[Effect of distal ischemic preconditioning on cardiovascular events in adult patients with hip fracture one year after operation].

OBJECTIVE: To investigate the effect of remote ischemic preconditioning (RIPC) on major adverse cardiovascular events (MACE) in elderly patients with hip fracture 1 year after operation. METHODS: Total of 314 elderly patients with hip fracture of gradeⅡand Ⅲ for American Society of Anesthesiologists (ASA) were treated by surgical operation from April 2015 to May 2020 including 116 males and 198 females, the age ranged from 60 to 76 years old. The subjects were divided into intervention group and control group according to whether received RIPC. Among them, 157 cases in intervention group included 56 males and 101 females with an average age of (68.12±7.13) years old and 157 cases in control group included 60 males and 97 females with an average age of (68.24±7.05) years old. Both groups were given routine anesthesia. The intervention group was treated with RIPC on the basis of routine anesthesia. The MACE events 1 year after operation in two groups were compared and analyzed. RESULTS: The OR values of RIPC for myocardial infarction, heart failure, stroke, nonfatal cardiac arrest, coronary revascularization, severe arrhythmia, peripheral artery thrombosis, readmission of cardiovascular disease, and all-cause death in patients with hip fracture one year after operation were 1.269, 1.304, 0.977, 1.089, 1.315, 1.335, 0.896, 0.774, 1.191, respectively, but there was no significant difference (P>0.05). CONCLUSION: RIPC did not significantly affect and change the occurrence of major cardiovascular adverse events within 1 year after hip fracture surgery. The long term impact of RIPC on clinical cardiovascular outcomes in non cardiac surgery needs to be confirmed in appropriate randomized clinical trials.

A highly stable chain-based EuIII metal-organic framework as a turn-on and blue-shift luminescent sensor for dipicolinic acid.

The development of a rapid and selective method for the identification of dipicolinic acid (DPA), a specific biomarker in Bacillus anthracis spores, is of great importance for the avoidance of anthrax infection. Herein, a chain-based EuIII metal-organic framework with the formula {[Eu3(BTDB)3(µ3-OH)3(H2O)]·solvents}n (JXUST-38, H2BTDB = (benzo[c][1,2,5]thiadiazole-4,7-diyl)dibenzoic acid) was obtained using 2-fluorobenzoic acid as the pH regulator. JXUST-38 exhibits good chemical and thermal stability and can specifically recognize DPA in N,N-dimethylformamide solution through luminescence enhancement and blue-shift effects with a detection limit of 0.05 µM. Furthermore, the significant luminescence enhancement and blue shift under UV lamps are obviously observable by the naked eye. The luminescence sensing mechanism is attributed to absorbance-induced enhancement between JXUST-38 and DPA. Test paper and mixed-matrix membrane based on JXUST-38 are designed for DPA detection. In addition, the feasibility of using JXUST-38 in biosensing is discussed in detail.

Highly pH-Responsive Sensor Based on a EuIII Metal-Organic Framework with Efficient Recognition of Arginine and Lysine in Living Cells.

A lanthanide-based three-dimensional metal-organic framework with excellent water, acid/base, and solvent stability, namely {[(CH3)2NH2]0.7[Eu2(BTDBA)1.5(lac)0.7(H2O)2]·2H2O·2DMF·2CH3CN}n (JXUST-29, H4BTDBA = 4',4‴-(benzo[c][1,2,5]thiadiazole-4,7-diyl)bis([1,1'-biphenyl]-3,5-dicarboxylic acid), Hlac = lactic acid), has been synthesized and characterized. Since the N atoms of the thiadiazole group will not coordinate with lanthanide ions, JXUST-29 has a free basic N-site accessible to small H+ ions, which allows it to be used as a promising pH fluorescence sensor. Interestingly, the luminescence signal was significantly enhanced, with an approximately 54-fold enhancement in the emission intensity when the pH value was increased from 2 to 5, which is the typical behavior of pH probes. In addition, JXUST-29 can also be used as a luminescence sensor to detect l-arginine (Arg) and l-lysine (Lys) in an aqueous solution through fluorescence enhancement and the blue-shift effect. The detection limits were 0.023 and 0.077 µM, respectively. In addition, JXUST-29-based devices were designed and developed to facilitate detection. Importantly, JXUST-29 is also capable of detecting and sensing Arg and Lys in living cells.

CHA2DS2-VASc score as a prognostic indicator in patients with atrial fibrillation undergoing coronary stenting.

