Akutes Koronarsyndrom und Entzündung

Inflammation plays a pivotal role in atherosclerosis and coronary heart disease. Inflammatory processes of the coronary arterial wall are involved in plaque formation, progression and, finally, plaque instability consecutively leading to the clinical manifestations of stable coronary artery disease or acute coronary syndromes (unstable angina, non-ST elevation and ST elevation myocardial infarction). Acute coronary syndromes result from plaque rupture or erosion leading to local thrombus formation with consecutive necrosis of myocytes due to ischemia, which is associated with widespread and diffuse pancoronary and panmyocardial inflammation. Accordingly, markers of myocardial necrosis (e. g., cardiac troponins) do have crucial diagnostic and prognostic value. In case of troponin-negative acute coronary syndromes, however, markers of inflammation emerged as potentially useful tools for risk stratification. C-reactive protein has been shown to serve as a powerful predictor of future cardiovascular events following acute coronary syndromes, even if troponins are not (yet) positive. Moreover, a variety of pro- (soluble CD40 ligand, placental growth factor, interleukin-6, pregnancy-associated plasma protein A, myeloperoxidase, monocyte chemoattractant protein-1) and anti-inflammatory markers (interleukin-10, activin A) have been suggested to provide relevant prognostic information in patients with acute coronary syndrome. However, the clinical utility of these novel markers has not been established so far.     

Increased circulating cytokines in patients with myocarditis and cardiomyopathy.

OBJECTIVES--To elucidate the potential role of cytokines in the pathogenesis of cardiomyopathy and myocarditis. BACKGROUND--Experimental studies show that certain cytokines depress myocardial contractility and that tumour necrosis factor-alpha plays an important part in the pathogenesis of myocardial injury in animal models of viral and autoimmune myocarditis. METHODS--Plasma interleukin 1-alpha, interleukin 1-beta, interleukin-2, interleukin-6, tumour necrosis factor-alpha, tumour necrosis factor-beta, granulocyte-macrophage colony stimulating factor, granulocyte colony stimulating factor, macrophage colony stimulating factor, interferon-alpha and interferon-gamma were measured in 13 patients with acute myocarditis, 23 patients with dilated cardiomyopathy, 51 patients with hypertrophic cardiomyopathy, nine patients with acute myocardial infarction, 18 patients with angina pectoris, 12 patients with essential hypertension and 17 healthy controls. RESULTS--Increased concentrations of cytokines were not detected in the controls. In patients with acute myocarditis, interleukin 1-alpha was detected in 23% (mean (SD) 25 (11) pg/ml), tumour necrosis factor-alpha in 46% (61 (31) pg/ml), and macrophage colony stimulating factor was 2.5 (1.8) ng/ml (normal 1.9 (0.4)). In patients with dilated cardiomyopathy, tumour necrosis factor-alpha was detected in 35% (402 (555) pg/ml). In patients with hypertrophic cardiomyopathy, interleukin-2 was detectable in 14% (2318 (4738) pg/ml) and tumour necrosis factor-alpha ws detected in 20% (992 (1517) pg/ml). The concentration of macrophage colony stimulating factor was raised in patients with acute myocardial infarction. Granulocyte colony stimulating factor was often increased in myocarditis, cardiomyopathies, acute myocardial infarction, and angina pectoris--suggesting activation of macrophages and/or endothelial cells--but this increase was not specific to these diseases. Increased concentrations of cytokines were not found in patients with essential hypertension. CONCLUSION--These results suggest that cytokines may play a part in the pathogenesis of myocardial injury in myocarditis and cardiomyopathies and that further studies to explore the potential pathogenetic role of cytokines in myocardial diseases may be warranted.     

