Right ventriculo-arterial (RV-VA) coupling expressed as a ratio of ventricular contractility to afterload (Ees/Ea) provides an integrated assessment of the efficiency of the pulmonary vascular—right ventricular unit. In previous work our group has demonstrated deterioration in cardiovascular magnetic resonance (CMR)-derived indices of VA coupling in patients undergoing lung resection. In patients, however, exploration of the mechanisms underlying uncoupling (i.e. the relative contributions of changes in contractility and afterload) is challenging, requiring expensive, invasive techniques. In this study we sought to use the Aplysia CardioVascular Lab haemodynamic simulator1 to explore in silico the mechanisms of uncoupling observed after lung resection. Demographic and haemodynamic data [including stroke volume (SV) and end-systolic volume (ESV)] were obtained from 15 patients enrolled in a CMR study examining RV-VA function before and on Day 2 after lung resection. Coupling was derived as the ratio of SV to ESV.2 Physiological adaptations were run for each patient within the simulator both before and after simulated lung resection (simulated by reducing the number of pulmonary blood vessels in the simulated patients in proportion to the volume of lung resected according to a 19-segment model of the pulmonary tree). The ratio of SV/ESV fell after both real and simulated lung resection implying deterioration in RV-VA coupling. The median SV/ESV fell by –0.14 [inter-quartile range (IQR), –0.34 to 0.01; P=0.02] in vivo and by –0.10 (IQR, –0.29 to –0.08; P<0.01) in silico; bias for the difference 0.01 (LOA –0.62 to 0.62), concordance 81.8%. Within the simulation this was attributable to a significant increase in Ea (P<0.01 for change; association between change in Ea and SV/ESV r=–0.9, P<0.01). There was, however, no association between changes in SV/ESV in real and simulated patients (r=0.32, P=0.24), and no association between simulated changes in Ea after lung resection and observed changes in SV/ESV in patients (r=–0.11, P=0.69). The mechanism of postoperative RV dysfunction after lung resection is widely believed to be the result of increased afterload, although this has not been demonstrated in clinical studies. The lack of association observed between simulated changes in Ea and changes in coupling seen in patients suggests that the mechanism of postoperative un-coupling is not simply related to the mechanical effect of a reduced pulmonary vasculature as would have been simulated according to the electrical analogue model within Aplysia. We hypothesise that an acute inflammatory injury to the RV impairs RV contractility and contributes to postoperative RV dysfunction, a mechanism which would not have been demonstrated by the computational model. 1.Broome M, Maksuti E, Bjallmark, et al. Biomed Eng Online 2013; 12: 692.Sanz J, Garcia-Alvarez A, Fernandez-Friere L. Heart 2012; 98: 238–43
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