BACKGROUND: Patients with atrial fibrillation (AF) and coronary stenting had a poor prognosis. This study aimed to assess the accuracy of CHA2DS2-VASc score for predicting and grading adverse clinical outcomes in this population. METHODS: We reviewed the clinical data of all patients with previously documented nonvalvular AF who underwent coronary stenting between January 2010 and June 2015 in 12 hospitals of Beijing, China. The study population was divided into three groups: 1) Low CHA2DS2-VASc score, ≦ 2 points, 2) Intermediate score, 3-4 points, and 3) High score, ≧ 5 points. Major adverse cardiac/cerebrovascular events (MACCE) were defined as a composite of all-cause death, nonfatal myocardial infarction, repeat revascularization and ischemic stroke/systemic thromboembolism (IS/SE). RESULTS: A total of 2394 patients (men: 72.3% vs. women: 27.7%, median age: 67 years) were included, with the CHA2 DS2-VASc score of 3.6 ± 1.6. The median follow-up duration was 36.2 months. All-cause mortality increased 3 folds from the low score (4.8%) to the high score group (15.8%). The high score group had more IS/SE (7.4%) and MACCE (26.3%). The CHA2 DS2-VASc score ≧ 5 points was independently associated with all-cause death (hazard ratio [HR]: 2.303, 95% confidence interval [CI]: 1.492- 3.555), IS/SE (HR: 4.169, 95% CI: 2.216-7.845) and MACCE (HR: 1.468, 95% CI: 1.113-1.936) on multivariate Cox proportional hazards regression. The area under the receiver operating characteristic curve of the CHA2DS2-VASc score was 0.644 (95% CI: 0.624-0.663) for all-cause death, 0.647 (95% CI: 0.627-0.666) for IS/SE, and 0.592 (95% CI: 0.572-0.611) for MACCE. DISCUSSION: CHA2DS2-VASc score was a reliable prognostic indicator in patients with AF and coronary stenting.

Predictive models for adverse clinical outcomes in Chinese patients with atrial fibrillation undergoing percutaneous coronary intervention with stenting.

OBJECTIVE: This study aimed to evaluate predictors for adverse cardiovascular outcomes in patients with atrial fibrillation (AF) undergoing coronary stenting. METHODS: We retrospectively recruited consecutive patients with previously documented non-valvular AF who underwent coronary stenting between January 2010 and June 2015 in 12 hospitals of Beijing, China. Major adverse cardiac/cerebrovascular events (MACCE) were a composite of all-cause death, non-fatal myocardial infarction, repeat revascularization, and ischaemic stroke/systemic thromboembolism (IS/STE). Major bleeding referred to grade 2 or higher of Bleeding Academic Research Consortium criteria. RESULTS: A total of 2394 patients (men: 72.3% vs. women: 27.7%, median age: 67 years) were included. The CHA2DS2-VASc and HAS-BLED were 3.6 ± 1.6 and 1.9 ± 0.7, respectively. The median follow-up duration was 36.2 months. There were 230 (9.6%) deaths, 96 (4.0%) IS/STE, 426 (17.8%) MACCE, and 72 (3.0%) major bleeding. Multivariate Cox regression yielded predictive models for (1) all-cause death: diabetes, prior myocardial infarction, chronic kidney disease (CKD), ST-segment elevation myocardial infarction (STEMI) at presentation, heart failure, no use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and statins; (2) IS/STE: advanced age, prior history of ischaemic stroke and intracranial haemorrhage; (3) MACCE: prior history of myocardial infarction and ischaemic stroke, CKD, STEMI, heart failure, and no statin use; (4) major bleeding: prior major bleeding, prior myocardial infarction, CKD and use of oral anticoagulants. CONCLUSION: Chinese patients with AF and coronary stenting had high mortality and incidence of MACCE. We compiled separate predictive models for all-cause death, IS/STE, MACCE, and major bleeding.

Desmoplakin and clinical manifestations of desmoplakin cardiomyopathy.

ABSTRACT: Desmoplakin (DSP), encoded by the DSP gene, is the main desmosome component and is abundant in the myocardial tissue. There are three DSP isoforms that assume the role of supporting structural stability through intercellular adhesion. It has been found that DSP regulates the transcription of adipogenic and fibrogenic genes, and maintains appropriate electrical conductivity by regulating gap junctions and ion channels. DSP is essential for normal myocardial development and the maintenance of its structural functions. Studies have suggested that DSP gene mutations are associated with a variety of hereditary cardiomyopathy, such as arrhythmia cardiomyopathy, dilated cardiomyopathy (DCM), left ventricular noncompaction, and is also closely associated with the Carvajal syndrome, Naxos disease, and erythro-keratodermia-cardiomyopathy syndrome with skin and heart damage. The structure and function of DSP, as well as the clinical manifestations of DSP-related cardiomyopathy were reviewed in this article.

