从“痰挟瘀血，遂成窠囊”探析急性心肌梗死进程中免疫炎症与NLR的演变及干预策略

[中图分类号］R259.422 [文献标志码]A [文章编号」0257-358X（2026）04-0352-09

AbstractThe occurnce and development of acute myocardial infarction（AMI）are closely related to the dynamic evolutionof immune inflammation.The neutrophil-lymphocyte ratio（NLR），asa novel indicator reflecting the balance of immune inflammation，，holdssignificant value in assessng the occurrence and progression of AMI.However，the intrinsic relationship between NLR abnormalitiesand theunderlying immune

inflammatoryimbalance，aswell asitsdynamic evolution during the course of AMI，remains to be furtherelucidated.Guided bythe theoryof“phlegm combined with blood stasis forming the Ke’nang（a pathological lesion characterized by coagulated phlegm and blood stasis）”，this article focuses on the high consistency in the pathological essence between the

“Ke'nang”and the“immune inflammation-thrombosis”network from the perspectiveof the interaction between thepathogenesisof deficiencyof healthy qi with phlegmand bloodstasis，andimmune inflammation，and explores the associations between them and the occurrence and development of AMI.The dynamic imbalance of immune inflammation is the microscopic manifestationof the pathogenesis of deficiencyof healthy qi with phlegmandblood stasis，andabnormal NLR canserveasa potential microscopic indicator for identifying this pathogenesis and judging the prognosis.Based on this，a therapeutic strategy centered on regulating qi， activating blood circulation，resolving phlegm，andeliminatingblood stasisis furtherproposed forthecritical stageof theacute phase of AMIcharacterized by the binding of phlegmand blood stasisand the formation of the Ke'nang，offering new insights for the clinical diferentiation and treatment of AMI.

Keywordsacute myocardial infarction（AMI）；immune inflammation ;neutrophil-lymphocyte ratio（NLR）; deficiency of healthy qi with phlegm and blood stasis;Ke'nang

急性心肌梗死（AMI是一种严重危害人类健康的心血管急症，其发生过程如下：在冠状动脉粥样硬化的基础上，经多种代谢性危险因素长期作用，冠状动脉内膜受损、脂质沉积形成斑块；由某些因素触发，斑块破裂，血小板大量活化、黏附、聚集，形成血栓；血栓阻塞冠状动脉管腔，导致冠状动脉血供急剧减少或中断，相应心肌出现缺血性损伤，进而发展为心肌坏死。（剩余16510字）