Elevated blood pressure (BP) levels are important in predicting primary and secondary prevention of stroke, but not much is known about the role of elevated BP in the acute stroke situation. The most recent American Heart Association guidelines recommend that emergency administration of antihypertensive agents be withheld unless the diastolic blood pressure is >120 mm Hg or the systolic blood pressure (SBP) is >220 mm Hg.

Prof. John Potter, University of East Anglia, Norwich, UK, presented data from the Control of Hypertension and Hypotension Immediately Post-Stroke (CHHIPS) pilot study, which assessed the safety and effectiveness of lowering BP following acute stroke in patients aged >18 years with symptom onset <36 hours lasting more than 60 minutes, a clinical diagnosis of suspected stroke (neuroimaging required within 72 hours of randomization), and SBP >160 mm Hg. Subjects were randomly assigned to receive lisinopril (n=57; dose range 5–15 mg), labetalol (n=56; dose range 50–150 mg BID) or matching placebo (n=59) for 14 days. BP was measured at 30-minute intervals for 8 hours, then at 24 hours and 2 weeks. Treatment dose was administered orally and titrated at 4 and 8 hours in non-dysphagic patients, while dysphagic patients received sublingual lisinopril or intravenous labetalol during the first 3 days, then either orally or via NG/PEG tube. The primary study endpoint was the proportion of dead/dependent patients (defined as a modified Rankin Scale [mRS] of >3 at 2 weeks post-stroke). Secondary endpoints included casual BP changes (at 24 hours and 2 weeks), treatment discontinuations and withdrawals, serious adverse events (SAEs), early (<72 hours) neurological deterioration (NIHSS increase ≥4/death), fatal and non-fatal stroke recurrence, and mortality at 3 months.

The active treatment group had a greater decline in SBP within the first 24 hours compared with placebo (21 mm Hg, 95% CI 17–25 vs 11 mm Hg, 95% CI 5–17, respectively; p=0.004). Significant differences in SBP declines between patients on active treatment versus those receiving placebo continued at 2 weeks (31 mm Hg vs 24 mm Hg, respectively; p<0.05). Neither active treatment was associated with deterioration in neurological status at 72 hours. Discontinuations, withdrawals, and adverse events were similar in the active and placebo treatment groups. There was no difference in death/dependency at 2 weeks between the active treatment group (61%) and the placebo group (59%; p=0.82). There were borderline reductions in 90-day mortality in favor of active treatment (p=0.05; Hazard Ratio 2.2; 95% CI 1.0–5.0), but the small number of events precluded firm conclusions.

The CHHIPS pilot data suggest that early use of anti-hypertensives following acute strokes significantly lowers BP compared with placebo without causing serious adverse effects or an early increase in stroke severity and may reduce long-term mortality. These results need to be confirmed in larger trials.