Conjugated bilayer structure of the homogeneous solid-liquid interface of metals.

The concept of "interfacial region" has long prevailed for over half century for describing the homogeneous solid-liquid (SL) interface of metals, but its intrinsic structure is still unclear due to the homogeneity. In this study, we reveal, for the first time, the intrinsic structure of these homogeneous SL interfaces consisting of two conjugated monoatomic layers of interfacial solid (IS) and interfacial liquid (IL) with a certain degree of corrugation via molecular dynamics simulations. We named it as the conjugated bilayer structure (CBS). In the framework of CBS, only the IS + IL bilayer plays stepwise transition roles from the solid to the liquid, which defines the four-terrace nature of the interface and act simultaneously as the boundaries of the bilateral bulk phases. The inherent diffuse nature of the "interfacial region" is proven originating from the corrugation of the IS + IL bilayer and its four-terrace nature. More importantly, the CBS also explains that the interfacial free energy originates mainly from the increase in the potential energy of the IS layer relative to its counterpart bulk solid instead of the previously argued entropy loss of the liquid phase. After all these verifications and interpretations, the CBS was verified as the intrinsic structure of the homogeneous SL interface of metals. Accordingly, we argue that the concept of CBS also resolves the volume-bearing flaw of the "interfacial region" concept and can definitively locate the intrinsic surface according to the capillary wave theory.

Recent approaches to His-Purkinje system pacing.

OBJECTIVE: Physiologic cardiac pacing is a novel technique which has been largely popularized in recent decades. His bundle pacing (HBP) has been long considered the most physiologic pacing method; however, with the widespread implementation of this method, its disadvantages have become apparent. In this context, left bundle branch pacing (LBBP)-directly engaged in the His-Purkinje system-has been foreseen as the best pacing method to mimic physiologic activation patterns. This review aimed to summarize recent approaches to physiologic cardiac pacing. DATA SOURCES: This review included fully peer reviewed publications up to July 2018, found in the PubMed database using the keywords "His bundle branch pacing," "right ventricular pacing," and "physiologic pacing." STUDY SELECTION: All selected articles were in English, with no restriction on study design. RESULTS: The HBP has been studied worldwide, and is currently considered the most physiologic pacing method. However, it has disadvantages, such as high pacing threshold, unsatisfactory sensing and long procedure times, among others. Although LBBP is theoretically superior to HBP, the clinical relevance of this difference remains under debate, as few large randomized clinical trials with LBBP have been published. CONCLUSIONS: Although HBP indeed appears to be the most physiologic pacing method, it has certain shortcomings, such as high pacing threshold, difficult implantation due to specific anatomic features, and others. Further studies are required to clarify the clinical significance of LBBP.

Overexpression of microRNA-590-3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF-κB signaling pathway by binding to RIPK1.

Ischemic heart disease is widely considered as a major health threat, which causes a high number of deaths every year worldwide. Much evidence has shown that oxidative stress (OS) is implicated in the pathogenesis of ischemia-reperfusion injury (IRI). This study aims to evaluate the effect of miR-590-3p on the OS of IRI mice through the nuclear factor kappa-B (NF-κB) signaling pathway by targeting receptor-interacting protein kinase 1 (RIPK1). IRI mouse models were established for extracting myocardial tissues and isolating myocardial cells. The expression of inflammatory related-factors was detected by enzyme-linked immunosorbent assay, and superoxide dismutase (SOD) and malondialdehyde (MDA) in tissues were determined. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were performed to assess the role of miR-590-3p in the expression of NF-κB-related factors and apoptosis-related factors. Besides, the regulatory effects of miR-590-3p on myocardial cell proliferation and apoptosis were also assessed. According to the obtained results, we found that IRI mice displayed higher expression of tumor necrosis factor-α, interleukin (IL)-6, and interferon-γ, lower expression of IL-10 in serum, a decreased SOD level, and an increased MDA level. In addition, RIPK1 was determined as a target gene of miR-590-3p. After transfection of overexpressed miR-590-3p or si-RIPK1, declined RIPK1, NF-κB, Toll-like receptor 4, caspase-3, FasL, p53, and c-myc levels, increased B-cell lymphoma-2 level, promoted cell proliferation, promoted cell cycle distribution and inhibited apoptosis of myocardial cells were found. Our study demonstrates that miR-590-3p can alleviate the OS of IRI mice through the inhibition of the RIPK1 and NF-κB signaling pathway. Thus, miR-590-3p represents a potential target for IRI repair.

