Surgically induced angiogenesis to compensate for hemodynamic cerebral ischemia.
The ischemic brain may stimulate angiogenesis to compensate for impaired circulation. We examined the conditions promoting such angiogenesis to provide the basis for surgical treatment.
The degree of cerebral hemodynamic stress was studied in patients with moyamoya disease using the stable xenon-enhanced computed tomographic acetazolamide tolerance test and positron emission tomography. Patients were subjected to surgery in which scalp arteries were placed on the cerebral cortex without vessel-to-vessel anastomosis. Formation of the newly vascularized collateral network connecting the implanted artery to cortical arteries was assessed angiographically 12 to 17 months after surgery.
Preoperative average resting cerebral blood flow for cortex that developed revascularization of cortical arteries was not significantly different from that for cortex that did not. However, cortex that developed revascularization had an average preoperative increase of blood flow by acetazolamide treatment of -3.29 +/- 4.6 mL/min per 100 cm3 (n = 20), which was significantly less (P = .0034) than that of cortex that did not show revascularization (20.7 +/- 4.3 mL/min per 100 cm3; n = 9). Good revascularization developed when the cortex showed increase of blood flow by acetazolamide treatment of less than 0 (steal phenomenon). Preoperative positron emission tomography data indicated that revascularization developed when the cortex was under "misery perfusion." Postoperative hemodynamics were ameliorated by revascularization.
Angiogenesis to connect the implanted scalp arteries to the cerebral cortical arteries was selectively initiated when ischemia of hemodynamic origin existed.
- Copyright © 1994 by American Heart Association