Hypoxic pulmonary hypertension; the load on the right ventricle

2013 ◽  
Vol 98 (8) ◽  
pp. 1244-1246 ◽  
Author(s):  
P. McLoughlin ◽  
J. P. T. Ward
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
Hypoxic Pulmonary Hypertension ◽  
The Right

C-type natriuretic peptide expression and pulmonary vasodilation in hypoxia-adapted rats

1998 ◽  
Vol 275 (4) ◽  
pp. L645-L652 ◽  
Author(s):  
James R. Klinger ◽  
Farjaad M. Siddiq ◽  
Richard A. Swift ◽  
Cynthia Jackson ◽  
Linda Pietras ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
Natriuretic Peptide ◽  
Right Atrium ◽  
Chronic Hypoxia ◽  
Right Atrial ◽  
Mrna Levels ◽  
Hypoxic Pulmonary Hypertension ◽  
Pulmonary Arterial ◽  
The Right

Atrial and brain natriuretic peptides (ANP and BNP, respectively) are potent pulmonary vasodilators that are upregulated in hypoxia-adapted rats and may protect against hypoxic pulmonary hypertension. To test the hypothesis that C-type natriuretic peptide (CNP) also modulates pulmonary vascular responses to hypoxia, we compared the vasodilator effect of CNP with that of ANP on pulmonary arterial rings, thoracic aortic rings, and isolated perfused lungs obtained from normoxic and hypoxia-adapted rats. We also measured CNP and ANP levels in heart, lung, brain, and plasma in normoxic and hypoxia-adapted rats. Steady-state CNP mRNA levels were quantified in the same organs by relative RT-PCR. CNP was a less potent vasodilator than ANP in preconstricted thoracic aortic and pulmonary arterial rings and in isolated lungs from normoxic and hypoxia-adapted rats. Chronic hypoxia increased plasma CNP (15 ± 2 vs. 6 ± 1 pg/ml; P < 0.05) and decreased CNP in the right atrium (35 ± 14 vs. 65 ± 17 pg/mg protein; P < 0.05) and in the lung (3 ± 1 vs. 14 ± 3 pg/mg protein; P < 0.05) but had no effect on CNP in brain or right ventricle. Chronic hypoxia increased ANP levels fivefold in the right ventricle (49 ± 5 vs. 11 ± 2 pg/mg protein; P < 0.05) but had no effect on ANP in lung or brain. There was a trend toward decreased ANP levels in the right atrium (2,009 ± 323 vs. 2,934 ± 397 pg/mg protein; P = not significant). No differences in CNP transcript levels were observed between the two groups of rats except that the right atrial CNP mRNA levels were lower in hypoxia-adapted rats. We conclude that CNP is a less potent pulmonary vasodilator than ANP in normoxic and hypoxia-adapted rats and that hypoxia raises circulating CNP levels without increasing cardiopulmonary CNP expression. These findings suggest that CNP may be less important than ANP or BNP in protecting against hypoxic pulmonary hypertension in rats.

CMR markers for early right ventricular dysfunction in precapillary pulmonary hypertension

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Vos ◽  
T Leiner ◽  
A.P.J Van Dijk ◽  
F.J Meijboom ◽  
G.T Sieswerda ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Circumferential Strain ◽  
Peak Strain ◽  
Healthy Controls ◽  
Free Wall ◽  
Global Circumferential Strain ◽  
The Right ◽  
Rv Function

