<p>Cardiovascular diseases (CVDs) remain the major cause of morbidity and mortality amongst people of all ages across the world. Research suggests that the initiation and progression of CVDs are associated with antibiotic-induced gut dysbiosis. Antibiotics are primarily intended to be used to treat bacterial infections, which can alter gut microbiota (GM) composition, by lowering the abundance of beneficial bacteria, like <i>Firmicutes</i>,<i> Bacteroidetes</i>, and increasing the profusion of <i>Enterobacteriaceae</i>, leading to harm on gut health. Additionally, it reduces short-chain fatty acids (SCFAs) and bile acid metabolism, increases trimethylamine N-oxide (TMAO) production, intestinal permeability allowing lipopolysaccharide (LPS) and TMAO into systemic circulation. SCFAs play a key role in lipid metabolism, inflammation, and strengthening of the intestinal barrier, and participate in CVDs through FFAR2 and FFAR3 receptors, whereas dysbiosis reduces SCFAs levels and worsens these effects. TMAO enhances oxidative stress, inflammation, endothelial dysfunction, and cholesterol dysregulation, thus worsening CVDs. Furthermore, LPS develops systemic inflammation, insulin resistance, and endothelial dysfunction by activating the NF-κB pathway. Dysbiosis also affects bile acid synthesis, disrupting lipid and glucose metabolism, further participating in the progression of CVDs. This article aims to explore the role of gut dysbiosis in various CVDs, including congenital heart disease, hypertension, valvular heart disease, coronary heart disease, and heart failure. Furthermore, this article aims to bridge the knowledge gap regarding the gut-heart axis by exploring how antibiotics alter the gut microbiota homeostasis, further contributing to the development of CVDs and therapeutic interventions that reduce cardiovascular risks and restore the gut microbiota homeostasis.</p>