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The state of vascular endothelial damage caused by multiple risk factors is the pathological basis for the development of coronary heart disease (CHD). It persists throughout the course of disease. Toxic pathogen theory, which is based on the pathogenic characteristics of toxic pathogen, combined with the pathological progress of CHD, states that toxic pathogen is the key factor of vascular endothelial injury, ranging from potential toxic pathogens to apparent toxic pathogens. This is a complex dynamic process in which the heart vessel is the location of disease. In the chronic stable phase, "potential toxic pathogen hiding in the blood vessel" is the core pathogenic factor. Specifically, toxic factors gradually accumulate and hide in the blood vessel, corresponding to the abnormal expression of risk factors and related pathological factors, which chronically and insidiously damage the vascular endothelium and are the initiating factors of the disease. In the acute attack phase, apparent toxic pathogen damaging the blood vessel is the core pathogenesis factor. Specifically, the toxic pathogen is persistent and difficult to resolve and will damage the blood vessel, representing an episodic cardiovascular event based on the pathology of vulnerable plaques, and acute toxic pathogen can damage the vascular endothelium, which is a sign of deterioration of the disease. According to the appearance of toxic pathogen, different treatments should be given in different stages of CHD. The treatment of CHD in the stable stage focuses on reinforcing healthy qi to eliminate pathogenic factors to help to eliminate the pathological factors in the blood vessels and eliminate the source of the formation of toxic pathogen. The treatment of CHD in the unstable stage focuses on attacking and removing toxins to eliminate the tangible pathological evil and relieve the substantial damage to the blood vessels by the pathological entity. It has been found that herbal treatments under the guidance of toxic pathogen theory have shown great endothelial protective effects, thus improving CHD. [ABSTRACT FROM AUTHOR]