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International Journal of Stroke 19(3)
Figure 4. Cardiac pathologies in ESUS patients, not discovered with standard workup. (a) A 57-year-old female patient with
mechanic prosthetic valve (*), presenting with ESUS. LGE imaging shows extensive fibrosis of the posterior LA wall, interatrial
septum, and the origin of the right pulmonary vein (red arrowheads). (b) A 53-year-old woman with multiple ischemic strokes
and increased peripheral eosinophil count. Cine image (left) showed an apparently hypertrophied LV apex (white arrow). Early
post-contrast image (right) showed multiple LV and RV thrombi (red arrowheads). The clinical and imaging features were in
keeping with Loeffler myocarditis. (c) A 55-year-old male patient with a history of inferior infarction. The cine (left) and LGE
(right) images show a large pseudoaneurysm with a broad connection to the LV chamber (red dashed line) and a large, stratified
thrombus (*). (d) A 47-year-old woman with ESUS. The cine (left) and LGE (right) images show a heterogeneous, irregularly
shaped mass (*) of the anterior mitral leaflet, consistent with myxoma.
LA: left atrium; LV: left ventricle; RA: right atrium; RV: right ventricle; RVOT: right ventricular outflow tract; Ao: aortic root.
first-line left atrium assessment by TTE, including direct
visualization of fibrotic burden, seen as hyperintense
LGE areas on delayed enhancement images (Figure 4(a)).
In the reviewed studies, the atrial fibrotic burden was
associated with increased odds of stroke in patients with
known AF10 and outperformed the CHA2DS2-VASc score
for the prediction of LA thrombosis.10,11 Atrial LGE in
patients with ESUS was significantly greater than in controls6,9
and was comparable with AF patients,8,9 suggesting
the widespread presence of pro-arrhythmic and
thrombogenic substrates among the former. A total of
12% atrial LGE threshold was proposed to identify
patients at a higher risk of ESUS, independently of the
presence of FA,6,7 which could establish fibrotic burden
as a potential decision-making tool.47 A recently published
protocol for a prospective multicenter CARM-AF
study will aim to identify patients with ESUS at risk of
future thromboembolism due to atrial cardiomyopathy
through non-invasive CMR and ECG data.48
The unparalleled soft-tissue contrast and robust temporal
resolution of CMR allow reliable detection and characterization
of a variety of LV embolic sources (Figure 4(b) to
(d)). CMR can accurately detect LV thrombi, which appear
International Journal of Stroke, 19(3)
markedly hypointense on early and delayed enhancement
images,49 and reliably differentiate them from tumors and
other cardiac masses (Figure 4(d)).12 CMR also allowed to
identify LV pathologies associated with thrombus formation
and increased risk of embolic stroke,14 including cardiomyopathies,
where altered cardiac morphology and
hemodynamic changes promote pro-thrombogenic environment
(Figure 4(b)),50 and previously undiagnosed myocardial
infarction characterized by subendocardial or
transmural distribution of hyperintense LGE on delayed
enhancement CMR (Figure 4(c)).15
The Trial of ORG 10172 in Acute Stroke Treatment
(TOAST) classification required an atherosclerotic plaque
causing a ⩾50% stenosis in a large brain-supplying artery
for the definition of large-artery atherosclerotic stroke.51
However, it becomes increasingly apparent that the assessment
of atherosclerotic plaques in ESUS should include a
broader set of plaque characteristics associated with substantial
embolic risk.52 In-depth tissue characterization by
MRI allows to identify a variety of high-risk plaque features
classified as AHA-LT VI plaques, including fibrous
cap rupture, lipid-rich necrotic core, intraluminal thrombus,
and IPH (Figure 5).53
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