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Mechanisms of Exercise Intolerance in Heart Failure with Preserved Ejection Fraction Barry A

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Mechanisms of Exercise Intolerance in Heart Failure with Preserved Ejection Fraction Barry A 20 BORLAUG BA Circulation Journal REVIEW Official Journal of the Japanese Circulation Society http://www.j-circ.or.jp Mechanisms of Exercise Intolerance in Heart Failure With Preserved Ejection Fraction Barry A. Borlaug, MD Approximately half of patients with heart failure (HF) have a preserved ejection fraction (HFpEF), and with the chang- ing age and comorbidity characteristics in the adult population, this number is growing rapidly. The defining symptom of HFpEF is exercise intolerance, but the specific mechanisms causing this common symptom remain debated and inadequately understood. Although diastolic dysfunction was previously considered to be the sole contributor to exercise limitation, recent studies have identified the importance of ventricular systolic, chronotropic, vascular, en- dothelial and peripheral factors that all contribute in a complex and highly integrated fashion to produce the signs and symptoms of HF. This review will explore the mechanisms underlying objective and subjective exercise intoler- ance in patients with HFpEF. (Circ J 2014; 78: 20 – 32) Key Words: Aging; Diastolic dysfunction; Exercise; Heart failure; Hemodynamics eart failure (HF) represents an enormous worldwide health problem, afflicting 6 million Americans, 15 Review of Basic Hemodynamics H million Europeans, and quite possibly over 35 mil- Cardiovascular hemodynamics, reviewed in detail elsewhere,25,26 lion Asians.1 Half of patients with HF have preserved ejection are fundamentally dictated by cardiac-specific properties, au- fraction (HFpEF), and with current secular trends in the age- tonomic tone, and external forces that modulate cardiovascular distribution and comorbidity profiles of the adult population, performance (afterload and preload). Afterload can be broadly the prevalence of HFpEF is growing relative to HF with re- defined as the forces that oppose cardiac ejection. Afterload is duced EF (HFrEF) by 1% per year.2 Exercise intolerance is the often incorrectly conceptualized as arterial blood pressure, but cornerstone clinical expression of HF, and exercise capacity is is more accurately reflected as systolic wall stress or aortic similarly impaired in HFpEF and HFrEF.3 However, in con- input impedance. The use of wall stress is problematic because trast to HFrEF, there is no proven effective treatment for it is potently affected by ventricular properties, as wall stress HFpEF.4 The reasons for this disparity are manifold, but is directly related to chamber dimension and inversely to wall among them, incomplete understanding of the pathophysiol- thickness. The ideal measure of afterload would be com- ogy looms large. Initial mechanistic paradigms focused on left pletely independent of the ventricle. Aortic input impedance ventricular (LV) diastolic dysfunction as the dominant mecha- provides a measure of the total vascular opposition to ejection nism driving HFpEF,5 but numerous recent studies have iden- that is independent of the heart, but is cumbersome to use tified abnormalities in LV systolic function, right ventricular because it is expressed in the frequency domain and is there- (RV) function, chronotropic incompetence, abnormal system- fore difficult to use with time-domain measures of ventricular ic and pulmonary vasodilation, endothelial dysfunction, and function. Effective arterial elastance (Ea) is an alternative abnormalities in the periphery.6–24 To make progress in the time-domain measure that incorporates both mean resistive treatment of HFpEF, these different mechanisms require fur- and oscillatory components of arterial load and is defined by ther study. An important paradigm regarding HFpEF that has the ratio of endsystolic arterial pressure to stroke volume emerged in recent years is that the presence of normal cardio- (SV). Ea is directly related to mean systemic vascular resis- vascular homeostasis at rest in no way guarantees preservation tance (SVR) and heart rate (HR) and inversely related to total of reserve capacity under physiologic stressors, the most com- arterial compliance. mon of which in daily life is physical exercise. Accordingly, Preload can be defined by the magnitude of distention or detailed understanding the mechanisms of exercise reserve “stretching” of ventricular myocytes prior to contraction, which intolerance is critical to appreciating the complex pathophysi- dictates the extent of myofiber shortening in the subsequent ology of HFpEF. In this review, I shall review the roles of contraction. Preload is often erroneously conceptualized in cardiac, vascular, and noncardiovascular systems in limiting practice as being