8 research outputs found

    Cardiovascular disease in rheumatic diseases:A focus on cardiac function in Ankylosing Spondylitis

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    Nurmohamed, M.T. [Promotor]Peters, M.J.L. [Copromotor]Horst-Bruinsma, I.E. van der [Copromotor]Kamp, O. [Copromotor

    Insights into cardiac involvement in ankylosing spondylitis from cardiovascular magnetic resonance

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    Item does not contain fulltextOBJECTIVE: To evaluate cardiac involvement in patients with ankylosing spondylitis using cardiac magnetic resonance (CMR). METHODS: Patients with ankylosing spondylitis without cardiovascular symptoms or known cardiovascular disease were screened by transthoracic echocardiography (TTE) for participation in this exploratory CMR study. We prospectively enrolled 15 ankylosing spondylitis patients with an abnormal TTE for further tissue characterisation using late gadolinium enhancement (LGE) and T1 mapping. T1 mapping was used to calculate myocardial extracellular volume (ECV). Disease activity was assessed by C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) measurements. RESULTS: In the total of 15 included patients, 14 had a complete CMR exam (mean age 62 years, 93% male and mean disease duration 21 years). Left ventricular (LV) diastolic dysfunction was the most common finding on TTE (79%), followed by aortic root dilatation (14%), right ventricular (RV) dilatation (7%) and RV dysfunction (7%). CMR revealed focal hyperenhancement in three patients (21%), all with a particular pattern of enhancement. LV dysfunction, as defined by a LV ejection fraction below 55%, was observed in five patients (36%). Myocardial ECV was correlated with the CRP concentration (R=0.78, p<0.01) and ESR level (RS=0.73, p<0.01). CONCLUSIONS: In patients with ankylosing spondylitis, CMR with cine imaging and LGE identified global LV dysfunction and focal areas of hyperenhancement. Myocardial ECV, quantified by CMR T1 mapping, was associated with the degree of disease activity. These results may suggest the presence of cardiac involvement in ankylosing spondylitis and may show the potential of ECV as a marker for disease monitoring

    Assessment of aortic stiffness in patients with ankylosing spondylitis using cardiovascular magnetic resonance

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    Contains fulltext : 207076.pdf (publisher's version ) (Closed access)To evaluate aortic stiffness in patients with ankylosing spondylitis (AS) using cardiovascular magnetic resonance (CMR) and to assess its association with AS characteristics and left ventricular (LV) remodeling. In this prospective study, 14 consecutive AS patients were each matched to two controls without cardiovascular symptoms or known cardiovascular disease who underwent CMR imaging for the assessment of aortic arch pulse wave velocity (PWV) at 1.5 Tesla. To enhance comparability of the samples, matching was done with replacement resulting in 20 unique controls. Only AS patients with abnormal findings on screening echocardiography were included in this exploratory study. Cine CMR was used to assess LV geometry and systolic function, and late gadolinium enhancement was performed to determine the presence of myocardial hyperenhancement (i.e., fibrosis). Aortic arch PWV was significantly higher in the AS group compared with the control group (median 9.7 m/s, interquartile range [IQR] 7.1 to 11.8 vs. 6.1 m/s, IQR 4.6 to 7.6 m/s; p < 0.001). PWV was positively associated with functional disability as measured by BASFI (R: 0.62; p = 0.018). Three patients (21%) with a non-ischemic pattern of hyperenhancement showed increased PWV (11.7, 12.3, and 16.5 m/s) as compared to the 11 patients without hyperenhancement (9.0 m/s, IQR 6.6 to 10.5 m/s; p = 0.022). PWV was inversely associated with LV ejection fraction (R: - 0.63; p = 0.015), but was not found to be statistically correlated to LV volumes or mass. Aortic arch PWV was increased in our cohort of patients with AS. Higher PWV in the aortic arch was associated with functional disability, the presence of non-ischemic hyperenhancement, and reduced LV systolic function

    Cardiovascular Risk in Rheumatoid Arthritis and Mechanistic Links: From Pathophysiology to Treatment

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    Cardiovascular Disease in Spondyloarthritides

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