Key result
Higher heart rate elevates carotid blood-flow energy loss ~2-fold, driven largely by viscous dissipation.
Why the study?
Carotid artery stenosis substantially alters local hemodynamics and can increase blood-flow energy loss, but the manner in which heart-rate-dependent inflow redistributes viscous loss, wall-related net loss, and Reynolds-stress transfer remained unclear.
How does heart-rate-dependent pulsatile inflow redistribute viscous loss, wall-related net loss, and Reynolds-stress energy transfer in patient-specific carotid artery stenosis?
How does heart-rate-dependent pulsatile inflow redistribute viscous loss, wall-related net loss, and Reynolds-stress energy transfer in patient-specific carotid artery stenosis?
In patient-specific carotid stenosis computational models, blood-flow energy loss increases with higher heart rates primarily due to viscous dissipation, while Reynolds-stress energy transfer behaves as a model-dependent interscale-transfer metric rather than a true physical turbulent-dissipation fraction.
Answers are grounded in this paper and cite their sources.
Higher heart rates may elevate viscous energy loss in carotid stenosis; hypothesis-generating and should not yet change practice.
Carotid artery stenosis substantially alters local hemodynamics and can increase blood-flow energy loss (BFEL). How heart-rate-dependent inflow redistributes viscous loss, wall-related net loss, and Reynolds-stress transfer remains unclear. Nine patient-specific carotid models spanning mild, moderate, and severe stenosis were examined using a bidirectional fluid–structure interaction framework. Flow-rate waveforms were converted to inlet velocities using case-specific common carotid artery areas; three-element Windkessel outlet models supported 27 simulations at 67, 100, and 140 beats per minute (bpm). Clinical Doppler ultrasound measurements were compared with predicted external and internal carotid velocity waveforms in one mild-stenosis case. A literature-based reconstructed phantom benchmark additionally assessed outlet-pressure predictions. Molecular viscous dissipation (Eμ), wall-related net energy loss (EW), and shear stress transport (SST)-modeled Reynolds-stress energy transfer (ERS) accounted for 10.14%–82.97%, 3.04%–32.81%, and 0.02%–66.37% of BFEL, respectively. Viscous loss dominated most cases, while BFEL generally increased from (3.0–10.5) × 10−5 J/cycle at 67 bpm to (5.4–17.7) × 10−5 J/cycle at 100 bpm and (7.0–23.0) × 10−5 J/cycle at 140 bpm, reflecting changes in flow magnitude and pulsatile timing. Wall-related loss varied comparatively little, whereas ERS responded strongly under selected conditions. In Case 7 at 140 bpm, ERS/BFEL was 66.37% with baseline SST and 62.52% with transition SST. A separate scale-resolving improved delayed detached-eddy simulation estimated mean-flow-to-fluctuation transfer and turbulence-associated irreversible dissipation at approximately 58.0% and 45.0% of BFEL, respectively. Thus, Reynolds-averaged Navier–Stokes-derived ERS is a model-dependent interscale-transfer metric rather than a physical turbulent-dissipation fraction.
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Yang et al. (2026) studied Carotid artery stenosis (mild, moderate, and severe) (n=9). Bidirectional fluid-structure interaction simulation at 67, 100, and 140 bpm vs. Clinical Doppler ultrasound measurements (in 1 mild-stenosis case), literature-based phantom benchmark, and scale-resolving IDDES was evaluated on Blood-flow energy loss (BFEL) and its components: molecular viscous dissipation (Eμ), wall-related net energy loss (EW), and Reynolds-stress energy transfer (ERS). Increasing heart rate from 67 to 140 bpm elevated carotid blood-flow energy loss from (3.0-10.5)x10^-5 to (7.0-23.0)x10^-5 J/cycle, dominated mostly by viscous dissipation (10.14%-82.97%).
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