Induced Hypertension

The ischemic penumbra shows impaired autoregulation, and appears to be particularly sensitive to blood pressure manipulation. The rationale for using induced hypertension as a stroke therapy is provided by early studies showing that raising mean arterial pressure results in improved cerebral perfusion within the penumbra, and a concomitant return of electrical activity. In animal models of focal cerebral ischemia, induced hypertension therapy was found to augment cerebral blood flow, attenuate brain injury, and improve neurological function [206, 207]. In humans with acute ischemic stroke, a spontaneous increase in blood pressure is common, and neurological deterioration can occur with "excessive" antihypertensive therapy [208]. Furthermore, a paradigm for induced hypertension for cerebral ischemia exists in the treatment of vasospasm after subarachnoid hemorrhage [209].

Based upon this rationale, recent trials have studied the effect of induced hypertension (using intravenous phenylephrine) on clinical and imaging outcomes in patients with acute stroke [210-212]. Patients with significant diffusion-perfusion "mismatch" on MRI, large vessel occlusive disease, and fluctuating neurological deficits were found to be more likely to respond, and improvement in tests of cortical function correlated with improved perfusion of corresponding cortical regions [213,214].A multi-

center randomized trial of induced hypertension is ongoing. The main concerns with induced hypertension therapy include the risk of precipitating intrac-erebral hemorrhage and worsening cerebral edema, particularly in patients with reperfusion, as well as systemic complications such as myocardial ischemia, cardiac arrhythmias, and ischemia from phenyle-phrine-induced vasoconstriction. Ultimately, this treatment might be more applicable to stroke patients who are not candidates for thrombolytic therapy.

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