The three phases of vasospasm.

We propose the theory that prolonged cerebral vasospasm involves three phases: (1) the initial muscular contraction of the arterial wall; (2) a secondary injury to the artery that consists of endothelial desquamation with adherence of platelets to te denuded internal elastic lamina and mural thrombus formation; and (3) the repair process, which is the proliferative endarteropathy that has been observed in autopsy specimens. Cerebral ischemia can be the end product of any of these three conditions. We have postulated a possible subcycle in the overall scheme by which adherence of platelets to the denuded internal elastic lamina of the artery provide a continuously replenishing supply of spasmogenic chemical factors to the mural receptors and stimulate prolonged contraction of the muscular layer. We propose that this cycle may be interrupted by the administration of heparin. To test this hypothesis, the records of 112 consecutive patients who received systemic heparin in conjunction with carotid ligation were compared with the results of carotid ligation reported in the Cooperative Study, in which heparin was not used. The incidence of ischemic complications in the group of patients receiving heparin was 6%, as compared to 23% in control group, with a concomitant reduction in mortality from 16% to 10%. The incidence of recurrent subarachnoid hemorrhage was slightly less in the patients receiving heparin than in patients in the Cooperative Study. We conclude that the data provide support for our hypothesis of the mechanism of prolonged cerebral vasospasm and cerebral ischemia associated with subarachnoid hemorrhage, and that systemic heparin may be used with relative safety in patients in whom the aneurysm if protected by partial carotid ligation.