Angiospasme

Vasospasm refers to a condition in which an arterial spasm leads to vasoconstriction. This can lead to tissue ischemia and tissue death (necrosis). Cerebral vasospasm may arise in the context of subarachnoid hemorrhage. Symptomatic vasospasm or delayed cerebral ischemia is a major contributor to post-operative stroke and death especially after aneurysmal subarachnoid hemorrhage. Vasospasm typically appears 4 to 10 days after subarachnoid hemorrhage. Along with physical resistance, vasospasm is a main cause of ischemia. Like physical resistance, vasospasms can occur due to atherosclerosis. Vasospasm is the major cause of Prinzmetal's angina. Normally endothelial cells release prostacyclin and nitric oxide (NO) which induce relaxation of the smooth muscle cells, and reduce aggregation of platelets. Aggregating platelets stimulate ADP to act on endothelial cells and help them induce relaxation of the smooth muscle cells. However, aggregating platelets also stimulate thromboxane A2 and serotonin which can induce contraction of the smooth muscle cells. In general, the relaxations outweighs the contractions. In atherosclerosis, a dysfunctional endothelium is observed on examination. It does not stimulate as much prostacyclin and NO to induce relaxation on smooth muscle cells. Also there is not as much inhibition of aggregation of platelets. In this case, the greater aggregation of platelets produce ADP, serotonin, and thromboxane A2. However the serotonin and the thromboxane A2 cause more contraction of the smooth muscle cells and as a result contractions outweigh the relaxations.> Vasospasm can occur in a wide variety of peripheral vascular beds under poorly understood mechanisms. Prinzmetal angina, Buerger's disease, contrast mediated selective renal vasospasm, hypercoagulability and cryoglobulinemia likely represent just a few of the known pieces of this puzzling phenomena. Ischemia in the heart due to prolonged coronary vasospasm can lead to angina, myocardial infarction and even death.