Serum tumour necrosis factor-alpha,interleukin-2 and interleukin-10 activation in stable angina and acute coronary syndromes

BACKGROUND: Dynamic instability of coronary atherosclerotic plaque results in the development of both unstable angina and myocardial infarction. The aim of the study was to investigate the dynamics of serum concentrations of tumour necrosis factor (TNF)alpha, interleukin (IL)-10, and IL-2 in patients with myocardial infarction (MI) and unstable angina (UA) as compared to stable angina (SA) patients and healthy volunteers. METHODS: A total of 189 patients with coronary artery disease (CAD) were studied: 100 patients with SA (class II/III according to CCS), 57 patients with UA (Braunwald class IIIB; determinations at 6, 24, and 48 h after chest pain), and 32 patients with MI (determinations at admission, on the 7th and 30th days after MI). Twenty healthy volunteers acted as controls. RESULTS: Serum TNFalpha levels were elevated in all CAD groups (SA: 17.3+/-4; UA: 18.7+/-4; MI: 22.0+/-3 pg/ml; p<0.001) in comparison to the controls (8.3+/-1.4 pg/ml). However, the highest values were characteristic of MI patients, especially values obtained at admission (p<0.01 versus SA and UA). Mean serum concentrations of IL-2 were significantly higher in patients with MI and UA (89.6+/-40; 87.0+/-24 pg/ml, respectively; p<0.01) when compared to SA and the control group (58.3+/-49; and 51.5+/-39, respectively). Serum IL-10 levels were also higher in MI and UA patients. Levels of IL-2 and IL-10 measured following chest pain in unstable patients, as well as their consecutive determinations in MI patients did not show any change dynamics, that is, they were persistently elevated. CONCLUSIONS: When compared to stable CAD and healthy subjects, acute coronary syndromes are associated with long-term increase of serum concentrations of pro- and anti-inflammatory cytokines. It seems likely that sudden CAD progression leading to acute coronary syndromes is triggered/accompanied by prolonged immune activation.     

Role of interleukin-17 and interleukin-17-induced cytokines interleukin-6 and interleukin-8 in unstable coronary artery disease

BACKGROUND: Atherosclerosis is a chronic inflammatory disease and interleukins are considered to play a key role in the chronic vascular inflammatory response that is typical of atherosclerosis. The serum levels of several of these cytokines have been found to positively correlate with coronary arterial disease and its sequelae. AIM: The aim of our study was to evaluate the levels of a comparatively new cytokine IL-17, in patients with stable and unstable coronary artery disease in order to assess whether unstable coronary artery disease patients had higher IL-17 levels. MATERIALS AND METHODS: We analyzed the concentrations of IL-17, IL-6, IL-8 and IL-10 using enzyme-linked immunosorbent assay and heat-sensitive C-reactive protein using latex particle-enhanced immunoturbidimetry in 58 consecutive unselected patients divided into three groups: stable angina (n=14), unstable angina (n=24) and acute myocardial infarction (n=20). We further compared them with 20 healthy controls. These 58 patients were also angiographically studied and divided into two groups: simple lesion (n=22) and complex lesion (n=36), on the basis of the coronary plaque morphology. RESULTS: Our results show increased concentrations of the proinflammatory cytokines IL-17, IL-6, IL-8 and heat-sensitive C-reactive protein, and decreased concentration of IL-10 in plasma of unstable angina and acute myocardial infarction patients. Plasma concentration of IL-17 was also positively correlated with plasma concentrations of IL-6 and heat-sensitive C-reactive protein. Our findings further showed that IL-17 values were higher in patients having angiographically visible complex types of lesions but no difference was observed between complex and simple lesion morphology patients. CONCLUSION: In conclusion, these findings point towards a role of inflammation in the form of increased activity of IL-17, IL-6 and IL-8 in patients of unstable angina and acute myocardial infarction and thus suggest that IL-17-driven inflammation may play a role in the promotion of clinical instability in patients with coronary artery disease.     

Cytokines in patients with ischaemic heart disease or myocardial infarction

BACKGROUND: Cytokines are responsible for the modulation of immunological and inflammatory processes as well as proliferative responses and apoptosis. It has been recently suggested that such cytokines as interleukin 6 (IL-6), soluble interleukin 6 receptor (sIL-6R) and anti-inflammatory cytokines such as interleukin 10 (IL-10) may play a significant role in the pathogenesis of acute coronary syndromes. AIM: To assess serum concentration of IL-6, sIL-6R and IL-10 in patients with ischaemic heart disease or acute myocardial infarction (AMI). METHODS: The study group consisted of 74 patients (25 females, 49 males, aged 40-69 years) divided into three groups; group I - 18 patients with AMI (up to 12 hours from the onset of symptoms), group II - 31 patients with unstable angina and group III - 25 patients with stable angina. The control group consisted of 20 healthy subjects. RESULTS: The IL-6 and sIL-6R serum levels were significantly higher in patients from groups I and II compared with patients from group III and controls, whereas the IL-10 serum concentration was similar in all studied groups. In patients with acute coronary syndromes serum concentrations of examined cytokines were positively correlated with acute inflammatory phase parameters and classical risk factors such as body mass index, blood pressure and lipid levels. CONCLUSIONS: IL-6 and sIL-6R are markers of acute coronary syndromes and may be used for the identification of high-risk patients with unstable angina or AMI.     

