Abstract
Pulmonary hypertension in the setting of heart failure with preserved ejection fraction (PH‐HFpEF) is a growing public health problem that is increasing in prevalence. While PH‐HFpEF is defined by a high mean pulmonary artery pressure, high left ventricular end‐diastolic pressure and a normal ejection fraction, some HFpEF patients develop PH in the presence of pulmonary vascular remodeling with a high transpulmonary pressure gradient or pulmonary vascular resistance. Aging, increased left atrial pressure and stiffness, mitral regurgitation, as well as features of metabolic syndrome, which include obesity, diabetes, and hypertension, are recognized as risk factors for PH‐HFpEF. Qualitative studies have documented that patients with PH‐HFpEF develop more severe symptoms than those with HFpEF and are associated with more significant exercise intolerance, frequent hospitalizations, right heart failure, and reduced survival. Currently, there are no effective therapies for PH‐HFpEF, although a number of candidate drugs are being evaluated, including the soluble guanylate cyclase stimulator, phosphodiesterase type 5 inhibitor, sodium nitrite, and endothelin receptor antagonist. In this review we attempt to provide an updated overview of recent findings pertaining to the pulmonary vascular complications in HFpEF in terms of clinical definitions, epidemiology, and pathophysiology. Mechanisms leading to pulmonary vascular remodeling in HFpEF, a summary of pre‐clinical models of HFpEF and PH‐HFpEF, and new candidate therapeutic strategies for the treatment of PH‐HFpEF, are summarized.
Prevalence and pathophysiology of PH in patients with HFpEF. LV = left ventricle; LVEDP = left ventricular end‐diastolic pressure; LA = left atrium; PV = pulmonary vein; PA = pulmonary artery/arterial; PVR = pulmonary vascular resistance; RV = right ventricle.
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