BackgroundPatients 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.ObjectivesTo investigate the association between newly developed HAP and pre-existing AF, and to identify whether AF is an independent risk factor for HAP.MethodsHospital 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.ResultsAmong 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.ConclusionWe 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.

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.

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.

BackgroundMyocardial 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 presentationIn present study, we reviewed four cases with myocardial bridge and no stenosis of coronary artery, which included acute coronary syndrome and sudden cardiac arrest.ConclusionsThese cases indicated that cardiac events in patients with myocardial bridge may be associated with coronary spasm, myocardial supply/demand mismatch or cardiac arrest.Electronic supplementary materialThe online version of this article (doi:10.1186/s12872-015-0158-2) contains supplementary material, which is available to authorized users.

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.