Leukocyte expression of heme oxygenase-1 [hmox1] varies inversely with severity of tricuspid regurgitation in acute pulmonary embolism

Jeffrey Kline, Nury M. Steuerwald, John A. Watts, Mark Courtney, Herbert L. Bonkovsky

Research output: Contribution to journalArticle

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Abstract

Objective Pulmonary embolism (PE) can cause intracardiac hemolysis and increased plasma hemoglobin and arginase-1, which can worsen pulmonary vasoconstriction. We test the hypothesis that patients with PE that causes tricuspid regurgitation (TR), indicative of higher pulmonary arterial pressures, have decreased leukocyte expression of hmox-1 compared with patients with PE and no TR and patients without PE. Design Prospective, noninterventional study. Patients Normotensive patients with suspected PE (n = 87) who underwent CT pulmonary angiography and transthoracic Doppler-echocardiography. Measurements Significant TR was defined as a jet velocity > 2.7 m/s. Leukocyte expression of hmox-1, haptoglobin, haptoglobin related gene, the haptoglobin receptor, CD163 and cox-2 genes were assessed by quantitative rtPCR, and the hmox-1 promoter was examined for the - 413 A → T SNP and GT repeat polymorphisms. Results Of the 44 (50%) with PE +, 22 had TR +, and their mean pulmonary vascular occlusion (39 ± 32%) did not differ significantly from patients who were TR - (28 ± 26%, P = 0.15). Patients with PE + and TR + had significantly lower expression of hmox-1 and haptoglobin genes than patients without PE + and no TR. Expression of hmox-1 varied inversely with TR velocity (r<sup>2</sup> = 0.45, P < 0.001) for PE + (n = 22) but not patients without PE. Hmox-1 expression did not vary significantly with genotype. Cox-2 did not differ between groups and had no correlation with TR. Conclusions Severity of TR varied inversely with hmox-1 expression, suggesting that hmox-1 expression affects pulmonary vascular reactivity after PE.

Original languageEnglish
Pages (from-to)769-774
Number of pages6
JournalThrombosis Research
Volume136
Issue number4
DOIs
StatePublished - Oct 1 2015

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Tricuspid Valve Insufficiency
Heme Oxygenase-1
Pulmonary Embolism
Leukocytes
Haptoglobins
Lung
Blood Vessels
Pulmonary Valve Insufficiency
Genes
Arginase
Doppler Echocardiography
Hemolysis
Vasoconstriction
Single Nucleotide Polymorphism
Echocardiography
Arterial Pressure
Hemoglobins
Genotype
Prospective Studies

Keywords

  • Fibrinolysis
  • Haptoglobin
  • Heme oxygenase
  • Hemolysis
  • Pulmonary hypertension

ASJC Scopus subject areas

  • Hematology

Cite this

Leukocyte expression of heme oxygenase-1 [hmox1] varies inversely with severity of tricuspid regurgitation in acute pulmonary embolism. / Kline, Jeffrey; Steuerwald, Nury M.; Watts, John A.; Courtney, Mark; Bonkovsky, Herbert L.

In: Thrombosis Research, Vol. 136, No. 4, 01.10.2015, p. 769-774.

Research output: Contribution to journalArticle

Kline, Jeffrey ; Steuerwald, Nury M. ; Watts, John A. ; Courtney, Mark ; Bonkovsky, Herbert L. / Leukocyte expression of heme oxygenase-1 [hmox1] varies inversely with severity of tricuspid regurgitation in acute pulmonary embolism. In: Thrombosis Research. 2015 ; Vol. 136, No. 4. pp. 769-774.
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abstract = "Objective Pulmonary embolism (PE) can cause intracardiac hemolysis and increased plasma hemoglobin and arginase-1, which can worsen pulmonary vasoconstriction. We test the hypothesis that patients with PE that causes tricuspid regurgitation (TR), indicative of higher pulmonary arterial pressures, have decreased leukocyte expression of hmox-1 compared with patients with PE and no TR and patients without PE. Design Prospective, noninterventional study. Patients Normotensive patients with suspected PE (n = 87) who underwent CT pulmonary angiography and transthoracic Doppler-echocardiography. Measurements Significant TR was defined as a jet velocity > 2.7 m/s. Leukocyte expression of hmox-1, haptoglobin, haptoglobin related gene, the haptoglobin receptor, CD163 and cox-2 genes were assessed by quantitative rtPCR, and the hmox-1 promoter was examined for the - 413 A → T SNP and GT repeat polymorphisms. Results Of the 44 (50{\%}) with PE +, 22 had TR +, and their mean pulmonary vascular occlusion (39 ± 32{\%}) did not differ significantly from patients who were TR - (28 ± 26{\%}, P = 0.15). Patients with PE + and TR + had significantly lower expression of hmox-1 and haptoglobin genes than patients without PE + and no TR. Expression of hmox-1 varied inversely with TR velocity (r2 = 0.45, P < 0.001) for PE + (n = 22) but not patients without PE. Hmox-1 expression did not vary significantly with genotype. Cox-2 did not differ between groups and had no correlation with TR. Conclusions Severity of TR varied inversely with hmox-1 expression, suggesting that hmox-1 expression affects pulmonary vascular reactivity after PE.",
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T1 - Leukocyte expression of heme oxygenase-1 [hmox1] varies inversely with severity of tricuspid regurgitation in acute pulmonary embolism

