An evidence of brain-heart disorder: mental stress-induced myocardial ischemia regulated by inflammatory cytokines.

OBJECTIVE: Underlying Coronary Artery Disease (CAD) complicated by Mental Stress-Induced Myocardial Ischemia (MSIMI) has been linked with an increased risk for adverse cardiovascular events and even sudden death. However, the underlying mechanisms of MSIMI remain unknown. In this study, we investigated cytokine levels at baseline inflammation status and during acute inflammatory responses to mental stress in patients with known CAD who presented with MSIMI. METHOD: 77 patients with known CAD were recruited and all underwent echocardiography before and during arithmetic stress task. MSIMI was diagnosed by new or worsening wall motion abnormalities greater than or equal to a 5% reduction of left ventricle ejection fraction. Inflammatory markers were measured both before and immediately after the Mental Stress (MS) by ELISA kits. Repeated measures models were used to report the responses and mixed linear regression models were used to report the differences between MSIMI negative and positive patients. RESULT: MS induced a significant increase in Stromal Cell-Derived Factor-1α (SDF-1α) and Monocyte Chemoattractant Protein-1 (MCP-1) in all subjects; 20.78% of the patients with known CAD developed MSIMI during the arithmetic task. MSIMI positive patients had significantly lower baseline levels of Interleukin-1ß (IL-1ß) and Tumor Necrosis Factor-α (TNF-α), but a higher response in levels of SDF-1α than MSIMI negative patients. CONCLUSION: MS can induce acute inflammatory responses. MSIMI is associated with lower levels of IL-1ß and TNF-α at baseline and higher levels of SDF-1α in response to MS.

Beneficial effects of trimetazidine on expression of serotonin and serotonin transporter in rats with myocardial infarction and depression.

BACKGROUND: Trimetazidine is an anti-ischemic drug that can inhibit platelet aggregation and regulate serotonin (5-hydroxytryptamine [5-HT]) release. The purpose of this study was to investigate the therapeutic effects of trimetazidine on 5-HT and serotonin transporter (SERT) expression in experimentally induced myocardial infarction (MI), depression, and MI + depression. MATERIALS AND METHODS: Eighty Sprague Dawley (SD) rats were randomly divided into a trimetazidine group and a saline group of 40 rats each. The trimetazidine group was given trimetazidine pretreatment for 4 weeks, while the saline group received saline for 4 weeks. Both groups were then subdivided into four subgroups (n=10), which were each subjected to a unique disease condition: sham surgery, MI, depression, or MI + depression. All rats were sacrificed 3 days thereafter, and serum and platelet levels of 5-HT and SERT were assessed. In addition, we experimented with trimetazidine posttreatment. Twenty SD rats underwent MI surgery, and were then randomly divided into a treatment and a saline group (n=10 each). For 4 weeks post-surgery, the trimetazidine group was given trimetazidine, while the saline group received saline. Serum and platelet levels of 5-HT and SERT were assessed. RESULTS: Pretreatment with trimetazidine: in the nontreatment saline group, MI, depression, and MI + depression showed significant declines (P<0.05) in both serum and platelet 5-HT levels compared to sham. Trimetazidine treatment significantly increased serum and platelet 5-HT levels in the MI, depression, and MI + depression (P<0.05) subgroups compared to their counterparts in the saline group. Results for SERT were heterogeneous between serum and platelets. Trimetazidine treatment significantly decreased serum levels of SERT in the sham surgery subgroup (P<0.05), while significantly increasing levels in depression rats, compared to control (P<0.05). In platelets, trimetazidine significantly decreased SERT in sham surgery, MI, depression, and MI + depression rats, compared to control (P<0.05). This contrast suggests that trimetazidine has opposite effects in serum and platelet SERT levels for the three disease models. Post-surgery trimetazidine: increased serum 5-HT (P<0.05) and serum SERT (P<0.05) were observed, compared to control. In platelets, trimetazidine decreased both 5-HT and SERT compared to control, significantly (P<0.05) for 5-HT, but not significantly for SERT (P>0.05). CONCLUSION: Trimetazidine has a regulatory effect on 5-HT and SERT in the serum and platelets. Because of the downstream effects of this regulation on blood vessel function and myocardial protection, trimetazidine may be a therapeutic or preventive agent in several disease processes, including MI, depression, and the comorbidity between these two diseases. Further investigation, aimed at exploring the clinical potential of trimetazidine, is therefore warranted.

