Berberine Protects Against Simulated Ischemia/Reperfusion Injury-Induced H9C2 Cardiomyocytes Apoptosis In Vitro and Myocardial Ischemia/Reperfusion-Induced Apoptosis In Vivo by Regulating the Mitophagy-Mediated HIF-1α/BNIP3 Pathway.

Berberine (BBR) has a variety of pharmacological activities and is widely used in Asian countries. However, the clinical application of BBR still lacks scientific basis, what protective mechanism of BBR against myocardial ischemia-reperfusion injury (MIRI). In vitro experiments, BBR pretreatment regulated autophagy-related protein expression, induced cell proliferation and autophagosome formation, and reduced the mitochondrial membrane potential (ΔΨm) increase in H9C2 cells. In vivo experiments, BBR reduced the myocardial infarct size, decreased cardiomyocyte apoptosis, and markedly decreased myocardial enzyme (CK-MB, LDH, and AST) activity-induced I/R. In addition, upon BNIP3 knockdown, the regulatory effects of BBR on the above indicators were weakened both in H9C2 cells and in vivo. Luciferase reporter and ChIP assays indicated that BBR mediated BNIP3 expression by enhancing the binding of HIF-1α to the BNIP3 promoter. BBR protects against myocardial I/R injury by inducing cardiomyocytes proliferation, inhibiting cardiomyocytes apoptosis, and inducing the mitophagy-mediated HIF-1α/BNIP3 pathway. Thus, BBR may serve as a novel therapeutic drug for myocardial I/R injury.

Berberine attenuates mitochondrial dysfunction by inducing autophagic flux in myocardial hypoxia/reoxygenation injury.

Berberine (BBR) is routinely prescribed in many Asian countries to treat diarrhea. Evidence from both animal and clinical investigations suggests that BBR exerts diverse pharmacological activities, including antidiabetic, antineoplastic, antihypertensive, and antiatherosclerotic effects. This study aimed to explore the cardioprotective mechanisms of BBR and to elucidate the modulations between autophagy and mitochondrial function during hypoxia/reoxygenation (H/R) in H9c2 cells. The degree of autophagic flux was assessed by pretreating H9c2 cells with BBR prior to H/R exposure and measuring the expression levels of Beclin-1 and green fluorescent protein (GFP)-labeled LC3B fusion proteins as well as the LC3II/LC3I ratio. The mitochondrial membrane potential (△Ψm) in H9c2 cells was evaluated by detecting rhodamine-123 fluorescence using flow cytometry. The results revealed that pretreatment with BBR upregulated autophagic flux and protected against the loss of the △Ψm in H9c2 cells subjected to H/R. We conclude that BBR attenuates mitochondrial dysfunction by inducing autophagic flux.

Y-box protein 1 promotes hypoxia/reoxygenation- or ischemia/reperfusion-induced cardiomyocyte apoptosis via SHP-1-dependent STAT3 inactivation.

Cardiomyocyte apoptosis induced by hypoxia and ischemia plays important roles in heart dysfunction after acute myocardial infarction (AMI). However, the mechanism of apoptosis induction remains unclear. A previous study reported that Y-box protein 1 (YB1) is upregulated after myocardial hypoxia/reoxygenation or ischemia/reperfusion (H/R or I/R, respectively) injury; however, whether YB1 is associated with H/R-induced cardiomyocyte apoptosis is completely unknown. In the present study, we investigated the roles of YB1 in H/R-induced cardiomyocyte apoptosis and the possible underlying molecular mechanisms. In vitro, H/R treatment upregulated the YB1 expression in H9C2 cells, whereas YB1 knockdown inhibited H/R-induced cardiomyocyte apoptosis and induced H9C2 cell proliferation via Src homology region 2 domain-containing phosphatase 1 (SHP-1)-mediated activation of signal transducer and activator of transcription 3 (STAT3). In vivo, YB1 knockdown ameliorated AMI, reducing infarct size, cardiomyocyte apoptosis, and oxidative stress, via SHP-1-mediated inactivation of STAT3. Additionally, YB1 knockdown inhibited H/R- or I/R-induced oxidative stress in vitro and in vivo. H/R and I/R increase YB1 expression, and YB1 knockdown ameliorates AMI injury via SHP-1-dependent STAT3 inactivation.

Effects of miR-181a targeting XIAP gene on apoptosis of cardiomyocytes induced by hypoxia/reoxygenation and its mechanism.

