The kynurenine pathway (KP) plays a crucial role in tryptophan metabolism, with its downstream metabolites involved in various physiological and pathological processes. Indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO) are the initial enzymes of the KP, with IDO being particularly significant in cardiovascular diseases. Elevated concentrations of KP metabolites, such as kynurenine (KYN) and 3-hydroxykynurenine, have been observed in plasma across conditions like atherosclerosis, hypertension, and acute myocardial infarction. KYN and its metabolites exhibit complex roles in inflammation, acting both as inhibitors and stimulators of inflammatory responses. In atherosclerosis, upregulation of IDO stimulates KYN production, exacerbating vascular inflammation and foam cell formation. Conversely, in arterial calcification, KYN-mediated AhR activation alleviates osteogenic differentiation of vascular smooth muscle cells. In cardiac remodeling, KYN-AhR activation worsens pathological left ventricular hypertrophy and fibrosis. Interventions targeting components of the KP, such as IDO inhibitors and downstream metabolites, show cardiovascular protective effects. This review highlights the mechanistic roles of the KP in coronary atherosclerosis, arterial calcification, and myocardial diseases, emphasizing its potential diagnostic, prognostic, and therapeutic value in cardiovascular diseases.The kynurenine pathway (KP) plays a crucial role in tryptophan metabolism, with its downstream metabolites involved in various physiological and pathological processes. Indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO) are the initial enzymes of the KP, with IDO being particularly significant in cardiovascular diseases. Elevated concentrations of KP metabolites, such as kynurenine (KYN) and 3-hydroxykynurenine, have been observed in plasma across conditions like atherosclerosis, hypertension, and acute myocardial infarction. KYN and its metabolites exhibit complex roles in inflammation, acting both as inhibitors and stimulators of inflammatory responses. In atherosclerosis, upregulation of IDO stimulates KYN production, exacerbating vascular inflammation and foam cell formation. Conversely, in arterial calcification, KYN-mediated AhR activation alleviates osteogenic differentiation of vascular smooth muscle cells. In cardiac remodeling, KYN-AhR activation worsens pathological left ventricular hypertrophy and fibrosis. Interventions targeting components of the KP, such as IDO inhibitors and downstream metabolites, show cardiovascular protective effects. This review highlights the mechanistic roles of the KP in coronary atherosclerosis, arterial calcification, and myocardial diseases, emphasizing its potential diagnostic, prognostic, and therapeutic value in cardiovascular diseases.