Glycaemic Control in Patients Undergoing Percutaneous Coronary Intervention: What Is the Role for the Novel Antidiabetic Agents? A Comprehensive Review of Basic Science and Clinical Data

Figures

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  Figure 1. Pathophysiological mechanisms of hyperglycaemia-induced vascular damage. AGE, advanced glycation end products; PKC, protein kinase C; e-NOS, endothelial nitric oxide synthase; VEGF, vascular endothelial grow factor; ICAM-1, intercellular adhesion molecule-1; VCAM-1, vascular cell adhesion molecule-1; PUMA, p53 upregulated modulator of apoptosis; PTEN, phosphatase and TENsin homolog deleted on chromosome 10; TIGAR, TP53-Induced Glycolysis and Apoptosis Regulator; NO, nitric oxide; TxA2, Thromboxane A2; TF, tissue factor; GP, glycoprotein; MAPK, mitogen-activated protein kinase; BMK, big MAPK; PI3K, Phosphoinositide 3-kinases; NF-kB, nuclear factor kappa B; IRS-1, insulin receptor substrate 1; KLF-4, Kruppel Like Factor 4; ERK, extracellular signal-regulated kinase; BCL, B-cell lymphoma; Bft, Bacteroides fragilis toxin; MAC, membrane attack complex; LFA-1, lymphocyte function-associated antigen 1; MCP-1, monocyte chemoattractant protein-1; IL, interleukin; TNF, tumour necrosis factor.

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  Figure 2. Peri-procedural and long-term stent-related complications favored by an abnormal glycaemic status.

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  Figure 3. Potential mechanisms of benefit of novel antidiabetic agents in the setting of PCI. PCI, percutaneous coronary intervention; GLP-1 RAs, glucagon-like peptide 1 receptor agonist; DPP4i, dipeptidyl peptidase-4 inhibitors; SGLT-2i, sodium-glucose cotransporter-2 inhibitors; NO, nitric oxide; ROS, reactive oxygen species; EPCs, endothelial progenitor cells; MMPs, matrix metalloprotease; VSMCs, vascular smooth muscular cell.