Altered left ventricular–arterial coupling precedes pump dysfunction in early heart failure.

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. [ABSTRACT FROM AUTHOR]