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Prolactinomas are the most common neuroendocrine tumors of the pituitary and the leading cause of hyperprolactinemia. Dopamine Receptor Agonists (DAs), particularly cabergoline (CAB), effectively reduce prolactin levels and tumor volume, and are therefore the first-line therapy for prolactinomas. With long-term cabergoline use, adverse effects may become more consequential for some patients. Cabergoline-Associated Valvulopathy (CAV) primarily affects the mitral, tricuspid, and aortic valves, although its underlying mechanisms remain unclear. The potential link between CAB use and Valvular Heart Disease (VHD) in patients with prolactinomas remains controversial. This review summarizes current understanding of CAV and explores potential molecular mechanisms, including CAB's modulation of catecholaminergic, serotonergic, and Transforming Growth Factor-beta (TGF-β) related signaling pathways, along with inflammatory pathways. By integrating clinical patterns with mechanistic plausibility, we aim to support practical surveillance decisions and improve the long-term safety of CAB therapy in patients with prolactinomas.