No long-lasting or intermittent mast cell activation in acute coronary syndromes

BACKGROUND: Unstable coronary syndromes, such as acute myocardial infarction and unstable angina pectoris are mostly due to rupture of an atherosclerotic plaque. Recently mast cells were found to participate actively in the inflammatory process of atherosclerosis by excreting proteolytic and pro-inflammatory substances with the ability to cause plaque instability and rupture. Mast cell activity can be determined by measuring serum levels of tryptase, as has been demonstrated in patients with anaphylaxis and mastcytosis. HYPOTHESIS: Acute coronary events (acute myocardial infarction and unstable angina pectoris) are associated with increased mast cell activity, reflected by elevated serum tryptase levels. METHODS: Serum levels of tryptase were determined in the following three groups of patients: 13 patients with acute myocardial infarction, 10 patients with unstable angina pectoris, and 14 patients without ischaemic cardiovascular disease who were used as controls. Patients with known IgE mediated allergic diseases and/or anti-histaminical drugs were excluded. RESULTS: The groups were comparable for sex, blood pressure, smoking and cholesterol levels. The controls tended to be younger (P=0.05). Levels of tryptase did not differ between patients with acute myocardial infarction (7.9+/-4.6 microg/l), unstable angina pectoris (6.0+/-2.1 microg/l) or controls (6.9+/-4.1 microg/l), nor could a relation with levels of C-reactive protein be demonstrated. CONCLUSION: Serum levels of tryptase are not elevated in patients with acute coronary syndromes. This implies that increased mast cell activity, if any, in unstable coronary syndromes is not reflected systemically. Other, more specific methods will be needed to determine the activity of the mast cell in vivo.     

Systemic inflammatory markers in acute coronary syndrome: association with cardiovascular risk factors and effect of early lipid lowering

BACKGROUND: Evidence for statin therapy in prevention of coronary artery disease is overwhelming. In spite of theoretical benefits, any additional advantage of its early introduction in the management of acute coronary syndrome is, however, uncertain. We therefore investigated differences between plasma levels of the systemic inflammatory markers intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, C-reactive protein and interleukin-6 in patients presenting with unstable angina or acute myocardial infarction, and assessed whether the 30-day levels of these markers are influenced by early instigation of the HMG-CoA reductase inhibitor pravastatin. MATERIALS AND METHODS: 170 (134 male) patients presenting with acute coronary syndrome, but without previous statin therapy, participated. Blood was taken within 24 h of onset of ischaemic pain and again at 30 days. In all, 87 (71 male) participants were treated with pravastatin (20-40 mg daily) and 83 (63 male) with a matched placebo. RESULTS: At presentation, interleukin-6 was higher in males than in females (P=0.008) and lower in those with a pre-existing history of myocardial infarction (P=0.038). C-reactive protein and interleukin-6 were greater in myocardial infarction, but this difference was lost at 30 days. Thirty-day changes in all parameters were inversely related to level at presentation but not to treatment with pravastatin. Hypertension (P=0.011) and smoking (P=0.042) were associated with elevation of C-reactive protein with no difference between unstable angina or acute myocardial infarction. The effect of these individual factors was cumulative. CONCLUSIONS: Interleukin-6 was greater in acute myocardial infarction than in unstable angina; E-selectin was positively associated with a previous myocardial infarction and inversely related to age. We found no effect of early introduction of pravastatin on systemic inflammatory markers 30 days after acute coronary syndrome.     

