Blood pressure variability and parenchymal hematoma after endovascular thrombectomy: effect modification by recanalization status and cerebral small vessel disease burden.
We investigated the association between post-thrombectomy blood pressure variability (BPV) and parenchymal hematoma (PH), and whether this relationship is modified by persistent vessel patency and cerebral small vessel disease (CSVD) burden.
We analyzed 302 patients with acute ischemic stroke who underwent endovascular thrombectomy. PH was defined as confluent hemorrhage with a mass effect. BPV was assessed using 2-h blood pressure measurements during the first 24 h. Parameters included the maximum, minimum, mean, range, standard deviation, coefficient of variation, and successive variation of systolic, diastolic, and pulse pressure (PP). CSVD burden was quantified using the total CSVD score and dichotomized into none-to-mild (score 0-1) and moderate-to-severe (score 2-4). Multivariable logistic regression models were used to evaluate associations and interaction effects.
PH occurred in 78 patients (25.8%). Among BPV parameters, pulse pressure successive variation (PPSV) showed favorable model performance and was selected for interaction analyses. Significant interactions were observed between PPSV and persistent vessel patency (Pinteraction = 0.003) and between PPSV and CSVD burden (Pinteraction = 0.007). In stratified analyses, higher PPSV was associated with PH in patients with sustained major vessel patency (OR, 2.67 [95% CI, 1.79-3.97]; p < 0.001) and in those with none-to-mild CSVD (OR, 2.61 [95% CI, 1.74-3.94]; p < 0.001) but not in those with persistent occlusion or moderate-to-severe CSVD.
Increased post-thrombectomy BPV, particularly PP variability, was independently associated with PH, with effects modified by persistent vessel patency and CSVD burden. These findings suggest individualized blood pressure management based on macrovascular persistent vessel patency and underlying microvascular integrity.
We analyzed 302 patients with acute ischemic stroke who underwent endovascular thrombectomy. PH was defined as confluent hemorrhage with a mass effect. BPV was assessed using 2-h blood pressure measurements during the first 24 h. Parameters included the maximum, minimum, mean, range, standard deviation, coefficient of variation, and successive variation of systolic, diastolic, and pulse pressure (PP). CSVD burden was quantified using the total CSVD score and dichotomized into none-to-mild (score 0-1) and moderate-to-severe (score 2-4). Multivariable logistic regression models were used to evaluate associations and interaction effects.
PH occurred in 78 patients (25.8%). Among BPV parameters, pulse pressure successive variation (PPSV) showed favorable model performance and was selected for interaction analyses. Significant interactions were observed between PPSV and persistent vessel patency (Pinteraction = 0.003) and between PPSV and CSVD burden (Pinteraction = 0.007). In stratified analyses, higher PPSV was associated with PH in patients with sustained major vessel patency (OR, 2.67 [95% CI, 1.79-3.97]; p < 0.001) and in those with none-to-mild CSVD (OR, 2.61 [95% CI, 1.74-3.94]; p < 0.001) but not in those with persistent occlusion or moderate-to-severe CSVD.
Increased post-thrombectomy BPV, particularly PP variability, was independently associated with PH, with effects modified by persistent vessel patency and CSVD burden. These findings suggest individualized blood pressure management based on macrovascular persistent vessel patency and underlying microvascular integrity.