急性冠脉综合征危险因素与冠状动脉病变严重程度相关性分析

【摘要】 目的 探讨急性冠状动脉综合征(ACS)患者危险因素与冠状动脉病变严重程度的相关性。方法 纳入于我院心脏中心行急诊经皮冠状动脉介入治疗(PCI)的ACS患者296例,采用Gensini评分评价冠状动脉病变严重程度,对比分析不同程度冠脉病变患者的基线资料特点,应用双变量相关分析、多元线性逐步回归和Logistic回归分析ACS危险因素与冠状动脉病变严重程度之间的相关性。结果 (1)冠状动脉中、重度病变组患者的年龄、低密度脂蛋白胆固醇(LDL-L)、N末端B型钠尿肽前体（NT-ProBNP）、高敏C反应蛋白(hs-CRP)、高敏肌钙蛋白T(hs-cTnT)、肌酸激酶同工酶(CK-MB)水平、Gensini评分均高于轻度病变组,差异均有统计学意义(均P＜0.05)。重度病变组患者的空腹血糖(FBG)水平高于轻度病变组,肌酸激酶同工酶(CK-MB)、Gensini评分水平高于中度病变组,差异均有统计学意义(均P＜0.05)。(2)双变量相关分析发现ACS患者危险因素中LDL-C、FBG、NT-ProBNP、hs-CRP、CK-MB与冠状动脉Gensini评分均呈正相关(相关系数r值分别为0.206、0.240、0.524、0.617、0.291,均P<0.05),HDL-C与Gensini评分负相关(r＝-0.286,P＜0.05)。(3)多元线性逐步回归分析提示NT-ProBNP、hs-CRP、CK-MB为冠状动脉Gensini评分独立预测因子(β分别为0.161、0.127、0.144,均P＜0.05)。(4)多元Logistic回归分析示,NT-ProBNP和hs-CRP与冠脉病变程度独立相关,0R(95%CI)分别为1.015(1.000～1.210),1.028(1.001～1.155),均P＜0.05。结论 急性冠脉综合征患者NT-ProBNP、hs-CRP水平与Gensini评分呈正相关,是冠状动脉病变程度的独立危险因素。     

Women and coronary heart disease risk factors

The prevalence of cardiovascular risk factors among women is high and cardiovascular risk factors often occur in clusters. Strong relationships between exposure to cigarette smoke, physical inactivity, hypertension, and abnormal levels of lipoproteins and homocysteine and subsequent coronary heart disease (CHD) in women are evident from many studies, while the impact of menopause, psychosocial factors, and inflammatory markers is less clear and requires further study. Observational studies document that smoking cessation reduces CHD risk among persons with and without existing CHD, and that moderate levels of physical activity are associated with lower CHD risk. Clinical trials over the last decade have convincingly shown that treatment of hypertension and dyslipidemia reduces CHD risk in both genders, but many women (and men) with hypertension and dyslipidemia remain either untreated or under-treated.     

Genetic risk factors and restenosis after percutaneous coronary interventions

Restenosis is the major limitation of percutaneous coronary interventions. Depending on the form of intervention and patients' characteristics, 20 to 50% of the treated patients incur significant restenosis. Restenosis is caused by a complex and only partially understood cascade of events. Thrombus formation at the injury site, formation of the neointima as a result of the migration and proliferation of smooth muscle cells (SMC) and extracellular matrix production, as well as constrictive remodeling of the vessel wall contribute by a variable degree to restenosis. Restenosis is not a random event but it affects selectively a certain subset of patients. These patients have some peculiar characteristics that help to identify the presence of a higher risk for restenosis. Conventional patient-related factors account only for a relatively small portion of the predictive power, much more contribution comes from lesion and procedural characteristics. There is increasing evidence that inherited factors may explain at least part of the excessive risk for restenosis observed in certain patients. Evidence exists that gene polymorphisms may lead to quantitative or functional alterations of the respective gene products. Recent studies have also found significant associations between several polymorphic alleles encoding for proteins with a relevant role in the process of lumen renarrowing and restenosis after percutaneous coronary interventions. The best studied polymorphisms in this regard are those of the genes encoding for angiotensin-converting enzyme and platelet glycoprotein-IIIa. Completed or ongoing studies have focused on polymorphisms of genes encoding for proteins interfering with lipid metabolism, hemostasis, nitric oxide production, inflammatory mechanisms, SMC proliferation and matrix production. The results of this research will have considerable pathophysiological and therapeutical implications for the battle against restenosis.     

