Cerebral Perfusion Pressure is Maintained in Acute Intracerebral Hemorrhage: A CT Perfusion Study

BACKGROUND AND PURPOSE:Although blood pressure reduction has been postulated to result in a fall in cerebral perfusion pressure in patients with intracerebral hemorrhage, the latter is rarely measured. We assessed regional cerebral perfusion pressure in patients with intracerebral hemorrhage by using CT perfusion source data.MATERIALS AND METHODS:Patients with acute primary intracerebral hemorrhage were randomized to target systolic blood pressures of <150 mm Hg (n = 37) or <180 mm Hg (n = 36). Regional maps of cerebral blood flow, cerebral perfusion pressure, and cerebrovascular resistance were generated by using CT perfusion source data, obtained 2 hours after randomization.RESULTS:Perihematoma cerebral blood flow (38.7 ± 11.9 mL/100 g/min) was reduced relative to contralateral regions (44.1 ± 11.1 mL/100 g/min, P = .001), but cerebral perfusion pressure was not (14.4 ± 4.6 minutes⁻¹ versus 14.3 ± 4.8 minutes⁻¹, P = .93). Perihematoma cerebrovascular resistance (0.34 ± 0.11 g/mL) was higher than that in the contralateral region (0.30 ± 0.10 g/mL, P < .001). Ipsilateral and contralateral cerebral perfusion pressure in the external (15.0 ± 4.6 versus 15.6 ± 5.3 minutes⁻¹, P = .15) and internal (15.0 ± 4.8 versus 15.0 ± 4.8 minutes⁻¹, P = .90) borderzone regions were all similar. Borderzone cerebral perfusion pressure was similar to mean global cerebral perfusion pressure (14.7 ± 4.7 minutes⁻¹, P ≥ .29). Perihematoma cerebral perfusion pressure did not differ between blood pressure treatment groups (13.9 ± 5.5 minutes⁻¹ versus 14.8 ± 3.4 minutes⁻¹, P = .38) or vary with mean arterial pressure (r = −0.08, [−0.10, 0.05]).CONCLUSIONS:Perihematoma cerebral perfusion pressure is maintained despite increased cerebrovascular resistance and reduced cerebral blood flow. Aggressive antihypertensive therapy does not affect perihematoma or borderzone cerebral perfusion pressure. Maintenance of cerebral perfusion pressure provides physiologic support for the safety of blood pressure reduction in intracerebral hemorrhage.

Patients with intracerebral hemorrhage (ICH) most often present with elevated blood pressure (BP), but acute treatment remains controversial.^1,2 Despite the results of recent randomized controlled trials of BP management demonstrating no excess of adverse clinical events,^3,4 many physicians are reluctant to aggressively use antihypertensive agents in the acute phase of ICH. This relucence is primarily based on persisting theoretic concerns that there is a zone of tissue at risk for ischemic injury surrounding the acute hematoma.⁵ In addition, more recent MR imaging studies have suggested that subacute ischemic injury occurs in areas remote from the hematoma, including borderzone (BZ, also known as watershed) regions.^6–11 The etiology of these ischemic injuries has been postulated to be hemodynamic compromise secondary to BP reduction.¹⁰ Studies of CBF in the perihematoma region indicate that this region is relatively hypoperfused, but not severely enough to result in ischemia.^12–14 Previous PET studies have demonstrated that the perihematoma region is, in fact, hypometabolic, likely secondary to the primary brain injury, and that the oxygen extraction fraction is not elevated, indicating the absence of misery perfusion.^12,15 Nonetheless, it is possible that reduction of BP will result in a fall in cerebral perfusion pressure (CPP), subsequently precipitating ischemia.¹⁶ In the Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial (ICH ADAPT), we demonstrated that acute BP reduction is not associated with a significant fall in CBF.¹⁷ It has been demonstrated, however, that CPP is more sensitive than CBF or CBV to changes in blood pressure.¹⁸ The relationship between CPP and BP reduction in patients with intracerebral hemorrhage is unknown.Global CPP is normally calculated as the difference between the mean arterial pressure and intracranial pressure, which requires insertion of an intraventricular manometer. Monitoring of intracranial pressure and CPP is generally reserved for patients with a decreased level of consciousness and/or obstructive hydrocephalus requiring ventricular drainage. In these cases, current consensus guidelines recommend that BP be titrated to ensure that CPP is between 50 and 70 mm Hg.^19,20 In addition, global CPP may not reflect local variations in intracranial pressure due to the mass effect of a hematoma, particularly in small hematomas.²¹ Measurements of regional CPP might inform clinical BP management decisions. With PET, it has been demonstrated that CPP can be calculated as a ratio of CBF to CBV.¹⁸ We adapted this technique by using CTP source data from ICH ADAPT to assess local CPP in acute ICH. We tested the hypothesis that aggressive antihypertensive therapy reduces CPP in the perihematoma and borderzone regions.