Atherosclerosis, a chronic inflammatory cardiovascular disease, leads to arterial constriction caused by the accumulation of lipids, cholesterol, and various substances within artery walls. Such plaque can rupture, resulting in a blood clot that obstructs major arteries and may initiate myocardial infarction, ischemic stroke, etc. Atherosclerotic plaque formation begins with the accumulation of foam cells and macrophages within the intima layer of the arterial wall. At the latter stage, the smooth muscle cells migrated from deeper artery wall layers, contributing to the fibrous cap formation and plaque stabilizing. A developed plaque gradually enters the lumen and narrows down the lumen to impede blood flow. We introduce a two-phase and macroscopic model to investigate the progression of plaque growth in its advanced stage and analyze the minimum gap (Lumen Clearance) within an atherosclerotic artery so that blood cells can pass through. Cardiac troponin, a high specificity and sensitivity biomarker, facilitates early detection of elevated myocardial infarction, ischemic stroke risks, etc. This study aims at establishing a relationship between the troponin concentration in atherosclerotic arteries and their internal clearance, which could significantly improve our understanding of disease progression. Our observations show that the plaque undergoes rapid evolution in its initial stages, gradually slowing down over time to reach a stable state. A positive correlation exists between the maximum plaque depth and cardiac troponin concentration in the blood. However, the lumen clearance exhibits the opposite behavior. The speed of blood cells slows down at an enhanced plaque depth within atherosclerotic arteries.
