?-blockade benefits patients following a subarachnoid haemorrhage

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.

The Burden of the Systemic Inflammatory Response Predicts Vasospasm and Outcome after Subarachnoid Hemorrhage

“…In fact, those treated with steroids had a higher incidence of SIRS, largely driven by an association of both with surgical interventions. Adrenergic-blocking agents, which temper the intense sympathetic activation after SAH, and statins, which stabilize endothelial function and reduce CRP, have been shown in small human studies to significantly reduce vasospasm and improve outcome after SAH [41][42][43]. In fact, statins upregulate nitric oxide synthesis, reduce adhesion molecule expression and inhibit leukocyte migration in experimental SAH [44]; their promising acute effects may largely be mediated through their modulation of the inflammatory cascade [45].…”

Sympathetic activity and myocardial damage after stimulation of dorsal medulla and vagotomy in a novel animal model

“…Active release of catecholamine by the animal is closer to the real clinical condition than passive administration. Moreover, previous studies revealed that adrenergic blockers could significantly protect the myocardial damage from catecholamines [10,[35][36][37]. Our model can be used to test the protective effect of different adrenergic blockers on the myocardium in future studies.…”

Potential adverse effects of norepinephrine on cortical somatosensory-evoked potentials during carotid endarterectomy: a case report

“…The fact that our patient was also taking beta blockers may have conferred some degree of cerebral protection. Neil-Dwyer et al [12] showed the protective effects of beta blockade in a subarachnoid hemorrhage model of cerebral ischemia. Patients treated with beta blockers after a subarachnoid hemorrhage, which cause a local release of catecholamines, showed a more favorable outcome in one year of follow-up.…”