Hyperglycemia in the setting of coronary revascularization is associated with increased adverse cardiovascular events in patients with or without diabetes mellitus. Data suggest that acute peri-procedural hyperglycemia causes an increase in inflammation, platelet activity, and endothelial dysfunction and is associated with plaque instability and infarct size. While peri-procedural blood glucose level is an independent predictor of adverse outcomes in patients undergoing coronary revascularization, treatment strategies remain uncertain. Randomized clinical trials of glucose-insulin-potassium infusions have consistently shown no benefit, while those comparing insulin therapy versus standard of care have demonstrated mixed results, likely due to the failure to reach euglycemia with these strategies. Although no glucose-lowering agent has been shown to be superior in peri-procedural glycemic control, the continuation of clinically prescribed long-acting glucose-lowering medications in patients with diabetes mellitus prior to coronary angiography and possible percutaneous coronary intervention may be the simplest and most effective approach to maintain euglycemia and decrease the associated increase in inflammation and platelet activity. However, alternative strategies such as therapies targeted at the underlying mechanism of harm (e.g., more potent anti-platelet therapy, anti-inflammatory therapy) should also be considered and warrant further investigation.

Factors that underlie the clustering of metabolic syndrome traits are not fully known. We performed whole exome sequence analysis in kindreds with extreme phenotypes of early-onset atherosclerosis and metabolic syndrome and identified novel loss-of-function mutations in the gene encoding the pancreatic elastase CELA2A. We further show that CELA2A is a circulating enzyme that reduces platelet hyperactivation, triggers both insulin secretion and degradation, and increases insulin sensitivity. CELA2A plasma levels rise postprandially and parallel insulin levels in humans. Loss of these functions by the mutant proteins provides insight into disease mechanisms and suggests that CELA2A could be an attractive therapeutic target.

Although PCI relieves symptoms, the evidence base indicates that it does not prolong survival in SIHD.