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DOI: 10.12201/bmr.202604.00176

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  Abstract: Coronary heart disease is generally classified in traditional Chinese medicine under “chest impediment” and “heart pain.” In clinical practice, it is not only characterized by obstruction of the heart vessels, but is also commonly accompanied by impaired myocardial energy supply, mitochondrial dysfunction, and progressive tissue injury. Earlier interpretations have focused mainly on phlegm turbidity, blood stasis, cold accumulation, and qi stagnation. These views are useful, yet they do not fully explain the chronic, recurrent, and mixed deficiency-excess nature of the disease. The theory of deficient qi retention and stagnation takes deficiency as the root and retention-stagnation as the manifestation. When heart qi is weak and gathering qi is insufficient, propulsion becomes impaired, blood flow slows, and body fluids fail to distribute normally. Over time, phlegm, stasis, turbidity, and toxin may develop internally, eventually obstructing the vessels and depriving the heart of nourishment. Modern studies indicate that AMP-activated protein kinase (AMPK) is a central regulator of myocardial energy sensing and metabolic balance, involved in glucose uptake, fatty acid oxidation, maintenance of mitochondrial homeostasis, and stress adaptation. In coronary heart disease, AMPK-related metabolic disturbance contributes to ischemic myocardial injury and also offers a possible microscopic explanation for the transition from impaired qi movement to endogenous retention and stagnation. On this basis, this paper integrates the theory of deficient qi retention and stagnation with current research on myocardial energy metabolism and AMPK, and proposes a continuous pathodynamic chain of “impaired qi movement–energy imbalance–endogenous retention and stagnation–aggravated injury,” in order to provide a broader theoretical perspective for the prevention and treatment of coronary heart disease with traditional Chinese medicine.

  Key words: coronary heart disease; deficient qi retention and stagnation; AMPK; myocardial energy metabolism; mitochondria

  Submit time: 29 April 2026

  Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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  1	2026-04-01	10.12201/bmr.202604.00176V1	Download

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