To investigate the effect of miR-181a targeting XIAP gene on the apoptosis of cardiomyocytes induced by hypoxia/reoxygenation (H/R) and its mechanism. The primary cultured cardiomyocytes were treated with hypoxia for 3 hours and reoxygenation for 4 hours to construct H/R cell model. The expression of miR-181a and XIAP messenger RNA in cardiomyocytes was detected by reverse-transcription polymerase chain reaction, and the expression of XIAP protein in cardiomyocytes was detected by Western blot analysis. H/R cardiomyocytes with low expression of miR-181a and overexpression of XIAP were constructed, and the effects of low expression of miR-181a and upregulation of XIAP on cardiomyocyte apoptosis were detected by flow cytometry. A dual luciferase reporter assay was used to detect the target relationship between miR-181a and XIAP. Further, H/R myocardial cells with low XIAP expression were constructed to observe the effect of downregulation of XIAP expression on apoptosis of myocardial cells with low expression of microarray-181a. The expression of apoptosis-related proteins Bax and Bcl-2 in myocardial cells was detected by Western blot analysis. After H/R treatment, the expression of microRNAs-181a was high but that of XIAP was low. The apoptosis of cardiomyocytes could be inhibited by both the low expression of miR-181a and the upregulation of XIAP. The results of dual luciferase reporter gene showed that XIAP was a potential target gene for miR-181a. The inhibitory effect of low expression of miR-181a on myocardial apoptosis could be reversed and the inhibitory effect of low expression of miR-181a on Bax protein expression and the promotion of Bcl-2 protein expression could be reversed by the downregulation of XIAP. MiR-181a can inhibit the apoptosis of hypoxic-reoxygenated cardiomyocytes by targeting XIAP to downregulate Bax and upregulate Bcl expression.

Identification of a peripheral blood long non-coding RNA (Upperhand) as a potential diagnostic marker of coronary artery disease.

BACKGROUND: Long non-coding RNAs (lncRNAs) have been confirmed to be involved in the pathologi-cal processes of multiple diseases. However, the characteristic expression of lncRNAs in peripheral blood of coronary artery disease (CAD) patients and whether some of these lncRNAs can be used as diagnostic biomarkers for CAD requires further investigation. METHODS: Six healthy and CAD individuals were selected for microarray analysis, and 5 differentially expressed lncRNAs were selected and confirmed in the second cohort consisting of 30 control individu-als and 30 CAD patients with different SYNTAX scores. Upperhand were verified in the third cohort consisting of 115 controls and 137 CAD patients. RESULTS: Thirty one lncRNAs were differentially expressed between the two groups, among whom, 25 were upregulated in the CAD group and 6 were downregulated. Four of the selected five lncRNAs were significantly upregulated in the CAD group, and Upperhand had the largest area under the curve (AUC). The diagnostic value of Upperhand was tested further, and it remained having a high diagnostic value. CONCLUSIONS: The expression level of Upperhand in peripheral blood of CAD patients is significantly higher than in control individuals, and is correlated with severity of CAD. Upperhand is a potential diagnostic biomarker of CAD, and when combined with TCONS_00029157, diagnostic value slightly increased.

The Diagnostic Value of Whole Blood lncRNA ENST00000550337.1 for Pre-Diabetes and Type 2 Diabetes Mellitus.

This study aims to investigate long noncoding RNA (lncRNA) as biomarker for pre-diabetes and T2DM. LncRNAs in the peripheral blood of 6 healthy individuals and 6 T2DM patients were collected for microarray analysis. Then 5 candidate biomarkers from the differentially expressed lncRNAs were chosen and verified in a larger independent cohort (control group=20; pre-diabetes group=20; and T2DM group=20). The diagnostic capacity of ENST00000550337.1 was further tested in the third cohort (control group, n=60; pre-diabetes group, n=63; and T2DM group, n=64). A total of 17 lncRNAs were found to be differentially expressed between the 2 groups. 14 lncRNAs of these were upregulated in T2DM patients and 3 were downregulated. 5 upregulated lncRNAs were selected as potential biomarkers and verified in the second cohort, and the expression levels of 3 lncRNAs increased gradually from the control group to the pre-diabetes group to the T2DM group. The diagnostic value of ENST00000550337.1 was then tested in the third cohort, and its high diagnostic value for pre-diabetes and T2DM was confirmed. LncRNA ENST00000550337.1 is a potential diagnostic biomarker for pre-diabetes and T2DM.

