Author + information
- Received October 28, 2009
- Revision received March 3, 2010
- Accepted March 9, 2010
- Published online September 7, 2010.
- Barry A. Borlaug, MD⁎ (, )
- Thomas P. Olson, PhD,
- Carolyn S.P. Lam, MBBS,
- Kelly S. Flood, RN,
- Amir Lerman, MD,
- Bruce D. Johnson, PhD and
- Margaret M. Redfield, MD
- ↵⁎Reprint requests and correspondence:
Dr. Barry A. Borlaug, Mayo Clinic and Foundation, 200 First Street SW, Rochester, Minnesota 55905
Objectives The purpose of this study was to comprehensively examine cardiovascular reserve function with exercise in patients with heart failure and preserved ejection fraction (HFpEF).
Background Optimal exercise performance requires an integrated physiologic response, with coordinated increases in heart rate, contractility, lusitropy, arterial vasodilation, endothelial function, and venous return. Cardiac and vascular responses are coupled, and abnormalities in several components may interact to promote exertional intolerance in HFpEF.
Methods Subjects with HFpEF (n = 21), hypertension without heart failure (n = 19), and no cardiovascular disease (control, n = 10) were studied before and during exercise with characterization of cardiovascular reserve function by Doppler echocardiography, peripheral arterial tonometry, and gas exchange.
Results Exercise capacity and tolerance were reduced in HFpEF compared with hypertensive subjects and controls, with lower VO2and cardiac index at peak, and more severe dyspnea and fatigue at matched low-level workloads. Endothelial function was impaired in HFpEF and in hypertensive subjects as compared with controls. However, blunted exercise-induced increases in chronotropy, contractility, and vasodilation were unique to HFpEF and resulted in impaired dynamic ventricular-arterial coupling responses during exercise. Exercise capacity and symptoms of exertional intolerance were correlated with abnormalities in each component of cardiovascular reserve function, and HFpEF subjects were more likely to display multiple abnormalities in reserve.
Conclusions HFpEF is characterized by depressed reserve capacity involving multiple domains of cardiovascular function, which contribute in an integrated fashion to produce exercise limitation. Appreciation of the global nature of reserve dysfunction in HFpEF will better inform optimal design for future diagnostic and therapeutic strategies.
Dr. Borlaug was supported by the Mayo Clinic Center for Translational Science Activities, the National Institutes of Health(UL RR024150), and the Marie Ingalls Career Development Award in Cardiovascular Research. Dr. Lerman serves on the advisory board for Itamar Medical. All other authors have reported that they have no relationships to disclose.
- Received October 28, 2009.
- Revision received March 3, 2010.
- Accepted March 9, 2010.
- American College of Cardiology Foundation