Abstract
s S143 Children’s Hospital, Columbus, OH; 2Qtest Labs, Columbus, OH; 3Cardiothoracic Surgery, Nationwide Children’s Hospital, Columbus, OH. Purpose: LVAD unloading seldom translates to normalized cardiac size or functional recovery. This study evaluated the intrinsic cardiovascular physiology of LVAD-supported ventricles via both load-independent function and myocardial loading as reflected by the arterial elastance (Ea). Normal ventricles were studied to avoid the confounders of myocardial dysfunction or remodeling present with heart failure to determine if there is a maladaptive cardiac signal during LVAD support. Methods: Healthy sheep were either implanted with an axial-flow LVAD (Heartmate II; Thoratec) via a left-thoracotomy (LVAD, n = 7) or served as shams (CTRL, n = 3). Animals were instrumented for LV/arterial pressures (via solid-state/fluid-filled catheters), LVAD and pulmonary artery flow (transit-time flow probes) and for the assessment of left-ventricular volume/ dimensions (sonometric crystals). Animals underwent continuous support for 8 weeks while systemic/ventricular hemodynamics, LV geometry and LV function were monitored in unsedated animals weekly. Atrial natriuretic peptide (ANP) plasma concentrations were measured weekly. Results: LVAD animals were supported at 5.7 ± 0.4 L/min (74 ± 2% of CO). When compared to CTRL, LVAD support resulted in immediately elevated Ea (2.7 ± 0.2 vs. 1.6 ± 0.1 mmHg/mL, P < 0.05) due to a paradoxical uncoupling of systemic hemodynamics (preserved aortic pressure, 91 ± 4 vs. 94 ± 5 mmHg) and decreased LV stroke-volume (LVSV, 34 ± 1 vs. 53 ± 5 mL, P < 0.05). Elevated Ea normalized over the the study (1.5 ± 0.1 mmHg/ml) as LVSV increased (34 ± 1 to 64 ± 2.3 mL, P< 0.01) as a consequence of increased end-diastolic volumes (63 ± 3.6 to 105 ± 8.2 mL) as Ea is a known driver of negative LV remodeling despite LVAD support. LVADdriven elevations in Ea were correlated with elevations in plasma ANP levels that also normalized with Ea over the study period (surgery, 510±380; wk 2 2380±340; wk 8 650±180 pg/mL) despite LV enlargement. Conclusion: LVAD support paradoxically produces an elevated Ea (arterial load) and static loading of the cardiomyocyte. As observed in congestive heart failure, uncoupled and elevated Ea translated to maladaptive LV remodeling and dysfunction in LVAD supported normal hearts potentially explaining poor cardiac reverse remodeling and recovery with continuous flow LVADs.
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