PULMONARY ARTERY STIFFNESS IN RACEHORSES AFFECTED BY EXERCISE-INDUCED PULMONARY HEMORRHAGE

Exercise-induced pulmonary hemorrhage (EIPH) is a common cause of poor performance in racehorses and reflects extreme exercise pressures and progressive changes of the pulmonary vessels. The aim of this thesis was to investigate whether pulmonary artery stiffness (PAS), a Doppler-derived index of pulmonary arterial elasticity, can be used as a practical, non-invasive indicator of pulmonary vascular involvement in Thoroughbred racehorses affected by EIPH. Several studies were conducted to provide a comprehensive overview of the pathophysiological background of EIPH and to refine diagnostic methodologies. First, the agreement between tracheal wash (TW) and bronchoalveolar lavage fluid (BALF) for EIPH assessment was evaluated in 172 poorly performing racehorses. TW and BALF provided similar information when hemorrhage was quantified using hemosiderophage-based metrics. A simplified TW Total Hemosiderin Score threshold was proposed to mirror BALF-based classification, allowing serial monitoring in field conditions when BALF is not feasible. Second, the interchangeability of TW and BALF for airway inflammatory phenotyping was assessed in 123 racehorses with EIPH. Some cell counts correlated, but agreement was insufficient to consider the samples equivalent. BALF remained necessary for accurate inflammatory profiling, while TW was better suited to estimating bleeding and monitoring EIPH itself. Third, PAS was measured in 40 Thoroughbreds using the left parasternal angled view of the right-ventricular outflow tract, and repeatability/reproducibility were assessed. Intra-operator agreement was excellent, while inter-operator agreement ranged from moderate to excellent. A systematic “window effect” was also observed: compared with the conventional right parasternal view already used for PAS measurement in equine medicine, the left view yielded shorter Acceleration Time (AT: 110 vs 151 ms), higher Maximal Frequency Shift (MFS: 2.6 vs 2.27 kHz), and higher PAS (23.8 vs 15.6 kHz·s⁻¹; all p<0.001). These findings likely underscore the influence of beam-flow alignment and indicate that PAS measurements obtained from different views are not interchangeable. Finally, PAS was evaluated in horses with and without EIPH, as classified by BALF cytology. The study included 40 horses affected by EIPH and 58 no-EIPH horses. Horses with EIPH showed significantly higher PAS values (22.26 ± 4.94 vs 19.06 ± 5.82 kHz/s; p = 0.006) and MFS (2.57 ± 0.34 vs 2.40 ± 0.43 kHz; p = 0.026), along with significantly shorter AT (114 [102–137] vs 137 [110–160] ms; p = 0.030) compared to no-EIPH horses. These findings are consistent with increased pulmonary vascular stiffness and reduced arterial compliance in EIPH, reflecting structural and functional alterations of the pulmonary vascular bed. Overall, the present project moves PAS from a physiological concept to a tool ready for clinical use. It describes how to measure PAS consistently in horses, explains left-right echocardiographic view differences, and demonstrates disease-related changes in conditions associated with pulmonary vascular remodeling, including EIPH. PAS can be added to standard echocardiography within minutes, monitored over time, and interpreted together with TW (for bleeding burden) and BALF (for inflammation) to support screening, follow-up, and management decisions in Thoroughbred racehorses.