5-Hydroxytryptamine Changes under Different Pretreatments on Rat Models of Myocardial Infarction and/or Depression.

BACKGROUND:: Psychocardiological researches have suggested a central role of 5-hydroxytryptamine (5-HT) on psychocardiological mechanism. This study aimed to further explore the central role of 5-HT and pretreatment effects of XinLingWan on rats with myocardial infarction (MI) and/or depression. METHODS:: Ninety Sprague-Dawley rats were randomly divided into three groups: MI group, depression group, and MI + depression group (n = 30 in each group). Each group was then divided into three subgroups (n = 10 in each subgroup): a negative control subgroup (NCS), a Western medicine subgroup (WMS), and a traditional Chinese medicine subgroup (TCMS), which were received pretreatment once a day for 4 weeks by saline, 20 mg/kg sertraline mixed with 2 ml saline, and 40 mg/kg XingLingWan mixed with 2 ml saline, respectively. Different rat models were established after different pretreatments. Rats were then sacrificed for detection of serum 5-HT, platelet 5-HT, 5-HT2A receptors (5-HT2AR), and serotonin transporter (SERT). Data were analyzed by one-way analysis of variance (ANOVA) and least-significant difference (LSD) testing. RESULTS:: MI group: compared with NCS, there was a significant increase in WMS and TCMS of serum 5-HT (176.15 ± 11.32 pg/ml vs. 334.50 ± 29.09 pg/ml and 474.04 ± 10.86 pg/ml, respectively, both P = 0.000), platelet 5-HT (129.74 ± 27.17 pg/ml vs. 322.24 ± 11.60 pg/ml and 340.4 5 ± 17.99 pg/ml, respectively, both P = 0.000); depression group: compared with NCS, there was a significant increase in WMS and TCMS of serum 5-HT (194.69 ± 5.09 pg/ml vs. 326.21 ± 39.98 pg/ml and 456.33 ± 23.12 pg/ml, respectively, both P = 0.000), platelet 5-HT (175.15 ± 4.07 pg/ml vs. 204.56 ± 18.59 pg/ml and 252.03 ± 22.26 pg/ml, respectively, P = 0.004 and P = 0.000, respectively); MI + depression group: compared with NCS, there was a significant increase in both WMS and TCMS of serum 5-HT (182.50 ± 10.23 pg/ml vs. 372.55 ± 52.23 pg/ml and 441.76 ± 23.38 pg/ml, respectively, both P = 0.000) and platelet 5-HT (180.83 ± 11.08 pg/ml vs. 221.12 ± 22.23 pg/ml and 265.37 ± 29.49 pg/ml, respectively, P = 0.011 and P = 0.000, respectively). CONCLUSIONS:: By elevating the amount of 5-HT and modulating 5-HT2AR and SERT levels in serum and platelets, XinLingWan and sertraline were found to exert pretreatment effect on rat models of MI and/or depression.

Association between coronary heart disease and erectile dysfunction in Chinese Han population.

To investigate the association between coronary heart disease (CHD) and erectile dysfunction (ED) in Chinese Han population. Patients who went to the andrological out-patient clinic of our hospital between August 1, 2015 and May 1, 2016 and met all eligible criteria were enrolled in this study. The patients diagnosed as ED using self-administered International Index of Erectile Function-5 (IIEF-5) questionnaire were considered as case group and others were considered as control. The cases were categorized as mild, moderate, and severe ED. Subjects were interviewed for the history of CHD. Uni- and multivariate logistic regression models were used to calculate odds ratios (ORs) and corresponding 95% confidence intervals (CIs) using the SPSS 18.0 software. A total of 240 participants (56 ED patients and 184 controls) were enrolled. CHD prevalence was higher in cases without statistical significance (OR = 1.20, 95%CI = 0.63-2.29; p = 0.58). Results of adjusted analysis also showed a non-significantly increased risk (OR = 1.25, 95%CI = 0.55-2.85; p = 0.59). Stratified analysis by severity of ED revealed similar results. This study suggests no significant association exists between CHD and ED in Chinese Han population.

