Pulmonary Hypertension in Heart Failure Preserved Ejection Fraction

Introduction

An elevation of left ventricular diastolic and pulmonary venous pressure is typical of heart failure (HF) regardless of left ventricular (LV) ejection fraction. Normal left ventricular diastolic function keeps both pressures low (<12 mm Hg), although some increase may be observed during stress conditions, such as volume overload¹ and exercise.² When these changes occur within a range of transient periods and in a normal heart, they are well tolerated because of the pulmonary vasculature ability to recruit and distend the capillary network.³

Heart failure with preserved ejection fraction (HFpEF) is a condition presenting, by definition, with an impaired relaxation and stiffened myocardium, which is in part consequence of an increased load to the left ventricle attributable to the stiff arterial system and resulting in a well-defined ventricular–vascular uncoupling. These main hemodynamic alterations expose the lung vasculature to pressure-induced challenges whose most immediate acute threat is pulmonary edema.⁴ In the long term, the sustained backward hemodynamic transmission, along with the potential contribution of mitral insufficiency, increases the pulsatile loading on the right ventricle (RV)⁵ and triggers pulmonary hypertension (PH) development and symptom exacerbation.⁶ Thus, as a consequence of hemodynamic and functional perturbations, PH-HFpEF develops as a more advanced corollary of diastolic HF, leading to abnormal phenotypes of the lung microcirculation,^7,8 the arterial system, and right heart function^9–11 (Figure 1).