Tim-1+ B cells suppress T cell interferon-gamma production and promote Foxp3 expression, but have impaired regulatory function in coronary artery disease.

Atherosclerosis and its associated coronary artery disease (CAD) represent another chronic low-grade inflammatory disorder. Regulatory B cells (Bregs) possess essential functions in maintaining peripheral tolerance and inhibiting pathogenic inflammation through IL-10. Here, we investigated one subset of Bregs, Tim-1+ B cell, and its role in atherosclerosis and CAD patients. In healthy individuals, IL-10-producing B cells were predominantly found in the Tim-1+ B cells. Upon stimulation of the B cell receptor (BCR) and Toll-like receptor 9 (TLR-9) by anti-BCR antibodies and CpG, respectively, the Tim-1+ B cells could further upregulate IL-10 expression. In contrast, the Tim-1+ B cells were present at normal frequency in CAD patients, but showed impaired capacity to upregulate IL-10 with or without BCR + CpG stimulation. The stimulated Tim-1+ B cells from healthy individuals also suppressed expression of interferon gamma (IFN-γ), an atherogenic cytokine in T cells, in an IL-10-dependent fashion, and strongly promoted the expression of Foxp3 in naive CD4+ CD45RO- T cells. In contrast, the Tim-1+ B cells from CAD patients were unable to suppress IFN-γ secretion, and only minimally increased the expression of Foxp3 in naive CD4+ CD45RO- T cells. Despite this, the frequency of Tim-1+ B cells in the atherosclerotic lesions from CAD patients was inversely correlated with the frequency of IFN-γ-expressing T cells. Together, these results demonstrated that CAD patients presented an inflammatory disorder in regulatory B cells, which could be used as a therapeutic target.

Triterpenoids from the bark of Dysoxylum hainanense and their anti-inflammatory and radical scavenging activity.

A phytochemical investigation on the 70% EtOH extract of the bark of Dysoxylum hainanense resulted in the isolation of four new triterpenoids, dysoxyhaines A-D (1-4). Structural elucidation of all the compounds were performed by spectral methods such as 1D and 2D (1H1H COSY, HMQC, and HMBC) NMR spectroscopy, in addition to high resolution mass spectrometry. The isolated components were evaluated in vitro for anti-inflammatory activities for Cox-1 and Cox-2, and radical scavenging potential using ABTS·+ and DPPH test. As a result, nor seco-olean type triterpenoid 1 exhibited significant anti-inflammatory potential, while tirucallane triterpenoids 3 and 4 showed radical scavenging activities.

Decrease in circulating myeloid dendritic cell precursors in patients with intracranial large artery atherosclerosis.

Intracranial large artery atherosclerosis (ILAA) is a major cause of ischemic cerebrovascular disease. The aim of this study was to investigate whether the levels of circulating dendritic cell precursors (DCP) could reflect the severity of intracranial large artery atherosclerosis (ILAA). For this purpose, a series of angiography were taken to determine the severity and extent of coronary artery and intracranial large artery stenosis, and flow cytometry were taken to determine the levels of circulating mDC precursors and pDC precursors in patients with severe intracranial large artery atherosclerosis (ILAA) (n = 101) and mild intracranial large artery atherosclerosis (ILAA) (n = 123) according to the angiography. Circulating mDC precursors were lower in patients with severe intracranial large artery atherosclerosis (ILAA) than in mild intracranial large artery atherosclerosis (ILAA) (P < 0.05), but circulating pDC precursors were not significant differences (P > 0.05). According to these data, circulating mDC precursors could predict the severity of ILAA, which also could be able to reflect the severity of ILAA.

Hypertensive vascular remodeling was inhibited by Xuezhikang through the regulation of Fibulin-3 and MMPs in spontaneously hypertensive rats.