The effects of tanshinone IIA on hypoxia/reoxygenation-induced myocardial microvascular endothelial cell apoptosis in rats via the JAK2/STAT3 signaling pathway.

OBJECTIVE: This study aims to investigate the effects of tanshinone IIA on hypoxia/reoxygenation (H/R)-induced myocardial microvascular endothelial cell (MMEC) apoptosis in rats. METHODS: MMECs from 10-days aged rats were isolated, cultured and identified, which were then divided into following groups: control group, control+tanshinone IIA (50µM) group, H/R model group, H/R+tanshinone IIA (5µM) group, H/R+tanshinone IIA (50µM) pre-treatment group, H/R+AG490 (50µM) pre-treatment group and H/R+AG490 (50µM)+tanshinone IIA (50µM) pre-treatment group. MTT assay, TUNEL staining and flow cytometry were used to measure the cellular viability and apoptosis. Western-blot were performed to detect protein expressions in JAK2/STAT3 signaling pathway. RESULTS: Compared with control group, H/R group showed decreased cell viability, increased apoptosis rate, increased proportions of cells into G0/G1 phase, decreased proportions of cells in S phase and G2/M phase, as well as up-regulated expressions of JAK2, STAT3, p53, Bax, Caspase-3, pJAK2 and pSTAT3, and down-regulated Bcl-2 expression (all P<0.05). Compared with H/R group, H/R+tanshinone IIA (5µM) group, H/R+tanshinone IIA (50µM) group H/R+AG490 (50µM) group and H/R+AG490 (50µM)+tanshinone IIA (50µM) group had increased cell viability, decreased apoptosis rate, reduced proportions of cells into G0/G1 phase, elevated proportions of cells in S phase and G2/M phase, as well as down-regulated expressions of JAK2, STAT3, p53, Bax, Caspase-3, pJAK2 and pSTAT3, elevated expression of Bcl-2 (all P<0.05). The most remarkable changes were observed in H/R+AG490 (50µM)+tanshinone IIA (50µM) group. CONCLUSION: Tanshinone IIA may attenuate H/R-induced MMEC apoptosis in rats by inhibiting the JAK2/STAT3 signaling pathway and regulating the expressions of p53, Bax, Caspase-3 and Bcl-2, which may provide a protective effect of tanshinone IIA for MMECs.

Time Rate of Blood Pressure Variation Is Associated With Endothelial Function in Patients With Metabolic Syndrome.

The time rate of blood pressure (BP) variation indicates the speed of BP fluctuations. Previous studies have demonstrated that the time rate of BP variation was associated with target organ damage. However, the association between time rate of BP variation and endothelial function has not been evaluated.24-hour ambulatory blood pressure monitoring (ABPM) was performed in 61 patients with metabolic syndrome. Time rate of BP variation was calculated from BP recordings of ABPM. Endothelial function was assessed using reactive hyperemia-peripheral arterial tonometry index (RHI) by EndoPat2000. Multiple linear regression models were used to detect the association between time rate of BP variation and RHI.Among all the subjects (n = 61), the multiple linear regression models revealed that the daytime rate of systolic blood pressure (SBP) variation was independently associated with RHI (ß = -0.334, P = 0.008). A 0.1 mmHg/minute increase in the daytime rate of SBP variation correlated with a decline of 0.20 in RHI. The same effect was also found in the subjects with eGFR ≥ 60 mL/ (minute*1.73 m(2)). A greater association was found in those who were not taking a statin, ß-blocker, ACEI/ARB, or diuretic and those without diabetes compared with those with any antihypertensive medication or with diabetes. Other ambulatory blood pressure parameters and central hemodynamics were not found to be associated with RHI.Our findings have shown that the daytime rate of SBP variation was associated with endothelial function in patients with metabolic syndrome, independent of other BP parameters and central hemodynamics.