Tumor necrosis factor-alpha gene -308G>A polymorphism is associated with ST-elevation myocardial infarction and with high plasma levels of biochemical ischemia markers

OBJECTIVES: As is well known, acute myocardial infarction presents two electrocardiogram (EKG) patterns, ST-elevation (STEMI) and no ST-elevation (NSTEMI), characterized by different coronary artery thrombotic occlusion. Growing evidence shows that inflammation plays a central role in the pathogenesis of acute myocardial infarction. Among the factors that promote inflammation and arterial thrombosis, one of the most important is the proinflammatory cytokine tumor necrosis factor-alpha. The expression of this cytokine is modulated by a polymorphism located at nucleotide -308 of tumor necrosis factor-alpha promoter gene. The objective of our study is to verify whether tumor necrosis factor-alpha -308 polymorphism is associated with risk of acute myocardial infarction (STEMI and NSTEMI) or with biochemical myocardial ischemia markers, such as troponin I, creatine kinase-MB, lactate dehydrogenase and myoglobin. METHODS: We analyzed tumor necrosis factor-alpha -308 polymorphism in a total of 603 study participants: 293 elderly patients affected by acute myocardial infarction (STEMI and NSTEMI) and 310 healthy controls. RESULTS: We found that individuals carrying the tumor necrosis factor-alpha -308 AG+AA genotypes are significantly more represented among acute myocardial infarction patients affected by STEMI than among NSTEMI patients (OR = 1.86, 95% CI 1.08-3.21, p = 0.027) and healthy controls (OR = 1.64, 95% CI 1.03-2.64, p = 0.046). Furthermore, the patients carrying tumor necrosis factor-alpha -308 AG+AA genotypes displayed significant increased levels of biochemical myocardial ischemia markers. CONCLUSIONS: Our study shows a significant association between the tumor necrosis factor-alpha -308 polymorphism and the occurrence of STEMI, and suggests that the tumor necrosis factor-alpha -308 polymorphism could play a role in the pathogenesis of cardiac ischemic damage, AA+AG genotype carrier individuals being likely to be affected by more severe ischemic damage than the rest of the population.     

非ST段抬高型急性冠状动脉综合征介入治疗对心功能的影响

非ST段抬高型急性冠状动脉综合征包括不稳定型心绞痛和非ST段抬高型急性心肌梗死。非ST段抬高型急性冠状动脉综合征患者往往伴有心功能不全,严重影响患者生存质量和预后。近年来研究表明介入治疗可以使狭窄闭塞的冠状动脉再通,心肌得到再灌注,对非ST段抬高型急性冠状动脉综合征患者心功能改善有很大帮助。     

Intracoronary temperature in patients with coronary artery disease

OBJECTIVES: Measurements of changes in plaque temperature may predict plaque rupture. The present study investigated variations in temperature within the atherosclerotic coronary artery using a pressure guide wire with thermal sensor (dual sensor guide wire). METHODS AND RESULTS: Seventy-seven patients (78 lesions), who had no significant lesion at the orifice of the culprit coronary artery, were studied. The patients had acute myocardial infarction (22 patients), unstable angina pectoris (20 patients), and stable angina pectoris (35 patients). The thermal sensor was calibrated at the orifice of the coronary artery, and then inserted into the culprit coronary artery. deltaT was defined as the difference between the intracoronary temperature at the position of the pressure gradient and at the orifice. deltaT was higher in patients with acute myocardial infarction and unstable angina pectoris than in patients with stable angina pectoris (0.09 +/- 0.07 and 0.07 +/- 0.07 vs 0.03 +/- 0.04 degrees C, p < 0.001, p = 0.02, respectively). There was no significant difference in deltaT between patients with acute myocardial infarction and unstable angina pectoris (p = 0.48). Patients with acute myocardial infarction and unstable angina pectoris showed a significant relationship between deltaT and C-reactive protein (r = 0.59, p = 0.0004). CONCLUSIONS: The variations in intracoronary temperature of the culprit coronary arteries in patients with acute coronary syndrome were higher than those in patients with stable angina pectoris. These variations may be related to inflammation of vulnerable plaque.     