Fibulin-3, an extracellular glycoprotein, has been suggested as having functions in vessels. In hypertension, extracellular matrix, matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) play important roles in cardiovascular remodeling. However, the role of Fibulin-3 as an extracellular glycoprotein in hypertensive vascular remodeling remains unclear. Our study was to determine whether Fibulin-3 and TIMPs/MMPs would affect vascular structure during hypertension and the treatment of Xuezhikang. Thirty spontaneously hypertensive rats (SHRs) aged 8 weeks were randomized to three groups: SHRs control group (SHRs group, n=10), group treated with low dose Xuezhikang (XZK-L, 20 mg/kg/d, n=10) and group treated with high dose Xuezhikang (XZK-H, 200 mg/kg/d, n=10), the normal group was comprised of ten Wistar-Kyoto (WKY) rats of the same age. We showed that serum nitric oxide (NO) in control group was significantly lower than WKY group (P<0.05). Concomitantly, serum oxidized low-density lipoprotein (ox-LDL) was higher than WKY group (P<0.05). The treatment of high dose Xuezhikang significantly dicreased ox-LDL, left ventricular mass index (LVMI) and Wall-to-lumen area ratio (W/L) of thoracic aorta (P<0.05), while serum NO was significantly increasing (P<0.05). Moreover, the expressions of Fibulin-3 and MMP-2, 9 at both protein and mRNA levels were significantly higher in thoracic aorta of SHRs group compared to WKY group by immunohistochemistry and western blotting (P<0.05). However, the levels of Fibulin-3 and MMP-2, 9 were significantly decreased in XZK-H group compared to control group (P<0.05). The level of TIMP-3 had no significance difference between SHRs and WKY groups (P>0.05). So the levels of Fibulin-3 and MMP-2, 9 in SHRs could be inhibited by Xuezhikang. Furthermore, a strong correlation in transcript expression was established between Fibulin-3, and MMP-2 (r=0.81, P<0.05) and MMP-9 (r=0.92, P<0.05) through immunohistochemistry. In summary, the overexpression of Fibulin-3 and MMP-2, 9 levels were associated with hypertension and vascular remodeling and inhibited by Xuezhikang. Fibulin-3 is a candidate in the pathogenesis of cardiovascular remodeling in hypertension.

Validation of the Andon KD-5917 automatic upper arm blood pressure monitor, for clinic use and self-measurement, according to the European Society of Hypertension International Protocol revision 2010.

OBJECTIVE: To validate the Andon KD-5917 automatic upper arm blood pressure monitor according to the European Society of Hypertension International Protocol revision 2010. MATERIALS AND METHODS: Sequential same-left-arm measurements of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were obtained in 33 participants using the mercury sphygmomanometer and the test device. According to the validation protocol, 99 pairs of test device and reference blood pressure measurements (three pairs for each of the 33 participants) were obtained in the study. RESULTS: The device produced 73, 98, and 99 measurements within 5, 10, and 15 mmHg for SBP and 86, 98, and 99 for DBP, respectively. The mean ± SD device-observer difference was 3.07 ± 3.68 mmHg for SBP and -0.89 ± 3.72 mmHg for DBP. The number of patients with two or three of the device-observer difference within 5 mmHg was 26 for SBP and 29 for DBP, and no patient had a device-observer difference within 5 mmHg. CONCLUSION: The Andon KD-5917 automatic upper arm blood pressure monitor can be recommended for clinical use and self-measurement in an adult population on the basis of the European Society of Hypertension International Protocol revision 2010.

Polymorphism of stromal cell-derived factor-1 selectively upregulates gene expression and is associated with increased susceptibility to coronary artery disease.

