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Title
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Late gadolinium enhancement CMR in primary mitral regurgitation
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Author
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Abstract
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| Aims The appropriate timing for surgery in severe asymptomatic primary mitral regurgitation (MR) remains controversial. It has been shown that late gadolinium enhancement on cardiovascular magnetic resonance (LGE CMR), which may identify myocardial fibrosis, is associated with a worse outcome in various cardiomyopathies. We sought to investigate the prevalence and significance of delayed enhancement in primary MR. Methods We prospectively included 41 patients with at least moderate primary MR and without overt signs of left ventricular (LV) dysfunction. Patients with evidence of coronary artery disease, arrhythmias or significant concomitant valvular disease were excluded. All patients were scheduled for transthoracic echocardiography and LGE CMR. Results A total of 39 patients had interpretable LGE CMR images. Among them, 12 (31%) had late contrast uptake of the LV wall. LGE CMR showed an infarct pattern in three patients, a pattern of mid-wall fibrosis in seven patients and two patients had a combined pattern. Patients with delayed enhancement on CMR had significant higher LV diameters (LV end-systolic diameter 39 +/- 4 vs. 34 +/- 5 mm, P = 0.002; LV end-diastolic diameter 57 +/- 5 vs. 50 +/- 5 mm, P = 0.001). There was a trend towards a higher indexed left atrial volume (55 +/- 21 vs. 44 +/- 13 mL/m(2), P = 0.06). By contrast, there was no significant association between myocardial contrast uptake and age, LV ejection fraction and MR severity. Conclusion Left ventricular remodelling seems to be associated with the presence of delayed enhancement on CMR in primary MR. Further data are needed to determine whether LGE CMR can predict a less favourable outcome or could improve risk stratification in asymptomatic primary MR. |
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Language
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English
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Source (journal)
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European journal of clinical investigation. - Berlin
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Publication
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Berlin
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2014
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ISSN
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0014-2972
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DOI
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10.1111/ECI.12306
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Volume/pages
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44
:9
(2014)
, p. 840-847
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ISI
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000341624500004
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Full text (Publisher's DOI)
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Full text (publisher's version - intranet only)
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