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Afterload Sensitivity of Continuous-Flow Left Ventricular Assist Devices and Abolition of Frank-Starling Forces Under Strain.

A 62-year-old man presented with symptomatic lowflow alarms 2 months post-insertion of HeartWare HVAD continuous-flow left ventricular assist device for ischemic cardiomyopathy. He underwent right heart catheterization with simultaneous recording of pump flow and radial arterial pressure. Baseline measurements revealed normal pulmonary artery wedge pressure (9 mmHg) and right atrial pressure (RAP, 5 mmHg). The mean arterial pressure was 90 mmHg and pump flow 3.1 L/minute. Valsalva maneuver at baseline (Figure [A]) resulted in reduced—but not abolished—flow pulsatility during late stage 2, and slightly reduced mean arterial pressure to a nadir of 81 mmHg immediately upon release (stage 3). Administration of glyceryl trinitrate resulted in significantly reduced mean arterial pressure (78 mmHg) and pump flow (2.6 L/minute) and slightly decreased pulmonary artery wedge pressure (5 mmHg). Repeat Valsalva (Figure [B]) produced rapid, complete, and sustained abolition of pump flow pulsatility commencing in early stage 2 with associated severe, symptomatic hypotension (nadir 54 mmHg), before a very gradual restoration of both arterial pressure and pump flow pulsatility in stage 4. The phenomenon of flow-flatlining during Valsalva maneuver has been previously described in continuous-flow left ventricular assist device patients, with the basic mechanism hypothesized to be reduction in FrankStarling forces to the point of zero ventricular contraction (V0). 1 The phenomenon is associated with reduced afterload, likely due to more efficient diastolic ventricular emptying by the inherently afterload-sensitive continuous-flow left ventricular assist device,2 contributing to progressive reduction in preload until V0 is reached. In some cases, steady-state may be obtained at V0, with ongoing efficient pump flow preventing restoration of Frank-Starling forces, causing sustained hypotension. This vignette highlights the hemodynamic consequences of flow-flatlining, profound in some cases, and the contributory effect of afterload-reducing vasoactive medications. Moreover, it illustrates a coupling of preload, afterload and Frank-Starling forces that is unique to continuous-flow left ventricular assist device physiology and a direct consequence of their unphysiological afterload sensitivity.2