Abstract Introduction Precapillary pulmonary hypertension (pPH) causes right ventricular (RV) pressure overload inducing RV remodeling, often resulting in dysfunction and dilatation, heart failure, and ultimately death. The ability of the right ventricle to adequately adapt to increased pressure loading is key for patients' prognosis. RV ejection fraction (RVEF) by cardiac magnetic resonance (CMR) is related to outcome in pPH patients, but this global measurement is not ideal for detecting early changes in RV function. Strain analysis on CMR using feature tracking (FT) software provides a more detailed assessment, and might therefore detect early changes in RV function. Aim 1) To compare RV strain parameters in pPH patients and healthy controls, and 2) to compare strain parameters in a subgroup of pPH patients with preserved RVEF (pRVEF) and healthy controls. Methods In this prospective study, a CMR was performed in pPH patients and healthy controls. Using FT-software on standard cine images, the following RV strain parameters were analyzed: global, septal, and free wall longitudinal strain (GLS, sept-LS, free wall-LS), time to peak strain (TTP, as a % of the whole cardiac cycle), the fractional area change (FAC), global circumferential strain (GCS), global longitudinal and global circumferential strain rate (GLSR and GCSR, respectively). A pRVEF is defined as a RVEF &gt;50%. To compare RV strain parameters in pPH patients to healthy controls, the Mann-Whitney U test was used. Results 33 pPH-patients (55 [45–63] yrs; 10 (30%) male) and 22 healthy controls (40 [36–48] yrs; 15 (68%) male) were included. All RV strain parameters were significantly reduced in pPH patients compared to healthy controls (see table), except for GCS and GCSR. Most importantly, in pPH patients with pRVEF (n=8) GLS (−26.6% [−22.6 to −27.3] vs. −28.1% [−26.2 to −30.6], p=0.04), sept-LS (−21.2% [−19.8 to −23.2] vs. −26.0% [−24.0 to −27.9], p=0.005), and FAC (39% [35–44] vs. 44% [42–47], p=0.02) were still significantly impaired compared to healthy controls. The RV TTP was significantly increased in pPH patients compared to healthy controls (47% [44–57] vs. 40% [33–43], p≤0.001). Conclusions Several CMR-FT strain parameters of the right ventricle are impaired in pPH patients when compared to healthy controls. Moreover, even in pPH patients with a preserved RVEF multiple RV strain parameters (GLS, sept-LS, and FAC) remained significantly impaired, and TTP significantly prolonged, in comparison to healthy controls. This suggests that RV strain parameters may be used as an early marker of RV dysfunction in pPH patients. Funding Acknowledgement Type of funding source: None

scholarly journals The Role of G Protein-Coupled Receptors in the Right Ventricle in Pulmonary Hypertension

2018 ◽  
Vol 5 ◽  
Author(s):  
Gayathri Viswanathan ◽  
Argen Mamazhakypov ◽  
Ralph T. Schermuly ◽  
Sudarshan Rajagopal
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
G Protein ◽  
G Protein Coupled Receptors ◽  
The Right ◽  
G Protein Coupled

scholarly journals Right Ventricular Function in Acute Respiratory Distress Syndrome: Impact on Outcome, Respiratory Strategy and Use of Veno-Venous Extracorporeal Membrane Oxygenation

2022 ◽  
Vol 12 ◽  
Author(s):  
Matthieu Petit ◽  
Edouard Jullien ◽  
Antoine Vieillard-Baron
Keyword(s):  
Pulmonary Hypertension ◽  
Extracorporeal Membrane Oxygenation ◽  
Right Ventricle ◽  
Pulmonary Circulation ◽  
Distress Syndrome ◽  
Cor Pulmonale ◽  
Prone Positioning ◽  
Acute Cor Pulmonale ◽  
Membrane Oxygenation ◽  
The Right

Acute respiratory distress syndrome (ARDS) is characterized by protein-rich alveolar edema, reduced lung compliance and severe hypoxemia. Despite some evidence of improvements in mortality over recent decades, ARDS remains a major public health problem with 30% 28-day mortality in recent cohorts. Pulmonary vascular dysfunction is one of the pivot points of the pathophysiology of ARDS, resulting in a certain degree of pulmonary hypertension, higher levels of which are associated with morbidity and mortality. Pulmonary hypertension develops as a result of endothelial dysfunction, pulmonary vascular occlusion, increased vascular tone, extrinsic vessel occlusion, and vascular remodeling. This increase in right ventricular (RV) afterload causes uncoupling between the pulmonary circulation and RV function. Without any contractile reserve, the right ventricle has no adaptive reserve mechanism other than dilatation, which is responsible for left ventricular compression, leading to circulatory failure and worsening of oxygen delivery. This state, also called severe acute cor pulmonale (ACP), is responsible for excess mortality. Strategies designed to protect the pulmonary circulation and the right ventricle in ARDS should be the cornerstones of the care and support of patients with the severest disease, in order to improve prognosis, pending stronger evidence. Acute cor pulmonale is associated with higher driving pressure (≥18 cmH2O), hypercapnia (PaCO2 ≥ 48 mmHg), and hypoxemia (PaO2/FiO2 &lt; 150 mmHg). RV protection should focus on these three preventable factors identified in the last decade. Prone positioning, the setting of positive end-expiratory pressure, and inhaled nitric oxide (INO) can also unload the right ventricle, restore better coupling between the right ventricle and the pulmonary circulation, and correct circulatory failure. When all these strategies are insufficient, extracorporeal membrane oxygenation (ECMO), which improves decarboxylation and oxygenation and enables ultra-protective ventilation by decreasing driving pressure, should be discussed in seeking better control of RV afterload. This review reports the pathophysiology of pulmonary hypertension in ARDS, describes right heart function, and proposes an RV protective approach, ranging from ventilatory settings and prone positioning to INO and selection of patients potentially eligible for veno-venous extracorporeal membrane oxygenation (VV ECMO).