Targeting HMGB1 ameliorates cardiac fibrosis through restoring TLR2-mediated autophagy suppression in myocardial fibroblasts.

BACKGROUND: Extracellular high-mobility group box 1 (HMGB1) has been identified as playing a critical role in the pathogenesis of tissue fibrosis. However, the underlying mechanism of its involvement in cardiac fibrosis is still not well-defined. Here, we aim to investigate whether toll-like receptor 2 (TLR2) contributes to the extracellular HMGB1-mediated development and progression of cardiac fibrosis. METHODS: A mouse model of cardiac fibrosis was induced by subcutaneous injection of isoproterenol (ISO). Glycyrrhizic acid (GA), an inhibitor of HMGB1 derived from natural products, was simultaneously administered by intraperitoneal injection. Echocardiography, H&E and Sirius red staining were used to evaluate cardiac function and fibrosis. The myocardial expression of autophagy-associated proteins was examined using immunoblotting. Cardiac fibroblasts were treated with different concentrations of HMGB1 to examine the expression levels of α-SMA, collagen I and autophagy markers. Interactions of HMGB1/TLR2 and α-SMA/p62 were examined by immunoprecipitation and immunofluorescence. RESULTS: ISO-treated mice showed characteristic cardiac fibrosis, increased expression and co-localization of HMGB1 and TLR2, as well as impaired autophagic signals in myocardial tissues, which could be prevented by silencing TLR2. Exogenous administration of HMGB1 blocked the autophagic flux in fibroblasts, which caused extensive accumulation of collagen I and α-SMA. In addition, cardiac fibrosis was alleviated by GA treatment through abrogating the interaction between HMGB1 and TLR2. CONCLUSIONS: Our study suggests that the interaction between TLR2 and HMGB1 contributes to the pathogenesis of cardiac fibrosis via suppressing fibroblast autophagy, and that inhibiting HMGB1 with GA provides therapeutic benefits for the treatment of fibroproliferative heart diseases.

Biofilm-Related Genes: Analyses in Multi-Antibiotic Resistant Acinetobacter Baumannii Isolates From Mainland China.

BACKGROUND Acinetobacter baumannii is an important nosocomial pathogen which shows a high level of mortality risk. Several papers have reported biofilm formation as a well-known pathogenic mechanism in A. baumannii infections and exceptional antibiotic resistance. The study aims to explore the potential relationships between biofilm-related genes and antimicrobial resistance. MATERIAL AND METHODS Samples from 122 patients with lower respiratory tract infections of A. baumannii were collected at Fujian Longyan First Hospital from January 2013 to September 2014. A. baumannii was isolated from sputum specimens. Biofilm-related genes including abaI, csuE, ompA, and bla-PER1 were analyzed by PCR. The minimum inhibitory concentration method was used to determine the sensitivity of each strain to antibiotics. RESULTS The clinical manifestations of A. baumannii-induced lower respiratory tract infections lacked specificity. Infected patients were most commonly admitted to intensive care units (54.9%) and frequently had chronic obstructive pulmonary disease (27.0%). The detection rates of abaI and csuE were both 59.8%, and those of ompA and bla-PER1 were 100% and 0%, respectively. After genetic testing, antimicrobial resistance to amikacin, ampicillin/sulbactam, and 14 other types of antimicrobials was higher in abaI- and csuE-positive strains than in abaI- and csuE-negative strains (P<0.05). CONCLUSIONS The findings of our study suggest that abaI- and csuE-positive Acinetobacter baumannii strains are associated with a higher incidence of antibiotic resistance in 14 types of antimicrobials.

Sequential changes of endoplasmic reticulum stress and apoptosis in myocardial fibrosis of diabetes mellitus-induced rats.

