The objective of this study was to define alterations in ventricular-arterial (V-A) coupling early in the development of tachycardia-induced heart failure (HF). Although HF is characterized by impaired V-A coupling, the temporal relationship of these derangements to overt left ventricular (LV) dysfunction is unknown. Six anesthetized dogs instrumented with LV manometers and piezoelectric crystals were studied before and after 24 h of rapid ventricular pacing (RVP). V-A coupling was indexed by the ratio between the end-systolic pressure-volume relation slope (endsystolic elastance, E(ES)) and effective arterial elastance (E(A)), and mechanical efficiency by the ratio of stroke work (SW) to pressure-volume area (PVA). After RVP, there was no significant depression of LV function, but E(A) and total peripheral resistance (R(T)) were increased (P < 0.05), indicating increased arterial load. After RVP, E(ES)/E(A) and SW/PVA were maintained during unstressed conditions, but upon changes in load induced by phenylephrine, E(ES)/E(A) declined more precipitously with equivalent increases in R (T) (slope E(ES)/E(A)-R(T) relation -16.7 +/- 4.6 vs -5.8 +/- 4.0 ml/mmHg.min, P < 0.025). Furthermore, after RVP there was significant (P < 0.05) blunting of dobutamine-induced augmentation of E(ES), E(ES)/E(A), and SW/PVA. Thus, after RVP there was a distinct loss of V-A coupling reserve during afterload and catecholamine stress. V-A coupling defects occur early in the development of tachycardia-induced HF prior to significant pump dysfunction, and are manifested primarily during hemodynamic and inotropic stress.