Fig 1.
Theoretical analysis of the impact of left ventricular assist device (LVAD) on pressure-volume loop in a normal left ventricle.
The solid line represents the baseline pressure-volume (PV) loop. In partial LVAD support (p-LVAD), LVAD decreases left ventricle (LV) end-diastolic volume and increases mean arterial pressure (AP), which in turn increases end-systolic volume (dotted line). On the other hand, total LVAD support (t-LVAD) markedly lowers LV pressure to below AP yielding an extremely small PV area (double line). EDPVR, end-diastolic pressure volume relation; ESPVR, end-systolic pressure volume relation;.
Fig 2.
Diagram of the left ventricular assist device (LVAD) used in this experiment.
The inlet and outlet cannulas were inserted into the LV apex and left femoral artery (LFA), respectively. These cannulas were connected to a centrifugal pump and an in-line ultrasonic flow probe was placed in the LVAD circuit to measure LVAD flow continuously.
Table 1.
Impact of level of left ventricular assist device (LVAD) support on hemodynamics in normal dogs.
Fig 3.
Representative pressure-volume loops at 3 levels of left ventricular assist device (LVAD) support in a normal dog.
The solid line represents pressure-volume (PV) loop with no LVAD support (Control). Partial LVAD support (p-LVAD) decreases left ventricle (LV) end-diastolic volume and increases mean arterial pressure (AP), thus PVA does not decrease much (dotted line). On the other hand, total LVAD support (t-LVAD) lowers LV pressure to below AP and markedly reduces PVA (double line).
Fig 4.
Impact of level of left ventricular assist device (LVAD) support on pressure-volume area and myocardial oxygen consumption in normal dogs.
Open bar, hatched bar and closed bar indicate no LVAD support (Control), partial LVAD support (p-LVAD) and total LVAD support (t-LVAD), respectively. Data are expressed as means ± SD. p-LVAD marginally reduces PVA, while t-LVAD markedly decreases pressure-volume area (PVA). In addition, t-LVAD markedly reduces myocardial oxygen consumption (MVO2) by more than 55%. *p < 0.05 versus Control; †p < 0.01 versus Control; ‡p<0.01 versus p-LVAD.
Table 2.
Impact of level of left ventricular assist device (LVAD) support on hemodynamics in a dog model of ischemia-reperfusion.
Fig 5.
Impact of LVAD support level on infarct size in a dog model of ischemia reperfusion.
(A): Representative left ventricular (LV) sections after staining with Evan’s blue and TTC. The area at risk (red) and the infarct area (white) were traced and measured by using an image analyzer. (B): Quantification of risk area in LV. There are no difference among three groups. (C): Assessment of infarct ratio (infarct area/risk area, %). Compared to control (no LVAD support, n = 6), p-LVAD (n = 5) moderately lowers the infarct ratio (p = 0.011), while t-LVAD (n = 5) strikingly decreases the infarct ratio by more than 80% (p<0.01). (D): Changes in serum creatine kinase-MB (CK-MB) 300 min after reperfusion in the three groups. (B-D): Data are expressed as means ± SD. *p < 0.05 versus Control; †p < 0.01 versus Control; ‡p<0.01 versus p-LVAD.
Fig 6.
Simulation study with normal and depressed LV systolic function.
(A): Simulated PV loop of LV with normal (solid line, maximum elastance: 7 mmHg/ml) and depressed (dashed line, maximum elastance: 1 mmHg/ml) systolic function. Mean circulatory filling pressure was fixed in both systolic conditions (6.4 mmHg). (B): The relationship between LVAD support flow and changes in PVA in normal (solid line) and depressed (dashed line) LV systolic function. PVA at baseline (no LVAD support) were normalized at 100% in each group. Both “a” and “b” indicate the inflection point which circulation turns to total LVAD from partial LVAD support. The rate of decrease in PVA by partial LVAD support (baseline PVA to that of “a” and “b”) is much lower in depressed LV (-27%) than in normal LV (-54%).