Peripheral blood circular RNA hsa_circ_0124644 can be used as a diagnostic biomarker of coronary artery disease.

The aim of the present study was to investigate the expression of circular RNAs (circRNAs) in the peripheral blood of coronary artery disease (CAD) patients and the potential use of circRNAs as diagnostic biomarkers of CAD. We first analysed peripheral blood circRNAs of 12 CAD patients and 12 control individuals by RNA microarray and found that 22 circRNAs were differentially expressed between these two groups: 12 were upregulated, and 10 were downregulated. Then, we selected 5 circRNAs as candidate biomarkers under stricter screening criteria and verified them in another group of subjects consisting of 30 control individuals and 30 CAD patients with different SYNTAX scores. These 5 circRNAs were all remarkably increased in the CAD group. Hsa_circ_0124644 had the largest area under the curve (AUC). We tested hsa_circ_0124644 in an independent cohort consisting of 115 control individuals and 137 CAD patients. After we included the risk factors for CAD, the AUC slightly increased from 0.769 (95% confidence interval = [0.710-0.827], P < 0.001) to 0.804 ([0.751-0.857], P < 0.001), and when combined with hsa_circ_0098964, the diagnostic value slightly increased. Taken together, our results suggest that hsa_circ_0124644 can be used as a diagnostic biomarker of CAD.

Enhanced effect of VEGF165 on L-type calcium currents in guinea-pig cardiac ventricular myocytes.

The mechanisms of vascular endothelial growth factor 165 (VEGF165) on electrical properties of cardiomyocytes have not been fully elucidated. The aim of this study is to test the hypothesis that VEGF165, an angiogenesis-initiating factor, affects L-type calcium currents (ICa,L) and cell membrane potential in cardiac myocytes by acting on VEGF type-2 receptors (VEGFR2). ICa,L and action potentials (AP) were recorded by the whole-cell patch clamp method in isolated guinea-pig ventricular myocytes treated with different concentrations of VEGF165 proteins. Using a VEGFR2 inhibitor, we also tested the receptor of VEGF165 in cardiomyocytes. We found that VEGF165 increased ICa,L in a concentration-dependent manner. SU5416, a VEGFR2 inhibitor, almost completely eliminated VEGF165-induced ICa,L increase. VEGF165 had no significant influence on action potential 90 (APD90) and other properties of AP. We conclude that in guinea-pig ventricular myocytes, ICa,L can be increased by VEGF165 in a concentration-dependent manner through binding to VEGFR2 without causing any significant alteration to action potential duration. Results of this study may further expound the safety of VEGF165 when used in the intervention of heart diseases.

Hsa_circ_0054633 in peripheral blood can be used as a diagnostic biomarker of pre-diabetes and type 2 diabetes mellitus.

AIMS: The purpose of the current study was to investigate the characteristic expression of circular RNAs (circRNAs) in the peripheral blood of type 2 diabetes mellitus (T2DM) patients and their potential as diagnostic biomarkers for pre-diabetes and T2DM. METHODS: CircRNAs in the peripheral blood from six healthy individuals and six T2DM patients were collected for microarray analysis, and an independent cohort study consisting of 20 normal cases, 20 pre-diabetes patients and 20 T2DM patients was conducted to verify the five chosen circRNAs. We then tested hsa_circ_0054633 in a third cohort (control group, n = 60; pre-diabetes group, n = 63; and T2DM group, n = 64) by quantitative real-time polymerase chain reaction (Q-PCR). RESULTS: In total, 489 circRNAs were discovered to be differentially expressed between the two groups, and of these, 78 were upregulated and 411 were downregulated in the T2DM group. Five circRNAs were then selected as candidate biomarkers and further verified in a second cohort. Hsa_circ_0054633 was found to have the largest area under the curve (AUC). The diagnostic capacity of hsa_circ_0054633 was tested in a third cohort. After introducing the risk factors of T2DM, the hsa_circ_0054633 AUCs for the diagnosis of pre-diabetes and T2DM slightly increased from 0.751 (95% confidence interval [0.666-0.835], P < 0.001) to 0.841 ([0.773-0.910], P < 0.001) and from 0.793 ([0.716-0.871], P < 0.001) to 0.834 ([0.762-0.905], P < 0.001), respectively. CONCLUSIONS: Hsa_circ_0054633 presented a certain diagnostic capability for pre-diabetes and T2DM.

Safety and efficacy of rivaroxaban versus warfarin in patients undergoing catheter ablation of atrial fibrillation: a meta-analysis of observational studies.

