TY - JOUR
T1 - Impaired myocardial oxygen availability contributes to abnormal exercise hemodynamics in heart failure with preserved ejection fraction
AU - van Empel, Vanessa P M
AU - Mariani, Justin
AU - Borlaug, Barry A.
AU - Kaye, David M.
PY - 2014/12/2
Y1 - 2014/12/2
N2 - 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 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.
AB - 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 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.
KW - Exercise
KW - Heart failure
KW - Hemodynamics
KW - Myocardial oxygenation
KW - Preserved ejection fraction
UR - http://www.scopus.com/inward/record.url?scp=84939461162&partnerID=8YFLogxK
U2 - 10.1161/JAHA.114.001293
DO - 10.1161/JAHA.114.001293
M3 - Article
C2 - 25468660
AN - SCOPUS:84939461162
SN - 2047-9980
VL - 3
JO - Journal of the American Heart Association
JF - Journal of the American Heart Association
IS - 6
M1 - 001293
ER -