Novel imaging modalities in detection of cardiovascular involvement in ankylosing spondylitis
Tarih
2018Yazar
Akyuz, Aydin
Baykiz, Derya
Sarifakioglu, Banu
Alpsoy, Seref
Aycicek, Ozge
Gur, Demet Ozkaramanli
Ozaltun, Derya Necmiye
Guzel, Savas
Üst veri
Tüm öğe kaydını gösterÖzet
Objectives: The diagnosis of cardiovascular involvement in ankylosing spondylitis (AS) is usually delayed since conventional echocardiography relies mainly on the morphological alterations. The aim of this study was to evaluate the role of echocardiographic methods such as tissue Doppler and strain imaging of left ventricle (LV) and proximal aorta; and concentrations of biomarkers of cardiac fibrosis such as galectin-3 (Gal-3) and soluble suppression-of-tumorogenicity-2 (sST2) in determining early cardiovascular impairment in AS. Design: In this prospective study of 75 AS and 30 healthy subjects (mean age 41.7 +/- 10.1 years; 37.3% female), we determined layer-specific strain and strain rates in longitudinal, circumferential and radial axes for LV as well as transverse and longitudinal strains of proximal aorta; central pulse wave velocity(cPWV); plasma high sensitivity C-reactive protein(hsCRP), Gal-3 and sST2 levels. Results: Patients with AS had increased levels of hsCRP and sST2 when compared to healthy controls. cPWV, E and e' velocities; longitudinal strain and strain rates at all myocardial layers; and transverse strains of both anterior and posterior aortic walls were reduced in AS patients. Gal-3 levels with strain and strain rates at circumferential and radial axes were similar between the groups. Among all echocardiographic and clinical parameters, AS was independently associated with LV dysfunction (expressed by longitudinal strain of LV) and aortic impairment (expressed by transverse strain of anterior wall). Conclusions: This study demonstrates that functional impairment in AS occurs early in the disease course and strain imaging is an effective tool in discriminating involvement. sST2 may represent the link between inflammation and fibrosis in AS.
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