亚甲基四氢叶酸还原酶基因多态性及血中同型半胱氨酸和叶酸水平与冠心病的关系

目的　观察高同型半胱氨酸 (HCY)血症是否为中国人冠心病 (CHD)的一个独立危险因素 ,以及探讨亚甲基四氢叶酸还原酶 (MTHFR)基因多态性与冠心病的联系 ,并分析HCY、叶酸与MTHFR基因多态性间的相互关系。方法　选择CHD患者 16 1例 ,其中 15 4例行冠状动脉造影证实。正常对照 12 5例。应用荧光免疫偏振法测定血浆HCY ,放免法测定血清叶酸 ,分析MTHFR基因多态性。结果　CHD患者血浆HCY浓度显著高于对照组 [分别为 (15 2 4± 9 5 9)与 (11 4 3± 6 4 4 ) μmol L ,P <0 0 1]。logistic回归分析显示性别、年龄、脂蛋白B和高HCY血症是CHD发病的独立危险因素 ,高HCY血症的优势比 (OR)为 2 5 70 7,其 95 %的可信区间 1 30 0 3～ 5 0 82 5。CHD组MTHFR基因C6 77T突变TT型的频率为 2 9 2 % ,明显高于对照组 16 8% (P =0 0 15 )。CHD组T等位基因频率显著高于对照组 (P =0 0 0 4 )。CHD组和对照组TT型的血浆HCY水平明显高于CT和CC型 (P <0 0 0 1)。CHD组各基因型的HCY水平均高于对照组 (P <0 0 0 1～ 0 0 1)。多元逐步回归显示 :血清叶酸浓度、TT型与血浆HCY浓度独立相关。CHD组和对照组的TT型中 ,血清叶酸水平 <对照组中位数时的HCY水平显著高于叶酸≥中位数时的HCY值。叶酸 <中位数时 ,TT型HCY水平显著     

冠心病患者血浆淀粉样蛋白A水平的变化

目的分别观察冠心病患者血浆中淀粉样蛋白A(serum amyloid A,SAA)和HDL中SAA水平的变化,探讨SAA与动脉粥样硬化之间的关系。方法应用酶联免疫吸附测定法分别检测冠心病组65例及对照组62例血浆中SAA和HDL中SAA的水平,同时对2组其他心血管危险因素、血脂水平和hs-CRP进行比较。结果冠心病组高血压史、吸烟史、冠心病家族史和hs-CRP水平明显高于对照组(P<0.05),血浆中SAA和HDL中SAA含量明显高于对照组,分别为(15.93±12.04)mg/L vs(10.92±11.04)mg/L,(115.22±70.61)mg/L vs(35.92±25.42)mg/L,差异有统计学意义(P<0.001)。logistic回归分析lghs CRP的OR值3.449,95%CI:1.207～9.854;lgSAA的OR值5.909,95%CI:1.531～22.801。结论冠心病患者SAA水平在血浆和HDL中均明显升高,可能是冠心病发病的重要危险因素。     

同型半胱氨酸与冠心病的相关性及其机制探讨

目的　探讨血浆同型半胱氨酸 (HCY)与冠心病 (CHD)的相关性、与CHD传统危险因素的关系及其致CHD的机制。方法　分别测定CHD患者 (10 5例 )及对照组 (32例 )血中HCY、内皮素(ET)、一氧化氮 (NO)、一氧化氮合酶 (NOS)水平及血脂各参数。结果　CHD组高同型半胱氨酸血症(HHCY)的发生率明显高于对照组 (49 5 %比 9 4 % ,P <0 0 1) ,CHD组HCY水平明显高于对照组[(15 2 9± 5 14 ) μmol L比 (10 6 6± 2 78) μmol L ,P <0 0 1]。多元回归分析显示HCY对CHD的相对危险度 (RR)为 1 397(95 %可信区间 :1 137～ 1 6 4 5 ,P <0 0 1) ,表明HCY为CHD的独立危险因素。HCY与年龄、甘油三酯有关 (P <0 0 5 )。HCY与ET呈正相关 (P <0 0 1) ,而与NO、NOS呈负相关 (P <0 0 1)。结论　HHCY是CHD的独立危险因素。HCY可能损伤血管内皮细胞 ,使血管内皮功能失调。     

