Computational fluid dynamics (CFD) simulations of patient-specific pulmonary vasculature revealed that intermediate-risk acute pulmonary embolism patients (n=6) showed significantly elevated hemodynamic resistance, power dissipation, and counts of vessels with low fractional flow reserve (FFR) compared to healthy controls (n=3). Critically, post-thrombectomy pressure normalization correlated with higher proximal power dissipation and low-FFR vessel counts pre-intervention, while persistently elevated post-procedure pressures linked to greater distal resistance. FFR count correlated significantly with both post-thrombectomy pulmonary pressure and cardiac index across all PE patients.
Pulmonary embolism kills roughly 60,000–100,000 Americans annually, yet the intermediate-risk tier—hemodynamically stable but physiologically stressed—remains a clinical decision minefield. Current risk stratification relies on echocardiography, troponins, and CT imaging, all of which offer limited mechanistic granularity. CFD-derived metrics borrowed from coronary artery disease management (notably FFR) could fill this gap by quantifying functional hemodynamic burden rather than merely anatomical clot burden. The finding that distal resistance—not proximal obstruction alone—predicts persistent post-thrombectomy hypertension is conceptually important, suggesting microvascular involvement may determine outcomes regardless of successful large-vessel clot removal.
However, this preprint has not yet been peer-reviewed, and the sample size (9 total subjects, 6 PE patients) is far too small to draw clinical conclusions. The steady-state inflow assumption also simplifies pulsatile pulmonary hemodynamics. This is exploratory, hypothesis-generating work—incremental in method but potentially paradigm-shifting in clinical application if validated at scale.
