Alterations in ventricular diastolic properties are commonly seen in the diseased heart, and have been extensively studied in coronary artery disease, congestive cardiomyopathy, and left ventricular hypertrophy due to pressure or volume overload. Acute increases in left ventricular (LV) diastolic pressure relative to volume occur regularly during the transient ischemia of angina pectoris and may contribute to the dyspnea and pulmonary congestion that commonly accompany this condition. Although the mechanism of this altered disastolic distensibility is debated, a substantial body of evidence favors a role for residual diastolic interaction between contractile elements in the ischemic heart. Congestive cardiomyopathy also appears to be associated with increased LV diastolic stiffness. While this may in part be related to fibrosis of the LV wall, shifts of the abnormal diastolic pressure-volume relation toward normal have been reported with sodium nitroprusside infusion or the beta-adrenergic agonist salbutamol, suggesting important contribution of physiologic factors to the increased resting LV stiffness in this condition. LV hypertrophy (LVH) is associated with increased effective diastolic chamber stiffness, but normalized LV diastolic stiffness is increased only in LVH due to chronic pressure overload. Possible explanations for these findings are discussed.