C-反应蛋白是急性冠脉综合征的一种危险因子

目的　研究急性冠脉综合征 (包括不稳定性心绞痛、急性心肌梗死和心源性猝死 )患者血清C 反应蛋白(CRP)浓度水平并与对照组 (即非急性冠脉综合征 ,包括稳定性心绞痛、陈旧性心肌梗死和正常体检人群 )比较 ,探讨CRP是否为急性冠脉综合征的一种危险因子。方法　用速率散射比浊法测定急性冠脉综合征患者和对照组血清CRP浓度 ,同时检测冠心病的常见危险因子并与CRP一起作Lo gistic回归分析。结果　①急性冠脉综合征患者血清CRP浓度 [18 5 0mg/L± 2 3 98mg/L (SE 2 5 1,n =91) ]显著高于对照组 [3 89mg/L± 7 14mg/L (SE 0 5 1,n =194 ) ](P <0 0 1)。②急性心肌梗死急性期患者CRP浓度 (18 6 5mg/L± 2 4 12mg/L)和不稳定性心绞痛CRP浓度 (17 95mg/L±2 4 10mg/L)显著高于正常对照组 (P <0 0 1)、稳定性心绞痛CRP浓度 (3 94± 7 5 0mg/L) (P <0 0 1)、急性心肌梗死患者恢复期 (5 93mg/L± 13 0 7mg/L) (P <0 0 1)和陈旧性心肌梗死患者 (4 5 7mg/L± 8 2 7mg/L) (P <0 0 1) ;稳定性心绞痛患者、急性心肌梗死患者恢复期和陈旧性心肌梗死患者之间CRP浓度无差别 (P >0 0 5 )并与正常人群比较无显著性差别 (P >0 0 5 )。③每增加CRP 5mg/L ,急性冠脉综合征发生危险增加到近 2倍 (用Logistic回归 ,OR     

冠心病患者C反应蛋白水平及其1059G/C基因多态性的研究

目的　研究中国汉族人群中血清高敏C反应蛋白 (CRP)水平及其 10 5 9G C基因多态性与冠状动脉造影证实的冠心病之间的关系。方法　采用免疫比浊法测定 35 6例冠状动脉造影患者的高敏CRP水平 ,同时应用聚合酶链反应 -限制性片段长度多态性 (PCR RFLP)核苷酸分型技术检测CRP的 10 5 9G C基因多态性 ,结合冠状动脉造影结果进行分析。结果　冠心病组的自然对数转换CRP(lnCRP)水平显著高于对照组 (P <0 0 5 ) ,以年龄、性别、吸烟、高血压、体重指数和lnCRP水平为自变量的Logistic回归分析显示 ,lnCRP水平 (OR =1 4 4,P <0 0 1)和体重指数 (OR =1 0 1,P <0 0 5 )与冠心病的危险性独立相关。 10 5 9G C基因多态性等位基因和基因型的分布频率符合Hardy Weinberg平衡 ( χ2 =0 2 97,P >0 0 5 )。两组的 10 5 9G C基因型和等位基因的分布趋势相同 ,差异无显著性 (P>0 0 5 )。C等位基因携带者的lnCRP水平低于GG基因型 [( 0 5 3± 1 0 1)比 ( 0 88± 0 99)lnmg L ;P =0 0 2 4],而冠状动脉病变程度不受 10 5 9G C基因多态性的影响 ( χ2 =1 374,P >0 0 5 )。结论　血清高敏CRP水平升高可能是中国汉族人冠心病发生的独立危险因素 ;CRP的水平可能受其 10 5 9G C基因多态性的影响。     

