2014
DOI: 10.1007/s11906-014-0501-5
|View full text |Cite
|
Sign up to set email alerts
|

Management of Pulmonary Hypertension due to Heart Failure with Preserved Ejection Fraction

Abstract: Heart failure with preserved ejection fraction (HFpEF) is a major cause of HF-related morbidity and mortality, with no medical therapy proven to modify the underlying disease process and result in improvements in survival. With long-standing pulmonary venous congestion, a majority of HFpEF patients develop pulmonary hypertension (PH). Elevated pulmonary pressures have been shown to be a major determinant of mortality in this population. Given the paucity of available disease-modifying therapies for HFpEF, ther… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

0
4
0

Year Published

2015
2015
2022
2022

Publication Types

Select...
5

Relationship

0
5

Authors

Journals

citations
Cited by 5 publications
(4 citation statements)
references
References 62 publications
0
4
0
Order By: Relevance
“…In contrast, a single‐center, placebo‐controlled, randomized trial reported significant improvements in PA pressure, RV function, and LV relaxation with sildenafil in patients with HFpEF and PH . In the absence of evidence‐based data, PDE5‐I cannot be recommended for the treatment of PH in HFpEF . Riociguat, a soluble guanylate cyclase stimulator that sensitizes guanylate cyclase through nitric oxide–dependent and –independent pathways, has been evaluated for the treatment of PH in HFpEF .…”
Section: Ph Phenotypementioning
confidence: 99%
“…In contrast, a single‐center, placebo‐controlled, randomized trial reported significant improvements in PA pressure, RV function, and LV relaxation with sildenafil in patients with HFpEF and PH . In the absence of evidence‐based data, PDE5‐I cannot be recommended for the treatment of PH in HFpEF . Riociguat, a soluble guanylate cyclase stimulator that sensitizes guanylate cyclase through nitric oxide–dependent and –independent pathways, has been evaluated for the treatment of PH in HFpEF .…”
Section: Ph Phenotypementioning
confidence: 99%
“…In PAH, the mean PAWP is ≤15mmHg, whereas in PH-LHD, the mPAWP is >15 mmHg [9]. This hemodynamic difference ensues from the chronic elevation in LV end-diastolic and left atrial pressure (LAP), which are triggers for the development of PH in HFpEF and HFrEF [36]. The elevation of pulmonary artery pressure (PAP) in the initial phase of the development of PH-HFpEF is, therefore, considered a passive reflection of LAP in the pulmonary circulation [37].…”
Section: Hemodynamic and Pathobiological Alterations In Ph-hfpefmentioning
confidence: 99%
“…HFpEF and HFrEF [36]. The elevation of pulmonary artery pressure (PAP) in the initial phase of the development of PH-HFpEF is, therefore, considered a passive reflection of LAP in the pulmonary circulation [37].…”
Section: Hemodynamic and Pathobiological Alterations In Ph-hfpefmentioning
confidence: 99%
“…Indeed, a substantial component of RV contractility is due to LV, through shared short axis fibers and trans-septal contribution. In HFpEF patients, despite normal ejection fraction (EF), LV evidences some degrees of impaired contractility (due to reduced longitudinal systolic function or diastolic dysfunction) and consequently impaired RV/ LV interactions (29). In this setting RV loses its ability to compensate the pressure overload, causing a ventricularvascular uncoupling.…”
Section: Rh Characteristicsmentioning
confidence: 99%