Elevated concentrations of pentraxin 3 are associated with coronary plaque vulnerability

Background

Inflammation is a critical contributing factor to the development and progression of atherosclerosis. Pentraxin 3 (PTX3) is produced abundantly in atherosclerotic lesions while C-reactive protein (CRP) is mainly produced in the liver. In this study, we investigated whether plasma levels of PTX3 might be a sensitive marker both for the severity of coronary artery disease and vulnerable plaques. Next, we determined whether assays for inflammatory molecules can be used to monitor the therapeutic effects of telmisartan on stabilization of vulnerable atherosclerotic plaques.

Methods and results

We measured PTX3 concentrations in the peripheral and coronary sinus plasma of 40 patients with angina pectoris (AP) and 20 control subjects. Next, in 28 patients with AP, we determined the correlation between levels of inflammatory molecules and the computed tomography (CT) density of plaques as a quantitative index of plaque vulnerability. There was no significant difference in peripheral plasma PTX3 concentrations between patients with AP and control subjects, while coronary sinus plasma PTX3 concentrations were significantly higher in AP patients than control subjects. The concentrations of PTX3 in coronary sinus and peripheral plasma correlated with Gensini scores as an index of severity of coronary atherosclerosis. Interestingly, there was a significantly negative correlation between plasma PTX3 concentrations and CT density (r = −0.67, p < 0.01). On the other hand, CT density did not correlate with the peripheral plasma concentrations of monocyte chemoattractant protein-1 (MCP-1) or high-sensitivity CRP (hsCRP). Furthermore, telmisartan treatment for 6 months decreased plasma concentrations of PTX3 but not those of MCP-1 or hsCRP in 12 patients with essential hypertension. Multivariate regression analysis revealed that changes in PTX3 levels were independent of blood pressure changes.

Conclusions

PTX3 is likely more specific than hsCRP as an indicator of coronary plaque vulnerability that could lead to plaque rupture.     

Elevation of plasma matrix metalloproteinase-9 in the culprit coronary artery in patients with acute myocardial infarction: clinical evidence from distal protection.

BACKGROUND: Although the elevation of circulating plasma matrix metalloproteinase (MMP)-9 levels in patients with acute myocardial infarction (AMI) has been documented, the origin of MMP-9 remains unclear. METHODS AND RESULTS: Plasma MMP-9 levels in both the peripheral circulation and coronary arteries were measured in patients with AMI (n=23) and with stable angina pectoris (SAP, n=10) during percutaneous coronary intervention (PCI) with a distal protection device. Blood samples were collected from the femoral artery (FA) and the coronary artery before (Initial) and after (Second) dilation of the culprit lesion. Coronary sinus blood samples were obtained immediately after PCI (n=7). Coronary artery plaque fragments were aspirated in patients with AMI (n=20) and compared with those from patients with SAP who underwent directional atherectomy (n=10). MMP-9 levels in Initial and Second were significantly higher in patients with AMI than in patients with SAP (p<0.01). In AMI patients MMP-9 levels were significantly higher in Initial than in the FA (p<0.05), and were further increased in Second (p<0.0001), whereas those in the coronary sinus were similar to the FA. Immunohistochemistry revealed augmented MMP-9 expression in the coronary artery plaque fragments from AMI patients. CONCLUSIONS: MMP-9 is mainly released into the coronary circulation from the coronary artery plaque in patients with AMI.     

Significance of soluble thrombomodulin in the coronary circulation of patients with coronary artery disease

OBJECTIVES: The relationship between plasma levels of soluble thrombomodulin, a probable marker for endothelial damage, and the severity of coronary atherosclerosis was investigated. METHODS: Plasma soluble thrombomodulin levels were evaluated in 160 patients(mean age 62 +/- 11 years) who underwent coronary angiography. Blood samples were obtained from the peripheral vein, ostium of the left coronary artery and coronary sinus. The levels of plasma thrombomodulin were measured by enzyme-linked immunosorbent assay. The change of thrombomodulin level in the coronary circulation (delta TM) was calculated as the coronary sino-arterial difference. Patients were classified into four groups according to the number of diseased vessels, and the severity of coronary atherosclerosis was evaluated with the modified Gensini score. RESULTS: Coronary sinus levels of thrombomodulin were significantly higher in the two or more vessel disease(VD) groups than in the no or one VD groups(p < 0.05). delta TM were significantly higher in the 2VD than in the 0VD groups(p < 0.05), and higher in the 3VD than in the 0VD or 1VD groups(p < 0.05). delta TM showed positive correlation with Gensini score for left coronary arteries(r = 0.347, p < 0.0001). CONCLUSIONS: The increment of thrombomodulin across the coronary circulation was significantly correlated with the severity of coronary atherosclerosis, suggesting a close association between the progression of coronary atherosclerotic stenosis and damage to the endothelial surface.     

