吸烟会增加心脏病复发的几率

希腊的研究人员发现,35岁以下的吸烟者若在心脏病发作后还不戒烟,再次引发心脏病的几率要比戒烟者高出三倍。     

肥胖是日后冠心病、糖尿病风险增加的独立因素

芝加哥一项新的研究表明，肥胖的中年人因心脏病／糖尿病住院或者死亡的风险更高，即使他们没有任何其他危险因素。     

研究发现遗传变异可增加心脏病的发作风险

日本科学家研究发现一种能引发炎症的基因变异可能会增加心脏病的发作风险,且该遗传性改变在已发生过心脏病的患者中较为常见。这种变异可能也与一种被称为泌乳素-2(galactin-2)的蛋白相关,且该蛋白可作为一种新的药物靶点以阻止心脏病的发作。     

被动吸烟增加儿童患鼻癌的风险

研究人员对父母患有肺癌的孩子做了调查，发现儿童期被动吸烟可能增加患鼻癌的危险，患膀胱癌和肾癌的发生率也有升高，可能是由于在母体子宫和哺乳时接触到了烟草中的致癌物。该结果已发表在《国际癌症杂志》的网络版上（http：//www3.interscience.wiley.com.doi：10.1002/ije.21387）。     

ICAM-1水平升高可增加先兆子痫妇女的心脏病危险

据近期出版的《高血压》杂志刊登的一项研究结果报道,细胞粘附分子-1(ICAM-1)浓度升高和先兆子痫的某些特点有可能导致有先兆子痫病史的妇女增加患冠心病(CHD)的危险性。     

研究证实ERT并不增加乳腺癌或心脏病风险

来自于国立卫生研究院(NIH)妇女健康促进会(WHI)的主要国际专家的初步研究结果显示,妇女接受为期7年的单一雌激素替代疗法(ERT)并不增加乳腺癌或心脏病风险。该结果与最初的妇女联合应用雌孕激素的研究结果有所差异。     

吃烤肉喝可乐会增加患骨癌的风险

烤肉味道鲜美、香气扑鼻.吃烤肉成为许多人聚会的首选.然而,据一项最新的科学研究显示,吃烤肉时如果搭配可乐,有导致骨癌的危险.     

母乳喂养可减少终生患心脏病的风险

母乳喂养似乎具有许多有益的效果，可减少终生患心血管疾病的风险。在青少年时期，经母乳喂养者的C-反应蛋白(CRP)水平和LDL／HDL比率明显低于接受代乳品喂养的同龄人。     

低剂量OC可增加心脏病发作和卒中的风险

维吉尼亚联邦大学（VCU）的一项研究发现，妇女在服用低剂量口服避孕药（OC）期间的心脏病发作和卒中的风险增加，但停药后这一风险即消失。     

不同年龄组冠心病危险因素的比较

目的 寻找不同年龄段冠心病发病危险因素的差异。方法 1991-03/1997-02在西京医院心内科住院确诊的434例冠心病患,按年龄分为3组,设计统一的调查表格,对一般社会经济化特征、冠心病常见危险因素以及冠状动脉造影（CAG）结果等进行调查和测量。比较3组间的危险因素的差异。结果 中年组、老年前期组和老年组的女性冠心病的比例分别为7.9%,9.1%和17.3%,吸烟率分别为81.2%,74.0%,62.6%,平均每日吸烟量分别为19.8,16.1和11.6支,家族心脑血管病史暴露率也随着年龄的增长而显下降,3组间有显差异。中青年组冠心病以典型心绞痛为主,老年冠心病则以不典型心绞痛为主。结论 不同发病年龄的冠心病患其危险因素的暴露水平有所不同,男性、吸烟和冠心病家庭史可能是冠心病提前发生的重要原因。     

Validation of the Framingham coronary heart disease prediction scores: results of a multiple ethnic groups investigation.

