Pathogenesis, histopathology, and mechanisms of pulmonary pathology secondary to chronic left heart failure in animals.

The pulmonary consequences of congestive heart failure in domestic animals, particularly from clinical and gross morphologic perspectives, have been described. However, the full spectrum of mechanistic and microscopic alterations, especially at the molecular and cellular levels, remains less well integrated in the context of veterinary pathology. We examine the pathogenesis and consequences of pulmonary hypertension secondary to left heart failure, in which chronic elevation of hydrostatic pressure triggers complex molecular, physiologic, and morphologic responses. These include the epithelial and endothelial stress response, molecular signaling, and interstitial remodeling. Although pulmonary edema is often referred to as the ultimate consequence of pulmonary venous hypertension, other critical yet underappreciated aspects also exist, such as pulmonary remodeling. We also explore the molecular mechanisms that can be activated during venous hypertension, offering a framework for understanding the continuum from reversible congestion to irreversible parenchymal injury. Describing the physiologic and morphologic patterns associated with cardiogenic lung disease not only enhances diagnostic precision, but also promotes a shared vocabulary for use among pathologists, clinicians, and cardiologists.