Plasma endothelin-1 in patients with stable or unstable angina

BACKGROUND: It has been documented that an elevated endothelin-1 (ET-1) plasma concentration is associated with an increased risk of serious coronary events and the presence of angiographically documented coronary artery disease (CAD). The results of a few studies which examined ET-1 plasma level in patients with stable or unstable angina, were inconclusive. AIM: To assess whether ET-1 blood concentration measured in the coronary sinus and peripheral vein is associated with clinical symptoms in patients with multi-vessel CAD. METHODS: The study group consisted of 23 patients with multi-vessel CAD of whom 11 had unstable angina and 12 - stable angina. Both groups were matched with regard to age, gender and the presence of cardio-vascular risk factors. Blood samples for ET-1 assessment were taken during coronary angiography simultaneously from the coronary sinus and femoral vein. ET-1 was measured using an immunoenzymatic method. RESULTS: ET-1 plasma level in the peripheral venous circulation was similar in patients with unstable or stable angina (0.45+/-0.18 pmol/L versus 0.46+/-0.14 pmol/L, NS) whereas ET-1 level in the coronary sinus was significantly higher in patients with unstable angina (1.44+/-0.47 pmol/L versus 0.34+/-0.17 pmol/L, p<0.05). CONCLUSIONS: ET-1 concentration in the coronary sinus is significantly higher in patients with unstable rather than stable angina which confirms the role of ET-1 in the pathogenesis of CAD. Our results suggest a possible future role of endothelin receptor blockers in the treatment of patients with unstable angina.     

冠心病患者血清VEGF水平的研究

目的 :观测冠心病患者血清血管内皮生长因子 （VEGF）的水平。方法 :行选择性冠脉造影 （SCA）的患者 6 0例 ,分为 4组 ,其中 SCA正常者 10例作为对照组 ,急性心肌梗死 （AMI）组 2 0例 ,陈旧性心肌梗死 （OMI）组 10例 ,心绞痛 （AP）组 2 0例 ,使用 EL ISA方法分别检测其血清 VEGF的水平。结果 :AMI患者血清 VEGF水平显著高于其它各组 （P<0 .0 1） ,且其 VEGF的水平与心肌梗死部位、病变血管及血管病变程度无关 ,AP、OMI组血清 VEGF略高于对照组 ,但无统计学差异 （P>0 .0 5 ）。结论 :AMI患者血清 VEGF水平升高。     

Role of circulating vascular endothelial growth factor and hepatocyte growth factor in patients with coronary artery disease

Vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) are thought to stimulate endothelial cell proliferation and induce angiogenesis in vivo. However, the precise mechanism responsible for VEGF and HGF release in patients with coronary artery disease is still unknown. We studied serum concentrations of VEGF and HGF in 20 patients with acute myocardial infarction (AMI), 20 patients with stable angina pectoris (AP) who had reversible perfusion defects on stress myocardial scintigraphy, and 16 patients with old myocardial infarction (OMI) who had no reversible defects on stress myocardial scintigraphy. The control group consisted of 20 patients with atypical chest pain who had angiographically normal coronary arteries. Serum VEGF and HGF concentrations were measured by enzyme-linked immunosorbent assay. Both the serum VEGF and HGF concentrations in the early stage of myocardial infarction in the patients with AMI were higher than those in the patients with AP and with OMI, and control patients. The VEGF concentration in the patients with AP was higher than in the patients with OMI, whereas the HGF concentration did not differ in the patients with AP and OMI. The VEGF concentration in AMI patients who had had preinfarction angina on admission was higher than that of patients who had had no preinfarction angina, whereas the HGF concentration did not differ between the two groups of patients. These results suggest that the serum VEGF concentration may reflect myocardial ischemia to a greater degree than the serum HGF concentration. Received June 9, 2000 / Accepted September 30, 2000     

