Can the hemodynamic model in heart failure be restored based on analysis of ventricular-arterial coupling?

The hemodynamic model was inappropriate to explain the disappointing effect of vasodilation and the beneficial effect of beta-blockade in chronic heart failure. A more nuanced hemodynamic analysis, taking both steady and pulsatile hemodynamics into consideration, improves insight into these apparently enigmatic effects. Of particular interest is the velocity of early systolic flow as a determinant of left ventricular afterload. Several drugs, in particular beta-blockers, directly or indirectly, influence the velocity of early systolic flow. Thus, the hemodynamic model in heart failure may deserve reconsideration.