Stromal cell-derived factor-1 (SDF-1) plays critical roles in vascular development and hematopoiesis. Here, we investigated the function of SDF-1 rs1801157G/A polymorphism in various immune cells and examined its association with susceptibility to coronary artery disease (CAD). Protein and mRNA levels of SDF-1 were tested in peripheral CD4+ T cell, CD8+ T cells, monocytes, and natural killer (NK) T cells from healthy donors with different genotypes of rs1801157G/A polymorphism. Prevalence of the polymorphism was compared between CAD patients and healthy controls. Data revealed that SDF-1 mRNA and protein were detectable in CD4+ T cells, CD8+ T cells, monocytes and NK T cells. Interestingly, both protein level and mRNA level of SDF-1 were significantly increased in the monocytes with rs1801157AA genotype, whereas the same phenomenon was not observed in the other three cell types. Blockage of CD14 completely inhibited the upregulation of SDF-1 in the monocytes with rs1801157AA genotype. Association analysis showed that frequencies of the rs1801157AA genotype and A allele were significantly higher in CAD cases than in controls (odds ratio [OR]=2.28, 95% confidence interval [CI], 1.50-3.29, p<0.0001, and OR=1.46, 95% CI, 1.21-3.73, p<0.0001, respectively). Also, prevalence of rs1801157AA genotype was further increased in cases with ST-elevation myocardial infarction (OR=1.65, 95% CI, 1.04-2.56, p=0.028). Our data suggest a novel pathway for regulating SDF-1 and a new risk factor for CAD.

[Impacts of establishment of chest pain center on the door-to-balloon time and the short-term outcome after primary percutaneous coronary intervention of patients with ST segment elevated myocardial infarction].

OBJECTIVE: To investigate the impact of the establishment of chest pain center (CPC) model based on the pre-hospital real-time tele-12-lead electrocardiogram on the door-to-balloon (D-to-B) time and short-term outcome after primary percutaneous coronary intervention (PPCI) of patients with ST-segment elevated myocardial infarction (STEMI). METHODS: A regular CPC was established with pre-hospital transmitted real-time 12-lead electrocardiogram system for pre-hospital diagnosis of STEMI and enabled the STEMI patients to bypass the emergency room and directly treated in the catheter lab to shorten the D-to-B time. The mean D-to-B time, the short-term outcome and medical costs were compared in PPCI patients before (93 cases, group A) and after (149 cases, group B) the establishment of CPC. RESULTS: After the establishment of CPC, the annual mean D-to-B time was significantly shortened [(127 ± 79) min in group A vs.(72 ± 23 )min in group B, P < 0.01], the shortest monthly mean D-to-B time was remarkably reduced in group B than in group A [(56 ± 11) min vs. (73 ± 14) min, P < 0.01]. The annual ratio of D-to-B below 90 minutes was significantly increased from 62.4% (58/93) in group A to 91.9% (137/149) in group B (P < 0.05) . The in-hospital mortality rate tended to be lower and the incidence of heart failure during hospitalization was significantly reduced in group B compared with group A [3.4% (5/149) vs. 6.5% (6/93), P > 0.05; 14.1% (21/149) vs. 24.7% (23/93), P < 0.05]. The length of hospital stay was slightly shortened from (8.98 ± 4.89) days to (7.79 ± 5.43) days (P > 0.05). Corrected mean medical cost went down by 9.4% (P < 0.05). CONCLUSION: The establishment of CPC may significantly shorten the D-to-B time, improve the short-term outcome and reduce the hospitalization cost for PPCI patients with STEMI.

Evaluation on the efficacy and safety of domestic bivalirudin during percutaneous coronary intervention.