Changes of serum hepatocyte growth factor in coronary artery disease

Hepatocyte growth factor (HGF) is an endothelial cell specific growth factor involved in the repair of endothelial cells and collateral formation, however, the role for coronary artery disease is still unknown. We measured serum HGF level in various coronary artery diseases to examine the clinical significance. Serum HGF level was measured using the enzyme-linked immunosorbent assay method in patients with stable effort angina pectoris (n = 26), old myocardial infarction (n = 18), unstable angina pectoris (UAP; n = 10) and acute myocardial infarction (AMI; n = 21). As a control group, we selected 11 patients with neurocirculatory asthenia. Blood samples from peripheral veins were collected at cardiac catheterization before heparin administration. In the AMI group, blood samples were also collected at 48, 72 hr, 1, 2, 3 and 4 weeks from the peripheral veins and 48 and 72 hr after reperfusion from the coronary sinus. Serum HGF level was significantly higher in the UAP (0.41 +/- 0.12 ng/ml, p < 0.001) and AMI groups (0.38 +/- 0.26 ng/ml, p < 0.05) compared to the control group (0.19 +/- 0.09 ng/ml). Serum HGF level peaked 48 hr after reperfusion in both the peripheral veins (0.42 +/- 0.16 ng/ml) and coronary sinus (0.58 +/- 0.23 ng/ml) in the AMI group, with a significantly higher level in the coronary sinus than the peripheral veins (p < 0.05). No significant correlation between peak HGF level in the peripheral veins and peak creatine kinase (CK), CK-MB, ejection fraction and cardiac index was observed. Serum HGF was elevated in acute coronary syndrome, indicating advanced endothelial cell damage. HGF is produced, at least partially, in the heart in patients with AMI. Serum HGF level may be useful to detect endothelial cell damage rather than myocardial cell damage.     

Clinical implications of circulating soluble Fas and Fas ligand in patients with acute myocardial infarction.

BACKGROUND: Apoptotic cell death is the major form of myocardial damage produced by coronary ischemic events. OBJECTIVE: To assess whether circulating levels of soluble Fas (sFas), an inhibitor of apoptosis, and sFas ligand, an inducer of apoptosis, in patients with coronary artery disease are greater than normal. METHODS: Forty-seven patients [acute myocardial infarction (AMI) in 17, old myocardial infarction (OMI) in 15, stable angina in 15] and 10 normal control subjects participated in this study. Serum levels of sFas and sFas ligand in all patients were measured, and cardiac catheterizations were performed. RESULTS: Serum levels of sFas were greater than normal only in patients with AMI (4.6 +/- 1.6 ng/ml); the levels were significantly higher than those in patients with OMI (2.1 +/- 0.6 ng/ml) and stable angina (2.2 +/- 0.5 ng/ml), and in normal subjects (2.0 +/- 0.6 ng/ml; P < 0.0001). However, there was no difference among serum levels of sFas ligand for all groups. For patients with AMI, there was no significant correlation between serum levels of sFas and peak levels both of plasma creatine phosphokinase and of plasma myosin light chain type I as clinical indexes of infarct size. However, there were significant correlations between serum levels of sFas and both pulmonary artery wedge pressure (r = 0.767, P = 0.0003) and left ventricular end-diastolic pressure (r = 0.629, P = 0.03). CONCLUSIONS: Circulating sFas increases in concentration in relation to the severity of hemodynamic conditions in patients with AMI, but it is independent from size of infarct. Therefore, circulating sFas could play an important role as the marker of pathophysiologic conditions associated with cardiomyocyte apoptosis in AMI.     

