Parneet Grewal, MD
Jeong H-G, Kim BJ, Kim H, Jung C, Han M-K, Liebeskind DS, et al. Blood Pressure Drop and Penumbral Tissue Loss in Nonrecanalized Emergent Large Vessel Occlusion. Stroke. 2019;50:2677–2684.
Despite recent advances in acute stroke care, many patients with large vessel occlusion (LVO) are not eligible for, or remain non-recanalized after, endovascular treatment. Ischemic penumbra, which is the target of recanalization treatment strategies, is an area that stands on a fragile balance between viability of the ischemic brain tissue and cerebral perfusion, and fluctuations in blood pressure may disrupt this balance. Patients with persistent LVO can easily have regional blood flow fall below the lower limit of cerebral autoregulation in the acute phase and, hence, accumulate recurrent ischemic insults. In this retrospective analysis, the authors investigated whether increased blood pressure (BP) variability or a transient but severe drop in BP within 24 hours of onset significantly contributed to penumbral tissue loss in persistent LVO patients. They also aimed to determine whether the relationships are modified by Hypoperfusion Intensity Ratio (HIR) on baseline perfusion imaging.
This retrospective study included 80 participants with acute ischemic stroke admitted to a single center between January 2010 and March 2018 with symptomatic occlusion of middle cerebral artery or internal carotid artery in whom no intravenous or endovascular recanalization was attempted. All the participants were admitted within 24 hours of symptom onset and had National Institute of Health Stroke scale (NIHSS) ³ 4 with serial blood pressure measurements. Follow up CT or MR scans were performed on days 3-5 of admission to evaluate for hemorrhage conversion or extent of final infarct.
The mean age of the study population was 74.3 ± 13.2 years, the median onset to arrival time 9.7 hours (IQR, 4.9 – 12.2), median initial NIHSS was 14 (IQR, 8 – 9), median volume of infarction at baseline image 26.4 mL (IQR, 6.3 – 69.2), and penumbral volume 79.3 mL (IQR, 38.2 – 129.6). Clinical profiles were compared by HIR in the penumbra, which is a practical tool to estimate severity of ischemic insult to the vulnerable tissue, and were dichotomized into low (<0.5) and high (>0.5) with the high-HIR group having higher NIHSS at presentation, higher rate of cardioembolic infarcts, and larger volumes of initial infarct, ischemic penumbra, and diffusion perfusion mismatch. Fluctuations in BP during the first 24 hours significantly contributed to the penumbral tissue loss during the acute period with greater association with diastolic BP than systolic BP. Drastic drop in blood pressure from local maxima to minima (SBPdropmax and DBPdropmax) was also significantly associated with penumbral tissue loss during follow up imaging. These findings were consistent in both the high- and low-HIR groups at baseline perfusion imaging with higher penumbral tissue loss in the high-HIR group than in the low-HIR group (median 55.0% versus 18.5%; p <0.01).
The small number of patients and the retrospective design of this study limit generalizability, but the results of this study do play a considerable role in understanding effects of blood pressure on penumbral preservation in patients with non-recanalized LVO. Blood pressure management in the acute phase of ischemic stroke is not fully clear, and the ideal goal and timing of initiation of antihypertensive medications is mostly individualized on a case -by-case basis at different centers. This study has major clinical implications and suggests that reducing episodes of acute BP drops with frequent BP monitoring for non-recanalized patients can prevent irreversible penumbral tissue infarction.