BACKGROUND: Bivalirudin was widely used as an anticoagulant during coronary interventional procedure in western countries. However, it was not available in China before this clinical trial was designed. This randomized, single-blind and multicenter clinical trial aimed to evaluate the efficacy and the safety of domestic bivalirudin during percutaneous coronary intervention (PCI). METHODS: A randomized, single-blind, multicenter trial was designed. Elective PCI candidates in five centers were randomized into a bivalirudin group and a heparin group, which were treated with domestic bivalirudin and non-fractional heparin during the PCI procedure. The efficacy was evaluated by comparing the activated coagulation time (ACT), the procedural success rate (residual stenosis < 20% in target lesions without any coronary artery related adverse events within 24 hours after PCI), and the survival rate without major adverse cardiac events at 30 days after PCI between the two groups. Safety was evaluated by the major/minor bleeding rate. RESULTS: A total of 218 elective PCI patients were randomized into a bivalirudin group (n = 110) and heparin group (n = 108). Except for two patients needing additional dosing in the heparin group, the ACT values of all other patients in both groups were longer than 225 seconds at 5 minutes after the first intravenous bolus. Procedural success rates were respectively 100.0% and 98.2% in the bivalirudin group and heparin group (P > 0.05). Survival rates without major adverse cardiac events at 30 days after PCI were 100.0% in the bivalirudin group and 98.2% in the heparin group (P > 0.05). Mild bleeding rates were 0.9% and 6.9% (P < 0.05) at 24 hours, and 1.9% and 8.8% (P < 0.05) at 30 days after PCI in the bivalirudin group and heparin group respectively. There was one severe gastrointestinal bleeding case in the heparin group. CONCLUSIONS: Domestic bivalirudin is an effective and safe anticoagulant during elective PCI procedures. The efficacy is not inferior to heparin, but the safety is superior to heparin.

[Effect of ulinastatin on expressions of serum cardiac troponin I, myocardial tumor necrosis factor-alpha and endothelin-1 in septic rats].

OBJECTIVE: To investigate the myocardial protective effects of different dosage of ulinastatin (UTI) and the possible mechanism in septic rats. METHODS: Forty male Sprague-Dawley (SD) rats were randomly divided into five groups: control group, sham group, model group, UTI in low dose or high dose group. Cecal ligation and puncture (CLP) was adopted to reproduce animal model of sepsis. Left ventricular myocardium was harvested and blood samples were collected at 24 hours after successful establishment of animal model. Serum cardiac troponin I (cTnI), the contents of myocardial tumor necrosis factor-alpha (TNF-alpha) and endothelin-1 (ET-1) were measured, and myocardial pathological changes were observed. RESULTS: In the model group, the level of serum cTnI, and the expressions of myocardial TNF-alpha and ET-1 were much higher than those in control group [cTnI (microg/L): 7.58+/-0.53 vs. 1.05+/-0.21, TNF-alpha (pg/g): 945.6+/-72.0 vs. 238.2+/-35.2, ET-1 (pg/g): 776.8+/-123.9 vs. 170.1+/-28.3, all P<0.01]. There were no differences in the levels of serum cTnI, myocardial TNF-alpha and ET-1 between low dose UTI group and the model group [cTnI (microg/L): 7.21+/-0.51 vs. 7.58+/-0.53, TNF-alpha (pg/g): 910.5+/-96.6 vs. 945.6+/-72.0, ET-1 (pg/g): 714.0+/-66.7 vs. 776.8+/-123.9, all P>0.05]. However, serum cTnI, myocardial TNF-alpha and ET-1 were lower significantly in high dose UTI group than in model group [cTnI (microg/L): 4.30+/-0.84 vs. 7.58+/-0.53, TNF-alpha (pg/g): 430.5+/-75.6 vs. 945.6+/-72.0, ET-1 (pg/g): 377.1+/-39.0 vs. 776.8+/-123.9, all P<0.01]. CONCLUSION: High dose (but not low dose) UTI may protect myocardium from the damage resulted from sepsis in a rat model, probably by lowering expressions of TNF-alpha and ET-1.

[The clinical application of the emergency remedial transthoracic cardiac pacing used by a steel wire loop electrode].

