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Effects and mechanisms of glucose-insulin-potassium on post-procedural myocardial injury after percutaneous coronary intervention

OBJECTIVE: To evaluate the effects and mechanisms of glucose-insulin-potassium (GIK) on post-procedural myocardial injury (PMI) after percutaneous coronary intervention (PCI). METHODS: A total of 200 non-diabetic patients with documented coronary heart disease (CHD) were divided into the Group GIK a...

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Detalles Bibliográficos
Autores principales: HAO, Yi-Dan, HAO, Peng, WANG, Zheng, ZHAO, Ying-Xin, ZHOU, Zhi-Ming, LIU, Yu-Yang, JIA, De-An, HAN, Hong-Ya, HU, Bin, SHEN, Hua, GAO, Fei, PAN, Guo-Zhong, GUO, Zhen-Feng, YANG, Shi-Wei, ZHOU, Yu-Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Science Press 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7568045/
https://www.ncbi.nlm.nih.gov/pubmed/33117419
http://dx.doi.org/10.11909/j.issn.1671-5411.2020.09.004
Descripción
Sumario:OBJECTIVE: To evaluate the effects and mechanisms of glucose-insulin-potassium (GIK) on post-procedural myocardial injury (PMI) after percutaneous coronary intervention (PCI). METHODS: A total of 200 non-diabetic patients with documented coronary heart disease (CHD) were divided into the Group GIK and Group G, with 100 patients in each group. Patients in Group G were given intravenous infusion of glucose solution 2 hours before PCI. As compared, patients in Group GIK were given GIK. RESULTS: Both post-procedural creatine phosphokinase isoenzyme MB (CK-MB; 62.1 ± 47.8 vs. 48.8 ± 52.6 U/L, P = 0.007) and cTnI (0.68 ± 0.83 vs. 0.19 ± 0.24 ng/mL, P < 0.001) in Group GIK were significantly higher than those in Group G. In Group G, 9.0% and 4.0% of patients had post-procedural increases in CK-MB 1-3 times and > 3 times, which were significantly lower than those in Group GIK (14.0% and 7.0%, respectively; all P values < 0.01); 13.0% and 7.0% of patients had post-procedural increases in cTnI 1-3 times and > 3 times, which were also significantly lower than those in Group GIK (21.0% and 13.0%, respectively; all P < 0.001). Pre-procedural (10.2 ± 4.5 vs. 5.1 ± 6.3, P < 0.001) and post-procedural rapid blood glucose (RBG) levels (8.9 ± 3.9 vs. 5.3 ± 5.6, P < 0.001) in Group G were higher than those in Group GIK. In adjusted logistic models, usage of GIK (compared with glucose solution) remained significantly and independently associated with higher risk of post-procedural increases in both CK-MB and cTnI levels > 3 times. Furthermore, pre-procedural RBG levels < 5.0mmol/L were significantly associated with higher risk of post-procedural increases in both CK-MB and cTnI levels. CONCLUSIONS: In non-diabetic patients with CHD, the administration of GIK may increase the risk of PMI due to hypoglycemia induced by GIK.