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Comparative Study
. 2013 Jan;19(1):50-9.
doi: 10.1016/j.cardfail.2012.11.005.

A possible role for systemic hypoxia in the reactive component of pulmonary hypertension in heart failure

Bryan J Taylor  1 , Cesar R Mojica, Thomas P Olson, Paul R Woods, Robert P Frantz, Bruce D Johnson
Affiliations
Comparative Study

A possible role for systemic hypoxia in the reactive component of pulmonary hypertension in heart failure

Bryan J Taylor et al. J Card Fail. 2013 Jan.

Abstract

Background: The mechanisms underlying the reactive component of pulmonary hypertension (PH) in heart failure (HF) are unclear. We examined whether resting systemic oxygen levels are related to pulmonary hemodynamics in HF.

Methods and results: Thirty-nine HF patients underwent right heart catheterization. Subsequently, patients were classified as having: 1) no PH (n = 12); 2) passive PH (n = 10); or 3) reactive PH (n = 17). Blood was drawn from the radial and pulmonary arteries for the determination of PaO(2), SaO(2), PvO(2), SvO(2), and vasoactive neurohormones. PaO(2) and PvO(2) were lower in reactive PH versus no PH and passive PH patients (65.3 ± 8.6 vs 78.3 ± 11.4 mm Hg and 74.5 ± 14.0 mm Hg; 29.2 ± 4.1 vs 36.2 ± 2.8 mm Hg and 33.4 ± 2.3 mm Hg; P < .05). SaO(2) and SvO(2) were lower in reactive PH versus no PH patients (93 ± 3% vs 96 ± 3%; 51 ± 11% vs 68 ± 4%; P < .05), but not different versus passive PH patients. The transpulmonary pressure gradient (TPG) was inversely related to PaO(2), PvO(2), SaO(2), and SvO(2) in the reactive PH patients only (r ≤ -0.557; P < .05). Similarly, plasma endothelin-1 correlated with PaO(2), PvO(2), SvO(2) (r ≤ -0.495), and TPG (r = 0.662; P < .05) in reactive PH patients only.

Conclusions: Systemic hypoxia may play a role in the reactive component of PH in HF, potentially via a hypoxia-induced increase in endothelial release of the vasoconstrictor endothelin-1.

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Figures

Fig. 1
Fig. 1
Scatter-plots showing the relationships between individual subject values of transpulmonary pressure gradient (TPG) (mean pulmonary artery pressure – mean pulmonary capillary wedge pressure) and partial pressure of arterial oxygen (PaO2), partial pressure of mixed venous oxygen (PvO2), arterial oxygen saturation (SaO2) and mixed venous oxygen saturation (SvO2) in HF patients without pulmonary hypertension (PH) (n = 12).
Fig. 2
Fig. 2
Definitions are the same as in Fig. 1. Scatter-plots showing the relationships between individual subject values of TPG and PaO2, PvO2, SaO2 and SvO2 in HF patients with passive PH (n = 10).
Fig. 3
Fig. 3
Definitions are the same as in Fig. 1. Scatter-plots showing the relationships between individual subject values of TPG and PaO2, PvO2, SaO2 and SvO2 in HF patients with reactive PH (n = 17). *P < 0.05, **P < 0.01, significant relationship between two parameters
Fig. 4
Fig. 4
Scatter-plots showing the relationships between individual subject (n = 17) values of TPG and plasma levels of endothelin-1, angiotensin-II, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), epinephrine and norepinephrine in HF patients with reactive PH only. **P < 0.01, significant relationship between two parameters.
Fig. 5
Fig. 5
Scatter-plots showing the relationships between individual subject (n = 17) values of plasma endothelin-1 (ET-1) and PaO2, PvO2, SaO2 and SvO2 in HF patients with reactive pulmonary hypertension only. *P < 0.05, **P < 0.01, significant relationship between two parameters.
See this image and copyright information in PMC

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