OBJECTIVE: To explore an effective method of emergency remedial cardiac pacing and evaluate its clinical application. METHODS: The transthoracic cardiac pacing was used by a steel wire loop electrode to 18 patients with cardiac arrest or serious bradycardia, after a routine cardiac pacing was failed by way of jugular or subclavian vein. RESULTS: It is a simple procedure used by steel wire loop. All the pacing had been successfully captured the hearts except 5 cases without capturing. There were 3 cases of cardiac arrest, 2 cases of cardiac arrest after electric defibrillation, 1 case of cardiac arrest after electric shock because of ventricular running and all the 5 cases of severe cardiac bradycardia due to serious atrioventricular block caused by high blood potassium were survived. Eight cases of cardiac arrest were successful capture, that was due to the short period of time from cardiac arrest to ventricle puncture than that of 5 cases of ventricular pacing which was not successful [(17.6+/-4.6) minutes vs. (26.4+/-5.4) minutes, P<0.05]. CONCLUSION: The steel wire loop electrode is a safe and reliable emergency cardiac pacing method, which contribute to the rapid establishment of an effective emergency cardiac pacing. When the conventional intravenous cardiac pacing was not successful, the method of emergency transthoracic cardiac pacing used by steel wire loop electrode should be bold and use to improve the successful rate of resuscitation.

[Expression of B7-related protein-1 on human coronary artery endothelial cells and its clinical significance].

OBJECTIVE: To study the effect of oxidized low density lipoprotein (ox-LDL) on the expression of B7-related protein-1 (B7RP-1) on human coronary artery endothelial cells (HCAECs). METHODS: HCAECs were incubated in the presence of 100 mg/L ox-LDL for 24 h, and B7RP-1 expression levels were determined using fluorescence reverse transcription PCR (RT-PCR) and Western blotting. RESULTS: B7RP-1 expression was detected HCAECs, with spots of fluorescence signals distributing on the cell membrane as observed under fluorescence microscope. RT-PCR with B7RP-1 specific primers yielded products of expected size (496 bp). Western blotting identified B7RP-1 expression in the HCAECs as a cell-associated protein with an apparent molecular mass of 70,000. Treatment of the cells with ox-LDL significantly increased B7RP-1 expression at both the mRNA and protein levels (P<0.05). CONCLUSION: B7RP-1 is expressed on the membrane of HCAECs. ox-LDL can promote up-regulate the expression of B7RP-1, which might be one of the immunopathogenesis of atherosclerosis.

[Expression of ICOSL on human coronary artery endothelial cells and its being interferentialed by ox-LDL].

AIM: To study the expression of inducible co-stimulator ligand(ICOSL) on human coronary artery endothelial cells(HCAEC) and its being interferentialed by oxidized low density lipoprotein(ox-LDL). METHODS: ICOSL expression levels were determined by the fluorescence, reverse transcription PCR (RT-PCR) and Western blot, respectively. RESULTS: The ICOSL mRNA OD values of control and 100 mg/L ox-LDL group was 0.071+/-0.035 and 0.186+/-0.044, respectively. The Western blot A values of control and 100 mg/L ox-LDL group was 10.88+/-1.53 and 16.03+/-4.08, respectively. ox-LDL increased expression of ICOSL mRNA and protein(P<0.05). CONCLUSION: ICOSL can express on the HCAEC. ox-LDL can up-regulate the expression of ICOSL.

[Effects of oxygen and calcium on the expression of wild-type and mutated hypoxia-inducible factor-1alpha eukaryotic vectors in HEK293 cells].

OBJECTIVE: To study the effects of oxygen and calcium on the expression of eukaryotic vectors harboring wild-type or mutated hypoxia-inducible factor-1alpha (HIF-11alpha) in HEK293 cells. METHODS: HEK293 cells were transiently transfected with pcDNA3.1+/HIF-11alpha, pcDNA3.1+/HIF-11alpha-564Ala and pcDNA3.1+/HIF-11alpha-564Ala-803Ala via lipofectin. Western blotting were used to detect HIF-11alpha protein after normoxic or hypoxic exposure of the transfected HEK293 cells in the presence or absence of Ca(2+). The levels of vascular endothelial growth factor (VEGF) mRNA in the transfected cells in normoxic condition was detected using RT-PCR. RESULTS: The levels of HIF-11alpha protein and VEGF mRNA increased in HEK293 cells transfected with the vectors harboring mutated HIF-11alpha, but not in the cells transfected with wild-type HIF-11alpha vectors in normoxia. Hypoxia increased the levels of HIF-11alpha protein in the cells transfected with wild-type HIF-11alpha vectors, which was inhibited by the application of Ca(2+). Ca(2+) showed no inhibitory effect on HIF-11alpha levels in HEK293 cells transfected with the vectors containing mutated HIF-11alpha. CONCLUSION: The protein products of pcDNA3.1+/HIF-11alpha-564Ala and pcDNA3.1+/HIF-11alpha- 564Ala-803Ala in HEK293 cells enhance the cell tolerance to oxygen and protease.