急性冠状动脉综合征中C反应蛋白的临床意义及阿司匹林的作用

为探讨Ｃ反应蛋白与急性冠状动脉综合征的关系及阿司匹林对其的影响,观察４６例急性心肌梗死患者、４０例不稳定性心绞痛虱及４２例稳定性心绞痛患者的Ｃ反应蛋白浓度以及不同剂量的阿司匹林对心肌梗死患者Ｃ反应蛋白浓度的影响。结果发现心肌梗死及不稳定性心绞痛患者的Ｃ反应蛋白浓度较稳定性心绞痛患者显著增高（Ｐ〈０．００１）。小剂量（每天３００ｍｇ）阿司匹林可降低心肌梗死患者的Ｃ反应蛋白浓度（Ｐ〈０．０５）。提示Ｃ反应蛋白浓度可作为评价急性冠状动脉综合征患者预后的一个参考指标。     

Serum profiles of matrix metalloproteinases and their tissue inhibitor in patients with acute coronary syndromes. The effects of short-term atorvastatin administration

There is increasing evidence that abnormal cytokine expression and increased metalloproteinase activity are implicated in the pathophysiology of acute coronary syndromes. This study investigates the serum profiles of representative metalloproteinases (MMP-1, -2, -9) and their tissue inhibitor (TIMP-1) in patients with myocardial infarction (MI) and unstable angina (UA) in relation to circulating proinflammatory cytokine (TNF-alpha and IL-6) activity. Furthermore, we examined the effects of a 30-day treatment with atorvastatin on serum levels of these inflammatory factors. Serum concentrations of MMP-1, -2, -9, TIMP-1, IL-6 and TNF-alpha were measured (enzyme-linked immunosorbent assay (ELISA) method) in 23 acute myocardial infarction patients and 20 unstable angina patients on 0 day, 1st, 3rd, 7th and 30th day after admission. Sixteen normal volunteers were used as healthy controls. Additionally, 12 patients of myocardial infarction group and 11 patients of unstable angina group were treated with atorvastatin (20 mg/day) for 30 days in a randomized design. In patients with myocardial infarction and unstable angina, serum levels of MMP-2, -9, TIMP-1, TNF-alpha and IL-6 were significantly higher than those of healthy controls in all time frames (p<0.05). In the group of unstable angina patients, we observed a statistically significant reduction in the levels of MMP-9, TIMP-1 and IL-6 after the 30-day atorvastatin administration. Our results suggest that serum MMPs, TIMP-1 and proinflammatory cytokines play an important role in the pathophysiology of the acute coronary syndromes. The reduction of these factors by short-term atorvastatin administration may provide a new insight into the pleiotropic effects of statins on unstable coronary artery disease.     

The heart in fatal unstable angina pectoris

Compared to patients with sudden coronary death and acute myocardial infarction, relatively little morphologic data has been reported in patients with unstable angina pectoris. This article reviews necropsy data collected from one laboratory on unstable angina pectoris. From these data, several observations are appropriate: (1) Patients with unstable angina as a group have more coronary narrowing by atherosclerotic plaque than do patients with sudden coronary death or acute or healed myocardial infarction. (2) Patients with unstable angina have a much higher frequency of severe narrowing of the left main coronary artery than do patients in other coronary subsets. (3) The coronary atherosclerotic plaques in unstable angina consist primarily of fibrous tissue, and they are more similar to those found in patients with sudden coronary death than in patients with acute myocardial infarction. (4) The frequency of acute coronary lesions (thrombi, plaque rupture, and plaque hemorrhage) is similar to that observed in patients with sudden coronary death and significantly less than that observed in acute myocardial infarction. (5) The frequency of multiluminal channels throughout the major coronary arteries is significantly higher in unstable angina compared to sudden coronary death or acute myocardial infarction. (6) The major epicardial arteries and the heart are smaller in patients with unstable angina than in patients with sudden coronary death or acute myocardial infarction. (7) The left ventricular cavity is usually of normal size in patients with unstable angina and therefore left ventricular function is usually normal.     