C-反应蛋白、内皮功能变化与急性冠状动脉综合征相关性研究

目的　探讨 C-反应蛋白及肱动脉流量介导的血管舒张在急性冠状动脉综合征中的变化及其相关性。方法　急性冠状动脉综合征 (ACS)组 5 1例 ,其中急性心肌梗死 (AMI) 15例 ,不稳定性心绞痛 (U AP) 36例 ;选择 2 2例冠状动脉造影除外冠心病的患者为对照组。用速率散射比浊法测血清 C-反应蛋白 (CRP) ,用高分辨率超声测肱动脉反应性充血引起的流量介导血管扩张 (FMD)与硝酸甘油介导的血管扩张 (NTG)。结果　 ACS组 CRP高于对照组(0 .94± 1.45 mg/ dl vs0 .2 7± 0 .2 1mg/ dl,P<0 .0 5 ) ,AMI亚组 CRP明显高于 UAP亚组与对照组 (1.6 4± 1.82mg/ dl vs0 .6 5± 1.17m g/ dl、 0 .2 7± 0 .2 1m g/ dl,P<0 .0 5 ) ,UAP亚组高于对照组 (0 .6 5± 1.82 m g/ dl vs0 .2 7±0 .2 1m g/ dl,P>0 .0 5 )。ACS组的 FMD明显低于对照组 (4 .6 1± 2 .2 1mm vs9.2 3± 3.45 mm,P<0 .0 5 ) ,而 NTG与对照组比较则无差别。经 logisitic回归分析 ,CRP的风险比值 (OR)值大于 1,是 ACS的危险因素 ,FMD的 OR值小于 1,是 ACS的保护因素。经前进法观察 CRP与 FMD在急性冠脉综合征中的作用是相互独立的。结论　急性冠状动脉综合征患者 C-反应蛋白升高 ,内皮功能受损 ,二者是 ACS发生的独立危险因素     

冠心病及其高危患者血管功能无创性检测的临床意义

目的 :探讨冠心病和具有冠心病危险因素患者的血管内皮和平滑肌功能无创性检测的临床意义。方法 :采用高分辨超声技术 ,检测 90例健康成人 (正常对照组 )、110例有冠心病危险因素者 (危险因素组 )和 71例冠心病患者 (冠心病组 )在反应性充血时及含服硝酸甘油后的肱动脉内径变化。结果 :危险因素组和冠心病组血流介导的肱动脉舒张 (FMD)均明显低于正常对照组 [(4 .79± 3.93) %和 (2 .4 4± 2 .94 ) %比 (8.76± 4 .33) % ,均P <0 .0 1];冠心病组硝酸甘油引起的肱动脉舒张 (NID)明显低于正常对照组 [(16 .5 8± 6 .2 6 ) %比 (2 3.6 2±8.5 5 ) % ,P <0 .0 1],但危险因素组的NID与正常对照组无统计学意义 [(2 0 .5 0± 7.30 ) %比 (2 3.6 2± 8.5 5 ) % ,P >0 .0 5 ]。多元逐步回归分析显示 :FMD与年龄、肱动脉基线内径和收缩压呈负相关 ,与高密度脂蛋白胆固醇呈正相关 ;而NID与肱动脉基线内径呈负相关 ,与FMD呈正相关。结论 :血管内皮功能失调是动脉粥样硬化临床前的早期表现 ,而血管平滑肌功能损害常提示患者已存在明显动脉粥样硬化病变     

阵发性心房颤动局灶性消融治疗后复发的危险因素与预测

目的　确定阵发性心房颤动 (房颤 )局灶性消融治疗后复发的危险因素与预测因子。方法　连续 74例接受局灶性消融治疗的阵发性房颤 ,通过单因素和多因素分析对 11项临床和射频消融指标与房颤复发之间的关系进行研究。结果　平均随访 (12 4± 6 6 )个月 ,5 1例 (6 8 9% )房颤复发。单因素分析确定的与复发有关的因素包括 :年龄 [(5 3 0± 13 9)对 (4 5 0± 11 6 )岁 ,P <0 0 5 ]、左心房前后径 [(39± 5 )对 (36± 3)mm ,P =0 .0 1]、异位灶数目 [(1.6± 0 .7)对 (1.2± 0 .4)个 ,P <0 .0 1]和总X线透视时间 [(4 3± 9)对 (38± 9)min ,P <0 0 5 ]等 4种 ;但经Logistic多因素逐步回归分析后仅有异位灶数目 (OR 3 7;95 %CI 1 2～ 11 1;P <0 0 5 )和左心房前后径 (OR 1 2 ;95 %CI 1 0～ 1 4;P <0 0 5 )为消融后复发的独立预测因子。结论　多异位灶起源和左心房增大是阵发性房颤局灶性消融后复发的独立预测因素     

