ArticleThrombosis research2015
Leukocyte expression of heme oxygenase-1 [hmox1] varies inversely with severity of tricuspid regurgitation in acute pulmonary embolism.
Article in Thrombosis research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Inhaled nitric oxide to control platelet hyper-reactivity in patients with acute submassive pulmonary embolism.Nitric oxide : biology and chemistry · 2020Trial
- Randomized trial of inhaled nitric oxide to treat acute pulmonary embolism: The iNOPE trial.American heart journal · 2017Trial
- Inhaled Nitric Oxide as an Adjunct to Thrombolytic Therapy in a Patient with Submassive Pulmonary Embolism and Severe Hypoxemia.Case reports in critical care · 2019Article
- Pulmonary vasodilation in acute pulmonary embolism - a systematic review.Pulmonary circulationReview
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
objectivePulmonary 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.
designProspective, 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 >2.7m/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.
resultsOf 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(2)=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.
conclusionsSeverity of TR varied inversely with hmox-1 expression, suggesting that hmox-1 expression affects pulmonary vascular reactivity after PE.
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