Early experimental ischemia reduces left ventricular ejection time and stroke volume due to early relaxation of the ischemic area and compensatory shortening of non-ischemic regions.
A marked decrease in the duration of left ventricular ejection time and a drop in stroke volume were observed in the dog during the first 30–60 sec of experimental occlusion of the left descending coronary artery. It has been found that these changes in ventricular performance result from additional displacement (shortening) of the non-ischaemic parts of the left ventricle leading to early dissipation of wall tension. This additional displacement is evoked by shortening of the time-to-peak tension and early relaxation of the ischaemic area. The mechanism described in this paper is proposed as a model of ventricular performance during coronary pain.
Lewartowski et al. (1974) studied this question.