C反应蛋白增高在心房颤动中的意义

目的 :探讨C反应蛋白 (CRP)增高在心房颤动 (房颤 )发病中的意义。方法 :应用免疫比浊法测定 96例诊断为房颤患者血清CRP水平 ,与对照组比较 ,并对房颤按持续时间、病因不同分设亚组 ,进行统计学分析。结果 :房颤组、对照组血清CRP水平分别为 (4 .30± 2 .87)、(1.15± 0 .90 )mg L ,两组相比P <0 .0 5。器质性、孤立性房颤者CRP水平分别为 (5 .0 6± 1.92 )、(4 .37± 1.32 )mg L ,均高于对照组 ,P <0 .0 5。持续性、永久性房颤者CRP水平分别为 (5 .6 0± 1.80 )、(5 .0 0± 1.6 0 )mg L ,均高于阵发性房颤 [(3.30± 1.2 0 )mg L],P <0 .0 5。结论 :CRP增高反映的炎症状态可能促进房颤发生 ,以及呈持续性发作。     

高同型半胱氨酸血症与冠脉病变的关系

目的　了解血清同型半胱氨酸 (Hcy)水平与冠脉病变的关系。方法　用断面调查的方法收集经冠状动脉造影确诊的冠心病患者 10 2例、非冠心病患者 5 2例 ,用高效液相色谱测定血清Hcy水平。 结果　冠脉病变与男性、吸烟、糖尿病及血清Hcy升高明显相关 ;冠心病组患者Hcy水平 [(19 6 8± 10 0 5 ) μmol/L]明显高于非冠心病组[(11 33± 4 17) μmol/L],P <0 0 1。冠心病合并糖尿病组冠脉病变程度较对照组明显严重。多元Logistic回归分析证实Hcy和糖尿病的比势比 (OR)均大于 1,并有显著差异。用前进法观察偏回归系数证实这两个因素是冠脉病变的独立危险因素。结论　血清Hcy升高和罹患糖尿病是导致冠脉病变的重要而各自独立的危险因素。     

Hyperhomocysteinemia is an independent risk factor in young patients with coronary artery disease in southern China

Background

Elevated plasma homocysteine (Hcy) is considered to be a risk factor of coronary artery disease (CAD), although this is still controversially discussed. This study investigated the role of Hcy in young patients with CAD in southern China.

Methods

A total of 146 consecutive patients (aged ≤?55 years) with angiographically proven CAD were enrolled in the study and 138 age-matched non-CAD individuals were included as the control group. Hcy levels were measured by enzymatic assay. Hyperhomocysteinemia (HHcy) was defined as Hcy ≥?15 µmol/l. A 10-year CAD risk was calculated using the Framingham risk score (FRS) modified according to the National Cholesterol Education Program Adult Treatment Panel III.

Results

There were significant differences between the CAD and control groups with regard to male sex (P?<?0.01), smoking history (P?<?0.05), and triglyceride levels (TG, P?<?0.05), but no remarkable difference in other conventional risk factors (all P?>?0.05). Hcy and high-sensitivity C-reactive protein (hs-CRP) levels were significantly higher in the CAD group than those in the control group (both P?<?0.05). The FRS and estimated 10-year absolute CAD event risk were low in both groups and did not show a statistical difference. Multivariate logistic regression showed that male sex (odds ratio, OR, 3.68; 95?% confidence interval, 95?% CI, 1.54–10.01), smoking (OR, 2.54; 95?% CI, 1.15–5.36), TG (OR, 1.30; 95??% CI, 1.08–3.06), hs-CRP (OR, 3.74; 95?% CI, 1.72–12.21), and HHcy (OR, 2.03; 95?% CI, 1.26–5.83) were independently correlated with CAD in young patients.

Conclusion

HHcy is an important independent risk factor for CAD in young patients in southern China after adjusting for other risk factors.     

High attributable risk of elevated C-reactive protein level to conventional coronary heart disease risk factors: the Third National Health and Nutrition Examination Survey

