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Published on: February 17, 2013
Regional myocardial perfusion after experimental subarachnoid hemorrhage
J G Zaroff1, G A Rordorf, J S Titus
1Cardiac Units, Massachusetts General Hospital and Harvard Medical School, Boston, Ma 02114, USA.
Insights
Cardiac injury after subarachnoid hemorrhage (SAH) can cause regional left ventricular dysfunction. This study found dysfunction occurred without myocardial hypoperfusion, suggesting a novel mechanism beyond ischemia.
Area of Science:
- Cardiology
- Neurology
- Pathophysiology
Background:
- The cause of cardiac injury following subarachnoid hemorrhage (SAH) is debated.
- Animal models suggest catecholamine release, while others propose myocardial ischemia due to coronary issues or hypertension.
Purpose of the Study:
- To investigate cardiac injury in SAH independent of myocardial hypoperfusion.
- To establish a canine model for SAH-induced cardiac and coronary circulation changes.
Main Methods:
- Experimental subarachnoid hemorrhage (SAH) model in dogs (n=9) with controls (n=5).
- Evaluated cardiac function using ECG, hemodynamics, 2D echocardiography, and myocardial contrast echocardiography.
- Assessed coronary circulation via angiography and regional myocardial blood flow measurements.
Main Results:
- Regional wall motion abnormalities were observed in 8/9 SAH dogs versus 1/5 controls (P=0.02).
- Coronary angiography showed no evidence of coronary artery disease or spasm.
- Myocardial hypoperfusion was not detected by blood flow or contrast echocardiography.
Conclusions:
- Subarachnoid hemorrhage induces a distinct regional left ventricular dysfunction.
- This dysfunction occurs without evidence of myocardial hypoperfusion in this experimental model.
- Further research is needed to elucidate the specific mechanisms of SAH-related cardiac injury.
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.
