Admission Heart Rate and Mortality in Critically Ill Patients with Acute Aortic Dissection.

The association between admission heart rate (HR) and the mortality of critically ill patients with acute aortic dissection (AAD) remains unclear.The data were extracted from the Medical Information Mart for Intensive Care (MIMIC-III) database. Cox regression models and Kaplan-Meier (KM) survival curve were used to explore the association between admission HR and 90-day, 1-year, and 3-year mortality in patients with AAD. Sensitivity analyses were conducted to assess potential bias.A total of 374 eligible AAD patients were included and divided in 4 groups according to admission HR (HR ≤ 70, 71-80, 81-90, and > 90 beats per minute (bpm) ). The patients with AAD in the group with HR > 90 bpm had higher 90-day, 1-year, and 3-year mortality than those in the groups with HR ≤ 70, 71-80, and 81-90 bpm. After adjusting for age, sex, BMI, systolic blood pressure, diastolic blood pressure, SOFA score, SAPSII score, Stanford type, hypertension, coronary artery disease, liver disease, atrial fibrillation, valvular disease, intensive care unit mechanical ventilation, aortic surgery, and thoracic endovascular aortic repair, patients with admission HR > 90 bpm had a higher risk of 90-day, 1-year, and 3-year mortality [adjusted hazard ratio, 95% confidence interval, 5.14 (2.22-11.91) P < 0.001; 4.31 (2.10-8.84) P < 0.001; 3.01 (1.66-5.46) P < 0.001] than those with HR 81-90 bpm. The 90-day, 1-year, and 3-year mortality were similar among the groups with HR ≤ 70, 71-80, and 81-90 bpm.Admission HR > 90 bpm was independently associated with all-cause mortality in critically ill AAD patients, either type A or B aortic dissection.

A Simple Scoring System for Quick, Accurate, and Reliable Early Diagnosis of Hand, Foot, and Mouth Disease.

BACKGROUND To construct an accurate, reliable, and simple scoring system of improving HFMD diagnosis. MATERIAL AND METHODS Based on the following 3 steps, a simple scoring diagnostic system was built: (1) we selected basic markers (age and sex), markers recommended in HFMD diagnosis guidelines, and significant biomarkers among severity groups found in a large dataset; (2) we used positive constituent ratio for determining scores of each marker; and (3) we applied receiving operating curve in an external dataset to determine the optimal cut-off score. RESULTS The selected markers were sex, age, fever, skin rashes, nervous system disorder, respiratory system disorder, digestive system disorder and cardiopulmonary complications, C-reactive-protein, White Blood Cell, Creatinine Kinase, Creatinine Kinase Isoenzyme, Gamma-Glutamyl Transpeptidase, Albumin, Globulin, Albumin/Globulin Ratio, Natrium, Chloride, Calcium, and Glucose. A simple scoring system with 3.9684 as the lower cut-off was constructed. The AUC was 0.918 (95% CI: 0.874-0.963, P<0.01). The sensitivity, specificity, and Youden Index, which were based on the validation dataset of 200 subjects (80 cases, 120 non-cases with skin rashes or fever), were 0.95, 0.90, and 0.85, respectively. CONCLUSIONS This simple scoring system is an effective method to diagnose HFMD.

Myocardia ischemia associated with a myocardial bridge with no significant atherosclerotic stenosis.

BACKGROUND: Myocardial bridge refers to the myocardial tissue with which the coronary artery is partly covered. Though it has long been regarded to be benign, patients with myocardial bridges may present with myocardial ischemia, acute coronary syndromes, coronary spasm, sudden cardiac arrest or even sudden death. CASE PRESENTATION: In present study, we reviewed four cases with myocardial bridge and no stenosis of coronary artery, which included acute coronary syndrome and sudden cardiac arrest. CONCLUSIONS: These cases indicated that cardiac events in patients with myocardial bridge may be associated with coronary spasm, myocardial supply/demand mismatch or cardiac arrest.

Association of Impaired Fasting Blood Glucose With Triple Coronary Artery Stenosis and Myocardial Infarction Among Patients With Coronary Artery Stenosis.