BACKGROUND: C-reactive protein (CRP), a marker of systemic inflammation, is predictive of coronary heart disease (CHD) events. However, the extent to which high CRP levels (>3 mg/L) may be attributable to high cholesterol levels and other CHD risk factors has not been well defined. METHODS: The prevalence of high CRP levels in the third National Health and Nutrition Examination Survey (n = 15 341) was studied using CHD risk-factor cut points designated as abnormal (total cholesterol values, >or=240 mg/dL [>or=6.22 mmol/L]; fasting blood glucose levels, >or=126 mg/dL [>or=6.99 mmol/L]; blood pressure, >or=140/90 mm Hg; body mass index [BMI], >or=30 kg/m(2); high-density lipoprotein cholesterol values, <40 mg/dL [<1.04 mmol/L] for men and <50 mg/dL [<1.30 mmol/L] for women; triglyceride levels, >or=200 mg/dL [>or=2.26 mmol/L]; current smoking status) or borderline (total cholesterol values, 200-239 mg/dL [5.18-6.19 mmol/L]; fasting blood glucose levels, 100-125 mg/dL [5.55-6.94 mmol/L]; blood pressure, 120-139/80-89 mm Hg; BMI, 25.0-29.9 kg/m(2), and triglyceride values 150-199 mg/dL [1.70-2.25 mmol/L], former smoking status), or normal. RESULTS: Weighted multiple logistic regression analysis demonstrated that high CRP level was significantly more common with obesity (odds ratio [OR], 3.78; 95% confidence interval [CI], 3.28-4.35]), overweight (OR, 1.88; 95% CI, 1.62-2.18), and diabetes (OR, 1.91; 95% CI, 1.54-2.38) and that high CRP level was rare in the absence of any borderline or abnormal CHD risk factor in men (4.4%) and women (10.3%). Overall, the risk of elevated CRP level attributable to the presence of any abnormal or borderline CHD risk factor was 78% in men and 67% women. CONCLUSIONS: These data suggest that elevated CRP levels in the general population are in large measure attributable to traditional CHD risk factors. Moreover, CRP level elevation is rare in the absence of borderline or abnormal risk factors. As such, CRP measurements may have limited clinical utility as a screening tool beyond other known CHD risk factors.     

静息心率与冠心病发病危险因素聚集性的关联

本文探讨了静息心率与冠心病发病危险因素高血压、高纤维蛋白原血症、高甘油三酯血症、高血糖聚集性的关联。发现超重（ＢＭＩ≥２５）及（或）男＞４５岁，女＞５５岁人群，平均静息心率＞８８次／分钟组上述两个以上危险因素聚集发生机率较６０次／分钟组增加约５０％。多因素Ｌｏｇｉｓｔｉｃ回归分析表明，调整年龄、体重指数两混杂因素影响后，在心率＞８８次／分钟人群则这种危险性仍明显增加（ＯＲ＝４．３，９５％可信限２．１～８．７），提示在超重及较年长人群中心率可能是一个简单的冠心病危险因素聚集发生的临床标志。     

Association of C-reactive protein with coronary heart disease risk factors in patients with type 2 diabetes mellitus

The assessment of markers of systemic inflammation, such as C-reactive protein (CRP) and interleukin 6 (IL6), could be used to identify persons at high risk of coronary heart disease (CHD). This study evaluates the relationship of CRP and IL6 with CHD risk factors in patients with type 2 diabetes mellitus (DM) with CHD and age and sex matched type 2 DM controls without CHD. CRP, IL-6, total plasma homocysteine (tHcy), lipoprotein (a) [Lp(a)] and sialic acid (SA) were determined in 55 type 2 diabetic patients with CHD and 51 age- and sex-matched type 2 diabetic controls without CHD. Multivariate and logistic regression analyses were used to relate these markers with CHD risk factors. CRP (P=0.02) and tHcy (P=0.03) were significantly higher in patients with CHD compared with the control group even after correction for age and sex. IL6, Lp(a), SA and lipid parameters were not significantly different between the two groups of patients. After adjustment for potential confounders, the odds ratio (OR) for elevated CRP was 2.00 (95% confidence interval [CI], 1.12-3.58) (P=0.02) but the OR for IL6 was 3.41 95% CI, 0.70-17.17 (P=0.14). Partial correlation analyses of CRP and IL6 with other variables showed significant correlation of CRP with tHcy, and SA in patients with CHD only. Our results support the inclusion of CRP (high-sensitivity assay), in the risk assessment of diabetic subjects.     

