Mitral regurgitation following myocardial infarction is one of the most serious complications. Therefore, early detection of the mitral regurgitation occurring in myocardial infarction must help in directing a treatment for it and in improving its prognosis. This study was conducted to establish a new clue of predicting mitral regurgitation complicated on myocardial infarction. Acute myocardial infarction and quantitatively measurable mitral regurgitation were made in 14 normal canine hearts to determine hemodynamics. Acute myocardial infarction was produced by ligating the anterior descending branch of the left coronary artery at its proximal one third and filling the branch distal to the ligation with 2 % -agar solution. Mitral regurgitation was through an external shunt from the apex of the left ventricle to the left atrial appendage. Hemodynamics were altered on production of myocardial infarction as follows: decrease of aortic and left ventricular pressures, increase of left atrial pressure and LVEDP, decrease of LV-max. dp/dt, and decrease of cardiac output and LV-SW. Hemodynamic alterations were as follows in a heart with mitral regurgitation superimposed on myocardial infarction. Mitral regurgitation was twice as much as cardiac output of heart with myocardial infarction: increase of left atrial pressure and LVEDP, increase of total stroke volume with decrease of effective stroke volume, increase of LV-max. dp/dt, increase of aortic and left ventricular systolic pressure. With increase of mitral regurgitation amounting 4 times as much as the cardiac output of a heart with only myocardial infarction, hemodynamics changed as follows: further decrease of effective stroke volume and LV-SW, decrease of aortic and left ventricular pressure, and no change in LV-max. dp/dt. Analysis of the aortic and left ventricular pressure tracings revealed shortening of the rapid ejection period, resulting in reduced ratio of this period to cardiac cycle. It was concluded that pressure tracing of the aorta or left ventricle would reflect hemodynamics altered when mitral regurgitation was complicated with myocardial infarction. Namely, it is conceivable that mitral regurgitation occurred in a patient with myocardial infarction when the pressure tracing showed shortening of the rapid ejection period. Therefore, monitoring of the arterial pressure tracing is available even in a less-equipped institute and yields indispensable information that mitral regurgitation did develop in a patient with myocardial infarction.