Effects of Hemoglobin on Pulmonary Arterial Pressure and Pulmonary Vascular Resistance in Patients with Chronic Emphysema

Nakamura, Akira; Kasamatsu, Norio; Hashizume, Ikko; Shirai, T; Hanzawa, Suguru; Momiki, Shigeru; Sasaki, Kohsuke; Kinoshita, Masao; Okada, Osamu; Kuriyama, Takayuki

doi:10.1159/000067463

Cited by 37 publications

(22 citation statements)

References 9 publications

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“…45 Additionally, if proper alignment cannot be obtained, a true tricuspid regurgitation velocity may be underestimated. Higher hemoglobin concentration may directly contribute to elevated pulmonary artery pressure in patients with chronic emphysema, 46 and it is conceivable that an expanded blood volume contributed to elevated estimated systolic pulmonary artery pressure in the patients with Chuvash polycythemia in this study. Higher hemoglobin and increased blood viscosity may result in fewer patients with measurable tricuspid regurgitation among VHL R200W homozygotes.…”

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confidence: 73%

Pulmonary artery pressure and iron deficiency in patients with upregulation of hypoxia sensing due to homozygous VHLR200W mutation (Chuvash polycythemia)

et al. 2011

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BackgroundPatients with Chuvash polycythemia, (homozygosity for the R200W mutation in the von Hippel Lindau gene (VHL)), have elevated levels of hypoxia inducible factors HIF-1 and HIF-2, often become iron-deficient secondary to phlebotomy, and have elevated estimated pulmonary artery pressure by echocardiography. The objectives of this study were to provide a comprehensive echocardiographic assessment of cardiovascular physiology and to identify clinical, hematologic and cardiovascular risk factors for elevation of tricuspid regurgitation velocity in children and adults with Chuvash polycythemia. Design and MethodsThis cross-sectional observational study of 120 adult and pediatric VHL R200W homozygotes and 31 controls at outpatient facilities in Chuvashia, Russian Federation included echocardiography assessment of pulmonary artery pressure (tricuspid regurgitation velocity), cardiac volume, and systolic and diastolic function, as well as hematologic and clinical parameters. We determined the prevalence and risk factors for elevation of tricuspid regurgitation velocity in this population and its relationship to phlebotomy. ResultsThe age-adjusted mean ± SE tricuspid regurgitation velocity was higher in VHL R200W homozygotes than controls with normal VHL alleles (2.5±0.03 vs. 2.3±0.05 m/sec, P=0.005). The ageadjusted left ventricular diastolic diameter (4.8±0.05 vs. 4.5±0.09 cm, P=0.005) and left atrial diameter (3.4±0.04 vs. 3.2±0.08 cm, P=0.011) were also greater in the VHL R200W homozygotes, consistent with increased blood volume, but the elevation in tricuspid regurgitation velocity persisted after adjustment for these variables. Among VHL R200W homozygotes, phlebotomy therapy was associated with lower serum ferritin concentration, and low ferritin independently predicted higher tricuspid regurgitation velocity (standardized beta=0.29; P=0.009). ConclusionsChildren and adults with Chuvash polycythemia have higher estimated right ventricular systolic pressure, even after adjustment for echocardiography estimates of blood volume. Lower ferritin concentration, which is associated with phlebotomy, independently predicts higher tricuspid regurgitation velocity (www.clinicaltrials.gov identifier NCT00495638).Key words: pulmonary hypertension, tricuspid regurgitation velocity, ferritin, VHL, hypoxia inducible factor.Citation: Sable CA, Aliyu ZY, Dham N, Nouraie M, Sachdev V, Sidenko S, Miasnikova GY, Polyakova LA, Sergueeva AI, Okhotin DJ, Bushuev V, Remaley AT, Niu X, Castro OL, Gladwin MT, Kato GJ, Prchal10 JT, and Gordeuk VR. Pulmonary artery pressure and iron deficiency in patients with upregulation of hypoxia sensing due to homozygous VHLR200W mutation (Chuvash polycythemia). Haematologica 2012;97(2):193-200. doi:10.3324/haematol.2011