Role of coronary risk factors in blood thrombogenicity and acute coronary syndromes

Recent advances in basic science have linked some systemic risk factors to endothelial dysfunction which gives rise to atherosclerotic disease and triggers the progression of thrombotic complications. Superficial erosion of the stenotic plaque can be observed in one-third of acute coronary syndromes (ACS). In these cases the presence of classic risk factors such as diabetes mellitus, hypercholesterolemia and smoking favor a state of "vulnerable blood" or high risk. Increased thrombogenicity can exacerbate thrombus formation and is able to trigger an ACS. The vessel endothelium regulates contractile, mitogenic and thrombotic activities of the vessel wall. Risk factors impair both homeostasis and hemostasis of the vessel wall and promote inflammatory signals. Platelet and monocyte activation favors the expression of tissue factor (TF), thus triggering the coagulation cascade with thrombin generation and clot formation. Increased blood thrombogenicity linked to classic risk factors may be associated with circulating TF levels which are much higher than those observed in healthy subjects without risk factors. These observations not only emphasize the usefulness of aggressive management of risk factors but open a new avenue for future studies to devise therapeutic strategies to treat ACS by inhibiting TF expression.     

Genetic risk factors for chronic obstructive pulmonary disease

Cigarette smoking is clearly the major risk factor for chronic obstructive pulmonary disease. However, only a minority of cigarette smokers develops chronic obstructive pulmonary disease, indicating that other factors are involved. Family and twin studies suggest that at least some of those factors are genetic. This article reviews the genes investigated as potential risk factors for this disease, focusing on the recent literature. The only established genetic risk factor for chronic obstructive pulmonary disease is homozygosity for the Z allele of the alpha1 -antitrypsin gene. There is increasing evidence that heterozygotes for the Z allele may also be at increased risk. Variants in genes involved in xenobiotic metabolism, antioxidation, and the inflammatory response have also been associated with chronic obstructive pulmonary disease. Thus, the genetic basis for chronic obstructive pulmonary disease has begun to be elucidated, and it is likely that several genes will be implicated in the pathogenesis of this disease.     

Genetic risk factors for chronic obstructive pulmonary disease

Numerous epidemiologic studies have indicated that there is a genetic basis to COPD. This result suggests that COPD develops in genetically susceptible individuals after sufficient exposure to cigarette smoke. At present, most of the genes that contribute to the genetic component to COPD are unknown. alpha 1-Antitrypsin deficiency is clearly a risk factor for COPD, but the other genetic associations with this disease must be considered as tentative. The key to establishing that a gene modifies the risk for a disease is replication of the association in different populations. This is a difficult task, however, because different genetic risk factors may be present in different populations. In addition, these genetic factors may interact with each other and with environmental risk factors, obscuring the effect of the gene on the phenotype. Apart from alpha 1-AT only the GST-M1, VDBP and CFTR genes have been implicated as risk factors in more than one population. Identification of other candidate genes awaits further understanding of the pathogenesis of COPD at the molecular level. There is good evidence that the propensity to smoke cigarettes and the likelihood of quitting smoking are influenced by genetic factors. This information may be useful in efforts directed toward cessation; however, most of the genetic studies so far have shown a rather small effect. The responses to hypoxia and hypercapnia also seem to be influenced by genetic factors. Identification of the genes involved could yield important insights into the pathogenesis of COPD and may highlight new targets for therapeutic intervention for this debilitating disease.     

Genetic risk factors of chronic obstructive pulmonary disease

Cigarette smoking is the major risk factor for chronic obstructive pulmonary disease (COPD). However, only a minority of cigarette smokers develop symptomatic disease. Family and twin studies suggest that genetic factors also contribute to the development of COPD. We present a detailed literature review of the genes which have been investigated as potential risk factors for this disease.     

