Recent genome-wide association studies have implicated both cardiac and pulmonary vein-related genes in the pathogenesis of asthma. Since cardiac cells are not present in lung airways or viewed to affect the immune system, interpretation of these findings in the context of more well-established contributors to asthma has remained challenging. However, cardiomyocytes are present in the lung, specifically along pulmonary veins, and recent murine models suggest that cardiac cells lining the pulmonary veins may contribute to allergic airway disease. Notably, the cardiac cell-junction protein αT-catenin (αT-cat, CTNNA3), which is implicated in occupational and steroid-resistant asthma by clinical genetic data, appears to play an important role in regulating inflammation around the cardiac cells of pulmonary veins. Beyond the potential contribution of pulmonary veins, clinical data directly examining cardiac function through echocardiography have found strong associations between asthmatic phenotypes and the mechanical properties of the heart. Together, these data suggest that targeting the function of cardiac cells in the pulmonary veins and/or heart may allow for novel and potentially efficacious therapies for asthma, particularly in challenging cases of steroid-resistant asthma.