Genetic Correlations Between Systolic and Diastolic Pulmonary Arterial Pressure in Beef Cattle

Abstract Pulmonary hypertension is a historical issue in high elevation beef production and is increasingly occurring in moderate elevation beef finishing systems (i.e., feedlots). Pulmonary arterial pressure (PAP) is the mean pressure (mmHg) measure in the pulmonary artery and is an indicator of pulmonary hypertension. To measure PAP, a certified veterinarian threads a catheter through the jugular vein to the heart and into the pulmonary artery. A total of 3 measures are recorded, including mean pulmonary arterial pressure (mPAP), systolic pulmonary arterial pressure (sPAP), and diastolic pulmonary arterial pressure. Systolic pressure is the pressure in the pulmonary artery during the contraction of the heart, whereas diastolic pressure is the pressure in the pulmonary artery during relaxation of the heart. For cattle living in high elevations, the Beef Improvement Federation Guidelines outline the risk of an individual by accounting for the elevation of the test and range of elevations at which that animal is expected to survive based on mPAP. The objective of this study was to estimate the genetic correlations between systolic and diastolic PAP. The data consisted of 1,352 animals with a mPAP, sPAP, and dPAP measured from 2011 to 2015. The systolic pulmonary arterial pressure has a mean of 65.4 ± 15.95 mmHg. The diastolic pulmonary arterial pressure has a mean of 18.2 ± 11.22 mmHg. Data were analyzed using a multiple trait, mixed effect animal model using the statistical software package ASReml 3.0. Fixed effects in the model included sex, birth year, wean date, and yearling date. Individual animal was included as the random effect. The respective heritabilities from the model were mPAP at 0.13 ± 0.05, sPAP at 0.9 ± 0.05 and dPAP at 0.09 ± 0.05. The phenotypic correlation between systolic and diastolic PAP was 0.18 ± 0.03, and the genetic correlation was 0.46 ± 0.32. The phenotypic correlation between sPAP and mPAP was 0.49 ± 0.02, and the genetic correlation was 0.69 ± 0.21. The phenotypic correlation between dPAP and mPAP was 0.83 ± 0.01, and the genetic correlation was 0.93 ± 0.07. Previous research with sPAP and dPAP has been conducted in humans, investigating methods to predict the likelihood of a person of developing pulmonary hypertension. These results provide a foundation to focus on how sPAP and dPAP impact the mPAP and current selection tools for a PAP measure and if the additional information could be useful for selection.