Fazekas, Joseph F.; Alman, Ralph W.; Ticktin, Howard E.; Ehrmantraut, Wilfred R.; Savarese, Charles J.
February 1964
Angiology;Feb1964, Vol. 15 Issue 2, p63
Academic Journal
Although modalities proposed for management of cerebral vascular disease have been freely borrowed from those employed in coronary artery disease, surprisingly little attention has been accorded the striking similarities between the ischemic syndromes involving these two vital structures. The bases for these similarities undoubtedly relate to the high oxygen requirements of heart and brain and to anatomical and physiologic characteristics of their respective vasculatures. The natural course of the individual case of ischemic myocardial or cerebral disease cannot be predicted nor can the value of available therapeutic modalities be accurately assessed. These uncertainties are due to our inability to measure quantitatively the rate of progression of the disease or the hemodynamic efficacy of spontaneous compensatory mechanisms. A significant number of patients with either coronary or cerebral vascular disease will have exhausted their homeostatic reserve so that minor reductions in oxygen delivery from whatever cause may produce clinically evident ischemia. In these cases, increase in perfusion pressure by administration of vasopressor agents may prove beneficial.


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