急性冠脉综合征患者血Th1/Th2漂移与冠脉病变特点及中医虚实证候的相关性

目的:探讨急性冠脉综合征（acute coronary syndrome,ACS）患者血Th1/Th2漂移与冠脉病变特点及胸痹虚实证候的相关性。方法:选取2010年5月~9月在山东省立医院及山东中医药大学第二附属医院心脏内科病房就诊行经皮冠状动脉造影(coronary arteriography,CAG)的患者66例,包括不稳定型心绞痛（unstable angina,UAP）患者22例、急性心肌梗死（acute myocardial infarction,AMI）患者11例、稳定型冠心病（SAP）患者33例,健康对照组20例。所有纳入对象均应用ELISA监测血干扰素γ（interferon-γ,IFN-γ）、白介素2 （interleukin-2,IL-2）、白介素4 （interleukin-4,IL-4）、白介素10（interleukin-10,IL-10）水平。冠状动脉造影采用Gensini积分、冠脉病变支数分析冠脉病变特点,并进行胸痹的辩证分型。结果: ①UAP组、AMI组患者IFN-γ、IL-2水平较SAP、正常对照组有显著升高（P<0.05）,且存在AMI组>UAP组>SAP组,然而,各组间IL-4、IL-10水平均无明显差异。②ACS组Gensini积分与SAP组比较有显著差异。UAP组、AMI组、SAP组患者IFN-γ、IL-2水平与Gensini积分均呈显著正相关;IL-4、IL-10水平与Gensini积分均呈负相关。③1支病变组与2支病变组之间IFN-γ、IL-2水平均无显著差异,但均较3支病变组细胞因子水平低（P<0.05）。2支病变组与3支病变组之间IL-4、IL-10水平均无显著差异,但均较1支病变组细胞因子水平低（P<0.05）。④中医虚证组IL-2、IFN-γ水平及Genisi积分均较实证组明显增高（P<0.05）。结论:①血Th1/Th2向Th1方向的漂移与ACS发生有关,与冠脉病变的程度是相关的。②虚证患者冠脉病变程度较实证患者严重。③IFN-γ、IL-2水平增高,可作为中医胸痹虚证微观辨证指标。     

The effects of metabolic syndrome versus infectious burden on inflammation, severity of coronary atherosclerosis, and major adverse cardiovascular events

BACKGROUND: The clinical predictors of inflammation in atherosclerosis remain controversial. The objective of this study was to compare the associations of metabolic factors vs. infectious burden (IB) with inflammation, the severity of coronary atherosclerosis, and major adverse cardiovascular events (MACEs). DESIGN, SETTING, AND PATIENTS: Coronary angiography with Gensini score was applied to assess the severity of coronary atherosclerosis in 568 patients with coronary artery disease. Metabolic syndrome (MS) score (0-5) was defined according to the modified criteria of National Cholesterol Education Program Adult Treatment Panel III. IB score (0-7) was defined as the number of seropositivities to several agents. RESULTS: IB score was not associated with plasma C-reactive protein (CRP) concentration, Gensini score, or the risk of MACE. In contrast, MS score significantly correlated with both plasma CRP concentration and Gensini score (P < 0.001 for both). MS score and plasma CRP concentration were also significantly associated with the risk of MACE (hazard ratios 1.51, P < 0.001; and 1.90, P = 0.002, respectively). CONCLUSION: Compared with IB, metabolic abnormalities have a more prominent association with the degree of inflammation, the severity of coronary atherosclerosis, and the risk of MACE in patients with coronary artery disease.     

Descending aorta wall volume and coronary artery disease: a comparative study using enhanced computed tomography of the chest and coronary angiography

The study examined the association between aortic wall volume (AWV) detected by enhanced computed tomography and coronary artery atherosclerosis observed on angiography. In 180 cases, AWV was measured as the total wall volume of a 7-cm portion of the descending thoracic aorta distal from the tracheal bifurcation. Coronary artery atherosclerosis was angiographically quantified by both Gensini score, in terms of the severity of coronary artery stenosis, and Extent score, in terms of the severity of coronary artery involvement. Mean AWV values between the patients with significant coronary artery stenosis and those without significant stenosis were 9.83+/-4.04 cm3 and 8.09+/-2.39 cm3, respectively (p<0.001). AWV was a significantly independent variable for significant coronary artery disease (p=0.0097) and an Extent score > or = 60 (p=0.0092). Calcification of AWV, however, was not associated with coronary atherosclerosis. The quantification of aortic atherosclerosis was useful for diagnosing coronary artery disease.     

