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Cardiovascular diseases (CVDs) represent a significant global public health challenge. Activation of the NLRP3 inflammasome contributes to CVD pathogenesis, while autophagy mitigates the condition by eliminating harmful metabolites. Furthermore, NLRP3 inflammasome and autophagy co-regulate CVDs by enhancing autophagic processes, inhibiting inflammasome activity, and reducing inflammatory responses, thus playing a pivotal role in the disease's pathophysiology. Certain pharmacological agents have been shown to inhibit NLRP3 inflammasome activity by promoting autophagy, thereby ameliorating disease pathology. This review underscores the critical roles of NLRP3 inflammasome and autophagy in CVDs and examines the regulatory effects of specific drugs on these processes.