Global Cardiovascular Reserve Dysfunction in Heart Failure with Preserved Ejection Fraction

By Barry A. Borlaug, T. Olson, C. Lam, K. Flood, A. Lerman, Bruce D. Johnson, M. Redfield. Journal of the American College of Cardiology, 2010

701 citations recorded by the source corpus.

Objectives 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 vasodilatation, 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 hypertensives and controls, with lower VO2 and cardiac index at peak, and more severe dyspnea and fatigue at matched low-level workloads. Endothelial function was impaired in HFpEF and in hypertensives 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. Conclusion 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.

Subfields: Cardiology and Cardiovascular Medicine, Complementary and alternative medicine

View Paper: https://www.semanticscholar.org/paper/b70be11e677e1e36632cc54fe3c052df6d07439e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

1. Barry A. Borlaug
2. W. Paulus
3. M. Redfield
4. C. Tschöpe
5. Joseph A. Hill

In Complementary and alternative medicine

1. W. Paulus
2. Barry A. Borlaug

Citations in the corpus

• Coronary Microvascular Rarefaction and Myocardial Fibrosis in Heart Failure With Preserved Ejection Fraction (2015, background): “HFpEF patients with EF 50% at diagnosis tended to have less severe CAD at autopsy (CAD total score 12 (7-14)) than HFpEF patients with EF 40-49% at HF diagnosis (12.”
• Heart failure with preserved ejection fraction: pathophysiology, diagnosis, and treatment. (2011, methodology): “These figures were created based upon previously published data in Borlaug et al.(28,33) Heart failure with preserved ejection fraction 675”
• A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation. (2013, positive): “Several recent studies emphasized the importance of a de fi cient systemic vasodilator response for the reduced exercise tolerance of HFPEF patients (33).”
• Effect of Phosphodiesterase-5 Inhibition on Exercise Capacity and Clinical Status in Heart Failure with Preserved Ejection Fraction: A Randomized Clinical Trial (2013, neutral): “Calcium channel blocker 66 (31) 35 (34) 31 (27)”
• Pathological Ventricular Remodeling: Mechanisms: Part 1 of 2 (2013, background): “In addition, impaired flow-mediated vasodilation has been observed, implicating endothelial dysfunction in HFpEF pathophysiology and suggesting the possibility of benefit with therapies targeting nitric oxide bioavailability.(13) Pulmonary hypertension is also associated with HFpEF, and elevated pul”