In recent years, numerous large-scale clinical trials have demonstrated that sodium-glucose cotransporter (SGLT) 2 inhibitors provide cardiovascular and renal protection regardless of diabetes status. Although SGLT1 is recognized as another primary isoform of SGLT, its precise role remains elusive. SGLT2 is highly expressed in the kidneys where it modulates glucose reabsorption, whereas SGLT1 is mainly expressed in the intestinal epithelium where it regulates dietary glucose uptake. Unlike SGLT2, which is minimally present in the heart, SGLT1 is abundantly expressed in the myocardium. SGLT1 may play a unique and supplementary role in glucose homeostasis. Thus, the targeting SGLT1 for inhibition could offer therapeutic benefits. During the early stages of cardiac injury, SGLT1 expression is considerably increased, ensuring an adequate energy supply to cardiac cells. However, preclinical research has indicated that prolonged SGLT1 overexpression may negatively affect the heart by triggering pathological mechanisms, such as cardiac inflammation, oxidative stress, fibrosis, apoptosis, and mitochondrial dysfunction. Thus, inhibiting SGLT1 could offer additional benefits beyond its effects on glucose absorption. Numerous clinical studies have demonstrated that SGLT1 inhibitors substantially benefit cardiovascular health by reducing the risks of cardiovascular mortality and hospitalization for heart failure (HF), regardless of the presence of diabetes or HF. Although the precise mechanisms underlying these beneficial effects are not fully understood, genetic models suggest that the malfunction of SGLT1 transporters adversely affects various tissues. This review explores both the positive and negative effects of SGLT1 inhibition on the heart. In addition, this review discusses potential mechanisms through which SGLT1 inhibition may confer cardiovascular protection on the basis of a thorough analysis of the fundamental research on SGLT1.