Insights Into Myocardial Oxygen Consumption, Energetics, and Efficiency Under Left Ventricular Assist Device Support Using Noninvasive Pressure-Volume Loops.
- Publication Type:
- Journal Article
- Citation:
- Circ Heart Fail, 2019, 12 (10), pp. e006191 - ?
- Issue Date:
- 2019-10
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BACKGROUND: Assessment of left ventricular (LV) recovery under continuous-flow LV assist device therapy is hampered by concomitant pump support. We describe derivation of noninvasive pressure-volume loops in continuous-flow LV assist device patients and demonstrate an application in the assessment of recovery. METHODS AND RESULTS: Using pump controller parameters and noninvasive arterial pressure waveforms, central aortic pressure, outflow conduit pressure gradient, and instantaneous LV pressure were calculated. Instantaneous LV volumes were calculated from echocardiographic LV end-diastolic volume accounting for the integral of pump flow with respect to time and aortic ejection volume derived from the pump speed waveform. Pressure-volume loops were derived during pump speed adjustment and following bolus intravenous milrinone to assess changes in loading conditions and contractility, respectively. Fourteen patients were studied. Baseline noninvasive LV end-diastolic pressure correlated with invasive pulmonary arterial wedge pressure (r2=0.57, root mean square error 5.0 mm Hg, P=0.003). Measured noninvasively, milrinone significantly increased LV ejection fraction (40.3±13.6% versus 36.8±14.2%, P<0.0001), maximum dP/dt (623±126 versus 555±122 mm Hg/s, P=0.006), and end-systolic elastance (1.03±0.57 versus 0.89±0.38 mm Hg/mL, P=0.008), consistent with its expected inotropic effect. Milrinone reduced myocardial oxygen consumption (0.15±0.06 versus 0.16±0.07 mL/beat, P=0.003) and improved myocardial efficiency (43.7±14.0% versus 41.2±15.5%, P=0.001). Reduced pump speed caused increased LV end-diastolic volume (190±80 versus 165±71 mL, P<0.0001) and LV end-diastolic pressure (14.3±10.2 versus 9.9±9.3 mm Hg, P=0.024), consistent with a predictable increase in preload. There was increased myocardial oxygen consumption (0.16±0.07 versus 0.14±0.06 mL O2/beat, P<0.0001) despite unchanged stroke work (P=0.24), reflecting decreased myocardial efficiency (39.2±12.7% versus 45.2±17.0%, P=0.003). CONCLUSIONS: Pressure-volume loops are able to be derived noninvasively in patients with the HeartWare HVAD and can detect induced changes in load and contractility.
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