Characteristics of stress tests and symptoms in patients with myocardial bridge and coronary artery spasm.

BACKGROUND: A relationship between coronary artery spasm (CAS) and myocardial bridge (MB) has been noticed. This study was designed to investigate the differences of stress tests and symptoms between CAS patients with or without MB. METHODS: Two hundred and sixteen patients with atypical chest pain who underwent coronary angiography and acetylcholine provocation test were divided into MB group (n=68) and nonmyocardial bridge group (NMB, n=148). The results of acetylcholine test, treadmill exercise electrocardiography, myocardial scintigraphy, and levels of plasma endothelin-1 and nitric oxide were compared between the two groups. RESULTS: Among these atypical chest pain patients, CAS was induced by acetylcholine in 85% MB patients and 53% NMB patients (P<0.001). A positive exercise electrocardiogram was identified in 71% MB patients and 8% NMB patients (P<0.001). Myocardial scintigraphy revealed ischemic changes in 67% MB patients and 9% NMB patients (P<0.001) and reverse redistribution in 87 and 69% (P<0.01), respectively. MB patients experienced exertional chest pain as well as at rest more frequently than NMB patients. Endothelin-1 levels were elevated in MB group complicated with CAS (P<0.01), whereas nitric oxide levels were reduced in the same cohort (P<0.05) compared with NMB group. CONCLUSION: MB might predispose to CAS in which endothelial dysfunction may play a part. CAS patients with MB usually present mixed chest pain and positive stress tests as well as reversal redistribution on myocardial scintigraphy whereas CAS patients without MB displayed chest pain at rest, negative stress test and reversal redistribution.

[Clinical features of coronary artery spasm patients with or without myocardial bridge].

OBJECTIVE: To investigate the clinical features of coronary artery spasm patients with or without myocardial bridge and explore the roles of endothelial dysfunction in these patients. METHODS: One hundred eighteen patients undergone acetylcholine provoking test were divided into myocardial bridge (MB) group (n = 26) and non-myocardial bridge (NMB) group (n = 92). The results of acetylcholine test, treadmill exercise electrocardiography, stress myocardial perfusion scintigraphy, plasma level of endothelin-1 and nitric oxide were compared between MB group and NMB group. RESULTS: Coronary artery spasm was induced in 21 patients in MB group (81%) and 52 patients in NMB group (57%, P < 0.05). Positive treadmill electrocardiography was obtained in 19 patients in MB group (73%) and 7 patients in NMB group (8%, P < 0.001). Ischemic perfusion defect in 20 (77%) and 9 patients (10%, P < 0.001) and reverse redistribution in 23 (88%) and 68 patients (74%, P > 0.05). Patients showed different clinical features in MB group and NMB group (more short-duration exertional angina and could not be readily released by nitroglycerine in MB group while more patients experienced long-lasting variant angina and symptoms could be readily released by nitroglycerine). Plasma endothelin-1 level was significantly higher [(132.1 +/- 6.5) ng/L vs. (108.5 +/- 8.2) ng/L, P < 0.01] while nitric oxide was significant lower [(84.7 +/- 17.5) ng/L vs. (99.8 +/- 18.2) ng/L, P < 0.05] in MB group compared to NMB group. CONCLUSION: MB patients were prone to coronary artery spasm partly due to endothelial dysfunction. Patients with MB and coronary artery spasm also showed classic clinical symptoms and positive stress tests for ischemia.

[Effect of porcine relaxin on NO production of human microvascular endothelial cells].