急性心肌梗死患者冠状动脉循环血线粒体偶联因子-6含量变化及意义

目的:研究急性心肌梗死(AMI)患者血清线粒体偶联因子-6(CF6)含量在冠状动脉循环中的变化。方法:用放免方法分别测定AMI患者与对照组冠状静脉窦、冠状动脉与外周血清中CF6浓度。结果:AMI患者冠状静脉窦、冠状动脉、外周静脉血清中CF6浓度较对照组差异均有统计学意义(P<0.01),AMI患者冠状静脉窦血清CF6较冠状动脉血清CF6明显升高,差异有统计学意义(P<0.01)。结论:AMI患者外周静脉、冠状动脉和冠状静脉窦血清CF6浓度明显增高,以冠状静脉窦血清CF6升高最明显。     

A decrease in the percentage of circulating mDC precursors in patients with coronary heart disease: a relation to the severity and extent of coronary artery lesions?

Inflammation plays a pivotal role in coronary heart disease. Dendritic cells (DCs) are principal players in inflammation and atherosclerosis. Although the percentage of circulating DC precursors in coronary heart disease have been investigated, circulating myeloid DC (mDC) and plasmacytoid DC (pDC) precursors have not been extensively studied, particularly in relation to the severity of coronary artery lesions in patients with coronary heart disease. In this study, we recruited controls (n = 29), patients with stable angina pectoris (SAP, n = 30), patients with unstable angina pectoris (UAP, n = 56), and patients with acute myocardial infarction (AMI, n = 50). The severity and extent of coronary artery lesions was evaluated by Gensini score, following coronary angiograms. The percentage of circulating mDC and pDC precursors was determined by fluorescence-activated cell sorting (FACS). Plasma levels of MCP-1 and MMP-9, which correlate with atherosclerosis and DC migration, were also measured. The percentage of circulating mDC precursors was reduced in patients with AMI and UAP compared with control and SAP patients, respectively (p < 0.01 for AMI vs. SAP and Control, p < 0.05 for UAP vs. SAP and Control). The percentage of circulating pDC precursors was not significant changed. The levels of plasma MMP-9 and MCP-1 and Genisi score were all increased in patients with AMI and UAP, compared to control and SAP patients, respectively (p < 0.01 for AMI vs. SAP and control, p < 0.05 for UAP vs. SAP and control). Overall, the percentage of circulating mDC precursors was negatively correlated with MCP-1 (p < 0.001), MMP-9 (p < 0.001) and Genisi scores (p < 0.001). Genisi scores were positively correlated with the levels of MCP-1 (p < 0.001) and MMP-9 (p < 0.001). Our study suggested that the percentage of circulating mDC precursors is negatively correlated with the severity and extent of coronary artery lesions in patients with coronary heart disease.     

急性心肌梗死患者血浆sST2水平与冠状动脉病变程度的相关性

目的探讨急性心肌梗死患者血浆白细胞介素1受体家族成员sST2浓度与冠状动脉狭窄严重程度的关系及意义。方法选择发病12 h内急诊经皮冠状动脉介入术术前的急性心肌梗死患者44名,采用酶联免疫吸附法检测患者血浆sST2浓度,根据造影结果对冠状动脉狭窄程度进行Gensini评分。分析sST2水平与冠状动脉病变程度和病变支数的关系。结果急性心肌梗死患者血浆中sST2水平随着冠状动脉Gensini评分增高而逐渐升高(P<0.001)。多支冠状动脉病变组血浆sST2浓度显著高于单支病变组(P<0.01)。sST2浓度与冠状动脉Gensini评分呈显著正相关(r=0.772,P<0.001)。结论急性心肌梗死患者血浆sST2水平可能成为预测冠状动脉狭窄严重程度的标志物。     

Imaging of subendocardial myocardial blood flow by dye-staining cardioscopy in patients with coronary artery disease

