Patients with acute myocardial infarction (AMI) often accompanied by admission hyperglycemia, which usually predicts a poor clinical outcomes for non-diabetes mellitus. Appropriate cut-point to identify high risk individuals in these patients remains controversial. One thousand six hundred ninety-eight non-diabetes AMI patients in this retrospective study were divided into 3 groups according to admission glucose levels (euglycemia group≤140 mg/dL, moderate hyperglycemia group 141–179 mg/dL, severe hyperglycemia group≥180 mg/dL). The primary endpoint of this study was all-cause in-hospital mortality rate. In-hospital motality related risk factors was analyzed by multivariate binary logistic regression analyses. All myocardial necrosis markers and Log NT-proBNP in severe hyperglycemia group were significantly higher than those in the other 2 groups. Logistic regression showed that independent predictors of the in-hospital mortality rate in non-diabetic patients with AMI were age (OR = 1.057, 95% CI 1.024–1.091, P < 0.001), logarithm of the N-terminal pro-brain natriuretic peptide (OR = 7.697, 95% CI 3.810–15.550, P < 0.001), insufficient myocardial reperfusion (OR = 7.654, 95% CI 2.109–27.779, P < 0.001), percutaneous coronary intervention (OR = 0.221, 95% CI 0.108–0.452, P < 0.001) and admission glucose (as categorical variable). Patients with moderate hyperglycemia (OR = 1.186, 95% CI 0.585–2.408, P = .636) and severe hyperglycemia (OR = 4.595, 95% CI 1.942–10.873, P = 0.001) had a higher all-cause in-hospital mortality rate compared with those with euglycemia after AMI in non-diabetic patients. The all-cause in-hospital mortality risk increases remarkably as admission glucose levels elevated in non-diabetic patients with AMI, especially in patients with admission glucose levels ≥180 mg/dL. Severe admission hyperglycemia could be regarded as prospective high-risk marker for non-diabetic AMI patients.

The aim of this study is to investigate the inter-scan reproducibility of kinetic parameters in atherosclerotic plaque using dynamic contrast-enhanced (DCE) cardiovascular magnetic resonance (CMR) in a multi-center setting at 3T.

Statin therapy has shown to deplete atherosclerotic plaque lipid content and induce plaque regression. However, how early the plaque lipid depletion can occur with low-density lipoprotein cholesterol (LDL-C) lowering in humans in vivo has not been fully described. We enrolled 43 lipid treatment naïve subjects with asymptomatic carotid atherosclerosis and LDL-C ≥ 100 and ≤ 250 mg/dl. Rosuvastatin 5–20 mg/day was used to lower LDL-C levels to < 80 mg/dl. Lipid profile and carotid MRI scans were obtained at baseline, 3, 12, and 24 months. Carotid plaque lipid-rich necrotic core (LRNC) and plaque burden were measured and compared between baseline and during treatment. Among the 32 subjects who completed the study, at 3 months, an average dose of rosuvastatin of 11 mg/day lowered LDL-C levels by 47% (125.2 ± 24.4 mg/dl vs. 66.7 ± 17.3 mg/dl, p < 0.001). There were no statistically significant changes in total wall volume, percent wall volume or lumen volume. However, LRNC volume was significantly decreased by 7.9 mm³, a reduction of 7.3% (111.5 ± 104.2 mm³ vs. 103.6 ± 95.8 mm³, p = 0.044). Similarly, % LRNC was also significantly decreased from 18.9 ± 11.9% to 17.9 ± 11.5% (p = 0.02) at 3 months. Both LRNC volume and % LRNC continued to decrease moderately at 12 and 24 months, although this trend was not significant. Among a small number of lipid treatment naïve subjects, rosuvastatin therapy may induce a rapid and lasting decrease in carotid plaque lipid content as assessed by MRI. ClinicalTrials.Gov numbers NCT00885872