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Pulmonary artery pressure and iron deficiency in patients with upregulation of hypoxia sensing due to homozygous VHLR200W mutation (Chuvash polycythemia)

et al. 2011

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“…Spleen contraction may temporarily contribute to the high Hb associated with secondary polycytemia, a common condition in COPD [28], which may have harmful consequences related to hyperviscosity and raised pulmonary arterial pressure [29]. Spleen contraction may be involved in exacerbation of shear stress imposed by atherosclerotic plaques and plaque ruptures by increasing blood viscosity during physiological and psychological stress [30,31], and clearly more research is needed to elucidated the spleen's role in regulation of stress related hemoconcentration.…”

Section: Hb (G/l)mentioning

confidence: 99%

Exercise induced hemoconcentration following spleen contraction in subjects with COPD

et al. 2015

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Background: The blood-boosting spleen contraction represents a potential protective response to hypoxia by raising the blood gas storage capacity. Human spleen contraction has been observed during exercise, apnea and simulated altitude resulting in ejection of stored red blood cells into circulation. High-altitude exposure has been shown to increase spleen contraction suggesting that long-term hypoxia may improve the response in humans. Subjects with COPD are often exposed to hypoxia, which limits their physical performance. However, it is not known if spleen contraction occurs in subjects with COPD. Our aim was to reveal whether subjects with COPD recruit the spleen erythrocyte reserve during mild exercise. Methods: SpO 2 , spleen volume and Hb were measured before and after 6 min walking test (6MWT) in 24 subjects with COPD. Results were analyzed for all subjects pooled and for subject groups with resting SpO 2 above and below 90 % separated and expressed as mean. Results: 6MWT reduced SpO 2 from 91 to 83 % and spleen volume from 254 to 181 mL, while Hb increased from 150 to 154 g/L (p = 0.001 for all). Compared to subjects with SpO 2 > 90 %, the group with SpO 2 < 90 % displayed the largest resting spleen volume (339 vs 202 mL; p = 0.001) and the most pronounced spleen volume reduction (139 vs 40 mL; p = 0.007). Conclusion: Exercise with hypoxia evokes spleen contraction in subjects with COPD and may represent a protective response during periods of hypoxia. The larger spleen volume and more pronounced contraction in the most hypoxic subjects may suggest long-term adaptation to hypoxia.

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“…[17][18][19] A retrospective analysis of 41 patients with emphysema revealed that increasing levels of Hb correlated with increasing PAP. 20 In contrast, some investigators have reported that augmentation of polycythaemia by exogenous human recombinant erythropoietin failed to worsen the severity of hypoxic pulmonary hypertension in rats. 21,22 As none of the current patients had resting hypoxaemia, the possibility of secondary polycythaemia was very low.…”

Section: Discussionmentioning

confidence: 97%

Pulmonary artery pressure in chronic obstructive pulmonary disease without resting hypoxaemia

Lee¹,

Oh²,

Seo

et al. 2011

int j tuberc lung dis

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THE DEVELOPMENT of pulmonary hypertension (PH) is often observed in advanced chronic obstructive pulmonary disease (COPD) and indicates a poor prognosis, with a 5-year survival rate of 20-36%. 1,2 PH primarily occurs in COPD patients with severe hypoxaemia; fortunately, however, the PH is typically mild. 3 Hypoxaemia increases pulmonary artery pres- S U M M A R Ysure (PAP) through hypoxic pulmonary vasoconstriction and vascular remodelling. 4 However, there is a poor correlation between lung function parameters and PAP, suggesting that factors other than airway obstruction and/or loss of alveolar surface may play a role in its aetiology.Recent studies have shown that a proportion of patients with only moderate airway obstruction have severe PH. 5,6 Disproportionate PH in COPD patients seems best defi ned as at least moderate elevation in SDL and YMO contributed equally to this article.

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Effects of Hemoglobin on Pulmonary Arterial Pressure and Pulmonary Vascular Resistance in Patients with Chronic Emphysema

Cited by 37 publications

References 9 publications

Pulmonary artery pressure and iron deficiency in patients with upregulation of hypoxia sensing due to homozygous VHLR200W mutation (Chuvash polycythemia)

Pulmonary artery pressure and iron deficiency in patients with upregulation of hypoxia sensing due to homozygous VHLR200W mutation (Chuvash polycythemia)

Exercise induced hemoconcentration following spleen contraction in subjects with COPD

Pulmonary artery pressure in chronic obstructive pulmonary disease without resting hypoxaemia

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