Inflammation amplifies this interplay; MI or HF release proinflammatory cytokines (e.g., IL-6 and TNF-α), triggering pulmonary endothelial injury, macrophage infiltration, and vascular remodeling, as observed in acute respiratory distress syndrome (ARDS) after cardiac insult.207,208 Oxidative stress from the ischemic myocardium generates ROS, further damaging alveolar‒capillary barriers and amplifying hypoxic pulmonary vasoconstriction.209. Here, TNF is linked to acute respiratory distress syndrome.