RT Journal Article
SR Electronic
T1 Endothelial function in contemporary patients with repaired coarctation of aorta
JF Heart
JO Heart
FD BMJ Publishing Group Ltd and British Cardiovascular Society
SP 1696
OP 1701
DO 10.1136/heartjnl-2014-305739
VO 100
IS 21
A1 R M Radke
A1 G-P Diller
A1 M Duck
A1 S Orwat
A1 D Hartmann
A1 T Thum
A1 H Baumgartner
YR 2014
UL http://heart.bmj.com/content/100/21/1696.abstract
AB Objective Previous studies have suggested endothelial dysfunction in adult patients after repair of aortic coarctation (CoA). It has been proposed to play a key role in the pathogenesis of arterial hypertension in the absence of re-coarctation. We aimed to assess the presence of endothelial dysfunction, the number of endothelial progenitor cells (EPC), and the levels of proinflammatory cytokines associated with endothelial injury in contemporary patients after CoA repair. Methods For this prospective observational study, 20 CoA patients and 22 healthy controls were recruited. Digital reactive hyperaemia was measured by peripheral arterial tonometry. Flow cytometry was used to quantify EPCs, and a comprehensive panel of laboratory markers of endothelial dysfunction was measured. Results Half the patients had known arterial hypertension requiring medical treatment. Indices of reactive hyperaemia showed no significant difference between CoA patients (1.96±0.32) and controlss (1.765±0.48) (p=0.82). Circulating EPCs, defined by the number of CD34+, CD34+/KDR+, CD34+/AC133+, CD34+/AC133+/KDR+ or CD34+/CD45− labelled cells were equally not significantly different between the groups. Furthermore, plasma levels of inflammatory mediators and markers of endothelial function (IL-6, IL-8, ICAM1 and VCAM1) were not significantly different between the groups, as were vascular endothelial growth factor levels (p>0.05, for all). Conclusions By contrast with earlier reports, no clinically significant difference in endothelial function between adult patients with coarctation repair and healthy controls could be demonstrated. Therefore, endothelial dysfunction may not necessarily be present in this population. Further studies are required to identify mechanisms and to develop strategies to avoid arterial hypertension in these patients.