Factors affecting early neurological deterioration after intravenous alteplase treatment for branch atheromatous disease.

Mizuno, Satoko; Deguchi, Ichiro; Takahashi, Shinichi; Arai, Noriko; Nakagami, Toru; Kimura, Ryutaro; Oryu, Kiichiro; Watanabe, Kaito; Ueda, Sae; Fujiwara, Shinako; Kato, Yuji; Hayashi, Takeshi; Suda, Satoshi

Background: Intravenous alteplase treatment is effective for acute cerebral infarction, irrespective of the stroke type. However, its value for branch atheromatous disease (BAD) remains unclear, and early neurological deterioration (END) can occur. Aim: To investigate factors affecting END after intravenous alteplase treatment in patients with acute BAD. Methods: This study included 40 consecutive patients diagnosed with cerebral infarction due to BAD in the lenticulostriate artery territory and treated with intravenous alteplase between April 2007 and March 2023. END was defined as an increase of ≥2 points in the total National Institutes of Health Stroke Scale score or ≥1 point in the motor items within 24 h post‐alteplase administration compared to the score at admission. Factors affecting END were retrospectively evaluated. Results: END was observed in 17 of the 40 patients (43%). The median time from the start of alteplase administration to the worsening of neurologic symptoms was 5 h. After intravenous alteplase treatment, the END group had a significantly lower 24‐h average systolic blood pressure (SBP, mean ± standard deviation mmHg) than the non‐END group (142.0 ± 15.2 vs. 149.4 ± 12.0, p < 0.001). The SBP at each time point (immediately before alteplase administration and every 2 h up to 24 h after alteplase administration) was significantly lower in the END than in the non‐END group at 2, 4, and 6 h after alteplase administration. Conclusions: When intravenous alteplase was administered for BAD, BP control after alteplase administration affected END. When alteplase is administered for BAD, it is important to control the blood pressure to maintain hemodynamics.

SYSTOLIC blood pressure; CEREBRAL infarction; CLINICAL deterioration; STROKE; BLOOD pressure

Neurology & Clinical Neuroscience, 2025, Vol 13, Issue 1, p57

2049-4173

Academic Journal

10.1111/ncn3.12848