Diastolic function in coronary artery disease is modified to a variable extent. There are distinct abnormalities produced during acute ischemia, and following myocardial infarction. The pathophysiology of diastolic abnormalities in these two syndromes is reviewed. During acute ischemia filling pressures of the left ventricle are increased. Pulmonary edema may be produced. Silent ischemia causes less of an increase in filling pressures. The diastolic pressure-volume relation is shifted in an upward manner with a variable contribution from altered myocardial relaxation, increased muscle stiffness, acute pericardial restriction, ventricular interaction, and acute chamber dilatation. The impairment of myocardial relaxation plays a central role and has been quantified in multiple clinical and experimental studies. Filling of the left ventricle during ischemia is altered due to the factors which shift the pressure-volume relation. The acute increase in left atrial pressure may increase filling rates somewhat surprisingly, given the reduced left ventricular compliance. Myocardial fibrosis following infarction may elevate filling pressures, but the degree of elevation is closely tied to the intravascular volume status. Shifts in the diastolic pressure-volume relation reflect a loss of chamber compliance due to an increase in muscle stiffness. Increased amounts of extracellular matrix, specifically collagen, produce this permanent increase in muscle stiffness which is central to the diastolic abnormalities in chronic coronary artery disease.