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<p>Stenosis in coronary arteries significantly alters local hemodynamics, but the combined effects of hypothermia‑induced viscosity changes and arterial stiffening remain underexplored. This study presents a comprehensive experimental investigation that simultaneously quantifies the hemodynamic and thermal burden of coronary stenosis under both normothermic (37&#xa0;°C) and hypothermic (29&#xa0;°C) conditions in a compliant, patient-specific model. Distilled water was employed as a Newtonian blood analog, with viscosity increasing from approximately 0.69 mPa·s at 37&#xa0;°C to 0.82 mPa·s at 29&#xa0;°C (~ 19% increase), providing a controlled thermo‑viscous perturbation as the primary independent variable. A pulsatile flow loop replicating physiological cardiac output was utilized, and pressure drops, wall shear stress (WSS), arterial compliance, vascular input impedance, fractional flow reserve (FFR), and Nusselt number were quantified across a heart‑rate range of 72–156&#xa0;bpm. Three principal novel findings were identified. First, this is the first experimental study to demonstrate that hypothermia alone can reduce FFR below the clinical ischemic threshold of 0.80 without any geometric alteration of the stenosis, with values reaching approximately 0.70 at resting heart rates, a finding with direct implications for the diagnostic accuracy of FFR assessment in hypothermic patients. Second, a novel power crossover phenomenon was identified at 132&#xa0;bpm, above which the hemodynamic power demand under hypothermia disproportionately surpasses normothermic levels, defining a specific vulnerability threshold during cold‑weather exertion. Third, the simultaneous quantification of WSS (peak ~ 240&#xa0;Pa at 29&#xa0;°C), vascular input impedance (Z ≈ 1.5 × 10¹⁰ Pa·s/m³), arterial compliance, and Nusselt number (Nu ≈ 250–280) within a single coupled experimental framework provides an integrative characterization of the hypothermic stenotic burden not previously available. These findings suggest that the combination of stenosis and cold exposure creates a “perfect storm” of high shear stress, increased cardiac afterload, and altered vascular mechanics, offering a fluid‑dynamical explanation for the increased risk of acute coronary syndromes during winter or therapeutic hypothermia.</p>

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Experimental investigation of hemodynamic and thermal implications of coronary stenosis under hypothermic conditions

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月2日

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  • Orhan Yildirim,
  • Sendoğan Karagoz,
  • Ömer Çomakli

摘要

Stenosis in coronary arteries significantly alters local hemodynamics, but the combined effects of hypothermia‑induced viscosity changes and arterial stiffening remain underexplored. This study presents a comprehensive experimental investigation that simultaneously quantifies the hemodynamic and thermal burden of coronary stenosis under both normothermic (37 °C) and hypothermic (29 °C) conditions in a compliant, patient-specific model. Distilled water was employed as a Newtonian blood analog, with viscosity increasing from approximately 0.69 mPa·s at 37 °C to 0.82 mPa·s at 29 °C (~ 19% increase), providing a controlled thermo‑viscous perturbation as the primary independent variable. A pulsatile flow loop replicating physiological cardiac output was utilized, and pressure drops, wall shear stress (WSS), arterial compliance, vascular input impedance, fractional flow reserve (FFR), and Nusselt number were quantified across a heart‑rate range of 72–156 bpm. Three principal novel findings were identified. First, this is the first experimental study to demonstrate that hypothermia alone can reduce FFR below the clinical ischemic threshold of 0.80 without any geometric alteration of the stenosis, with values reaching approximately 0.70 at resting heart rates, a finding with direct implications for the diagnostic accuracy of FFR assessment in hypothermic patients. Second, a novel power crossover phenomenon was identified at 132 bpm, above which the hemodynamic power demand under hypothermia disproportionately surpasses normothermic levels, defining a specific vulnerability threshold during cold‑weather exertion. Third, the simultaneous quantification of WSS (peak ~ 240 Pa at 29 °C), vascular input impedance (Z ≈ 1.5 × 10¹⁰ Pa·s/m³), arterial compliance, and Nusselt number (Nu ≈ 250–280) within a single coupled experimental framework provides an integrative characterization of the hypothermic stenotic burden not previously available. These findings suggest that the combination of stenosis and cold exposure creates a “perfect storm” of high shear stress, increased cardiac afterload, and altered vascular mechanics, offering a fluid‑dynamical explanation for the increased risk of acute coronary syndromes during winter or therapeutic hypothermia.