Background: The association between impaired fasting glucose level (IFG) and coronary heart disease (CAD) remain controversial. In the present study, we sought to ascertain a relationship of IFG with the number of diseased coronary artery and occurrence of myocardial infarction, among CAD cases. Methods: We studied 1,451 consecutive no-diabetic patients who underwent coronary angiography at the First Affiliated Hospital of Shantou University Medical College in Southern China. Demographic, biochemical, clinical and angiographic data were collected. Results: The prevalence of IFG was higher in patients with angiographically confirmed CAD than in subjects without angiographic evidence of CAD (33.4 versus 28.2%, p = 0.034). Compared with CAD cases without IFG, CAD cases with IFG had a higher odds ratio (OR) of having triple-vessel disease as opposed to having single- or double-vessel disease [OR = 1.53, 95% confidence interval (CI) = 1.13-2.07]. Furthermore, the occurrence of MI was higher in CAD cases with IFG than in CAD cases without IFG (OR = 1.73, 95% CI = 1.27-2.36). Conclusions: There is an association between IFG and a predisposition to severe CAD indicated by triple vessel disease or myocardial infarction.

Effects of osteopontin on functional activity of late endothelial progenitor cells.

The aim of this study is to investigate the effect of osteopontin (OPN) on functional activity of late endothelial progenitor cells (EPCs). Total mononuclear cells (MNCs) were isolated from human umbilical cord blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture plates. Late EPCs were positive for both 1,1-dioctadecyl-3,3,3,3-tetramethylindocarbocyanine-labeled acetylated low-density lipoprotein (DiI-acLDL) and fluorescein-isothiocyanate-conjugated Ulex europaeus agglutinin lectin (UEA-1). Expression of von Willbrand factor (vWF) and kinase insert domain receptor (KDR) were detected by indirect immunofluorescence staining. Late EPCs of 3-5 passages were treated for 24 h with OPN (to make a series of final concentration: 0.005 µg/ml, 0.01 µg/ml, 0.05 µg/ml, 0.5 µg/ml, 2.5 µg/ml), or vehicle control. The proliferation, migration, and in vitro vasculogenesis activity of late EPCs were assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, modified Boyden chamber assay and an in vitro angiogenesis assay, respectively. Late EPCs adhesion assay was performed by replating cells on fibronectin-coated plates, and then adherent cells were counted. Incubation with OPN dose-dependently inhibited the proliferative, adhesive, and in vitro vasculogenesis capacity and increased migratory activity of late EPCs.

Nicotine improves the functional activity of late endothelial progenitor cells via nicotinic acetylcholine receptors.

The aim of this study is to investigate whether nicotinic acetylcholine receptors (nAChRs) are involved in the modulation of functional activity of late endothelial progenitor cells (EPCs) induced by nicotine. Total mononuclear cells (MNCs) were isolated from human umbilical cord blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture plates. Late EPCs were positive for 1,1-dioctadecyl-3,3,3,3-tetramethylindocarbocyanine-labeled acetylated low-density lipoprotein (DiI-acLDL) uptake and fluorescein-isothiocyanate-conjugated Ulex europaeus agglutinin lectin (UEA-1) binding. Expression of von Willbrand factor (vWF), kinase insert domain receptor (KDR), and α7 nAChR was detected by indirect immunofluorescence staining. Late EPCs of 3-5 passages were treated for 32 h with either vehicle or nicotine with or without pre-incubation of nAChR antagonism, mecamylamine, or α-bungarotoxin. The viability, migration, and in vitro vasculogenesis activity of late EPCs were assayed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, modified Boyden chamber assay, and in vitro angiogenesis assay, respectively. Late EPCs adhesion assay was performed by replating cells on fibronectin-coated plates, and then adherent cells were counted. Incubation with 10 nmol/L nicotine enhanced viable, migratory, adhesive, and in vitro vasculogenesis capacity of late EPCs. The effect of nicotine on late EPCs can be attenuated by mecamylamine or α-bungarotoxin. In conclusion, nicotine improves the functional activity of late EPCs via nAChRs.

