Abstract
Pulmonary hypertension (PH) is common in patients with heart failure (HF). The role of PH in patients with HF with reduced (HFrEF) and preserved (HFpEF) left ventricular ejection fraction (LVEF) has been extensively characterized during the last years. In contrast, the pathophysiology of HF with mid-range LVEF (HFmrEF), and in particular the role of PH in this context, are largely unknown. There is a paucity of data in this field, and the prevalence of PH, the underlying mechanisms, and the optimal therapy are not well-defined. Although often studied together there is increasing evidence that despite similarities with both HFrEF and HFpEF, HFmrEF also differs from both entities. The present review provides a summary of the current concepts of the mechanisms and clinical impact of PH in patients with HFmrEF, a proposal for the non-invasive and invasive diagnostic approach required to define the pathophysiology of PH and its management, and a discussion of future directions based on insights from mechanistic studies and randomized trials. We also provide an outlook regarding gaps in evidence, future clinical challenges, and research opportunities.
Highlights
Pulmonary hypertension (PH) in patients with left heart diseases is the most common form of PH [1]
The rationale underlying the creation of the HF with mid-range LVEF (HFmrEF) category had been as follows: on the one hand, the established HFrEF pharmacotherapy is based on studies that included patients up to an left ventricular ejection fraction (LVEF) of 40%, and on the other hand, it has been realized that in the large randomized “HF with preserved LVEF (HFpEF) studies,” which included patients with LVEF ≥40%/45%, those with LVEF
H2FPEF score:c doubling of the probability of HFpEF with each one-point increase aLVEF cut-offs adopted from the 2021 Universal Definition and Classification of Heart Failure [10]. bHeart Failure Association (HFA)-PEFF: score: composed of (a) septal or lateral peak early diastolic mitral annular velocity by tissue Doppler (e′), ratio of peak early diastolic transmitral velocity by pulsed wave Doppler (E) to e′ (E/e′), peak tricuspid regurgitant velocity, estimated systolic pulmonary artery pressure, or global longitudinal strain, (b) left atrial volume index (LAVI), left ventricular (LV), mass index (LVMI), or relative wall thickness, and (c) B-type natriuretic peptide (BNP), or N-terminal proBNP (NT-proBNP)
Summary
Pulmonary hypertension (PH) in patients with left heart diseases is the most common form of PH [1]. The presence of PH in this context typically reflects an advanced disease stage with exhausted compensatory mechanisms, which is associated with exercise intolerance and a poor prognosis [2]. Our understanding of the relatively new disease entity of HF with mid-range LVEF (or “mildy reduced” LVEF; HFmrEF) is still evolving, and the pathophysiology and clinical impact of PH in this context have not been defined yet [6]. Before HFmrEF was clearly defined as a distinct entity, these patients were often included in HFrEF or HFpEF studies on pathophysiology and therapy. We discuss HFmrEF in the context of concepts regarding PH in HFrEF vs HFpEF
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