equivalent to LV filling pressures (LVFP), exercise capacity in patients with HFpEF. when in fact, the most accurate measure of LV preload is chamber volume prior to the onset of isovolumic contraction Received August 28, 2013; revised manuscript received October 30, 2013; accepted November 11, 2013; released online December 3, 2013 The Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN, USA Mailing address: Barry A. Borlaug, MD, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. E-mail: [email protected] ISSN-1346-9843 doi: 10.1253/circj.CJ-13-1103 All rights are reserved to the Japanese Circulation Society. For permissions, please e-mail: [email protected] Circulation Journal Vol.78, January 2014 Exercise Intolerance in HFpEF 21 (LV end-diastolic volume, LVEDV). Filling pressures are re- with exertion is, not surprisingly, metabolic demand for O2, lated to preload by the compliance properties of the heart and and studies dating back over 50 years have shown that in gen- the kinetics of relaxation, especially at higher HRs. Preload is eral, for each 1 ml increase in VO2, there is an approximately affected by venous return, diastolic function, the right heart, 6 ml increase in QC in healthy humans.30,31 and the pericardium. SV increases by approximately 40% during upright exer- The ventricle can be characterized by its capacity to eject cise, owing to both augmentation in LVEDV and reduction in blood (systolic function) and to fill with blood (diastolic func- LV endsystolic volume (ESV).29 Increases in RV EDV occur tion). Systolic function reflects the heart’s pumping ability and in response to enhanced venous return mediated by muscle and is most often measured clinically by the EF. However, EF ventilatory pumps, and possibly dynamic reductions in blood varies directly with preload and inversely with afterload (as is volume in the large-capacity splanchnic veins.27 This increase true of all measures of systolic shortening or thickening). Al- in venous return to the thorax during early exercise is opti- ternative measures that account for both preload and afterload, mally coupled to 2 compliant ventricles that can accommodate such as LV endsystolic elastance (Ees), stress-corrected frac- increases in EDV without excessive rises in ventricular filling tional shortening, or preload-recruitable stroke work are more pressure (end-diastolic pressures, EDP). Net ventricular cham- specific measures of LV chamber contractility that are inde- ber compliance (change in volume per change in pressure) is pendent of load. related to chamber volumes as well to factors within the car- Diastolic function is often dichotomized into “active” and diac myocyte (eg, cytosolic calcium levels, titin phosphoryla- “passive” functions, though these distinctions are arbitrary and tion and isotype expression), the extracellular matrix (collagen there is considerable overlap between them. “Active” function content and cross-linking), the right heart and the pericardi- generally refers to early diastolic processes involved in cross- um.32 Increases in EDV lead to increased stretch of cardiac bridge detachment, calcium reuptake and rapid pressure decay myocytes that serves to enhance the force of contraction via during isovolumic relaxation and early filling. Active diastolic the Frank-Starling mechanism. To allow the ventricle to fill to function is usually measured by the time constant of early dia- a larger EDV in a shorter interval of time, without pathologic stolic pressure decay (τ) or the velocity/extent of tissue motion increases in EDP, there is exercise-induced enhancement in during early filling. Passive diastolic function generally refers early diastolic relaxation, suction and untwist that is mediated to the mechanical properties of heart muscle that dictate the predominantly by adrenergic stimulation.33 Recent research degree of pressure elevation to achieve a given preload vol- indicates that LV chamber stiffness can be dynamically re- ume (end-diastolic chamber elastance or Eed, an approxima- duced by cyclic adenosine monophosphate- (cAMP) and cy- tion for the slope of the end-diastolic pressure-volume rela- clic guanosine monophosphate- (cGMP) dependent phosphor- tionship). Eed is determined by stiffness within the cardiac ylation of macromolecules in the cardiac myocyte, such as myocytes as well as the extracellular matrix, chamber, and titin,34–36 though it is unknown if this protein phosphorylation pericardium. affects elastance (stiffness) acutely during exercise. Protein If systolic and diastolic ventricular properties are held con- kinase C also phosphorylates titin, but in contrast to the stant, an isolated increase in afterload will increase blood pres- cAMP- and cGMP-dependent pathways, PKC phosphoryla- sure and decrease SV, whereas an isolated increase in preload tion increases stiffness.37 Titin
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