OBJECTIVE: To observe effect of porcine relaxin(pRLX) on NO production of human microvascular endothelial cells(HMVECs) and discuss its possible mechanism. METHODS: iNOS and cNOS expression of HMVECs with or without pRLX were detected using western blotting. NO production of HMVECs with pRLX at different concentration or different time were determined by method of Griess. NO production of pRLX of HMVECs plus Non-selective NOS inhibitor NG-monomethyl-L-arginine(L-NMMA), selective iNOS inhibitor aminoguanidine(AG) or nuclear factors-kappaB (NF-kappaB) inhibitor pyrrolidine dithiocarbamate(PDTC) were also analysed. RESULTS: pRLX promoted iNOS protein expression of HMVECs, but not cNOS protein expression. NO production of HMVECs was promoted by pRLX on concentration-dependent pattern instead of time-dependent one. AG, L-NMMA and PDTC were showed to block the effect of pRLX on NO production of HMVECs. CONCLUSION: pRLX promote iNOS expression and NO production of HMVECs.

Resting Chest Pain, Negative Treadmill Exercise Electrocardiogram, and Reverse Redistribution in Dipyridamole Myocardial Perfusion Scintigraphy Might be the Features of Coronary Artery Spasm.

BACKGROUND: Coronary artery spasm usually attacks while at rest and the diagnosis depends on provoking tests which mostly are invasive, expensive and not practical. Previous investigations demonstrated that in most patients with coronary artery spasm, treadmill exercise electrocardiography (TEEC) did not induce any ischemic changes, and myocardial perfusion scintigraphy (MPS) showed reverse redistribution (RR). HYPOTHESIS: Combination of resting chest pain, negative TEEC and RR might be a rational noninvasive set to predict coronary artery spasm. METHODS: Patients with chest pain at rest, no significant coronary artery stenosis, and willing to undergo acetylcholine test were included. TEEC, dipyridamole and rest thallium-201 MPS were performed before or after coronary angiography. The patients were divided into spasm and nonspasm groups by acetylcholine test. The clinical features and results of TEEC and MPS were compared between the spasm and nonspasm groups. RESULTS: Acetylcholine test was performed in 92 patients and coronary artery spasm was successfully provoked in 68 patients. Positive TEEC was induced in only 4 patients in the spasm group. RR was present in totally 77 patients and 68 of them were from the spasm group. By a combination of resting chest pain, negative TEEC and RR to diagnose coronary artery spasm, the sensitivity and specificity were 94% and 96% respectively. CONCLUSION: Combination of resting chest pain, negative TEE and RR appears to be a rational noninvasive set to predict coronary artery spasm.

[Comparison of plasma low-density lipoprotein and oxidized low-density lipoprotein levels with coronary lesion severities in patients with coronary artery disease].

OBJECTIVE: To explore the relationship between plasma low-density lipoprotein (LDL) and oxidized low-density lipoprotein (ox-LDL) levels and the severity of coronary atherosclerosis. METHODS: Fasting plasma ox-LDL was measured by enzyme-linked immunosorbent assay and plasma LDL was measured by biochemical autoanalyser in 31 patients with coronary artery spasm (CAS group, chest pain with positive acetylcholine provocation test but without significant coronary artery stenosis), 35 patients with stable angina pectoris (SAP group) and 24 healthy persons (control group). RESULTS: Plasma LDL levels were similar between CAS and SAP groups but significantly higher than that in control group. Plasma ox-LDL levels significantly increased in proportion to coronary lesion severities [SAP (575 +/- 219 microg/L) > CAS (299 +/- 117 microg/L) > control (218 +/- 35 microg/L)]. In SAP group, plasma ox-LDL level was also significantly higher in multi-vessel disease group than that in single-vessel disease group (672 +/- 92 vs. 462 +/- 72 microg/L, P < 0.05). CONCLUSION: Plasma ox-LDL but not LDL level is significantly correlated to the severity of coronary atherosclerosis and should therefore be the focused therapy target in patients with coronary artery disease.