Congestive heart failure may result from cardiovascular overload, from systolic or from diastolic dysfunction. Diastolic left ventricular dysfunction may result from structural resistance to filling such as induced by pericardial constraint, right ventricular compression, increased chamber stiffness (hypertrophy) and increased myocardial stiffness (fibrosis). A distinct and functional etiology of diastolic dysfunction is slow and incomplete myocardial relaxation. Relaxation may be slowed by pathological processes such as hypertrophy, ischemia and by asynchronous left ventricular function. The present contribution analyses the occurrence of slow and incomplete myocardial relaxation in response to changes in systolic pressure and in response to changes in venous return. The regulation of myocardial relaxation by load is critically dependent on the transition from myocardial contraction to relaxation, which occurs in dogs when 82% of peak isovolumetric pressure has developed or at a relative load of 0.82. This corresponds to early ejection in normal hearts, but is situated even before aortic valve opening in severely diseased hearts. When load is developed beyond this transition, relaxation becomes slow and even incomplete. This is load dependent diastolic dysfunction. Load dependent diastolic dysfunction occurs in normal hearts facing heavy afterload and in severely diseased hearts even with normal hemodynamic parameters. This dysfunction should contribute to elevating filling pressures in most patients with severe congestive heart failure. This dysfunction can be reverted by decreasing systolic pressures or by decreasing venous return. Load dependent diastolic dysfunction gives us an additional reason to aggressively treat CHF patients with diuretics and vasodilators.