The safety and efficacy of rivaroxaban in the periprocedural anticoagulation for patients undergoing catheter ablation of atrial fibrillation is not well established. We sought to systematically review this evidence using data from multiple studies. A thorough literature search was conducted in MEDLINE, EMABSE, Web of knowledge, clinicaltrials.gov, and the Cochrane library up to November 2014. Studies of at least 100 patients in rivaroxaban and warfarin groups were included. Nine observational studies were identified enrolling a total of 4,334 patients (1,210 treated with rivaroxaban and 3,124 with warfarin). The primary outcomes were thromboembolic events and major bleeding. The fixed-effects model meta-analysis was performed and risk ratios (RRs) were calculated. No significant differences were found between patients treated with rivaroxaban and warfarin with regard to thromboembolic events (0.25% rivaroxaban vs. 0.29% warfarin; RR: 0.61; 95%CI: 0.21-1.76; P=0.36) and major bleeding (1.03% rivaroxaban vs. 1.83% warfarin; RR: 0.51; 95%CI: 0.26-1.00; P=0.05). This meta-analysis suggests that patients treated with rivaroxaban have a similar incidence of thromboembolic events and major bleeding compared to warfarin. Signals were seen favoring rivaroxaban; however, considering low events rates, more high-quality studies are necessary to thoroughly compare the two strategies.

Effects of thyroid dysfunction on the severity of coronary artery lesions and its prognosis.

BACKGROUND: Abnormal thyroid hormone metabolism influences the occurrence and progress of coronary heart disease (CHD). The aim of the present study was to analyze the severity of coronary artery lesions and the prognosis of thyroid dysfunction patients admitted for coronary angiography (CAG). METHODS: From July 2011 to July 2012, 605 consecutive patients with suspected coronary heart disease admitted for CAG were selected. The patients were divided into three groups, based on their thyroid function prior to CAG: euthyroid group (n=455 patients), low T3 syndrome group (n=96 patients), and hypothyroidism group (n=54 patients). All patients underwent CAG. Then the severity of coronary artery lesions was assessed by Gensini scores. All patients were followed up for major adverse cardiac events. RESULTS: The prevalence of CHD in low T3 syndrome group and hypothyroidism group was significantly higher than that in the euthyroid group (p<0.001 and p=0.004, respectively). Moreover, the severity of coronary artery lesions in low T3 syndrome group and hypothyroidism group was significantly greater than that in the euthyroid group (all p<0.001). Multinomial logistic regression analysis demonstrated that low T3 syndrome was an independent risk factor of coronary artery moderate [odds ratio (OR)=4.268, 95% CI: 3.294-7.450, p=0.016] and severe (OR=4.294, 95% CI: 2.259-9.703, p<0.001) lesions. The mean duration of follow-up was 15.3±3.8 months; patients with thyroid dysfunction had a significantly worse prognosis as compared to those in the euthyroid group for the composite end-point (p<0.01). Moreover, the incidence of the composite end-point (all-cause death, non-fatal myocardial infarction, and coronary revascularization) was significantly higher in low T3 syndrome group and hypothyroidism group compared with that of in the euthyroid group (all p<0.001). CONCLUSIONS: The patients with hypothyroidism and low T3 syndrome had a high prevalence of CHD, increased severity of coronary artery lesions and poor prognosis.

The effect of low FT3 levels on coronary artery calcification and MACE in outpatients with suspected coronary artery disease.

OBJECTIVE: Considerable evidence suggests that thyroid dysfunction, especially hypothyroidism, may lead to coronary artery disease (CAD). The aim of this study is to investigate the effect of low serum levels of free triiodothyronine (FT3) on coronary artery calcification in outpatients with suspected CAD and the occurrence rate of major adverse cardiac events (MACE) in these patients. METHODS: A total of 588 outpatients with suspected CAD were enrolled in this study. The patients' blood samples were assayed for FT3, free thyroxine, thyroid stimulating hormone and serum lipids. On the basis of FT3 levels, these patients were divided into low FT3 (FT3<3.5 pmol/l; n=127) and normal FT3 (≥3.5 pmol/l; n=461) groups. Coronary artery calcification scores (CACS) were measured using dual-source computed tomography. The occurrence of MACE was recorded during the follow-up period (8-29 months) and their relationship with FT3 levels was investigated. RESULTS: Patients with low FT3 levels had higher CACS (337.52±339.36 vs. 194.89±347.29, P<0.001) and a higher incidence of MACE (7.9 vs. 2.2%, P=0.002) compared with those with normal FT3 levels (≥3.5 pmol/l). Logistic regression analysis showed that the FT3 levels are inversely associated with CACS (odds ratio=0.463, 95% confidence interval=0.282-0.761, P=0.002) and patients with CACS greater than 100 have lower FT3 levels than those with lower CACS (P<0.001). Kaplan-Meier analysis showed that patients with low FT3 levels have a higher incidence of MACE. CONCLUSION: FT3 levels were inversely associated with CACS and the incidence of MACE in patients with suspected CAD. A low FT3 level was an important predictor of the occurrence of MACE.

