As mentioned in Chapter 1, hypertension is the most important treatable risk factor for stroke, and antihypertensive treatment significantly reduces this risk. Half of all patients with stroke will have a history of hypertension, and up to 40% of patients are taking antihypertensive treatment when their stroke occurs.

Immediately after a stroke, a breakdown in cerebral autoregulation occurs. As a result, rapid decreases in blood pressure can cause a reduction in cerebral perfusion and a further extension of the stroke. For this reason, most authorities recommend that antihypertensive drugs should be withheld until the patient is ambulant; however, very little trial data is available on this point.

In the acute period after a stroke, casual levels of blood pressure are often high, with about 70% of patients having levels ≥140/90 mm Hg within the first 48 h of ictus. These levels usually subside over the next 10–14 days. In part, the increase may be simply the result of the stress of the stroke and of hospitalisation, but other mechanisms may also be responsible, including pre-existing hypertension and neurohumeral activation. The higher the blood pressure at presentation, the worse the outcome, although patients who are hypotensive also do badly. The international stroke trial reported a J-shaped relation between initial blood pressure and outcome, with early deaths increasing by 18% for every 10 mm Hg of admission systolic blood pressure below 150 mm Hg and by 4% for every 10 mm Hg above 150 mm Hg.

On a longer-term basis, in stroke survivors, there is a much closer relationship between the height of the blood pressure (Figure 10.1).

Blood pressure reduction in acute strokes

The value of blood pressure reduction in patients immediately following their stroke is controversial and there are wide international differences in clinical practice. Some studies of β blockers and calcium blockers used immediately after a stroke have shown no benefit, but these studies were small. It is possible that any benefits of blood pressure reduction were offset by harmful reductions in cerebral blood flow.

There is some evidence that the angiotensin blocking drugs (ACE inhibitors and ARBs) do not have adverse effects on cerebral blood flow immediately following a stroke, unlike the other antihypertensive drugs. The acute candesartan therapy in stroke survivors (ACCESS) trial suggested that the ARB, candesartan may be of benefit in patients with high blood pressure (200/110 mm Hg) within the first 48 h after cerebral infarction (Figure 10.2).

The results of the ACCESS trial are offset by the larger SCAST trial, which reported adverse outcomes with candesartan versus placebo in 2029 stroke patients (Figure 10.3).The SCAST investigators also included a meta-analysis in their paper of all the trials of blood pressure reduction following an acute stroke. Their conclusion was that there was a non-significant trend for acute blood pressure reduction to be harmful. The treatment to reduce blood pressure in acute stroke (<48 h) is probably only appropriate when blood pressure is persistently very high (>220/110 mm Hg), although no robust outcome data from clinical trials are available on this point.

There is now good evidence that intravenous thrombolysis with tissue plasminogen activators (TPA) does improve outcomes in patients with acute cerebral infarction, but this is only feasible if computed tomography or magnetic resonance imaging of the head is available within 2 h of stroke onset. If thrombolysis is given, then antihypertensive drugs – such as labetolol, nifedipine or intravenous sodium nitroprusside – will be needed if blood pressure is very high. Immediate reductions in blood pressure may also be beneficial in patients with proven cerebral haemorrhage, although there is little information on this point.