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The neurohormonal basis of pulmonary hypertension in heart failure with preserved ejection fraction
M. Obokata, GC. Kane, YNV. Reddy, V. Melenovsky, TP. Olson, P. Jarolim, BA. Borlaug,
Jazyk angličtina Země Velká Británie
Typ dokumentu klinické zkoušky, časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
R01 HL128526
NHLBI NIH HHS - United States
U10 HL110262
NHLBI NIH HHS - United States
T32 HL007111
NHLBI NIH HHS - United States
NLK
Free Medical Journals
od 1996 do Před 1 rokem
Open Access Digital Library
od 1996-01-01
PubMed
31513270
DOI
10.1093/eurheartj/ehz626
Knihovny.cz E-zdroje
- MeSH
- arteria pulmonalis fyziologie MeSH
- arteriální tlak fyziologie MeSH
- atriální natriuretický faktor krev MeSH
- cvičení fyziologie MeSH
- echokardiografie metody MeSH
- endotelin-1 krev MeSH
- hemodynamika fyziologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- peptidové fragmenty krev MeSH
- plicní hypertenze etiologie metabolismus patofyziologie MeSH
- prospektivní studie MeSH
- průřezové studie MeSH
- senioři MeSH
- spotřeba kyslíku fyziologie MeSH
- srdeční selhání komplikace patofyziologie MeSH
- studie případů a kontrol MeSH
- tepový objem fyziologie MeSH
- tolerance zátěže fyziologie MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- klinické zkoušky MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
AIMS: Pulmonary hypertension (PH) represents an important phenotype among the broader spectrum of patients with heart failure with preserved ejection fraction (HFpEF), but its mechanistic basis remains unclear. We hypothesized that activation of endothelin and adrenomedullin, two counterregulatory pathways important in the pathophysiology of PH, would be greater in HFpEF patients with worsening PH, and would correlate with the severity of haemodynamic derangements and limitations in aerobic capacity and cardiopulmonary reserve. METHODS AND RESULTS: Plasma levels of C-terminal pro-endothelin-1 (CT-proET-1) and mid-regional pro-adrenomedullin (MR-proADM), central haemodynamics, echocardiography, and oxygen consumption (VO2) were measured at rest and during exercise in subjects with invasively-verified HFpEF (n = 38) and controls free of HF (n = 20) as part of a prospective study. Plasma levels of CT-proET-1 and MR-proADM were highly correlated with one another (r = 0.89, P < 0.0001), and compared to controls, subjects with HFpEF displayed higher levels of each neurohormone at rest and during exercise. C-terminal pro-endothelin-1 and MR-proADM levels were strongly correlated with mean pulmonary artery (PA) pressure (r = 0.73 and 0.65, both P < 0.0001) and pulmonary capillary wedge pressure (r = 0.67 and r = 0.62, both P < 0.0001) and inversely correlated with PA compliance (r = -0.52 and -0.43, both P < 0.001). As compared to controls, subjects with HFpEF displayed right ventricular (RV) reserve limitation, evidenced by less increases in RV s' and e' tissue velocities, during exercise. Baseline CT-proET-1 and MR-proADM levels were correlated with worse RV diastolic reserve (ΔRV e', r = -0.59 and -0.67, both P < 0.001), reduced cardiac output responses to exercise (r = -0.59 and -0.61, both P < 0.0001), and more severely impaired peak VO2 (r = -0.60 and -0.67, both P < 0.0001). CONCLUSION: Subjects with HFpEF display activation of the endothelin and adrenomedullin neurohormonal pathways, the magnitude of which is associated with pulmonary haemodynamic derangements, limitations in RV functional reserve, reduced cardiac output, and more profoundly impaired exercise capacity in HFpEF. Further study is required to evaluate for causal relationships and determine if therapies targeting these counterregulatory pathways can improve outcomes in patients with the HFpEF-PH phenotype. CLINICAL TRIAL REGISTRATION: NCT01418248; https://clinicaltrials.gov/ct2/results? term=NCT01418248&Search=Search.
Brigham and Women's Hospital Harvard Medical School 75 Francis St Boston MA USA
Department of Cardiovascular Medicine Mayo Clinic and Foundation 200 1st Street SW Rochester MN USA
Institute for Clinical and Experimental Medicine IKEM Vídeňská 1958 9 Prague Czech Republic
Citace poskytuje Crossref.org
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