Atherosclerosis, a condition characterized by the accumulation of lipids and a culprit behind cardiovascular events, has long been studied. However, in recent years, there has been an increase in interest in its initiation, with researchers shifting focus from traditional pathways involving the vascular infiltration of oxidized lipids and towards the novel presence of chronic inflammatory pathways. The accumulation of pro-inflammatory cytokines, in combination with the activation of transcription factors, creates a positive feedback loop that drives the creation and progression of atherosclerosis. From the upregulation of the nod-like receptor protein 3 (NLRP3) inflammasome and the Notch and Wnt pathways to the increased expression of VEGF-A and the downregulation of connexins Cx32, Cx37, and Cx40, these processes contribute further to endothelial dysfunction and plaque formation. Herein, we aim to provide insight into the molecular pathways and mechanisms implicated in the initiation and progression of atherosclerotic plaques, and to review the risk factors associated with their development.

Hypertrophic cardiomyopathy is the most prevalent inherited cardiac condition, distinguished by an autosomal dominant inheritance pattern. Diagnosis can be achieved through echocardiography, cardiac magnetic resonance imaging, and genetic testing. Recently, significant advancements have occurred in pharmacological and invasive therapies that are transforming the management of hypertrophic cardiomyopathy, including the introduction of cardiac myosin inhibitors, radiofrequency ablation, and gene editing. Additional trials are being conducted on investigational therapies, with the results anticipated in the near future. This review aims to provide a concise overview of both currently approved and investigational treatments for hypertrophic cardiomyopathy.