The endoplasmic reticulum (ER) is an organelle in which proteins form their appropriate structures. However, several of these proteins become unfolded or misfolded when exposed to stimuli, including hyperglycemia, oxidative stress, ischemia, disturbance of calcium homeostasis and overexpression of abnormal proteins, which activates ER stress and the unfolded protein response (UPR). To date, investigations have demonstrated that ER stress is important in diabetic myocardial fibrosis by inducing cardiac cell apoptosis. Therefore, in the present study, the polymerase chain reaction, western blotting analysis and tissue staining were performed to identify the changes in UPR signaling proteins and apoptotic proteins in diabetic rats at different time points, and to determine whether the myocardial fibrosis is associated with ER-stress-mediated apoptosis using a diabetes mellitus (DM) rat model. It was found that the upregulation of ER stress markers and apoptotic molecules developed over time. It was also demonstrated that anti­apoptotic markers and proapoptotic markers were activated early following model establishment, and then decreased in months 4 and 5. The changes in myocardial fibrosis were found to accelerate in a time-dependent manner with apoptosis in the DM rats.

Genetic diversity and temporal dynamics of phytoplankton viruses in East Lake, China.

Phytoplankton viruses are important components of aquatic ecosystems. However, their prevalence and genetic diversity in marine and freshwater systems are largely under estimated owing to the immense size of water bodies and limitations in virus discovery techniques. In this study, we conducted a 1-year survey of phytoplankton virus communities by collecting surface water monthly from an inland lake (East Lake) in China between May 2012 and April 2013. We examined four phytoplankton viruses, i.e., myoviruses, podoviruses, siphoviruses, and phycodnaviruses, and seven sets of primers were used to target conserved genes within these four species. In this year-long investigation, a total of 358 different virus-related sequences from four virus families were obtained. All virus families were detected in all months, except for cyanopodoviruses, which were only identified during eight of the 12 months surveyed. Moreover, virus abundance and diversity changed dynamically over time. Phylogenetic analysis revealed that the majority of viral sequences from East Lake, China displayed distinct clustering patterns compared with published sequences. These results supported the existence of a highly diverse and unique phytoplankton virus community in East Lake, China.

Toll-like receptor 4 knockout protects against isoproterenol-induced cardiac fibrosis: the role of autophagy.

BACKGROUND: Toll-like receptor 4 participates in the process of acute heart injury. The underlying mechanisms of its protection are multifactorial, but we hypothesized that toll-like receptor-mediated autophagy control plays a vital role. The purpose of this study was to clarify the effect of autophagy on cardiac fibrosis. METHODS: Cardiac fibrosis was induced by subcutaneous isoproterenol (ISO) injection, and rapamycin was simultaneously administered orally for 14 days. Animal echocardiography was then used to evaluate the success of the cardiac fibrosis model, and the mice were killed after the echocardiography examination. RESULTS: Toll-like receptor 4 knockout (TLR4 KO) mice had better heart function than did wild-type (WT) mice (P < .05). Rapamycin treatment reduced the left ventricular ejection fraction to 23.5% (P < .05), and the collagen volume fraction of the ISO and ISO plus rapamycin groups was 5.9% and 25.9%, respectively, in TLR4 KO mice. Compared with the WT mice, Beclin 1 and autophagy were downregulated in TLR4 KO mice (P < .05); however, the ISO plus rapamycin group had higher autophagy activity than did the ISO group in TLR4 KO mice (P < .05). CONCLUSIONS: Our results suggest that TLR4 KO-induced cardioprotection against ISO-induced cardiac fibrosis is associated with reduced autophagy induction. Cardiac fibroblast autophagy participates in its own activation. The moderate inhibition of autophagic activity may be a new strategy for treating cardiac fibrosis.

Progressive decay of Ca2+ homeostasis in the development of diabetic cardiomyopathy.

BACKGROUND: Cardiac dysfunction in diabetic cardiomyopathy may be associated with abnormal Ca2+ homeostasis. This study investigated the effects of alterations in Ca2+ homeostasis and sarcoplasmic reticulum Ca2+-associated proteins on cardiac function in the development of diabetic cardiomyopathy. METHODS: Sprague-Dawley rats were divided into 4 groups (n = 12, each): a control group, and streptozotocin-induced rat models of diabetes groups, examined after 4, 8, or 12 weeks. Evaluations on cardiac structure and function were performed by echocardiography and hemodynamic examinations, respectively. Cardiomyocytes were isolated and spontaneous Ca2+ spark images were formed by introducing fluorescent dye Fluo-4 and obtained with confocal scanning microscopy. Expressions of Ca2+-associated proteins were assessed by Western blotting. RESULTS: Echocardiography and hemodynamic measurements revealed that cardiac dysfunction is associated with the progression of diabetes, which also correlated with a gradual but significant decline in Ca2+ spark frequency (in the 4-, 8- and 12-week diabetic groups). However, Ca2+ spark decay time constants increased significantly, relative to the control group. Expressions of ryanodine receptor 2 (RyR2), sarcoplasmic reticulum Ca2+-2ATPase (SERCA) and Na+/Ca2+ exchanger (NCX1) were decreased, together with quantitative alterations in Ca2+regulatory proteins, FKBP12.6 and phospholamban progressively and respectively in the diabetic rats. CONCLUSIONS: Ca2+ sparks exhibited a time-dependent decay with progression of diabetic cardiomyopathy, which may partly contribute to cardiac dysfunction. This abnormality may be attributable to alterations in the expressions of some Ca2+-associated proteins.