Tumor necrosis factor-alpha G-238A polymorphism and coronary artery disease risk: a meta-analysis of 4,222 patients and 4,832 controls.

BACKGROUND: The aim of the present study was to investigate the association between tumor necrosis factor-alpha (TNF-α) gene G-238A polymorphism and risk of coronary artery disease (CAD) using a meta-analytical approach. METHODS: The PubMed and Embase databases were searched for relevant publications up to January 13, 2015. Four authors (XPH, XDZ, XTZ, and ZJZ) independently selected the studies, extracted, and analyzed the data using the Comprehensive Meta-Analysis software. The sensitivity and subgroups analyses were also performed. Either a fixed effects or a random effects model was used to estimate pooled odds ratios (ORs) and their 95% confidence intervals (CIs). RESULTS: Finally, ten articles including eleven case-control studies involving 4,222 patients and 4,832 controls were yielded. The results indicated no significant association between G-238A polymorphism and CAD risk (A vs G: OR =1.08, 95% CI =0.89-1.30; AA vs GG: OR =1.15, 95% CI =0.59-2.25; GA vs GG: OR =1.14, 95% CI =0.88-1.48; AA vs [GG + GA]: OR =1.09, 95% CI =0.56-2.14; (GA + AA) vs GG: OR =1.11, 95% CI =0.90-1.38). In the subgroup analyses, similar results were obtained with overall populations. The sensitivity analyses showed that the overall results were robust. No publication bias was detected. CONCLUSION: Based on current evidence, we can conclude that TNF-α G-238A polymorphism might not be associated with CAD risk.

Changes of Serotonin (5-HT), 5-HT2A Receptor, and 5-HT Transporter in the Sprague-Dawley Rats of Depression, Myocardial Infarction and Myocardial Infarction Co-exist with Depression.

BACKGROUND: To evaluate whether serotonin (5-HT), 5-HT2A receptor (5-HT2AR), and 5-HT transporter (serotonin transporter [SERT]) are associated with different disease states of depression, myocardial infarction (MI) and MI co-exist with depression in Sprague-Dawley rats. METHODS: After established the animal model of four groups include control, depression, MI and MI with depression, we measured 5-HT, 5-HT2AR and SERT from serum and platelet lysate. RESULTS: The serum concentration of 5-HT in depression rats decreased significantly compared with the control group (303.25 ± 9.99 vs. 352.98 ± 13.73; P = 0.000), while that in MI group increased (381.78 ± 14.17 vs. 352.98 ± 13.73; P = 0.000). However, the depression + MI group had no change compared with control group (360.62 ± 11.40 vs. 352.98 ± 13.73; P = 0.036). The changes of the platelet concentration of 5-HT in the depression, MI, and depression + MI group were different from that of serum. The levels of 5-HT in above three groups were lower than that in the control group (380.40 ± 17.90, 387.75 ± 22.28, 246.40 ± 18.99 vs. 500.29 ± 20.91; P = 0.000). The platelet lysate concentration of 5-HT2AR increased in depression group, MI group, and depression + MI group compared with the control group (370.75 ± 14.75, 393.47 ± 15.73, 446.66 ± 18.86 vs. 273.66 ± 16.90; P = 0.000). The serum and platelet concentration of SERT in the depression group, MI group and depression + MI group were all increased compared with the control group (527.51 ± 28.32, 602.02 ± 23.32, 734.76 ± 29.59 vs. 490.56 ± 16.90; P = 0.047, P = 0.000, P = 0.000 in each and 906.38 ± 51.84, 897.33 ± 60.34, 1030.17 ± 58.73 vs. 708.62 ± 51.15; P = 0.000 in each). CONCLUSIONS: The concentration of 5-HT2AR in platelet lysate and SERT in serum and platelet may be involved in the pathway of MI with depression. Further studies should examine whether elevated 5-HT2AR and SERT may contribute to the biomarker in MI patients with depression.