This study was carried out to image subendocardial myocardial blood flow (SMBF) by dye-staining cardioscopy (DSC) in patients with coronary artery disease.In patients with epicardial coronary artery disease, SMBF plays a direct and critical role in determining the extent and severity of cardiac function and symptoms. If SMBF could be clinically imaged instantaneously, the effects of medical and interventional treatment on it can be directly evaluated. However, there are no clinically available methods for direct and real-time imaging of SMBF. Twenty-three patients [6 with chest pain syndrome (CPS); 3 with vasospastic angina pectoris (VSA); 9 with angina pectoris due to organic coronary stenosis (AP); 5 with old myocardial infarction OMI)] underwent DSC of the left ventricle by selective intracoronary injection of 1 mL of 2.5% Evans blue dye solution (EB). Five patients with acute myocardial infarction (AMI) underwent DSC before and after coronary stent deployment. The endocardial surface was stained diffusely blue with EB indicating normal blood flow in patients with CPS; stained in a patchy fashion indicating patchy blood flow in patients with VSA; and stained in a patchy fashion or not stained indicating patchy or no blood flow in those with AP and OMI. Myocardial staining with EB was observed after coronary stent deployment in all patients with AMI, indicating restoration of the SMBF. It is evident that SMBF could be imaged by DSC. This imaging modality is useful for the evaluation of therapies and accurate guidance of transendocardial therapies of the ischemic myocardium.     

冠心病患者冠脉循环中血浆线粒体偶联因子-6含量与冠脉狭窄程度的相关性(英文)

目的：研究冠心病（CHD）患者冠脉循环中血浆线粒体偶联因子－6（MCF－6）含量与冠脉狭窄程度的相关性。方法：选择冠心病患者64例（冠心病组）,根据冠脉病变程度分为单支、双支、多支病变组;另选冠脉正常者20例作为正常对照组,用放免方法分别测定各组外周、冠状窦、冠状窦与主动脉根部血浆MCF－6浓度,并用多元线性逐步回归分析分析冠脉循环血浆MCF－6含量与冠脉狭窄程度的相关性。结果：冠心病患者外周、主动脉根部、冠状窦血浆MCF－6浓度较正常对照组均显著升高（P〈0．05）;冠心病组冠状窦血浆MCF－6浓度较主动脉根部及外周血的均显著升高[（402±56）pg／ml比（348±48）pg／ml比（340±51）pg／ml,P〈0．01];多支病变组的血浆MCF－6浓度较单支、双支病变组的显著升高（P〈0．05～0．01）;多元线性逐步回归分析显示冠状窦及主动脉根部血浆MCF－6浓度与Gensini积分均呈明显正相关（r=0．650,P〈0．01;r＝0．711,P〈0．01）。结论：线粒体偶联因子－6参与了冠心病的病理生理过程,在冠心病的发病过程中可能是一种较为重要的血管活性物质。     

急性心肌梗死患者血清高敏肌钙蛋白T及线粒体偶联因子-6含量的变化

目的观察急性心肌梗死（AMI）患者血清高敏肌钙蛋白T（hs-TnT）及线粒体偶联因子-6（CF6）含量在冠状动脉循环中的变化。方法纳入2009年4月到2011年3月期间我院收诊的AMI患者60例,同期选取冠脉造影结果无狭窄或狭窄程度〈50%的患者30例作为对照组。取两组受试者冠状静脉窦、冠状动脉与外周血清,分别采用发光免疫法和放射免疫法测定hs-TnT及CF6浓度。结果 AMI患者冠状静脉窦、冠状动脉与外周静脉血清中hs-TnT、CF6浓度与对照组相比,差异均有统计学意义（P〈0.01）;AMI患者冠状静脉窦血清hs-TnT、CF6较冠状动脉血清hs-TnT、CF6均值升高,差异有统计学意义（P〈0.01）。结论 AMI可导致冠脉循环hs-TnT和CF6浓度升高,二者可在一定程度上预测心肌梗死面积。     

Brachial arterial stiffness predicts coronary atherosclerosis in patients at risk for cardiovascular diseases

