Induced Hypertension

The phenomenon of cerebral autoregulation in the healthy brain maintains constant cerebral blood flow the face of wide fluctuations in arterial blood pressure. However, the ischemic brain loses its capacity to autoregulate and becomes sensitive to blood pressure manipulation. This is most relevant in the ischemic penumbra, where raising mean arterial pressure has been shown to improve cerebral perfusion, with a concomitant return of electrical activity. In animal models of focal cerebral ischemia, induced hypertension therapy augmented cerebral blood flow, attenuated

128,129

brain injury, and improved neurological function. , In humans, spontaneous hypertension is commonly observed in the setting of critical carotid artery stenosis, and lowering blood pressure can result in infarct extension and neurological deterioration.130 Induced hypertension is commonly used to improve perfusion in

FIGURE 5.5 (a) Comparison of ischemia-reperfusion profiles in various control and NBO groups. LDF cerebral perfusion data are calculated as a percentage of pre-ischemic baselines (mean ± S.D.). NBO did not lead to any statistically significant differences in ischemia or reperfusion. (b) Forty-eight-hour infarct volumes (mean + SD) in control transient ischemia rats compared with untreated permanent focal cerebral ischemia. In this model, the reperfusion window is about 1-2 hours. *p < 0.05 vs. permanent ischemia. (c) Forty-eight-hour infarct volumes (mean + S.D.) in NBO-treated transient ischemia rats compared with untreated permanent focal cerebral ischemia. NBO increased the reperfusion window to about 3-4 hours. *p < 0.05 vs. permanent ischemia. (Reprinted with permission from reference 124.)

FIGURE 5.5 (a) Comparison of ischemia-reperfusion profiles in various control and NBO groups. LDF cerebral perfusion data are calculated as a percentage of pre-ischemic baselines (mean ± S.D.). NBO did not lead to any statistically significant differences in ischemia or reperfusion. (b) Forty-eight-hour infarct volumes (mean + SD) in control transient ischemia rats compared with untreated permanent focal cerebral ischemia. In this model, the reperfusion window is about 1-2 hours. *p < 0.05 vs. permanent ischemia. (c) Forty-eight-hour infarct volumes (mean + S.D.) in NBO-treated transient ischemia rats compared with untreated permanent focal cerebral ischemia. NBO increased the reperfusion window to about 3-4 hours. *p < 0.05 vs. permanent ischemia. (Reprinted with permission from reference 124.)

the ischemic distal arterial territory in patients with vasospasm after aneurysmal subarachnoid hemorrhage.131

Based upon this rationale, the effect of pharmacologically induced hypertension on clinical and imaging outcomes is being investigated in patients with acute stroke.132-134 In one study, patients with significant diffusion-perfusion ''mismatch'' on MRI, large vessel occlusive disease, and fluctuating neurological deficits were found to be more likely to respond. Induced hypertension correlated with improved cortical cerebral

FIGURE 5.6 Serial MRI findings in a patient with cardio embolic right MCA stroke treated with NBO for 8 hours. Top: Baseline (pre-NBO) MRI, 13.1 hours postsymptom onset, shows a large DWI lesion, a larger MTT lesion, and MCA occlusion (arrow) on head MRA. Middle: A second MRI after 3.75 hours (during-NBO) shows 36% reduction in the DWI lesion, stable MTT deficit, and persistent MCA occlusion. Bottom: A third MRI after 24 hours (post-NBO) shows reappearance of DWI abnormality in some areas of previous reversal; MTT image shows partial reperfusion (39% MTT volume reduction, mainly in the ACA territory); MRA shows partial MCA recanalization. (Reprinted with permission from reference 126.)

FIGURE 5.6 Serial MRI findings in a patient with cardio embolic right MCA stroke treated with NBO for 8 hours. Top: Baseline (pre-NBO) MRI, 13.1 hours postsymptom onset, shows a large DWI lesion, a larger MTT lesion, and MCA occlusion (arrow) on head MRA. Middle: A second MRI after 3.75 hours (during-NBO) shows 36% reduction in the DWI lesion, stable MTT deficit, and persistent MCA occlusion. Bottom: A third MRI after 24 hours (post-NBO) shows reappearance of DWI abnormality in some areas of previous reversal; MTT image shows partial reperfusion (39% MTT volume reduction, mainly in the ACA territory); MRA shows partial MCA recanalization. (Reprinted with permission from reference 126.)

perfusion and improvement in clinical tests of cortical function.135,136 A two-center safety trial of pharmacologically induced hypertension enrolled 11 subjects. Raising mean arterial blood pressure to 30% above baseline resulted in an improvement of mean NIHSS from 10 to 8.4. Two patients developed asymptomatic postischemic brain hemorrhage and one patient showed evidence of myocardial infarction. Although these complications were not attributed to treatment in this trial, induced hypertension therapy has theoretical risks, including postischemic brain hemorrhage, myocardial ischemia, cardiac arrhythmias, and peripheral ischemia from vasopressor-induced vasoconstriction. A major limitation of induced hypertension as an acute stroke treatment is that it cannot be used as an adjunct to patients receiving thrombo-lysis because of the risk of precipitating intracerebral hemorrhage.

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