[Effect of pretreatment with qishen yiqi dropping pills on right cardiac function of patients undergoing valve replacement].

In this study, 120 patients with rheumatic heart disease undergoing valve replacement were randomly divided into the control group and the Qishen group, with 60 cases in each group. Before the operation, the control group was given routine heart and diuretic treatments and placebo of Qishen Yiqi dropping pills for seven days (0.5 g each time, three times a day); While the Qishen group was given Qishen Yiqi dropping pills for seven days (0.5 g each time after meal, three times a day) on the basis of the routine treatments. The right ventricular end-diastolic volume (RVEDV), end-systolic volume (RVESV), stroke volume (SV) and right ventricular ejection fraction (RVEF) were detected after the operation. The results showed that patients in the two groups showed significantly lower right ventricular end diastolic volume (RVEDV), right ventricular end systolic volume (RVESV) and stroke volume (SV) decreased than that before the operation, but with significantly higher Ejection fraction (RVEF) significantly than that before the operation. However, the Qishen group showed a significantly lower right heart function reduction than the control group, with the statistical significance in the differences (P < 0.05). This indicated that the pretreatment with Qishenyiqi Drop Pills showed a remarkable efficacy in the improvement of right ventricular function after valve replacement.

The electrophysiological effects of qiliqiangxin on cardiac ventricular myocytes of rats.

Qiliqiangxin, a Chinese herb, represents the affection in Ca channel function of cardiac myocytes. It is unknown whether Qiliqiangxin has an effect on Na current and K current because the pharmacological actions of this herb's compound are very complex. We investigated the rational usage of Qiliqiangxin on cardiac ventricular myocytes of rats. Ventricular myocytes were exposed acutely to 1, 10, and 50 mg/L Qiliqiangxin, and whole cell patch-clamp technique was used to study the acute effects of Qiliqiangxin on Sodium current (I Na), outward currents delayed rectifier outward K(+) current (I K), slowly activating delayed rectifier outward K(+) current (I Ks), transient outward K(+) current (I to), and inward rectifier K(+) current (I K1). Qiliqiangxin can decrease I Na by 28.53% ± 5.98%, and its IC50 was 9.2 mg/L. 10 and 50 mg/L Qiliqiangxin decreased by 37.2% ± 6.4% and 55.9% ± 5.5% summit current density of I to. 10 and 50 mg/L Qiliqiangxin decreased I Ks by 15.51% ± 4.03% and 21.6% ± 5.6%. Qiliqiangxin represented a multifaceted pharmacological profile. The effects of Qiliqiangxin on Na and K currents of ventricular myocytes were more profitable in antiarrhythmic therapy in the clinic. We concluded that the relative efficacy of Qiliqiangxin was another choice for the existing antiarrhythmic therapy.

[Effects of qishenyiqi gutta pills on calcium/calmodulin dependent protein kinase II in rats with renal hypertension].

