Fig 1.
Representative cases of the four types of LAA mechanism.
Diffusion-weighted image and time-of-flight MRA images of the four types of LAA mechanism: (A) Artery-to-artery embolization, (B) In-situ thrombosis, (C) Hypoperfusion, and (D) Branch atheromatous disease.
Table 1.
Baseline characteristics in END and non-END patients with acute ischemic stroke.
Table 2.
Multivariable analyses of the relationship between early neurological deterioration and inflammatory markers with/without stratification by stroke mechanism.
Fig 2.
Serum NLR according to the burden of the vascular lesions.
Patients with occlusive vascular lesions had the highest NLR levels (P = 0.033); serum NLR increased according to the degree of stenosis in a dose-response manner (P for trend = 0.006). Furthermore, serum NLR increased according to the number of vessel stenosis in a dose-response manner (P for trend = 0.038).
Fig 3.
Serum NLR according to stroke mechanism in patients with large-artery atherosclerosis.
Patients with in-situ thrombosis or hypoperfusion mechanisms had higher serum NLR levels than those with other stroke mechanisms.
Fig 4.
Comparison of serum NLR between patients with END and patients without END by LAA mechanism.
Patients with hypoperfusion (median NLR, 3.23 [2.67–3.71]) and in-situ thrombosis (median NLR, 2.88 [2.04–4.21]) mechanisms had higher NLR levels than those with artery-to-artery embolization (median NLR, 2.23 [1.56–3.57]) or branch atheromatous disease mechanisms (median NLR, 2.27 [1.45–3.60]). However, only in-situ thrombosis showed significant differences between the END group and the non-END group (P = 0.005).
Table 3.
Characteristics according to stroke mechanism in patients with large-artery atherosclerosis.