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OBJECTIVETo investigate the risk of acute myocardial infarction (AMI) following stress hyperglycemia after hip fracture.RESEARCH DESIGN AND METHODSFrom February 2007 to February 2012, we carried out a prospective observational analysis of 1,257 consecutive patients with no history of diabetes who suffered hip fractures. Fasting blood glucose (FBG) and glycosylated hemoglobin tests as well as electrocardiography, ultrasonic cardiography, and chest X-ray examinations were performed after admission. All selected hip fracture patients were divided into stress hyperglycemia and non-hyperglycemia groups according to their FBG, and the incidence of AMI was monitored.RESULTSAmong the patients enrolled, the frequency of stress hyperglycemia was 47.89% (602/1,257) and that of AMI was 9.31% (117/1,257), and the occurrence of AMI in the stress hyperglycemia group was higher than in the non-hyperglycemia group (12.46 vs. 6.41%, P < 0.05). In the stress hyperglycemia patients, FBG reached maximum levels at 2–3 days after hip fractures and then decreased gradually. The AMI incidence (62.67% [47/75]) of the stress hyperglycemia group was highest in the initial 3 days after hip fracture, significantly coinciding with the FBG peak time (P < 0.05). In all patients with AMI, non–ST-segment elevation myocardial infarction occurred more often than ST-segment elevation myocardial infarction (62.39% [73/117] vs. 37.61% [44/117]).CONCLUSIONSStress-induced hyperglycemia after hip fracture increased the risk of AMI.

The importance of monocyte/lymphocyte ratio (MLR) has been indicated in the initiation and progression of coronary artery disease. However, few previous researches demonstrated the relationship between MLR and plaque vulnerability. We aimed to investigate coronary non-culprit plaque vulnerability in patients with acute coronary syndrome (ACS) by optical coherence tomography (OCT). A total of 72 ACS patients who underwent coronary angiography and OCT test in Beijing Anzhen Hospital were included in this retrospective study. The plaque vulnerability and plaque morphology were assessed by OCT. The non-culprit plaque in high MLR group exhibited more vulnerable features, characterizing as thinner thickness of fibrous cap ( P = .013), greater maximum lipid core angle ( P = .010) and longer lipid plaque length ( P = .041). A prominently negative liner relation was found between MLR and thickness of fibrous cap (R = –0.225, P = .005). Meanwhile, the proportion of OCT-detected thin cap fibro-atheroma (TCFA) ( P = .014) and plaque rupture ( P = .017) were higher in high MLR group. Most importantly, multivariable logistic regression analysis showed MLR level was identified as an independent contributor to the presence of TCFA (OR:3.316, 95%: 1.448–7.593, P = .005). MLR could differentiate TCFA with a sensitivity of 60.0% and a specificity of 85.1%. Circulating MLR level has potential value in identifying the presence of vulnerable plaque in patients with ACS. MLR, as a non- invasive biomarker of inflammation, may be valuable in revealing plaque vulnerability.