OBJECTIVE: To explore the effects of qishenyiqi gutta pills on myocardial hypertrophy of left ventricle and calcium/calmodulin dependent protein kinase II (CAMK II) in rats with renal hypertension and elucidate its intervention mechanism for myocardial hypertrophy. METHODS: A total of 50 Wistar rats were randomly divided into 5 groups of sham-operation, control, high-dose qishenyiqi gutta pills, low-dose qishenyiqi gutta pills and valsartan (n = 10 each). The rat model of myocardial hypertrophy with renal hypertension was established by the 2-kidney 1-clip (2K1C) method. The experimental animals were divided into control, high-dose, low-dose and valsartan groups. At Week 5 postoperation, valsartan group received an oral dose of valsartan (30 mg×kg(-1)×d(-1)), high-dose and low-dose groups took qishenyiqi gutta pills (250 and 125 mg×kg(-1)×d(-1)) while sham-operation and control groups had the same dose of normal saline solution. Tail arterial pressure was detected weekly and continued for 8 weeks. At the end of Week 12, the animals were sacrificed to harvest myocardial tissue of left ventricle for detecting left ventricular mass index (LVMI). The collagen volume fraction (CVF) of myocardium was examined by Van Gieson staining, the activities of superoxide dismutase (SOD) and reactive oxygen species (ROS) were detected by enzyme-linked immunosorbent assay (ELISA) and the expression of CAMK II was detected by immunohistochemistry and Western blot. RESULTS: (1) Blood pressures were significantly higher in high-dose, low-dose and control groups than those in sham-operation and valsartan groups ((167.66 ± 11.48), (166.72 ± 13.51), (174.34 ± 14.52) vs (119.57 ± 6.30), (131.80 ± 12.49) mm Hg, P < 0.01). The changes of blood pressure had no significant difference between high-dose and low-dose groups. (2) LVMI and CVF increased significantly in high-dose, low-dose and valsartan groups versus sham-operation group (LVMI: (1.98 ± 0.16), (2.09 ± 0.14), (1.97 ± 0.17) vs (1.74 ± 0.17) g/kg; CVF: 0.94% ± 0.22%, 2.53% ± 0.61%, 0.81% ± 0.20% vs 0.45% ± 0.13%) (P < 0.01, P < 0.05), but decreased significantly versus control group (LVMI: (1.98 ± 0.16), (2.09 ± 0.14), (1.97 ± 0.17) vs (2.28 ± 0.28) g/kg; CVF: 0.94% ± 0.22%, 2.53% ± 0.61%, 0.81% ± 0.20% vs 4.73% ± 1.04%) (P < 0.01, P < 0.05). (3) The expression of CAMK II was significantly higher in high-dose, low-dose, valsartan and control groups than that in sham-operation group (65.9%, 95.3%, 84.8%, 160.1% vs 67.7%). And it was significantly lower in high-dose, low-dose and valsartan groups than that in control group (65.9%, 95.3%, 84.8% vs 160.1%). There was no statistical difference among high-dose, low-dose and valsartan groups. CONCLUSIONS: Qishenyiqi gutta pills may retard myocardial hypertrophy of left ventricle in rats with renal hypertension. And the mechanism is probably be correlated with its antioxidant activity and inhibited expression of myocardial CAMK II.

Increasing age associated with elevated cardio-ankle vascular index scores in patients with type 2 diabetes mellitus.

OBJECTIVE: The study investigated the relationship between arterial stiffness calculated using the cardio-ankle vascular index (CAVI), diagnosis of type 2 diabetes mellitus and type 2 diabetes-related cardiovascular complications, in patients with type 2 diabetes mellitus (type 2 diabetes) and nondiabetic patients. METHODS: A retrospective cross-sectional study was conducted in patients with type 2 diabetes and age-matched nondiabetic patients. CAVI was measured using an automatic vascular screening system. Parameters associated with type 2 diabetes and cardiovascular complications were also measured. RESULTS: A total of 51 patients with type 2 diabetes and 59 nondiabetic patients were enrolled in the study. Significantly higher CAVI scores were observed in patients with type 2 diabetes compared with nondiabetic patients (mean ± SD: 9.55 ± 1.13 versus 8.54 ± 0.94, respectively). Multivariate linear regression analyses demonstrated that age was the only significant factor influencing the CAVI score, in patients with type 2 diabetes. CONCLUSION: Patients with type 2 diabetes had an increased risk of arterial stiffness, based on the CAVI score, compared with nondiabetic patients; this, in turn, could increase their risk of developing other cardiovascular complications.

Association between the endothelial nitric oxide synthase gene Glu298Asp polymorphism and coronary heart disease: a meta­analysis of 39 case­control studies.