[Relationship of serum free T3 with the coronary artery calcification and major adverse cardiac events in patients with suspected coronary artery disease].

OBJECTIVE: To survey the association of serum free triiodothyronine (FT3) level with coronary artery calcification and major adverse cardiac events (MACE) in outpatients with suspected coronary artery disease (CAD). METHODS: A total of 577 outpatients with suspected CAD, who underwent dual-source computed tomography and FT3 detection were included, patients were followed up for 8-29 months for the major adverse cardiac events (death, MI, PCI, CABG). These patients were divided into low FT3 ( < 3.5 pmol/L, n = 126) and normal FT3 ( ≥ 3.5 pmol/L, n = 451) group based on the FT3 level, and divided into CACS > 100 (n = 235) and CACS ≤ 100 (n = 342) group based on the coronary artery calcium score (CACS). Related factors to CACS and MACE were analyzed using logistic regression (stepwise) analysis. RESULTS: CACS (146.7 (55.8, 599.1) vs. 34.8 (0, 261.9), P < 0.001) and MACE (7.9% (10/126) vs. 2.0% (9/451) , P = 0.003) were significantly higher in the low FT3 group than in normal FT3 group. Logistic regression analysis demonstrated that the FT3 levels are inversely associated with the CACS (OR = 0.442, 95%CI = 0.317-0.618, P < 0.001). Kaplan-Meier analysis displayed that patients with low FT3 levels had a lower cumulative survival rate than patients with normal FT3 levels (P = 0.005), and patients with CACS > 100 also had a lower cumulative survival rate than patients with CACS ≤ 100(P < 0.001). CONCLUSIONS: FT3 levels are associated with coronary artery calcification scores and the incidence rate of MACE in patients with suspected coronary artery disease. A low FT3 level is considered as an important risk factor of high calcification scores and MACE.

Suppression of rat Frizzled-2 attenuates hypoxia/reoxygenation-induced Ca2+ accumulation in rat H9c2 cells.

Growing evidence suggests that Ca(2+) overload is one of the major contributors of myocardial ischemia/reperfusion-induced injury. Since Frizzled-2 receptor, a seven transmembrane protein, transduces downstream signaling by specialized binding of Wnt5a to increase intracellular Ca(2+) release, this work aimed to investigate the effect of Frizzled-2 on Ca(2+) accumulation in H9c2 cells, which were subjected to hypoxia/reoxygenation to mimic myocardial ischemia/reperfusion. After exposing H9c2 cells to hypoxia/reoxygenation, we observed higher expression of Frizzled-2 and Wnt5a as compared to control group cells. Hypoxia/reoxygenation-induced intracellular Ca(2+) accumulation approached that of cells transfected with frizzled-2 plasmid. In cells treated with RNAi specifically designed against frizzled-2, intracellular Ca(2+) in both hypoxia/reoxygenation-treated cells and plasmid-treated cells were decreased. Rats that underwent ischemia/reperfusion injury exhibited increased intracellular Ca(2+) with high expression levels of Frizzled-2 and Wnt5a as compared to the sham group. Our data indicates that upon binding to Wnt5a, increased Frizzled-2 expression after hypoxia/reoxygenation treatment activated intracellular calcium release in H9c2 cells. Our findings provide a new perspective in understanding calcium overload in myocardial ischemia/reperfusion.

In vivo assessment of optimal viewing angles from X-ray coronary angiography.

