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Published on: January 4, 2013
Increased arterial pulsatility and progression of single subcortical infarction
Keon-Joo Lee1,2, Keun-Hwa Jung3,4, Chan-Young Park1,2
1Department of Neurology, Laboratory for Neurotherapeutics, Biomedical Research Institute, Seoul National University Hospital, 101, Daehangno, Jongno-gu, Seoul, 03080, South Korea.
Insights
Higher pulsatility index, a measure from transcranial Doppler, is linked to stroke progression in lacunar infarction patients, suggesting it may indicate vascular resistance and perfusion status.
Area of Science:
- Neurology
- Vascular Neurology
- Neuroimaging
Background:
- Subcortical infarctions, including lacunar and striatocapsular types, represent a significant cause of stroke.
- Understanding factors associated with stroke progression is crucial for patient management and therapeutic development.
Purpose of the Study:
- To investigate the association of clinical, laboratory, sonographic, and imaging parameters with the progression of single subcortical infarctions.
- To determine if the pulsatility index (PI) measured by transcranial Doppler is associated with stroke progression in different types of subcortical infarctions.
Main Methods:
- A cohort of 169 patients with lacunar (n=89) and striatocapsular infarctions (n=80) in the middle cerebral artery (MCA) territory were analyzed for stroke progression.
- Transcranial Doppler sonography was used to measure the pulsatility index (PI) from the ipsilateral M1 segment of the MCA.
Main Results:
- The striatocapsular infarction group showed more stroke progression compared to the lacunar infarction group.
- Progressive lacunar infarctions were associated with diabetes, higher HbA1c, and higher NIHSS scores.
- Higher MCA PI was observed in the lacunar infarction progression group (0.99±0.19 vs. 0.90±0.14, p=0.048) and independently associated with lacunar infarction progression (OR 1.51; p=0.024).
Conclusions:
- Elevated pulsatility index is associated with progression in lacunar infarction.
- Transcranial Doppler-derived PI may serve as an indicator of stroke progression by reflecting downstream arterial resistance and perfusion status.
- Distinct factors associated with stroke progression suggest different underlying pathophysiologies for lacunar versus striatocapsular infarctions.
Objective:
We investigated the association of clinical, laboratory, sonographic and imaging parameters, in the progression of single subcortical infarctions.
Methods:
Consecutive 169 patients with lacunar (n = 89) and striatocapsular infarctions (n = 80) in the middle cerebral artery (MCA) territory with nonstenotic MCAs were recruited and examined for stroke progression. The pulsatility index (PI) was measured by transcranial Doppler from ipsilateral M1.
Results:
The striatocapsular infarction group exhibited more stroke progression. The patients with progressive lacunar infarctions had more diabetes, higher HbA1c levels, and higher initial National Institutes of Health Stroke Scale (NIHSS) scores, and the patients with progressive striatocapsular infarctions had more hypertension, higher cholesterol levels, and higher NIHSS scores. The MCA PI was higher in the lacunar infarction patients with progression (0.99 ± 0.19 vs. 0.90 ± 0.14, p = 0.048), while the striatocapsular infarction patients did not differ according to progression. From a multivariate analysis, higher MCA PI were independently associated with lacunar infarction progression (by 0.1 increase, OR 1.51; 95 % CI 1.06-2.15; p = 0.024).
Conclusions:
Higher pulsatility was associated with progression in lacunar infarction. PI measured by transcranial Doppler sonography might reflect downstream arterial resistance and vascular/paravascular perfusion status and be a possible indicator of stroke progression.
Key Points:
• Higher pulsatility index was observed in progression group of lacunar infarction patients. • Higher pulsatility index seemed to be associated with progression in lacunar infarction patients. • Differences in the factors associated with stroke progression suggest different underlying pathophysiologies.
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