Management of High Blood Pressure in Acute Ischaemic Stroke

Elevated blood pressure (BP) is the most common clinical symptom of acute ischaemic stroke (AIS), a highly heterogeneous syndrome. The pathophysiology of high BP in stroke is complex and poorly understood. The hypertensive response in AIS reflects both stroke-related and nonspecific epiphenomena that vary over time and across patients. Extremes of BP as well as high BP variability have been associated with worse outcomes in observational studies. Importantly, the observed relationship between BP and stroke outcome may or may not be causally related. Antihypertensive therapy effectively reduces BP in AIS, but the available evidence is insufficient to guide therapeutic decisions and does not demonstrate that lowering BP reduces mortality or disability in patients not treated with reperfusion therapies. However, early reduction of BP in patients with AIS undergoing reperfusion therapy has been shown to be safe and effective, provided that aggressive BP reduction was avoided in patients who have undergone successful reperfusion. Importantly, cohorts of patients with AIS are highly heterogeneous, and the benefits of acute treatment for AIS are extremely time dependent. AIS patients with a history of hypertension experience worse outcomes, which may be explained by the harmful effect of the intracerebral renin-angiotensin system overactivation. Nevertheless, the management of BP immediately after stroke onset is still largely empirical, and the optimal BP management after AIS remains a challenge. Current guidelines propose early and modest BP lowering in AIS patients with BP ≥ 185/110 mmHg who are eligible for reperfusion therapies (avoiding BP > 180/105 mmHg after the procedure), and in AIS patients with BP ≥ 220/120 mmHg or with pre-existing comorbid conditions (e.g. acute heart failure, acute coronary syndrome, aortic dissection, preeclampsia) who are ineligible for reperfusion therapies. More research is needed to identify patients most likely to benefit from lowering BP in acute stroke, as well as the time window in which the response to treatment is likely be favourable. Subtyping of stroke according to the underlying cause, advanced neuroimaging tools enabling the assessment of infarct core volume, collateral sufficiency, person-specific local cerebral perfusion and metabolic demand, as well as a detailed individual history of the patient’s comorbidities, including identification of signs and symptoms of hypertensive target organ damage might all help to stratify BP policy in AIS in the future trials that are required.