冠心病新的危险因素

冠心病是目前全球范围最常见的心血管疾病 ,它的发生是由外界环境因素和内在的多基因调控异常共同作用的结果。已报道的冠心病危险因素有 2 0 0多种 ,包括我们已经熟悉的危险因素和一些新的危险因素。本文就冠心病的一些新的危险因素做一简述     

Stressful life events and depressive disorders as risk factors for acute coronary heart disease]

BACKGROUND: Several studies outlined the role of stressful life events in the pathogenesis of coronary heart disease. It has recently been emphasized the role of depression, both clinical and subclinical, in the course of myocardial infarction. The relationship between recent life events, major depression, depressive symptomatology and onset of acute coronary heart disease has been less considered. METHODS: Ninety-seven consecutive patients with first episode of coronary heart disease and 97 healthy subjects matched for sociodemographic variables were included. All patients were interviewed by Paykel's interview for recent life events, a semistructured interview for determining the psychiatric diagnosis of mood disorders, a semistructured interview for demoralization. Patients were assessed while on remission from the acute phase. The time period considered was the year preceding the first episode of coronary heart disease, and the year before interview for controls. RESULTS: Patients with acute coronary heart disease reported significantly more life events than control subjects (p < 0.001). All categories of events (except entrance events) were significantly more frequent. Thirty percent of patients were identified as suffering from a major depressive disorder; 9% of patients were suffering from minor depression, and 20% from demoralization. Even though there was an overlap between major depression and demoralization (12%), 17% of patients with major depression were not classified as demoralized and 7 % of patients with demoralization did not satisfy the criteria for major depression. Independently of mood disorders, patients have a higher (p < 0.001) mean number of life events than controls. With regard to life events, the same significant difference (p < 0.001) compared to controls applied to patients with and without mood disorders. CONCLUSIONS: Our findings emphasize the relationship between life events and acute coronary heart disease. These data, together with those regarding traditional cardiac risk factors, may have clinical and prognostic implications to be verified in longitudinal studies.     

Coronary heart disease mortality and coronary risk factors in Argentina

A marked increase in the coronary heart disease (CHD) mortality of working-age (35-64 years) men and women occurred in Argentina in the 1960s and 1970s. CHD is the leading cause of death in men. In 1978, Argentine men had also one of the highest CHD mortality rates (603.9/100,000) in international mortality statistics and Argentine women (155.2/100,000) were also at the top of these statistics. Stroke mortality has also increased in the younger age-group of men and women over the last decade. The high CHD and stroke mortality rates are compatible with a high prevalence of cardiovascular risk factors. Several surveys have demonstrated that mean serum total cholesterol levels are high, the prevalence of smokers is increasing and the proportion of adequately treated hypertensive patients is low. These results suggest that measures should be introduced to change the Argentine way of life to try to initiate a decline in cardiovascular mortality.     

Genetic factors modify the risk of developing beryllium disease

Chronic beryllium disease (CBD) is a debilitating, granulomatous lung disease that occurs in 1 to 5% of exposed workers. Beryllium stimulates a major histocompatibility Class II-restricted, TH1, CD4+ T cell-mediated immune response. The immunological component of the illness, coupled with the small subset of beryllium workers who develop disease, led researchers to hypothesize that genetic factors modify risk of disease. Analysis of human leukocyte antigen (HLA) genes, the T cell receptor, and tumor necrosis factor (TNF)-alpha focused on three critical steps in the development of beryllium specific immunity. Molecular epidemiological analysis of the association of HLA-DP, -DR, and -DQ has implicated HLA-DPB1E69 allelic variants in disease; however, its role in sensitization is unclear. A single report suggested association between HLA-DQB1G86 and progression from sensitization to disease. A beryllium-specific binding motif was identified in CBD-derived T cell clones. Beryllium-stimulated proliferation using HLA-DPB1*0201 and TCRAV22S1/TCRBVb3 T cell receptors (TCRs) confirmed beryllium specificity of these molecules. The G/A transition at -308 in the TNF-alpha promoter was associated with high concentrations of TNF-alpha in bronchoalveolar lavage and to disease severity. Although these studies are continuing, the data confirm the role of genetic factors in the cellular response to beryllium.