In-Silico Evaluation of Mechanical vs Myocardial Efficiency: Influence of Aortic Compliance and Heart Rate

Background: Over the past 50 years, studies have evaluated mechanical (ME) and myocardial efficiency (MyoEff) using the left ventricular pressure-volume (PV) construct. ME represents an engineering concept and includes potential energy (PE). MyoEff represents a metabolic parameter. The early calculation of MyoEff included the PE component. However, the metabolic cost of PE cannot be quantified in in-vivo and human settings. To resolve this, we compared two methods of calculating MyoEff using the PVA metric (MyoEff-PVA) and the stroke-work (SW) metric (MyoEff-SW). The other limiting step in the MyoEff metric is the calculation of myocardial oxygen consumption (MVO 2 ), which requires an invasive data collection. The Rooke & Feigl pressure-work index (1982) was developed to provide an estimate of myocardial oxygen consumption (eMVO 2 ) and has been shown to be significantly correlated with positron emission tomography (PET) derived MVO 2 . We investigated how 1) the impact of a loss in aortic compliance (C A ) impacts ME, MyoEff-PVA and MyoEff-SW and 2) how an increase in HR coupled with the loss in C A impacts the variables using our computational model (CM). Methods: A lumped parameter CM based on the 3-element Windkessel was created and the PV loop metrics were compared with previously published human PV loop data. Simulated vena-caval occlusions were performed during two phases: phase 1 (P1) was conducted at 80 bpm with five levels of C A (normal (N) to stiff (S)) while phase 2 (P2) was conducted at the N and S settings of C A during three heart rates (60/100/140 bpm). The ME, MyoEff-PVA and MyoEff-SW metrics were evaluated. Results: During P1, the loss in C A from the N to S setting led to increases in SW and PVA. As a result of the increase in SW (90.9%) and PVA (210%) across the five elevated levels of C A , eMVO 2 increased 49%, while ME decreased (15%). In contrast, increases in MyoEff-SW (28%) and MyoEff-PVA (50%) were observed. During P2, as HR increased to 100 and 140 bpm, coupled with a loss in C A from N to S, SW decreased (62 and 61%, respectively) while PVA decreased 54 and 52%. The increase in HR led to a loss in ME (18 and 19%). Coupled with the loss in SW and an increase in eMVO 2 (43 and 47%), MyoEff-SW decreased 74 and 74%. MyoEff-PVA decreased similarly (68% at both N and S settings) but from an elevated baseline value due to the large increase in PE. Conclusion: The results from our CM suggest that use of MyoEff-PVA overestimates myocardial efficiency. The loss in C A coupled with increases in HR impacts MyoEff-SW in an expected manner. The study reestablishes the utility of the noninvasive calculation of eMVO 2 allowing its use in the clinic. These findings need to be evaluated in those presenting with a variety of cardiac related disease. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.