*2.1.2 Pathophysiology*

CCS is a condition involving the relative stability of coronary atherosclerotic plaques, in the absence of an acute atherothrombotic event caused by plaque rupture or erosion. When progressive atherosclerotic plaques cause significant narrowing of the lumen of the coronary arteries (usually above 70% of the lumen diameter), symptoms can be present, most typically angina/shortness of breath during physical exertion and relief at rest [2].

When the lumen of a coronary artery is narrowed, the myocardial perfusion by this vessel is significantly reduced. Especially during physical exertion, the oxygen supply to the heart muscle is impaired while the oxygen demand increases. With this supply–demand imbalance, the heart muscle must depend on anaerobic metabolism to ensure normal function. It is anaerobic metabolic products such as LDH and adenosine that cause chest pain by stimulating the nerve endings of the coronary system. The long-term consequences of this ischemic heart condition are angina attacks during physical exertion, seriously affecting the quality of life as well as the patient's psyche; it may cause impaired LV function and risk of arrhythmias [3]. In addition to the main cause of myocardial hypoxia due to atherosclerosis which causes the narrowing of the coronary vessels, other factors such as vasospasm, especially small blood vessels, anemia, and decreased blood oxygen are also important causes of angina [4]. Factors affecting myocardial oxygen demand are heart rate, myocardial contractility, preload, and afterload. The increase in these factors increases the oxygen demand of the heart muscle and affects myocardial ischemia. Therefore, for the treatment of CCS, increased supply and/or decrease in myocardial oxygen demand along with antiplatelet therapy are core issues [1]*.*
