ABSTRACT
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.
ABSTRACT
BACKGROUND: Genetic susceptibility to the development of coronary artery disease (CAD) and myocardial infarction (MI) is well established. However, lack of replication, and difficulty in the identification of specific genes that underlie impressive linkage peaks remain challenges at the molecular level due to the heterogeneity of phenotype and their associated genotypes. We present two cases of first-degree family members of acute myocardial infarction (AMI) having similar clinical and angiographic features of obstructive coronary lesions at same anatomic locations. CASE PRESENTATION: The father presented with significant chest discomfort and loss of consciousness. The electrocardiogram (ECG) showed an acute anterior ST-segment-elevation myocardial infarction (STEMI). Coronary angiogram demonstrated a subtotal occlusion in the mid-left anterior descending (LAD) coronary artery. One week later, the son presented after an in-hospital cardiac arrest with pulseless electric activity preceded by significant chest pain and loss of consciousness. His ECG also showed an acute anterior STEMI. Catheterization revealed strikingly similar angiographic characteristics with his father: subtotal occlusion in the proximal to mid-LAD coronary artery. CONCLUSIONS: More considerations should be given to patients with similar phenotypic characterization in genetic studies of CAD/MI in the future.