Regional Myocardial Perfusion After Experimental Subarachnoid Hemorrhage

Abstract

Background and Purpose-The pathophysiology of cardiac injury after subarachnoid hemorrhage (SAH) remains controversial. Data from animal models suggest that catecholamine-mediated injury is the most likely cause of cardiac injury after SAH. However, researchers also have proposed myocardial ischemia to be the underlying cause, as a result of coronary artery disease, coronary artery spasm, or hypertension and tachycardia. To test the hypothesis that SAH-induced cardiac injury occurs in the absence of myocardial hypoperfusion, we developed an experimental canine model that reproduces the clinical and pathological cardiac lesions of SAH and defines the epicardial and microvascular coronary circulation. Methods-Serial ECG, hemodynamic measurements, coronary angiography, regional myocardial blood flow measurements by radiolabeled microspheres, 2D echocardiography, and myocardial contrast echocardiography were performed in 9 dogs with experimental SAH and 5 controls. Results-Regional wall motion abnormalities were identified in 8 of 9 SAH dogs and 1 of 5 controls (Fisher's Exact Test, Pϭ0.02) but no evidence was seen of coronary artery disease or spasm by coronary angiography and of significant myocardial hypoperfusion by either regional myocardial blood flow or myocardial contrast echocardiography. Conclusions-In this experimental model of SAH, a unique form of regional left ventricular dysfunction occurs in the absence of myocardial hypoperfusion. Future studies are justified to determine the cause of cardiac injury after SAH.

Electrocardiographic Changes in Patients with Acute Stroke: A Systematic Review

“…Animal models suggest that catecholamine-mediated injury is the cause of ECG abnormalities after a SAH. In a canine SAH model [43], regional cardiac wall motion abnormalities detected by echocardiography were found in 8 of 9 SAH dogs vs. 1 of 5 controls, and ischemic-like ECG changes were observed in 5 of 8 SAH dogs vs. 1 of 5 controls, but not all of these changes were accompanied by myocardial hypoperfusion.…”

Cardiac Troponin-I: A Predictor of Prognosis in Subarachnoid Hemorrhage

“…A previous study suggested that the etiology of cardiac injury in the majority of patients with SAH is due to reversible left ventricular systolic dysfunction rather than underlying obstructive coronary artery disease [7]. The mechanism of cardiac injury is thought to be secondary to a sudden surge in catecholamine levels [8][9][10] resulting in functional myocardial stunning [7] and focal contraction band necrosis. Therefore, neurocardiac injury is likely directly responsible for left ventricular dysfunction and elevated cardiac biomarkers [11].…”

Neurogenic Stunned Myocardium Associated with Reversible Posterior Leukoencephalopathy Syndrome

“…Normal cardiac perfusion is also demonstrated by myocardial contrast echocardiography in neurogenic-stunned myocardium initial MRI brain FLAIR demonstrates increased T2 signal in the bilateral frontal lobes, thalamus, and cerebellum (arrows). Bottom panel: repeat MRI brain FLAIR at 1 month confirms complete resolution of the previously seen T2 signal hyperintensities patients [6][7][8]. The more accepted theory explaining neurogenic-stunned myocardium is called the ''catecholamine hypothesis.''…”