Longitudinal assessment of cerebral infarcts and small vessel disease using magnetic resonance imaging in antiphospholipid syndrome: A single-centre retrospective study

Abstract

Introduction: Stroke is the most frequent arterial thrombosis in antiphospholipid syndrome (APS) with high rates of recurrence.

Methods and patients: A retrospective, single-centre 10-year review of patients with APS having sequential cerebral magnetic resonance imaging (MRI) was performed to describe ischaemic features in APS and associated disease risk factors and progression over time.

Results: A total of 120 patients and 307 scans were included with 67% of patients receiving vitamin K antagonists (VKA). Note that 65% of patients had baseline ischaemic features with white matter hyperintensities (WMH), as a feature of small vessel disease (SVD), seen in 79% of abnormal scans. Fifteen percent of patients had progressive ischaemic changes with 83% demonstrating progressive WMH and 33% new infarcts (predominantly lacunar) on sequential scans. Progression-free survival for progressive ischaemia was 88% at 5 years. Multivariate analysis showed longer follow-up was a risk for developing progressive ischaemia (odds ratio [OR] 1.43, 95% confidence interval [CI] 1.13-1.86, p = 0.005). Hypertension (56% vs. 30%, p = 0.04) and ischaemic heart disease (22% vs. 6%, p = 0.04) were more prevalent with progressive ischaemia. There was no difference in progression or bleeding events according to VKA therapeutic intensity.

Discussion: These results show SVD is a common feature of APS using MRI with progressive changes despite anticoagulation. Traditional risk factors for cerebrovascular disease were associated with progression.

Keywords: MRI; anticoagulation; antiphospholipid syndrome; imaging; stroke.

FIGURE 1

Flow chart of patient inclusion and magnetic resonance imaging (MRI) outcomes. APS, antiphospholipid syndrome; TAPS, thrombotic APS; OAPS, obstetric APS; WMH, white matter hyperintensities; CMB, cerebral microbleeds.

FIGURE 2

Kaplan–Meier curve of progression‐free survival to development of cerebral ischaemia: (A) all patients; (B) patients with asymptomatic scans.

FIGURE 3

Cerebral magnetic resonance imaging of patients with antiphospholipid syndrome showing infarction: (A) 3D fluid attenuated recovery sequence (FLAIR) image—right parietal gliosis consistent with cortical infarction (arrow); (B) axial T2 image—right thalamic infarct (arrow).

FIGURE 4

Cerebral magnetic resonance imaging of patients with antiphospholipid syndrome showing infarction: (A) axial T2 image—central pontine gliosis consistent with infarction and (B) axial diffusion weighted imaging (DWI) image with signal abnormality right internal capsule consistent with capsular infarction.

FIGURE 5

Cerebral magnetic resonance imaging of patients with antiphospholipid syndrome showing infarction. Deep watershed and separate cortical embolic infarcts by (A and B) T2 axial and (C and D) 2D fluid attenuated recovery sequence (FLAIR). Long arrows demonstrate deep watershed hyperintense foci (A and B) which were subsequently supressed on FLAIR imaging, confirming gliotic change secondary to infarction (C). Short arrows outline cortical infarction of the left anterior cerebral territory within the superior frontal gyrus (B and D).

FIGURE 6

Cerebral magnetic resonance imaging of patients with antiphospholipid syndrome showing watershed infarction—3D fluid attenuated recovery sequence (FLAIR) sequence confirming right external watershed territory infarct interposed between middle and posterior cerebral arterial territories.

FIGURE 7

Serial cerebral magnetic resonance imaging of a patient with antiphospholipid syndrome over a 10‐year period. (A) Initial axial fluid attenuated recovery sequence (FLAIR) sequence demonstrating deep watershed infarcts (B) coronal FLAIR sequence acquired 5 years after the initial scan, demonstrating a right occipitotemporal (posterior cerebral artery) territory embolic infarct. (C) Axial T2 sequence acquired 10‐years after the initial scan, demonstrating an external watershed infarct interposed between the middle and posterior cerebral arterial territories.