冠心病患者血浆血栓调节蛋白水平的测定及其临床意义

目的　测定冠心病患者血浆血栓调节蛋白 ( throm bom odulin,TM)水平并探讨其临床意义。方法　急性心肌梗死、不稳定型心绞痛、稳定型心绞痛三组患者及正常对照组 ,抽取血浆并用酶联免疫吸附试验测量其血浆 TM水平。结果　急性心肌梗死组、不稳定型心绞痛组、稳定型心绞痛组血浆 TM水平均高于正常对照组 ( P<0 .0 5 ) ;急性心肌梗死组与不稳定型心绞痛组间患者血浆 TM水平没有显著性差异 ( P>0 .0 5 ) ,但均高于稳定型心绞痛组和正常对照组 ( P<0 .0 5 )。结论　血浆可溶性 TM水平是反映冠心病患者内皮细胞损伤程度和范围的良好标志 ,对急性心肌梗死、不稳定型心绞痛、稳定型心绞痛的鉴别有一定的临床指导意义     

Increased production of inflammatory cytokines in patients with silent myocardial ischemia

OBJECTIVES

The aim of the study was to examine the inflammatory cytokines in patients with myocardial ischemia to evaluate whether silent ischemia patients exibit any particular cytokine pattern.

BACKGROUND

Silent myocardial ischemia is frequently observed in patients with coronary artery disease. Various endogenous mechanisms control a patient’s perceived intensity of pain. Among them, the inflammatory process and the related cytokine production are known to modulate the threshold for activating the primary afferent nociceptors.

METHODS

Seventy-eight patients with reproducible exercise-induced myocardial ischemia were studied: 34 symptomatic patients, with rest and/or stress angina; 44 asymptomatic patients, with no symptoms during daily life activities or during positive exercise stress test. Venous blood samples were taken from all patients to evaluate the expression of CD11b receptors both on neutrophils and monocytes. Frozen plasma samples (at −80°C) were used to quantify the anti-inflammatory (interleukin-4 and -10, transforming growth factor-β) and the proinflammatory cytokines (tumor necrosis factor-, interferon-γ, interleukin-1β and -6).

RESULTS

In asymptomatic patients lower CD11b receptor expression and higher concentration of anti-inflammatory cytokines were observed. Proinflammatory cytokine production was similar in the two groups.

CONCLUSIONS

The data suggest that an “anti-inflammatory pattern” of cytokine production correlates with silent ischemia and that the immune and inflammatory system activation may be crucial for angina symptoms.     

The determination of serum estradiol, testosterone and progesterone in acute myocardial infarction

The levels of serum estradiol, testosterone and progesterone were determined in 13 cases of acute myocardial infarction. Thirteen intensive care patients without coronary, hepatic or renal disease, 13 cases of unstable angina and 15 normal subjects. The patients were males ranging from 24 to 56 years of age, the average being 40.4 years. The levels of serum estradiol in the acute myocardial infarction and unstable angina groups were significantly higher than in the normal group, and no difference was found between the normal and intensive care patient. The testosterone levels were significantly lower in the acute myocardial infarction and unstable angina groups than in the normal group. Progesterone levels increased in acute myocardial infarction patients. The estradiol: testosterone ratio was considerably elevated in the acute phase of myocardial infarction, and in unstable angina patients. No difference was found between the intensive care patient and normal groups.     

急性心肌梗死与不稳定型心绞痛患者血栓前体蛋白和肌酸激酶的检测

为了解检测血栓前体蛋白对急性冠状动脉综合征转归的早期诊断价值 ,5 1例临床确诊冠心病患者分为不稳定型心绞痛和急性心肌梗死两组 ,采用酶联免疫吸附法检测各组血浆中血栓前体蛋白含量 ,采用干化学法同步检测患者血清磷酸肌酸激酶及其同工酶。结果发现 ,急性心肌梗死组 2 5例患者血栓前体蛋白均值为 9.9± 3.9mg L ,不稳定型心绞痛组 2 6例患者血栓前体蛋白均值为 2 .6± 1.7mg L ,前者明显升高 ,差别有显著性意义 (P <0 .0 1) ;急性心肌梗死组磷酸肌酸激酶均值为 5 95± 4 32u L ,磷酸肌酸激酶同工酶均值为 10 1± 74u L ,不稳定型心绞痛亚组磷酸肌酸激酶均值为 137± 4 0u L ,磷酸肌酸激酶同工酶均值为 10± 7u L ,前者亦明显升高 ,差别均有显著意义(分别为P <0 .0 5和P <0 .0 1)。结果提示 ,血栓前体蛋白对急性冠状动脉综合征具有早期诊断和鉴别价值     

