The 2019 ESC guidelines first introduced chronic coronary syndrome (CCS) as a more comprehensive, diagnostically and therapeutically demanding clinical entity than the previous term stable angina pectoris. It includes the clinical presentation of coronary artery disease (CAD) that occurs during a stable period of coronary disease, after or preceding acute coronary syndrome. CCS encompasses various clinical presentations of stable ischemic heart disease. Thanks to new insights into the pathophysiological mechanism of ischemia, CCS is not associated exclusively with obstructive atherosclerotic disease of the epicardial coronary arteries, but also with functional and structural disorders of the microcirculation, vasospasm and endothelial dysfunction, i.e. anginal disorders within the framework of angina/ischemia with no obstructive coronary artery disease (ANOCA/INOCA). Men have about 50% higher risk of developing CCS, but ANOCA/INOCA clinical entities are higher in women. Along with atherosclerotic vascular changes (risk factors: diabetes, arterial hypertension, obesity, dyslipidemia), nonvascular causes of CSS are increasingly being investigated in the pathogenesis of myocardial ischemia, such as myocardial metabolic disorders, coronary flow changes due to platelet activation, microembolization, and endothelial inflammation. According to the 2024 ESC guidelines, there are 5 categories of CSS: patients with proven coronary artery disease and anginal disorders during exercise, patients with anginal disorders (vasospasm or microcirculatory disease) but without obstructive coronary disease (ANOCA/INOCA), patients with stable symptoms after ACS or revascularization, patients with stable symptoms and heart failure of ischemic or cardiometabolic etiology, and the asymptomatic category in which CAD was detected by invasive or noninvasive imaging methods, due to other indications. It is crucial to identify and effectively manage all aspects of Chronic Stable Syndrome (CSS) promptly, as they often go undiagnosed despite causing significant morbidity, reduced quality of life, and cardiovascular complications such as arrhythmias, valvular diseases, heart failure, and major adverse cardiac events (MACE). Although there has been notable progress in understanding the mechanisms behind CSS and in current treatments—including lifestyle modifications—a considerable number of patients, particularly those asymptomatic, remain undetected. Additionally, further clinical research is needed to refine antianginal therapies and invasive coronary procedures, aiming for comprehensive and long-term stabilization of CSS. (