alexa Assessment of myocardial fibrosis and microvascular damage in systemic sclerosis by magnetic resonance imaging and coronary angiotomography.
Immunology

Immunology

Rheumatology: Current Research

Author(s): RodrguezReyna TS, MorelosGuzman M, HernndezReyes P, MonteroDuarte K, MartnezReyes C,

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Abstract OBJECTIVE: Cardiac involvement in SSc is characterized by myocardial fibrosis, arrhythmias and pericarditis. Prevalence studies have shown variable results. The objective of this study was to determine the prevalence of cardiac involvement in SSc patients using the non-invasive, highly sensitive diagnostic methods of cardiac MRI and coronary angiotomography. METHODS: We included 62 SSc patients and excluded those with heart disease prior to the onset of SSc, renal failure, diabetes mellitus, hyperlipidaemia, arterial hypertension, untreated thyroid disease, cor pulmonale, pregnancy or contraindications to performing cardiac MRI. All underwent clinical and laboratory evaluation, ECG, coronary angiotomography and cardiac MRI. RESULTS: The prevalence of myocardial fibrosis was 45\% and was higher in dcSSc (59\%) than in lcSSc patients (33\%; P = 0.04). The mean left ventricular ejection fraction (LVEF) was lower in patients with myocardial fibrosis (56\%) than in those without fibrosis (63\%; P = 0.0009); myocardial fibrosis on MRI was more frequent in the basal-septal segments of the LV. Seventy-nine per cent of patients had subendocardial perfusion defects and these were associated with higher ultrasensitive serum CRP values. There was no association of myocardial fibrosis or microvascular damage with atherosclerosis. CONCLUSION: The prevalence of myocardial fibrosis on MRI attributable to SSc is 45\%, is more frequent and severe in dcSSc patients, is associated with lower LVEF and affects mainly basal LV walls. Microvascular damage in SSc is common and is associated with elevated ultrasensitive CRP levels. Cardiac damage due to SSc is not associated with coronary artery disease. © The Author 2014. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oup.com. This article was published in Rheumatology (Oxford) and referenced in Rheumatology: Current Research

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