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Beta-blockade benefits patients following a subarachnoid haemorrhage
Insights
Early beta-blockade with propranolol significantly reduces neurological deficits and mortality in patients following subarachnoid hemorrhage. This treatment offers long-term benefits up to one year post-event.
Area of Science:
- Neurology
- Cardiology
- Pharmacology
Background:
- Subarachnoid hemorrhage (SAH) is linked to elevated catecholamines, myocardial damage, and poor outcomes.
- Beta-blockade, specifically propranolol, has shown potential in mitigating ECG changes and myocardial lesions post-SAH.
Purpose of the Study:
- To evaluate the impact of adrenergic blockade on morbidity and mortality in patients after subarachnoid hemorrhage.
- To assess the long-term effects of early beta-blockade treatment on neurological deficits and survival rates.
Main Methods:
- A randomized, double-blind, between-patients study involving 224 patients admitted within 48 hours of SAH.
- Patients received either an alpha-blocker (phentolamine) plus propranolol or placebo, or just propranolol or placebo, for three weeks.
- Outcomes were assessed at four weeks and one year, focusing on neurological deficit and mortality.
Main Results:
- The treated group showed significant improvements in neurological deficit (p=0.003) and reduced mortality (p=0.02) at four weeks.
- Patients receiving treatment had a better outcome after surgery (p=0.01).
- At one year, the treated group maintained significantly fewer neurological deficits (p=0.003), though the reduction in deaths was not statistically significant (p=0.09).
Conclusions:
- Early beta-blockade therapy provides significant benefits for patients with subarachnoid hemorrhage.
- Treatment with propranolol leads to fewer neurological deficits for up to one year post-SAH.
- Potential mechanisms include reduced plasma renin activity, prevention of myocardial damage, and decreased cerebral oxygen demand.
Abstract:
Previous studies have shown that ECG changes following a subarachnoid haemorrhage are associated with increased catecholamine levels, necrotic myocardial lesions, and a poor prognosis. Furthermore, beta-blockade using propranolol reverses some of the ECG changes and prevents necrotic myocardial lesions. This study was established to assess the affects of adrenergic blockade on morbidity and mortality following subarachnoid haemorrhage. Patients were admitted to the randomized double-blind between-patients study if they presented at the neurosurgical unit within 48 hours of a subarachnoid haemorrhage confirmed by lumbar puncture. Of 224 patients, the first 118 received an alpha-blocker, phentolamine 20 mg three-hourly, and either the beta-blocker propranolol 80 mg eight-hourly, or placebo. The last 106 patients received either propranolol or placebo. Treatment was continued for three weeks. Assessment at four weeks revealed significant improvements in the treated group for neurological deficit (p = 0.003) and death (p = 0.02). More treated patients underwent operation and those that did had a better outcome (p = 0.01). Assessment at one year showed that although patients had improved in both groups, patients in the treated group had significantly fewer neurological deficits (p = 0.003). There were fewer deaths in the treated group but this difference was not significant (p = 0.09). Possible mechanisms for this protective effect of propranolol may include a reduction in plasma renin activity, a reduction in pulmonary oedema, prevention of myocardial infarcts, and a reduction in cerebral oxygen requirements. It is concluded that early beta-blockade benefits patients with subarachnoid haemorrhage, in terms of fewer neurological deficits, for up to one year.