Year: 2013
Type: article
Abstract: To the Editor:
Measurements from humans and animal models with pulmonary embolism (PE) have demonstrated increases in multiple vasoconstrictive molecules, including prostaglandins, platelet-activating factor and leukotrienes [1]. Nitric oxide (NO), produced tonically by vascular endothelial nitric oxide synthase (eNOS), plays a pivotal role in maintaining a normal pulmonary vascular resistance under these conditions [2]. These facts underlie the construct hypothesis that in different subjects, PE can obstruct the same degree of pulmonary vasculature but manifest widely different pulmonary arterial resistances.
Preliminary evidence from animal models and humans suggests that acute PE is associated with intravascular haemolysis, related to the severity of PE [3–8]. Intravascular haemolysis liberates haemoglobin and diffusible haem, both of which directly bind NO. Ruptured erythrocytes also release large amounts of the enzyme arginase-1, which cleaves the eNOS substrate l-arginine, producing urea and l-ornithine.
We hypothesised that patients with acute PE that causes significant tricuspid regurgitation (TR) will have acutely increased plasma concentrations of arginase-1, decreased l-arginine and increased asymmetric dimethylarginine (aDMA) compared with patients who have mild PE without TR as well as patients without PE.
This was a secondary analysis of a four-centre prospective study of diagnostic accuracy conducted in patients with suspected PE (www.clinicaltrials.gov identifier NCT00368836) [9]. The enrolment and diagnostic criteria have been described previously [9]. Acute PE was considered present if two independent board-certified radiologists interpreted a filling defect consistent with acute PE on computed tomographic pulmonary angiography. Echocardiography was performed using techniques as previously described, …
Source: European Respiratory Journal
Language: English
Subfield: Internal Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2095836300