May 1, 2022Physiological ReportsOpen Access

Right ventricular myocardial energetic model for evaluating right heart function in pulmonary arterial hypertension

View Full Paper

Ask AI

Bookmark

Why the study?

PAH increases RV workload and decreases myocardial oxygen reserve, leading to poor cardiac output, prompting a novel model of RV work output based on RV hemodynamics and oxygen supply.

Does a novel right ventricular myocardial energetic model accurately estimate right ventricular total power output and efficiency in patients with pulmonary arterial hypertension?

Structured PICO

Does a novel right ventricular myocardial energetic model accurately estimate right ventricular total power output and efficiency in patients with pulmonary arterial hypertension?

Population

15 patients with idiopathic pulmonary arterial hypertension (IPAH) (14 female, 1 male, aged 26-71 years) and 6 adult male Dorset sheep (60 ± 3 kg) undergoing acute pulmonary banding with or without hypoxia.

Intervention

A novel adjusted right ventricular myocardial energetic model based on thermodynamic first principles to calculate RV power output specific to PAH.

Comparator

Original Elbeery et al. left ventricular energetic model applied to the right ventricle.

Outcome

Correlation (coefficient of determination, R2) between right ventricular O2 consumption and right ventricular total power output.surrogate

A novel thermodynamic model accurately estimates right ventricular total power output and highlights the vulnerability of PAH patients with compromised right coronary flow and high afterload.

Limitations

The small contribution of anaerobic energy sources (glycolysis) is considered to be negligible in the model.
Out of necessity, the non-zeroth harmonic stroke power is estimated using the method of Saouti et al. for clinical data, as QPA could not be directly measured in humans.

Implication

May inform RV workload assessment in PAH; leaves open clinical utility pending prospective validation.

Abstract

BACKGROUND: Pulmonary arterial hypertension (PAH) increases right ventricular (RV) workload and decreases myocardial oxygen reserve, eventually leading to poor cardiac output. This study created and assessed a novel model of RV work output based on RV hemodynamics and oxygen supply, allowing new insight into causal mechanisms of RV dysfunction. METHODS: The RV function model was built upon an earlier, left ventricular model and further adjusted for more accurate clinical use. The model assumes that RV total power output (1) is the sum of isovolumic and stroke power and (2) is linearly related to its right coronary artery oxygen supply. Thus, when right coronary artery flow is limited or isovolumic power is elevated, less energy is available for producing cardiac output. The original and adjusted models were validated via data from patients with idiopathic PAH (n = 14) and large animals (n = 6) that underwent acute pulmonary banding with or without hypoxia. RESULTS: = 0.86). Furthermore, the models demonstrate a significant inverse relationship between required oxygen consumption and RV efficiency (stroke power/total power) (p < 0.001). Lastly, higher NYHA class was indicative of lower RV efficiency and higher oxygen consumption (p = 0.013). CONCLUSION: Right ventricular total power output can be accurately estimated directly from pulmonary hemodynamics and right coronary perfusion during PAH. This model highlights the increased vulnerability of PAH patients with compromised right coronary flow coupled with high afterload.