A Microstructurally-Motivated Framework to Study Autoregulation in the Coronary Circulation
Coronary autoregulation is defined as the capability of the coronary circulation to maintain the blood supply to the heart over a range of perfusion pressures. This phenomenon is facilitated through intrinsic mechanisms that control the vascular resistance by regulating the mechanical function of smooth muscle cells. Understanding the mechanisms involved in coronary autoregulation is one of the most fundamental questions in coronary physiology.This paper presents a structurally-motivated coronary autoregulation model that uses a nonlinear continuum mechanics approach to account for the morphometry and vessel wall composition in two coronary trees in the subepicardial and subendocardial layers.The model is calibrated against diverse experimental data from literature and is used to study heterogeneous autoregulatory response in the coronary trees. This model drastically differs from previous models, which relied on lumped parameter model formulations, and is suited to the study of long-term pathophysiological growth and remodeling phenomena in coronary vessels.
Authors
- C. Alberto Figueroa (ORCID: https://orcid.org/0000-0002-3934-6506)
- Matthew Eden (ORCID: https://orcid.org/0000-0001-9409-8974)
- Domingo Uceda (ORCID: https://orcid.org/0000-0001-9916-8898)
- Victoria Sturgess (ORCID: https://orcid.org/0000-0002-7413-8657)
- Daniel Beard (ORCID: https://orcid.org/0000-0003-0974-2353)
- Johnathan D. Tune (ORCID: https://orcid.org/0000-0003-2959-0801)
- Seungik Baek (ORCID: https://orcid.org/0000-0003-2007-339X)
- Hamidreza Gharahi
Institutions
- University of North Texas (US)
- University of North Texas Health Science Center (US)
- University of Michigan (US)
- Michigan State University (US)
Publication Details
- Journal
- bioRxiv (Cold Spring Harbor Laboratory)
- Published
- 2025-12-05
- DOI
- https://doi.org/10.64898/2025.12.02.691683
- Primary Topic
- Coronary Interventions and Diagnostics
- Type
- article
- Field-Weighted Citation Impact
- 0.00