ABO blood groups and risk of deep venous thromboembolism in Chinese Han population from Chaoshan region in South China.

 Objectives: To demonstrate the prevalence of ABO blood groups with deep venous thromboembolism in Chinese Han population. METHODS: A retrospective study was conducted between January 2010 and March 2015 in The First Affiliated Hospital of Shantou University Medical College in Chaoshan District of Guangdong Province in South China. Eighty nine patients with confirmed diagnosis of deep venous thromboembolism were included. Frequency of blood groups was determined. Results: Of 89 patients with deep venous thromboembolism, 28 patients had blood group A (31.5%), 28 patients had blood group B (31.5%), 13 patients had blood group AB (14.6%), and 20 patients had blood group O (22.5%). Compared with O blood type, the odds ratios of deep venous thromboembolism for A, B and AB were 2.23 (95% CI, 1.27-3.91), 2.34 (95% CI, 1.34-4.09) and  4.43 (95% CI, 2.24-8.76). Conclusion: There is a higher risk of venous thromboembolism in non-O blood groups than O group.

Atrial Fibrillation Is an Independent Risk Factor for Hospital-Acquired Pneumonia.

BACKGROUND: Patients who were hospitalized for community-based pneumonia frequently had pre-existing atrial fibrillation (AF) and had subsequent cardiovascular complications. Whether patients who had AF would be susceptible to the development of hospital-acquired pneumonia (HAP) is a serious concern but this has not been investigated. In our clinics, we have made empirical observation of such susceptibility. OBJECTIVES: To investigate the association between newly developed HAP and pre-existing AF, and to identify whether AF is an independent risk factor for HAP. METHODS: Hospital data from 8657 sequentially admitted inpatients [1059 patients with AF and 7598 without AF (NAF)] were collected from the Department of Cardiology, First Affiliated Hospital of Shantou University Medical College, Shantou, China, from January 1, 2009 to December 31, 2011. Exclusion criteria were: having previous or current pneumonia, pacemakers, sick sinus syndrome and repeated hospitalization. The incidence of HAP (within 48 hours after hospitalization) was identified among all the patients. RESULTS: Among the AF patients, 274 had HAP (adjusted rate 25.64%) which was significantly higher than the 276 NAF patients who had HAP (adjusted rate 3.66%; P<0.001). The increased risk was also associated with high blood pressure, heart failure and age, but not with gender, smoking, coronary heart disease, diabetes, congenital heart disease. In addition, our multiple regression analysis indicates that AF is an independent risk factor for HAP. CONCLUSION: We have identified, for the first time, that AF is an important risk factor for HAP. Although additional clinical confirmation is needed, our data provide valuable evidence for use in prevention of HAP which is the most common cause of death from nosocomial infection.

Effects of urotensin II on functional activity of late endothelial progenitor cells.

Urotensin II (UII) is a potent vasoactive cyclic peptide which has multiple effects on the cardiovascular system. However, the effects of UII on late endothelial progenitor cells (EPCs) are still unclear. The aim of the present study is to investigate whether UII influences the functional activity of late EPCs. Late EPCs were isolated from human umbilical cord blood by Ficoll density gradient centrifugation and treated with UII (10(-10), 10(-9), 10(-8), 10(-7) and 10(-6)M), or vehicle control. Expression of urotensin II receptor (UT) in late EPCs was confirmed by indirect immunofluorescence staining. Late EPCs proliferation, migration and in vitro vasculogenesis activity were assayed with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, transwell chamber assay, and matrigel tube formation assay. Late EPCs adhesive assay was performed by replating cells on fibronectin-coated dishes, and then adherent cells were counted. Incubation with UII increased the migratory, adhesive and in vitro vasculogenesis capacity and inhibited the proliferative activity of late EPCs. Furthermore, these UII-mediated effects on late EPCs were attenuated by pretreatment with the UT antagonist urantide. These findings indicate that UII may exert multiple effects on functional activity of late EPCs through UT.