Pulmonary artery calcification in racehorses may be related to transient and repeated increases in arterial pressure during exercise

Abstract

Calcification of the pulmonary artery has been found in a large number of racing horses. The majority of calcified lesions are found immediately distal to the primary arterial bifurcation. Increased arterial wall stress levels have been previously demonstrated at these locations, with the wall stress levels increasing under intra-luminal pressures associated with exercise. We hypothesize therefore that the formation of calcified lesions is mediated by transient and repeated increases in pulmonary artery intra-luminal pressure. The presence of calcified lesions would likely further exacerbate the levels of wall stress, leading to growth of the lesions. A level of wall stress may exist above which calcified lesions form, and a second level may exist above which the calcified lesions grow at an increased rate. A computer model of pulmonary artery wall stress with calcified lesions was created, and wall stress levels were found to be greatest at the periphery of the calcified lesions. Osteo/chondrocyte-like cells have also been found at the periphery of the calcified lesions and could be responsible for collagen deposition and lesion growth, mediated by local wall stress levels. These increased levels of wall stress could place racehorses at a greater risk of acute pulmonary arterial rupture at the site of the calcified lesions, due to the high levels of intra-luminal pressure within the pulmonary artery during exercise. The hypothesis may also have implications in the etiology of human vascular diseases.