Regional myocardial perfusion after experimental subarachnoid hemorrhage
| Autor: | J G, Zaroff, G A, Rordorf, J S, Titus, J B, Newell, N J, Nowak, D F, Torchiana, H T, Aretz, M H, Picard, R L, Macdonald |
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| Rok vydání: | 2000 |
| Předmět: |
Tachycardia
medicine.medical_specialty Pathology Subarachnoid hemorrhage Heart Diseases Hemodynamics Myocardial Reperfusion Coronary artery disease Coronary circulation Electrocardiography Dogs Internal medicine medicine Animals cardiovascular diseases Advanced and Specialized Nursing medicine.diagnostic_test business.industry Subarachnoid Hemorrhage medicine.disease nervous system diseases Disease Models Animal medicine.anatomical_structure Angiography Cardiology Neurology (clinical) medicine.symptom Cardiology and Cardiovascular Medicine business Artery |
| Zdroj: | Stroke. 31(5) |
| ISSN: | 0039-2499 |
| Popis: | 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, P =0.02) 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. |
| Databáze: | OpenAIRE |
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