AIMS: To propose and validate a novel approach to determine the optimal angiographic viewing angles for a selected coronary (target) segment from X-ray coronary angiography, without the need to reconstruct the entire coronary tree in three-dimensions (3D), such that subsequent interventions are carried out from the best view. METHODS AND RESULTS: The approach starts with standard quantitative coronary angiography (QCA) of the target vessel in two angiographic views. Next, the target vessel is reconstructed in 3D, and in a very simple and intuitive manner, the possible overlap of the target vessel and other vessel segments can be assessed, resulting in the best view with minimum foreshortening and overlap. A retrospective study including 67 patients was set up for the validation. The overlap prediction result was compared with the true overlap on the available angiographic views (TEST views). The foreshortening for the views proposed by the new approach software viewing angle (SVA) and the views used during the stent deployment software viewing angle (EVA) were compared. Two experienced interventional cardiologists visually evaluated the success of SVA with respect to EVA. The evaluation results were graded into five values ranging from -2 to 2. The overlap prediction algorithm successfully predicted the overlap condition for all 235 TEST views. EVA was associated with more foreshortening than SVA (8.9% ± 8.2% vs. 1.6% ± 1.5%, p<0.001). The average evaluated point for the success of SVA was 0.94 ± 0.80 (p <0.001), indicating that the evaluators were in favor of the optimal views determined by the proposed approach versus the views used during the actual intervention. CONCLUSIONS: The proposed approach is able to accurately and quickly determine the optimal viewing angles for the online support of coronary interventions.

[A comparative study of target vessel assessments by three- and two-dimensional quantitative coronary X-ray angiography and visual estimation].

OBJECTIVE: To compare the efficacy of three-dimensional (3D) and two-dimensional (2D) quantitative coronary X-ray angiography (QCA) and visual estimation in the assessment of target vessels. METHODS: The radiographic data of 60 patients (65 vessel segments) receiving coronary angiography and interventional stent placement were retrospectively analyzed. The area stenosis, diameter stenosis, lesion length, and reference diameter assessed by Medis 3D QCA, Siemens 2D QCA and visual estimation were compared. RESULTS: Three-dimensional reconstruction was successfully performed for 65 vessel segments, and 3 target vessel were excluded due to the lack of a second angiographic view for 3D reconstruction. There were significant differences in the assessments of the area stenosis [(73.87 ∓ 8.98)% vs (79.10 ∓ 8.06)% vs (83.53 ∓ 8.19)%, P<0.001], lesion length (28.95 ∓ 17.31 mm vs 26.20 ∓ 16.04 mm vs 27.21 ∓ 16.58 mm, P<0.001), reference diameter (28.95 ∓ 17.31 mm vs 26.2 ∓ 16.04 mm vs 27.21∓16.58 mm, P<0.001) by 3D QCA, 2D QCA and visual estimation; the diameter stenosis assessed by 3D [(54.21 ∓ 9.48)%] and 2D QCA [(57.84 ∓ 10.17)%] also differed significantly (P=0.016). CONCLUSION: 3D QCA allows successful three-dimensional reconstruction of the target vessel and restores the actual dimensions of the vessel for a more accurate assessment of coronary artery disease than 2D QCA and visual estimation.

[Analysis of glucose levels and the risk for coronary heart disease in elderly patients in Guangzhou Haizhu district].

OBJECTIVE: To investigate the prevalence of diabetes and prediabetes and their association with the risk for coronary heart disease (CHD) in elderly residents in Haizhu District of Guangzhou. METHODS: Stratified random sampling was employed to select a total of 1800 resident aged 50 years or older in the region. The fasting fingertip blood glucose>5.6 mmol/L was used as the criterion for the initial screening. The data were collected from qualified subjects via scheduled questionnaire surveys, blood collection and testing, and physical examination. The subjects were divided into the 3 groups, namely normal blood glucose, prediabetes, and diabetes groups. The combination rates of the relevant risk factors (hypertension, hyperlipemia, obesity, and central obesity) were compared among the groups by Framingham Heart Study to predict the occurrence of CHD in 10 years. RESULTS: The incidence was 11.00% for prediabetes and 7.56% for diabetes in the elderly residents in Haizhu District. The occurrence of hypertension, hyperlipemia, obesity, and central obesity was significant higher in the prediabetes and diabetes group than in the normal blood glucose group, and showed no significant differences between the former two groups. The 10-year risks for CHD were markedly higher in both the prediabetes and diabetes groups than in the normal blood glucose group, but similar between the former two groups. CONCLUSION: Elderly patients with prediabetes and diabetes have significantly increased 10-year risk for CHD in comparison with those with normal blood glucose, but the risk is similar between the former two groups, indicating a close association of IGR (impaired fasting glucose+ impaired fasting glucose) with CHD. Early control of blood glucose is essential to the prevention and control of CHD.