Aortic pulse wave velocity (PWV) is a predictor of atherosclerosis. The percent mean pulse amplitude of the artery (%MPA) has been proposed as a novel marker of atherosclerosis. The present study evaluated the predictive value of PWV and the %MPA for coronary atherosclerosis. The severity of coronary atherosclerosis was evaluated using both the Gensini score and coronary calcium grade. Thirty-three patients with cardiovascular risk factors were assigned to those with significant coronary artery stenosis ((+)stenosis) group with the presence of > or = 75% coronary artery stenosis (n = 15; age: 68 +/- 7 years, mean +/- SD) or those without significant coronary artery stenosis ((-)stenosis) group (n = 18; age: 66 +/- 8 years). In each patient, the PWV and %MPA at the right brachial artery and both sides of the ankle were obtained using a non-invasive vascular screening device. The Gensini score and coronary calcium grade were higher in the +stenosis group than they were in the (-)stenosis group (P < 0.01 and P < 0.05, respectively). The brachial %MPA was lower in the (+)stenosis group than it was in the -stenosis group (P < 0.005). Both the Gensini score and the coronary calcium grade correlated with the brachial %MPA (r = 0.62, P = 0.0001 and P = 0.33, P = 0.030, respectively). Our observations suggest that brachial %MPA provides predictive values for coronary atherosclerosis in subjects at risk for cardiovascular disease.     

Serum hepatocyte growth factor predicts ventricular remodeling following myocardial infarction.

Hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) stimulate endothelial cell proliferation and induce angiogenesis, but the timing and significance of their release in patients with acute myocardial infarction (AMI) are unknown in relation to future left ventricular remodeling. Venous blood samples were obtained at admission and up to 3 weeks later in 40 patients with AMI and in 40 age- and sex-matched control subjects. Blood samples were also taken from the coronary sinus (CS) in 20 patients on day 7 following AMI. Left ventricular end-diastolic volume in the subacute (1 week) and chronic (3 months) phases was assessed by left ventriculography to identify the remodeling group (n=15), which was defined as an increase in left ventricular end-diastolic volume index > or =5 ml/m(2) relative to the baseline value. Serum HGF and VEGF concentrations were higher in newly admitted patients with AMI than in the controls (HGF, 0.33 +/-0.09 vs 0.24+/-0.08 ng/ml, p<0.01; VEGF, 92.2+/-43.1 vs 67.2+/-29.8 pg/ml, p<0.01), peaking on day 7 (HGF, 0.41+/-0.12; VEGF, 161.7+/-76.9), and gradually decreasing between days 14 and 21. The HGF concentration in the CS did not differ from the concentration in the periphery, but the VEGF concentration was significantly more abundant in the CS than in the peripheral sample on day 7 (p<0.05). The serum HGF concentration on day 7 was higher in the remodeling group than in the nonremodeling group (0.47 +/-0.13 vs 0.36+/-0.09 ng/ml, p<0.01), but there was no difference between the groups on admission, day 14 and day 21. The serum VEGF concentration did not differ between the remodeling and nonremodeling groups at any time. Thus, the serum HGF concentration on day 7 after AMI is mostly from noncardiac sources and predicts left ventricular remodeling.     

Impact of plasma adiponectin levels to the presence and severity of coronary artery disease in patients with metabolic syndrome

OBJECTIVES: Adiponectin is thought to serve a protective function for the coronary endothelium by inhibiting many of the crucial steps in atherosclerotic process. Previous research has indicated an increased risk of coronary artery disease (CAD) in patients with metabolic syndrome (MetS). The objective of this study was to investigate whether plasma adiponectin concentrations were associated with the presence and severity of CAD in patients with MetS undergoing coronary angiography. METHODS: We measured plasma adiponectin levels in 167 consecutive patients with MetS undergoing coronary angiography. The severity of coronary atherosclerosis was defined by using Gensini score system. RESULTS: CAD was found in 70.1% of the patients. Patients with significant CAD had lower plasma adiponectin concentrations than those without CAD (4.14+/-3.83 vs. 8.94+/-6.63 microg/ml, P<0.001). Multiple regression analysis demonstrated that plasma adiponectin level was independently associated with CAD (odds ratio: 0.86; 95% confidence interval: 0.78-0.94; P=0.001). Plasma adiponectin levels were inversely related to the Gensini score (rho: -0.480, P<0.001) and predicted the severity of coronary atherosclerosis independent of other risk factors (beta: -0.054; 95% confidence interval: -0.074--0.034; P<0.001). CONCLUSIONS: These findings suggest that hypoadiponectinemia may play a role in the development of coronary atherosclerosis and the observation of adiponectin levels may be indicative of the presence of significant CAD in patients with MetS.