AU - Kline, Jeffrey

AU - Steuerwald, Nury M.

AU - Watts, John A.

AU - Courtney, Mark

AU - Bonkovsky, Herbert L.

PY - 2015/10/1

Y1 - 2015/10/1

N2 - Objective Pulmonary embolism (PE) can cause intracardiac hemolysis and increased plasma hemoglobin and arginase-1, which can worsen pulmonary vasoconstriction. We test the hypothesis that patients with PE that causes tricuspid regurgitation (TR), indicative of higher pulmonary arterial pressures, have decreased leukocyte expression of hmox-1 compared with patients with PE and no TR and patients without PE. Design Prospective, noninterventional study. Patients Normotensive patients with suspected PE (n = 87) who underwent CT pulmonary angiography and transthoracic Doppler-echocardiography. Measurements Significant TR was defined as a jet velocity > 2.7 m/s. Leukocyte expression of hmox-1, haptoglobin, haptoglobin related gene, the haptoglobin receptor, CD163 and cox-2 genes were assessed by quantitative rtPCR, and the hmox-1 promoter was examined for the - 413 A → T SNP and GT repeat polymorphisms. Results Of the 44 (50%) with PE +, 22 had TR +, and their mean pulmonary vascular occlusion (39 ± 32%) did not differ significantly from patients who were TR - (28 ± 26%, P = 0.15). Patients with PE + and TR + had significantly lower expression of hmox-1 and haptoglobin genes than patients without PE + and no TR. Expression of hmox-1 varied inversely with TR velocity (r2 = 0.45, P < 0.001) for PE + (n = 22) but not patients without PE. Hmox-1 expression did not vary significantly with genotype. Cox-2 did not differ between groups and had no correlation with TR. Conclusions Severity of TR varied inversely with hmox-1 expression, suggesting that hmox-1 expression affects pulmonary vascular reactivity after PE.

AB - Objective Pulmonary embolism (PE) can cause intracardiac hemolysis and increased plasma hemoglobin and arginase-1, which can worsen pulmonary vasoconstriction. We test the hypothesis that patients with PE that causes tricuspid regurgitation (TR), indicative of higher pulmonary arterial pressures, have decreased leukocyte expression of hmox-1 compared with patients with PE and no TR and patients without PE. Design Prospective, noninterventional study. Patients Normotensive patients with suspected PE (n = 87) who underwent CT pulmonary angiography and transthoracic Doppler-echocardiography. Measurements Significant TR was defined as a jet velocity > 2.7 m/s. Leukocyte expression of hmox-1, haptoglobin, haptoglobin related gene, the haptoglobin receptor, CD163 and cox-2 genes were assessed by quantitative rtPCR, and the hmox-1 promoter was examined for the - 413 A → T SNP and GT repeat polymorphisms. Results Of the 44 (50%) with PE +, 22 had TR +, and their mean pulmonary vascular occlusion (39 ± 32%) did not differ significantly from patients who were TR - (28 ± 26%, P = 0.15). Patients with PE + and TR + had significantly lower expression of hmox-1 and haptoglobin genes than patients without PE + and no TR. Expression of hmox-1 varied inversely with TR velocity (r2 = 0.45, P < 0.001) for PE + (n = 22) but not patients without PE. Hmox-1 expression did not vary significantly with genotype. Cox-2 did not differ between groups and had no correlation with TR. Conclusions Severity of TR varied inversely with hmox-1 expression, suggesting that hmox-1 expression affects pulmonary vascular reactivity after PE.

KW - Fibrinolysis

KW - Haptoglobin

KW - Heme oxygenase

KW - Hemolysis

KW - Pulmonary hypertension

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