Regional myocardial perfusion after experimental subarachnoid hemorrhage

Background and Purpose-The pathophysiology of cardiac injury after subarach noid hemorrhage (SAH) remains controversial. Data from animal models sugges t that catecholamine-mediated injury is the most likely cause of cardiac in jury after SAH. However, researchers also have proposed myocardial ischemia to be the under lying cause, as a result of coronary artery disease, coron ary artery spasm, or hypertension and tachycardia. To test the hypothesis t hat SAM-induced cardiac injury occurs in the absence of myocardial hypoperf usion, we developed an experimental canine model that reproduces the clinic al and pathological cardiac lesions of SAH and defines the epicardial and m icrovascular coronary circulation. Methods-Serial EGG, hemodynamic measurements, coronary angiography, regiona l myocardial blood now measurements by radiolabeled microspheres. 2D echoca rdiography, and myocardial contrast echocardiography were performed in 9 do gs with experimental SAH and 5 controls. Results-Regional wall motion abnormalities were identified in 8 of 9 SAH do gs and 1 of 5 controls (Fisher's Exact Test, P=0.02) but no evidence was se en of coronary artery disease or spasm by coronary angiography and of signi ficant myocardial hypoperfusion by either regional myocardial blood flow or myocardial contrast echocardiography. Conclusions-In this experimental model of SAH, a unique form of regional le ft ventricular dysfunction occurs in the absence of myocardial hypoperfusio n. Future studies are justified to determine the cause of cardiac injury af ter SAH.