Mark R. Etherton, MD, PhD
In this entry, I discuss a recent publication by Mingli He and colleagues investigating the relationship between blood pressure control in the early phases poststroke and risk of subsequent cognitive dysfunction.
Poststroke cognitive dysfunction is common, occurring in ~25-50% of patients with acute ischemic stroke. The authors set out to explore the relationship between average systolic and diastolic blood pressure in the first 7 days poststroke and risk of cognitive dysfunction.
796 patients were included in the analysis. Mean systolic and diastolic blood pressure in the first 7 days poststroke was used to divide the population into quintiles for analysis against cognitive performance. Cognitive function was assessed with the Montreal Cognitive Assessment (MoCA) after admission and serially at 2 weeks, 3, 6, and 12 months.
The authors report a bipolar relationship whereby patients in the lowest and highest quintiles of systolic and diastolic blood pressure performed significantly worse on the MoCA compared to patients in the middle quintile (3 months Q1: 20.73, Q3 23.28, Q5 20.98; P value <0.001). Interestingly, this blood pressure relationship was not present at 2 weeks and had normalized at 12 months poststroke between quintiles. The authors then show that stroke subtype correlates with risk of poststroke cognitive dysfunction as patients with small-vessel occlusive mediated strokes had the lowest MoCA scores (17.21), and patients with stroke attributed to large-artery atheroembolism had the highest prevalence of poststroke cognitive impairment (see Figure). Building on a relationship between small-vessel disease and poststroke cognitive dysfunction, the authors show that increasing Fazekas score as a qualitative marker of white matter hyperintensity burden is associated with increased risk of poststroke cognitive impairment. This observation is especially intriguing as it underscores the relationship of small-vessel disease and poststroke cognitive dysfunction.
The underlying explanation for the self-limited association between high and low blood pressure and risk of poststroke cognitive dysfunction is unclear. Why do patients in the lowest and highest blood pressure quintiles have temporary poststroke cognitive dysfunction? The authors reportedly monitored for confounding poststroke depression; however, it is not clear if there was any difference in performance on the Hamilton Depression Scale-24 between quintiles. In addition, given the disparate results with stroke subtype and poststroke cognitive dysfunction, it is imperative to know whether there were differences in stroke subtype between the blood pressure quintiles. This point is suggested by Supplementary Table II, which shows a nonsignificant increase in posterior circulation-defined infarcts in Q1 compared to the other blood pressure quintiles. These questions limit interpretation into the mechanism for the observed relationship between early phase blood pressure and poststroke cognitive dysfunction.
In summary, these observations of a potential relationship between blood pressure in the early poststroke period and poststroke cognitive dysfunction are interesting and warrant further investigation. Identifying the mechanism for the relationship of early phase blood pressure and white matter injury with risk of poststroke cognitive dysfunction could impact the clinical care of this vulnerable population.