Abstract
Although the coronary sinus reducer (CSR) has emerged as a promising therapeutic intervention for patients with refractory angina, its underlying mechanistic basis remains incompletely understood. Specifically, how CSR affects microvascular hemodynamics, and O
2
transport under ischemic conditions, has not been established. To address this issue, we developed a multiscale computational framework that couples closed-loop coronary hemodynamics with an advection-diffusion model of O
2
transport to evaluate the effects of CSR across varying degrees of myocardial ischemia. Simulations show that CSO elevates coronary sinus (CS) pressure, increases venous-capillary pressure gradients, and induces retrograde venous flow that helps redistribute blood from non-ischemic territories to ischemic territory. This retrograde flow increases mean pO
2
in the ischemic capillary bed by 47% (3.14 ± 6.05 mmHg in severe ischemia to 4.63 ± 5.54 mmHg with CSO) and reduced the fraction of severely hypoxic capillaries from 76% to 58%, providing a partial alternative pathway for O
2
delivery when arterial inflow to capillaries is critically reduced. These results provide a quantitative mechanistic explanation for the clinical improvements observed with CSR therapy for patients who are not candidates for revascularization. Finally, this model highlights the impact of severity of arterial stenosis and microvascular O
2
transport on the therapeutic efficacy of the CSR.