射血分数保留的心力衰竭患者中，心肌氧供应受损会导致异常的运动血流动力学。
Impaired myocardial oxygen availability contributes to abnormal exercise hemodynamics in heart failure with preserved ejection fraction.
作者信息
van Empel Vanessa P M, Mariani Justin, Borlaug Barry A, Kaye David M
机构信息
Heart Failure Research Group, Baker IDI Heart and Diabetes Institute, Melbourne, Australia (V.M.E., J.M., D.M.K.) Department of Cardiovascular Medicine, Alfred Hospital, Melbourne, Australia (V.M.E., J.M., D.M.K.) Department of Cardiology, Maastricht University Medical Center, Maastricht, The Netherlands (V.M.E.).
Heart Failure Research Group, Baker IDI Heart and Diabetes Institute, Melbourne, Australia (V.M.E., J.M., D.M.K.) Department of Cardiovascular Medicine, Alfred Hospital, Melbourne, Australia (V.M.E., J.M., D.M.K.).
出版信息
J Am Heart Assoc. 2014 Dec 2;3(6):e001293. doi: 10.1161/JAHA.114.001293.
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 transition to impaired diastolic reserve. However, the contribution of other mechanisms affecting active and passive 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 supine-cycle 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.
背景
高血压是射血分数保留的心力衰竭（HFPEF）发生的常见危险因素。细胞外基质的渐进性积累被认为是导致舒张储备受损转变的基本病理生理机制。然而，影响舒张功能主动和被动成分的其他机制的作用尚未得到全面评估。在本研究中，我们调查了心肌氧输送受损在HFPEF病理生理学中的潜在作用。
方法和结果
HFPEF患者、血压控制良好的高血压患者和健康对照者在静息状态和仰卧位蹬车运动期间同时进行右心导管检查、超声心动图检查以及配对的动脉和冠状窦血气采样。尽管HFPEF患者的工作量较低（HFPEF与对照组、高血压组相比：43±8 与 114±12、87±14 W；P分别<0.001和P<0.05），但与健康和高血压对照组相比，HFPEF患者运动高峰时的肺毛细血管楔压明显更高（32±2 与 16±1 和 17±1 mmHg，均P<0.001）。运动期间，所有组的跨心脏氧梯度均显著增加；然而，HFPEF患者的运动高峰跨心脏氧梯度显著更低（P<0.05）。此外，与对照组相比，HFPEF患者经左心室作功校正的跨心脏氧梯度仍显著更低（P<0.001）。
结论
本研究提供了独特的数据，表明HFPEF患者运动时观察到的舒张储备异常可能部分是由于微血管功能障碍导致的心肌氧输送受损所致。需要进一步研究来证实这些发现的结构和功能基础，并研究潜在治疗方法对这种异常的影响。
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