Numerous studies have indicated that the human endothelial nitric oxide synthase (eNOS) gene Glu298Asp polymorphism is associated with coronary heart disease (CHD) susceptibility, however, their conclusions are inconsistent. The present meta­analysis aimed to evaluate the precise result by searching the PubMed database and using 39 case­control studies comprising 7489 cases and 7051 controls.Each study tested the association between the eNOS Glu298Asp polymorphism and CHD. A meta­analysis was then conducted using the Comprehensive Meta Analysis 2.2 software to calculate the pooled odds ratios (ORs) of five genetic models with 95% confidence intervals (CIs). Publication bias was also explored. The meta­analysis showed a significant association between the eNOS Glu298Asp polymorphism and CHD susceptibility for all the genetic models [Asp vs. Glu, OR 1.26, 95% CI 1.14­1.40, P<0.001; Asp/Asp vs. Glu/Glu, OR 1.58, 95% CI 1.23­2.02, P<0.001; Glu/Asp vs. Glu/Glu, OR 1.12, 95% CI 1.03­1.22, P=0.001; (Glu/Asp+Asp/Asp) vs. Glu/Glu, OR 1.17, 95% CI 1.07­1.27, P<0.001; Asp/Asp vs. (Glu/Glu+Glu/Asp), OR 1.59, 95% CI 1.25­2.03, P<0.001]. Subgroup and sensitivity analyses indicated that the result was robust. A weak publication bias was detected. The results indicated that the eNOS Glu298Asp polymorphism is a risk factor for developing CHD, particularly in the Asian population.

[The anti-athetotic effects of heme-L-lysinate in a rabbit model of atherosclerosis].

OBJECTIVE: To investigate the anti-atherotic effects of heme-L-lysinate in a rabbit model of atherosclerosis and related machanisms. METHODS: Adult rabbits were treated with 1% cholesterol diet (chol group, n = 8) or 1% cholesterol diet plus heme-L-lysinate (9 mgxkg(-1)xd(-1), Heme group, n = 8) or 1% cholesterol diet plus isotonic Na chloride (Na chloride group, n = 8) for 10 weeks. Eight rabbits fed with normal diet served as normal control. Aortic carbon monoxide (CO) was quantified spectrophotometrically by the formation of carboxyhaemoglobin (HbCO). Aortic heme oxygenase-1 (HO-1) and HSP70 mRNA and protein expressions were detected by RT-PCR and immunohistochemical staining. RESULTS: Aortic CO production and HO-1 activity were significantly increased in chol group and Na chloride group compared those in normal control group (P < 0.01). Aortic plaque area was significantly reduced in heme group (26.6% +/- 9.2%) than that in chol group (42.3% +/- 8.7%, P < 0.01). Aortic HO-1 expression, CO production and HSP70 were significantly increased in heme group than those in chol group and Na chloride group (all P < 0.01). CONCLUSIONS: Heme-L-lysinate could attenuate atherosclerotic progression through upregulating HO-1 and HSP70 expression and increasing CO production in this model.

[Evaluation of diagnosis and prediction of degree of coronary stenosis by CAVI].

OBJECTIVE: To investigate the relationship between CAVI (Cardio-Ankle vascular Index) and the degree of coronary artery stenosis in elderly patients with type 2 diabetes, the predictive value of CAVI were evaluated using the degree of coronary artery stenosis. METHODS: Relevant clinical data including CAMI, BMI, blood pressure, smoking, age, Sbp, Dbp, history and blood biochemistry test were collected in 60 years or older patients with coronary artery stenosis diagnosed by coronary angiography, and the 298 cases were divided into two groups, A group (CAVI > or = 9), B group (CAVI < 9), to investigate the correlativity among the level of CAVI and cardiovascular risk factors; at the same time all cases were assigned to group C (diabetes group) and group D (non-diabetic group), to analyse the change of CAVI in coronary artery stenosis patients complicated with diabetes mellitus. RESULTS: A total of 298 eligible patients with coronary artery stenosis were enrolled, including 163 non diabetics and 135 type 2 diabetics. The analysis result shows that there was a positive correlation among CAVI, old age, BMI, LDL-C, multi-vessel lesion, diabetes. CONCLUSION: The increase of CAVI was most highly related to the coronary artery stenosis. The level of CAVI might be a helpful predictive indexes to the severity of coronary atherosclerosis.