CONTEXT: The Framingham Heart Study produced sex-specific coronary heart disease (CHD) prediction functions for assessing risk of developing incident CHD in a white middle-class population. Concern exists regarding whether these functions can be generalized to other populations. OBJECTIVE: To test the validity and transportability of the Framingham CHD prediction functions per a National Heart, Lung, and Blood Institute workshop organized for this purpose. DESIGN, SETTING, AND SUBJECTS: Sex-specific CHD functions were derived from Framingham data for prediction of coronary death and myocardial infarction. These functions were applied to 6 prospectively studied, ethnically diverse cohorts (n = 23 424), including whites, blacks, Native Americans, Japanese American men, and Hispanic men: the Atherosclerosis Risk in Communities Study (1987-1988), Physicians' Health Study (1982), Honolulu Heart Program (1980-1982), Puerto Rico Heart Health Program (1965-1968), Strong Heart Study (1989-1991), and Cardiovascular Health Study (1989-1990). MAIN OUTCOME MEASURES: The performance, or ability to accurately predict CHD risk, of the Framingham functions compared with the performance of risk functions developed specifically from the individual cohorts' data. Comparisons included evaluation of the equality of relative risks for standard CHD risk factors, discrimination, and calibration. RESULTS: For white men and women and for black men and women the Framingham functions performed reasonably well for prediction of CHD events within 5 years of follow-up. Among Japanese American and Hispanic men and Native American women, the Framingham functions systematically overestimated the risk of 5-year CHD events. After recalibration, taking into account different prevalences of risk factors and underlying rates of developing CHD, the Framingham functions worked well in these populations. CONCLUSIONS: The sex-specific Framingham CHD prediction functions perform well among whites and blacks in different settings and can be applied to other ethnic groups after recalibration for differing prevalences of risk factors and underlying rates of CHD events.     

Mechanisms by which stress can lead to coronary heart disease

Much stress is of psychological origin and due to emotional arousal. The mechanisms by which anger, helplessness, or a sense of control and serenity exert their various neuroendocrine effects are discussed. Primacy is given to three systems; to the catecholamines, to testosterone and to cortisol. Evidence that they interact to accelerate the arteriosclerotic process is cited. The protective aspects of intimacy are discussed together with evidence that certain personality types promote it in the marital situation while others do not. It is suggested that the post-traumatic stress syndrome may relate to the coronary-prone personality for it involves an alexithymic disturbance of the emotional competence required for successful intimacy.     

Periodontal disease and coronary heart disease risk

CONTEXT: Research has suggested a relationship between periodontal disease and coronary heart disease (CHD), but data on the association between these 2 common conditions are inconclusive due to the possibility of confounding. OBJECTIVE: To evaluate the risk of CHD in persons with periodontitis, gingivitis, or no periodontal disease. DESIGN: Prospective cohort study. SETTING: The First National Health and Nutrition Examination Survey Epidemiologic Follow-up Study, conducted in 1982-1984, 1986, 1987, and 1992. PARTICIPANTS: A total of 8032 dentate adults aged 25 to 74 years with no reported history of cardiovascular disease, including 1859 individuals with periodontitis, 2421 with gingivitis, and 3752 with healthy periodontal tissues. MAIN OUTCOME MEASURE: First occurrence of death from CHD or hospitalization due to CHD, or revascularization procedures, obtained from death certificates and medical records, by baseline periodontal status. RESULTS: During follow-up, 1265 individuals had at least 1 CHD event, including CHD fatality (n = 468) or at least 1 hospitalization with a diagnosis of CHD (n = 1022), including coronary revascularization procedures (n = 155). After adjustment for known cardiovascular risk factors, gingivitis was not associated with CHD (hazard ratio, 1.05; 95% confidence interval, 0.88-1.26), while periodontitis was associated with a nonsignificant increased risk for CHD event (hazard ratio, 1. 14; 95% confidence interval, 0.96-1.36). CONCLUSION: This study did not find convincing evidence of a causal association between periodontal disease and CHD risk. JAMA. 2000;284:1406-1410.