Relaxin inhibit cardiac fibrosis induced by phorbol 12-myristate 13-acetate.

Relaxin is known to inhibit cardiac fibrosis. However, it is unclear whether relaxin could regulate the effects of Phorbol 12-myristate 13-acetate (PMA, PKC activator) on cardiac fibrosis. So the influence of relaxin on the cell proliferation and collagen expression induced by PMA in cultured cardiac fibroblasts was studied. It showed that PMA significantly increased cardiac fibroblasts proliferation, Type I pro-collagen protein expression, Type I pro-collagen mRNA expression, and rhRLX absolutely significantly decreased PMA induced effects on cardiac fibroblasts proliferation and Type I pro-collagen expressions, indicating that relaxin could inhibit cardiac fibrosis induced by PMA.

pH luminescence switching, dihydrogen phosphate sensing, and cellular uptake of a heterobimetallic ruthenium(II)-rhenium(I) complex.

A new heterobimetallic ruthenium(II)-rhenium(I) complex of [Ru(bpy)2(HL)Re(CO)3Cl](ClO4)2·6H2O (RuHLRe) {bpy = 2,2'-bipyridine and HL = 2-(4-(2,6-di(pyridin-2-yl)pyridin-4-yl)phenyl)-1H-imidazo[4,5-f][1,10]phenanthroline} was synthesised and characterised by elemental analysis, proton nuclear magnetic resonance spectroscopy, and mass spectrometry. The ground- and excited-state acid-base properties of RuHLRe were studied using UV-Vis absorption spectrophotometric and spectrofluorimetric titrations in a 100 : 1 (v/v) Britton-Robinson buffer-CH3CN solution combined with luminescence lifetime measurements. The complex exhibited two-step separate protonation-deprotonation processes in both the ground and excited states. The complex acted as pH-induced "off-on-off" luminescence switches (I(on)/I(off) = 31.0 and 14.6), with one of the switching actions being driven by pH variations over the physiological pH range (5.3-8.0). Importantly, cellular imaging and cytotoxicity experiments demonstrated that RuHLRe rapidly and selectively illuminated the membrane of HeLa cells over fixed cells and exhibited reduced cytotoxicity at the imaging concentration compared to the Re(I)-free parent Ru(II) complex. In addition, RuHLRe acted as an efficient "turn on" emission sensor for H2PO4(-) and "turn off" emission sensor for F(-) and OAc(-).

[The relationship between left ventricular diastolic function and arterial stiffness in diabetic coronary heart disease].

OBJECTIVES: By measuring left ventricular diastolic function and arterial stiffness, this study aims to probe into the effect of diabetes mellitus (DM) on left ventricular diastolic function and arterial stiffness, and evaluate the correlation between left ventricular diastolic function and arterial stiffness. METHODS: Seventy-six inpatients were enrolled. According to their coronary angiography, OGTT test results and past history of DM, patients were divided into controlled, CHD (coronary heart disease with no DM), and CHD + DM groups. Through invasive hemodynamic monitoring during left ventricular angiography, left ventricular end-diastolic pressure (LVEDP) and tau index were collected. Carotid-femoral pulse wave velocity (c-f PWV), reflected wave augmentation index (AIx@75) and other data reflecting the degree of arterial stiffness were collected bedside with non-invasive means. SPSS 18.0 was used for statistical analysis. RESULTS: No significant difference was found between groups for LVEDP, tau index, and AIx@75. In terms of c-f PMV, The CHD + DM group (8.79 ± 1.59) cm/s differed significantly from the CHD group (7.43 ± 1.42) cm/s and the controlled group (6.83 ± 1.14) cm/s. No correlations were found between c-f PMV and LVEDP or tau index. A positive correlation was found between AIx@75 and tau index. CONCLUSIONS: Compared with the controlled group and CHD patients with no DM, CHD + DM patients show worse arterial stiffness with no difference in ventricular diastolic function. There is a positive correlation between arterial stiffness and diastolic dysfunction.