Low molecular weight heparins and coronary artery disease

Coronary artery disease encompasses a wide spectrum of conditions including silent ischemia, exertional angina, unstable angina, and myocardial infarction. Acute coronary syndromes (unstable angina and myocardial infarction) are caused by the rupture of an atherosclerotic plaque, platelet activation, and fibrin deposition resulting in thrombosis. Aspirin and unfractionated heparin (UFH) have traditionally been the treatment of choice in patients with acute coronary syndromes; however, low molecular weight heparins (LMWHs) offer potential advantages over UFH. Available evidence indicates that LMWH is superior to UFH in reducing ischemic events or death in the acute phase of unstable angina or non-Q-wave myocardial infarction. Long-term therapy with lower doses of LMWH may not offer any advantage to aspirin in the prevention of coronary events or death. Major bleeding complications are similar for LMWH and UFH although minor bleeding complications are more common with LMWH, primarily due to injection-site hematomas. Finally, use of LMWH appears to be costeffective compared with UFH. The available evidence supports improved clinical outcomes, favorable safety profile, and cost savings associated with LMWH use in the management of unstable angina and non-Q-wave myocardial infarction and should be favored over UFH.     

C-Reactive Protein and Cardiovascular Diseases

C-reactive protein (CRP) is a unique risk marker and plays a role in the pathogenesis of inflammation and atherosclerosis. It is synthesized and secreted mainly by hepatocytes in response to interleukin-6 (IL-6) and either IL-1 or tumor necrosis factor-alpha. The average plasma half life of CRP is 19 hours. CRP activates complement, increases phagocytic activity of neutrophils, increases respiratory burst of neutrophils, and induces expression of adhesion molecules, synthesis of tissue factor, cytokines from monocytes and platelet aggregation. CRP is involved in development of atherosclerosis and thrombosis. High sensitive-CRP (hs-CRP) is a very novel biochemical marker. It is elevated in various conditions including: inflammation both acute and chronic, acute myocardial infarction, unstable angina, peripheral vascular diseases, diabetes, renal disease, hypertension, and cardiopulmonary bypass. A positive association has been reported between CRP levels and age, smoking, body mass, total cholesterol, lipoprotein a [Lp(a)], homocysteine and fibrinogen. It has a predictive value for the development of peripheral vascular disease, restenosis following percutaneous coronary interventions with or without stent implantation, and complications following cardiopulmonary bypass. Preprocedural high levels of plasma CRP are associated with high incidence of late adverse events (composite of cardiac death, nonfatal myocardial infarction, clinical occurrence of symptoms, progression of significant coronary lesion in vessels other then treated ones) after successful coronary stenting. Baseline levels of CRP predict risk of future myocardial infarction, and stroke in apparently healthy middle-aged men and women. CRP levels predict atherosclerotic vascular disease in patients with end-stage renal disease. Increased pretransplant CRP levels are associated with higher risk of acute rejection in transplant recipients. Various strategies to reduce the adverse effects of CRP have been discussed.     

冠状动脉支架术对冠心病患者血小板活化功能的影响

目的探讨冠心病患者行冠状动脉内支架置入术前后血小板活化指标的变化,了解冠心病不同临床类型支架置入数与血小板活化指标之间的关系。方法利用流式细胞术和单克隆抗体测定48例稳定型心绞痛、45例不稳定型心绞痛患者与37例急性心肌梗死患者外周血中血小板膜糖蛋白CD62p、CD63和凝血酶敏感蛋白的阳性表达率,并与45例冠状动脉造影正常者作对照分析。结果稳定型心绞痛患者、不稳定型心绞痛患者和急性心肌梗死患者支架置入后CD62p、CD63和凝血酶敏感蛋白的阳性表达率均显著高于支架置入前(P<0.01);不稳定型心绞痛组和急性心肌梗死组治疗前亦高于对照组(P<0.01),而稳定型心绞痛组治疗前与对照组比较差异无显著性(P>0.05)。稳定型心绞痛组和不稳定型心绞痛组CD62p、CD63和凝血酶敏感蛋白的阳性表达率与支架置入个数有关,置入支架越多阳性表达率越高。结论不稳定型心绞痛患者及急性心肌梗死患者存在血小板高活化状态、动脉粥样硬化斑块破裂以及急性血栓形成。支架置入术对冠状动脉内皮的损伤加强了血小板的活化,增加了血栓形成的风险。