The Scientific Basis for the Relations Between Pulsed‐Doppler Transmitral Velocity Patterns and Left Heart Chamber Properties

This article presents a didactic approach toward understanding the complex relations between transmitral flow patterns and cardiac properties. We start with some observations, obtained noninvasively, from normal and diseased human hearts, and supplement them with noninvasive and invasive observations from the dog laboratory. We then formulate a conceptual approach that is consistent with a physical interpretation of the data, and that enables us to clarify the roles of the active and passive properties of the left atrium and left ventricle. These basic concepts are incorporated into a computational model wherein the properties of the cardiovascular system can be varied to simulate physiological and pathological states of diastolic function to produce normal and abnormal ventricular flow patterns. We present examples of normal hearts, pressure overload hypertrophy, dilated failing hearts, and ventricles with poor compliance but apparently normal flow patterns. Various isolated perturbations of interest were performed in each of these conditions; and finally, we studied the effects on diastolic indices of a systematic variation of the time constant of ventricular relaxation, and of cardiac output. Among the interesting findings are: flow patterns that mimic mitral stenosis can be created by the properties of the ventricle as well as by the properties of the mitral apparatus; the A/E ratio is greater than normal in the dilated ventricle and in the hypertrophied ventricle with slowed relaxation; and in both conditions, the A/E ratio also increases with decreased cardiac output. Thus, changes in stroke volume, whether due to diastolic or to systolic function, will change indices of diastolic function. Finally, in concentric hypertrophy: large increases in atrial contractility are a necessary condition for large A/E ratios; and slowed ventricular relaxation by itself is incapable of producing a slowed deceleration of early filling; incomplete relaxation and myocardial viscoelasticity are also required.