Key result
Post-lung resection RV dysfunction stems from combined contractility loss and increased afterload in computational model.
Why the study?
The mechanisms of right ventricle dysfunction after lung resection remain unclear, particularly whether afterload increase or contractility loss is the underlying cause.
Does right ventricular dysfunction following lung resection primarily result from increased afterload or loss of contractility in a computational model?
Does right ventricular dysfunction following lung resection primarily result from increased afterload or loss of contractility in a computational model?
This first-of-its-kind computational model demonstrates that post-operative right ventricular dysfunction following lung resection likely results from a combination of contractility loss and afterload increase, which produce opposite changes in pulmonary pressures.
May inform targeted pressure measurements to differentiate RV dysfunction mechanisms post-lung resection; leaves open clinical validation of this model.
Functional limitation after lung resection surgery has been consistently documented in clinical studies, and right ventricle (RV) dysfunction has been hypothesized as a contributing factor. However, the mechanisms of RV dysfunction after lung resection remain unclear, particularly whether change in afterload or contractility is the underlying cause. This study reviews the clinical literature on this topic and proposes a lumped parameter model to simulate the effects of lung resection. Our model allowed us to isolate the two mechanisms and compare them. Subsequently, the simulation outputs were compared against the literature. Our rigorous approach included local and global sensitivity analyses to evaluate the effect of model parameters, both individually and collectively. The two mechanisms produced the same trends for all outputs except three: RV systolic pressure (RVSP) and pulmonary artery systolic and diastolic pressure (PASP and PADP) changed in opposite directions. Furthermore, our model indicates that obtaining pressure measurements in the clinic may help quantify the precise combination of the two mechanisms. This study presents the first mathematical model of the effect of lung resection on the cardiovascular system. Further refinement, combined with additional clinical data, will help us predict RV dysfunction and pave the way towards improving outcomes for lung cancer patients.
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Pant et al. (2026) studied Right ventricular dysfunction following lung resection. Simulated lung resection (afterload increase and RV contractility loss) vs. Pre-operative baseline (simulated healthy condition) was evaluated on Right ventricular volume and pressure changes. A computational model demonstrated that postoperative right ventricular dysfunction following lung resection likely results from a combination of right ventricular contractility loss and afterload increase.
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