Imaging the right ventricle in pulmonary hypertension

PVRI Review ◽  
2009 ◽  
Vol 1 (3) ◽  
pp. 180 ◽  
Author(s):  
AndrewJ Peacock ◽  
KevinG Blyth
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
The Right

scholarly journals Phenotyping the Right Ventricle in Patients with Pulmonary Hypertension

2009 ◽  
Vol 2 (4) ◽  
pp. 294-299 ◽  
Author(s):  
Marc A. Simon ◽  
Christopher Deible ◽  
Michael A. Mathier ◽  
Joan Lacomis ◽  
Orly Goitein ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
The Right

scholarly journals Brain natriuretic peptide inhibits hypoxic pulmonary hypertension in rats

1998 ◽  
Vol 84 (5) ◽  
pp. 1646-1652 ◽  
Author(s):  
James R. Klinger ◽  
Rod R. Warburton ◽  
Linda Pietras ◽  
Nicholas S. Hill
Keyword(s):  
Pulmonary Hypertension ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Systolic Pressure ◽  
High Rate ◽  
Hypoxic Pulmonary Hypertension ◽  
Ventricular Systolic Pressure ◽  
Hypoxic Conditions ◽  
Pulmonary Vasodilator ◽  
The Right

Brain natriuretic peptide (BNP) is a pulmonary vasodilator that is elevated in the right heart and plasma of hypoxia-adapted rats. To test the hypothesis that BNP protects against hypoxic pulmonary hypertension, we measured right ventricular systolic pressure (RVSP), right ventricle (RV) weight-to-body weight (BW) ratio (RV/BW), and percent muscularization of peripheral pulmonary vessels (%MPPV) in rats given an intravenous infusion of BNP, atrial natriuretic peptide (ANP), or saline alone after 2 wk of normoxia or hypobaric hypoxia (0.5 atm). Hypoxia-adapted rats had higher hematocrits, RVSP, RV/BW, and %MPPV than did normoxic controls. Under normoxic conditions, BNP infusion (0.2 and 1.4 μg/h) increased plasma BNP but had no effect on RVSP, RV/BW, or %MPPV. Under hypoxic conditions, low-rate BNP infusion (0.2 μg/h) had no effect on plasma BNP or on severity of pulmonary hypertension. However, high-rate BNP infusion (1.4 μg/h) increased plasma BNP (69 ± 8 vs. 35 ± 4 pg/ml, P < 0.05), lowered RV/BW (0.87 ± 0.05 vs. 1.02 ± 0.04, P < 0.05), and decreased %MPPV (60 vs. 74%, P < 0.05). There was also a trend toward lower RVSP (55 ± 3 vs. 64 ± 2, P = not significant). Infusion of ANP at 1.4 μg/h increased plasma ANP in hypoxic rats (759 ± 153 vs. 393 ± 54 pg/ml, P < 0.05) but had no effect on RVSP, RV/BW, or %MPPV. We conclude that BNP may regulate pulmonary vascular responses to hypoxia and, at the doses used in this study, is more effective than ANP at blunting pulmonary hypertension during the first 2 wk of hypoxia.

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