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Abnormal blood pathways in left ventricular cavity in acute myocardial infarction. Experimental observations with
1National Cardiovascular Center, Department of Cardiovascular Dynamics, Osaka, Japan.
Insights
Myocardial infarction causes abnormal blood flow in the left ventricle (LV), leading to hemostasis (blood pooling) in the apex. This regional hemostasis is a key mechanism in thrombus formation during heart attacks.
Area of Science:
- Cardiovascular Physiology
- Echocardiography
- Thrombosis Research
Background:
- Myocardial infarction (MI) can lead to thrombus formation within the left ventricular (LV) cavity.
- The precise mechanisms of regional hemostasis in the LV during MI remain incompletely understood.
Purpose of the Study:
- To investigate the blood flow dynamics and regional hemostasis within the LV cavity following coronary artery ligation in a canine model.
- To elucidate the role of altered blood flow in thrombus formation after myocardial infarction.
Main Methods:
- Contrast echocardiography was utilized to visualize blood flow patterns in the LV cavity of nine canines.
- Coronary artery ligation was performed to induce myocardial infarction, and blood flow was assessed before and after the procedure.
- Echocardiographic parameters were analyzed to identify areas of hemostasis and abnormal blood flow pathways.
Main Results:
- Before coronary ligation, contrast echoes exhibited normal spread throughout the LV cavity.
- After ligation, "smokelike" echoes indicating hemostasis were observed in the apical regions, particularly in dogs with apical akinesis or dyskinesis.
- Contrast echoes showed impaired apical penetration and altered flow patterns towards the outflow tract, with tachycardia exacerbating these abnormalities.
Conclusions:
- Apical myocardial infarction induces abnormal blood flow pathways within the left ventricle, resulting in regional hemostasis.
- This regionally altered hemodynamics and hemostasis in the LV apex are identified as a significant mechanism contributing to thrombus formation in myocardial infarction.
Abstract:
To elucidate the mechanism of regional hemostasis in the left ventricular (LV) cavity during myocardial infarction, the blood pathway in LV cavity was examined with contrast echocardiography injected from the left atrium before and after coronary ligation in nine canines. Before coronary ligation, contrast echoes spread over LV cavity with one rush. After ligation, smokelike echoes indicating hemostasis were observed at the apical middle of the LV cavity in five dogs with apical akinesis and at the apical area in four dogs with apical dyskinesis. The contrast echoes did not reach the apex within one diastolic period but turned upward to the outflow tract in the middle of the cavity in all dogs. In the cardiac beats that followed, some contrast echoes spread slowly toward the apex, forming a thin layer along the posterior wall in cases with akinesis but not in cases with dyskinesis. The area separated from the blood pathway developed where the smokelike echoes had been developed. Tachycardia exaggerated the abnormality of blood pathway and widened the contrast echo-free area. The abnormal pathway of the blood in apical myocardial infarction develops hemostasis in the apex. This should be one of the mechanisms of thrombus formation in myocardial infarction.