Abstract Body (Do not enter title and authors here): Introduction
Emergency PCI has reduced immediate death in STEMI patients. However, reperfusion therapy can cause intramyocardial hemorrhage (IMH) in 40% of STEMI patients and has emerged as a major predictor of adverse CV events. The mechanisms contributing to the development of IMH, however, are not understood.

Research Hypothesis
We hypothesize that hemodynamic forces (pressure variation and blood flow redistribution) influenced by the topological organization of coronary vasculature plays a major role in IMH development.

Goal
We tested our hypothesis by developing a computational model of the coronary vasculature to determine patient-specific coronary network topology biomarkers and hemodynamics associated with IMH.

Methods
Pre- and post-PCI coronary angiograms from STEMI patients (n=17) were stratified into 4 groups (IMH:H; Collaterals: C): H-/C+; H+/C-, H-/C-, and H+/C+). T2* MRI was used to identify IMH. Vascular topology and hemodynamics of the main branches of LCx and LAD and associated collaterals (if present) were determined. Computational model used input pressure of 100mmHg, 40mmHg threshold for IMH in microvasculature, and pressure-flow relationships.

Results
A higher density of vessels on angiograms in the H-/C+ group (91±15) vs H+/C- (47±19) with smaller vessel diameters (1.2±0.2mm (H-/C+) vs 1.6±0.4mm (H+/C-)) of shorter length (7.4±1.1mm vs 11±3.5mm) were observed. There were more 3^rd or 4^th order arterioles (41±6.7 vs. 21±8) with smaller diameters (0.72±0.6 vs. 0.9±0.2mm) in H-/C+ vs H+/C-. The Junctional Exponent (JE, a coronary network biomarker) was significantly lower in the H-/C+ vs other groups in pre-PCI (1.48±0.1 vs 1.74±0.02 H+/C- p=0.021; 1.79±0.12 H-/C- p=0.021; 1.6±0.12 H+/C+ p=0.008) and post PCI (1.44±0.11 vs 1.87±0.19 H+/C- p=0.02; 1.64±0.07 H-/C- p=0.04) except H+/C+ (1.58±0.11 H+/C- p=0.46) suggesting hemodynamically efficient branching structure in the H-/C+ group. Hemodynamic simulations indicated that prior to PCI, collaterals provide some tissue perfusion to the MI area whereas, after PCI, collaterals play minimal role in flow redistribution. Mean segment pressure was lower in the H-/C+ vs. H+/C- groups (55.6±4.2 vs. 60.8±7.7mmHg, p=0.41) whereas the terminal arterial flows were not different (p=0.94).

Conclusions
Our early findings support the notion that coronary network topology influences hemodynamic factors and contributes to the development of hemorrhagic MI.