netherlands, Utrecht, Netherlands
- National Health and Medical Research Council of Australia
- Victorian Government OIS Program
Background-Hypertension is a frequent risk factor for the development of heart failure with preserved ejection fraction (HFPEF). Progressive extracellular matrix accumulation has been presumed to be the fundamental pathophysiologic mechanism that leads to the components of diastolic function has not been comprehensively assessed. In this study, we investigated the potential role of impaired myocardial oxygen delivery in the pathophysiology of HFPEF. Methods and Results-Patients with HFPEF, those with controlled hypertension, and healthy controls underwent simultaneous right-heart catheterization, echocardiography, and paired arterial and coronary sinus blood gas sampling at rest and during supinecycle ergometry. Despite a lower workload (HFPEF vs control, hypertension: 43 +/- 8 versus 114 +/- 12, 87 +/- 14 W; P< 0.001 and P< 0.05, respectively), peak exercise pulmonary capillary wedge pressure was markedly higher in HFPEF patients compared with healthy and hypertensive controls (32 +/- 2 versus 16 +/- 1 and 17 +/- 1 mm Hg, both P< 0.001). During exercise, the transcardiac oxygen gradient increased significantly in all groups; however, the peak transcardiac oxygen gradient was significantly lower in HFPEF patients (P< 0.05). In addition, the left ventricular-work corrected transcardiac oxygen gradient remained significantly lower in HFPEF patients compared with controls (P< 0.001). Conclusion-The current study provides unique data suggesting that the abnormal diastolic reserve observed during exertion in HFPEF patients may, in part, be explained by impaired myocardial oxygen delivery due possibly to microvascular dysfunction. Further studies are required to confirm the structural and functional basis of these findings and to investigate the influence of potential therapies on this abnormality.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据