Why the study?
Does acute experimental coronary occlusion alter left ventricular mechanics and function in a dog heart model?
Does acute experimental coronary occlusion alter left ventricular mechanics and function in a dog heart model?
Deterioration of ventricular function after acute coronary occlusion is driven by additional series elasticity provided by ischaemic muscle and increased afterload.
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Suggests ischemic ballooning increases afterload and impairs LV function via series elasticity in dogs; leaves open human translation.
Ballooning of the ischaemic area, shortening of the circular segment length before ejection (SPE), dP/dt max, left ventricular systolic pressure (LVSP), and circular wall stress were recorded in the left ventricle of the dog heart during coronary occlusion. Occlusion of the artery was followed by quick development of ballooning paralleled by an increase in SPE and in the stress/LVSP ratio, and decrease in dP/dt max. It is concluded that deterioration of ventricular function was due to additional series elasticity provided by ischaemic muscle. This conclusion is mainly based on the increase in SPE parallel with the development of ballooning and decrease in dP/dt max. Stroke volume is additionally compromised by increase in afterload.
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Sędek et al. (1973) studied this question.
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