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

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Abstract

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 AR 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.

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Correspondence to Sumanth D. Prabhu.

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Prabhu, S. Altered left ventricular–arterial coupling precedes pump dysfunction in early heart failure. Heart Vessels 22, 170–177 (2007). https://doi.org/10.1007/s00380-006-0954-9

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