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 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.

Two weeks post-operative ultrasound examination of radio-cephalic arteriovenous fistulae to predict maturity in a Chinese population.

AIM: The aim of this study was to assess the accuracy of post-operative ultrasound examination for predicting wrist radio-cephalic arteriovenous fistula maturity. METHODS: All radio-cephalic arteriovenous fistulas performed in our hospital between October 2015 and December 2017 were included in this study. Ultrasound examination of radio-cephalic arteriovenous fistulas was performed 2 weeks post-surgery. Radio-cephalic arteriovenous fistula maturation was defined as successful cannulation of a fistula with two needles, delivery of blood via the access route at a flow rate ⩾200 mL/min for 4 h, and dialysis via fistulae in at least six consecutive sessions. RESULTS: Eighty-two wrist radio-cephalic arteriovenous fistulas were analyzed, of which 13 failed. Cephalic vein diameter >4.285 mm and brachial artery peak systolic velocity >134.75 cm/s were the best post-operative ultrasound predictors of radio-cephalic arteriovenous fistula maturity (p < 0.001 and p = 0.011, respectively). Receiver-operating characteristic curve analysis showed that the sensitivity and specificity of predicting radio-cephalic arteriovenous fistula maturation were 88.4% and 92.3% for cephalic vein diameter (area under the curve = 0.939), respectively, and 82.9% and 76.9% for brachial artery peak systolic velocity (area under the curve = 0.830), respectively. All assessments predicted radio-cephalic arteriovenous fistula maturity (post-operative positive predictive values: cephalic vein diameter = 98.4%, brachial artery peak systolic velocity = 95%) much better than radio-cephalic arteriovenous fistula failure (post-operative negative predictive values: cephalic vein diameter = 60%, brachial artery peak systolic velocity = 45.5%). CONCLUSION: Two weeks after surgery, a new wrist radio-cephalic arteriovenous fistula with a cephalic vein diameter >4.285 mm was considered suitable for dialysis. A high-risk arteriovenous fistula failure would benefit from early intervention.

The serum anion gap is associated with disease severity and all-cause mortality in coronary artery disease.

OBJECTIVE: To evaluate the associations between the serum anion gap (AG) with the severity and prognosis of coronary artery disease (CAD). METHODS: We measured serum electrolytes in 18,115 CAD patients indicated by coronary angiography. The serum AG was calculated according to the equation: AG = Na+[(mmol/L) + K+ (mmol/L)] - [Cl- (mmol/L) + HCO3- (mmol/L)]. RESULTS: A total of 4510 (24.9%) participants had their AG levels greater than 16 mmol/L. The serum AG was independently associated with measures of CAD severity, including more severe clinical types of CAD (P < 0.001) and worse cardiac function (P = 0.004). Patients in the 4th quartile of serum AG (≥ 15.92 mmol/L) had a 5.171-fold increased risk of 30 days all-cause death (P < 0.001). This association was robust, even after adjustment for age, sex, evaluated glomerular filtration rate [hazard ratio (HR): 4.861, 95% confidence interval (CI): 2.150-10.993, P < 0.001], clinical diagnosis, severity of coronary artery stenosis, cardiac function grades, and other confounders (HR: 3.318, 95% CI: 1.76-2.27, P = 0.009). CONCLUSION: In this large population-based study, our findings reveal a high percentage of increased serum AG in CAD. Higher AG is associated with more severe clinical types of CAD and worse cardiac function. Furthermore, the increased serum AG is an independent, significant, and strong predictor of all-cause mortality. These findings support a role for the serum AG in the risk-stratification of CAD.

Association of dysglycemia and all-cause mortality across the spectrum of coronary artery disease.

OBJECTIVE: To assess the association between fasting plasma glucose (FPG) and all-cause mortality across the spectrum of coronary artery disease (CAD). PATIENTS AND METHODS: The study included 18,999 patients during a study period of April 1, 2004, through October 31, 2010. The primary end points were in-hospital and follow-up all-cause mortality. According to the quartiles of FPG levels, patients were categorized into 4 groups: quartile 1, less than 5.1 mmol/L; quartile 2, 5.1 to less than 5.9 mmol/L; quartile 3, 5.9 to less than 7.5 mmol/L; and quartile 4, 7.5 mmol/L or greater. The conversion factor for units of plasma glucose is 1.00 mmol/L equals 18 mg/dL. Presented as mg/dL, the 4 quartile ranges of plasma glucose concentrations used in our data analysis are ≤90.0 mg/dL, 90.1-106.0 mg/dL, 106.1 mg/dL-135.0 mg/dL and ≥135.1 mg/dL. Quartile 1 was recognized as the lower glycemic group, quartiles 2 and 3 as the normoglycemic groups, and quartile 4 as the higher glycemic group. RESULTS: In patients with acute myocardial infarction, all-cause mortality for the dysglycemic groups was higher than for the normoglycemic groups: in-hospital mortality for quartiles 1, 2, 3, and 4 was 1.0%, 0.9%, 0.2%, and 1.5%, respectively (P=.001); follow-up mortality for quartiles 1, 2, 3, and 4 was 1.7%, 0.9%, 0.3%, and 1.8%, respectively (P<.001). In patients with stable CAD, no significant differences in mortality were found among groups. However, in patients with unstable angina pectoris, the normoglycemic groups had lower follow-up mortality and roughly equal in-hospital mortality compared with the dysglycemic groups. After adjusting for confounding factors, this observation persisted. CONCLUSION: The association between lower FPG level and mortality differed across the spectrum of CAD. In patients with acute myocardial infarction, there was a U-shaped relationship. In patients with stable CAD or unstable angina pectoris, mildly to moderately decreasing FPG level was associated with neither higher nor lower all-cause mortality.

The natural course of traumatic myocardial infarction in a young patient with angiographically normal coronary arteries.

A 23-year-old man with no history of heart disease was admitted to Beijing Anzhen Hospital Affiliated to Capital Medical University for an abnormal electrocardiogram of ST-T changes mimicking myocardial infarction. Catheterization revealed normal coronary and peripheral arteries. The echocardiogram and delayed enhancement cardiovascular magnetic resonance imaging indicated a markedly reduced left ventricular function and enlarged left ventricular cavity with evidence of fibrous tissue. Given the patient's history of multiple blunt trauma 7 years previously and acute myocardial infarction diagnosis at that time, he was diagnosed with traumatic myocardial infarction (TMI). We describe the natural course of such a patient with TMI. There is a possibility of spontaneous healing of coronary artery dissection induced by trauma. Although early revascularization may be helpful for preventing cardiac remodeling after TMI in some cases, more data are needed to compare the long-term outcome among different interventions in large sample cases.