Renin-angiotensin system polymorphisms and coronary events in familial hypercholesterolemia

The role of renin-angiotensin system polymorphisms as risk factors for coronary heart disease (CHD) is controversial. This study investigated their role in patients with heterozygous familial hypercholesterolemia (FH). Polymorphism frequencies for angiotensin-I-converting enzyme insertion/deletion (ACE I/D), angiotensinogen M235T, and angiotensin-II type I receptor (AG2R) A1166C were determined in 112 patients with FH and 72 patients with polygenic hypercholesterolemia, of whom 26.7% and 41.6%, respectively, had established CHD. None of the polymorphisms were associated with risk of CHD in patients with polygenic hypercholesterolemia in this study. Logistic regression analysis of risk factors for CHD in patients with FH identified male sex (odds ratio [OR]=3.03; 95% CI, 3.07 to 3.72; P=0.05), smoking (OR=2.91; 95% CI, 2.16 to 4.24; P=0.05), diastolic blood pressure (OR=3.70; 95% CI, 3.43 to 3.97; P=0.02), plasma glucose (OR=3.31; 95% CI, 3. 10 to 3.52; P=0.04), and the AG2R A1166C polymorphism as risk factors. The OR for the AG2R A1166C polymorphism was 2.26 (95% CI, 1.26 to 3.72; P=0.06) and increased to 3.10 (95% CI, 1.20 to 7.52; P=0.04) after adjustment for other risk factors. The AG2R A1166C polymorphism may interact with severe hypercholesterolemia and other risk factors to increase risk of CHD in FH patients.     

Maternal and paternal environmental risk factors, metabolizing GSTM1 and GSTT1 polymorphisms, and congenital heart disease

Congenital heart defects (CHDs) are the most prevalent of all birth malformations arising from the complex interplay of environmental exposures and genes. Modifiable environmental risk factors are still largely unknown, especially for paternal exposure. The aim of the present study was to examine the association between the environmental exposures of both parents and CHD risk and to explore the modification effect of metabolizing gene polymorphisms in children who lack the genetic capacity to produce the glutathione S-transferase (GST) GSTM1 and GSTT1 enzymes. A total of 330 parents of a child with CHD and 330 parents of a child without any congenital malformations were compared in terms of lifestyle habits and toxicant exposure. GST gene polymorphisms were investigated in 180 patients with CHD (104 males, age 4.9 ± 5.8 years). Paternal smoking (≥15 cigarettes/day) was significantly associated with CHD risk (odds ratio [OR] 2.1, 95% confidence interval [CI] 1.3 to 3.5, p = 0.002). Both maternal (OR 2.6, 95% CI 1.6 to 4.2, p <0.0001) and paternal (OR 2.5, 95% CI 1.6 to 3.8, p <0.0001) occupational/environmental exposures increased the risk of CHD. Also, a significant additive risk (OR 4.5, 95% CI 2.5 to 8.3, p <0.0001) was found when both parents were exposed to toxicants. Both maternal (OR 3.6, 95% CI 1.1 to 11.2, p = 0.03) and paternal (OR 3.3, 95% CI 1.0 to 10.8, p = 0.03) exposure to toxicants increased the CHD risk in children who carried the combined null GST genotypes. The effect for the combined null GST genotypes was also stronger (OR 6.5, 95% CI 1.5 to 28.0) when both parents were exposed. In conclusion, paternal smoking and exposure to toxicants for both parents affect the risk of children with CHD. Polymorphisms in GST genes can modify a person's risk of toxicant exposure-induced disease.     

Ten-year predicted coronary heart disease risk in HIV-infected men and women.

BACKGROUND: Highly active antiretroviral therapy (HAART), in addition to traditional vascular risk factors, may affect coronary heart disease (CHD) risk in individuals with human immunodeficiency virus (HIV) infection. METHODS: Among HIV-infected (931 men and 1455 women) and HIV-uninfected (1099 men and 576 women) adults, the predicted risk of CHD was estimated on the basis of age, sex, lipid and blood pressure levels, the presence of diabetes, and smoking status. RESULTS: Among HIV-infected men, 2% had moderate predicted risk of CHD (10-year CHD risk, 15%-25%), and 17% had high predicted risk (10-year CHD risk of > or = 25% or diabetes). Among HIV-infected women, 2% had moderate predicted CHD risk, and 12% had high predicted CHD risk. Compared with users of protease inhibitor-based HAART, the adjusted odds ratio (OR) for moderate-to-high risk of CHD was significantly lower among HAART-naive individuals (OR, 0.57; 95% confidence interval [CI], 0.36-0.89). Users of HAART that was not protease inhibitor based (OR, 0.74; 95% CI, 0.53-1.01) and former HAART users (OR, 0.68; 95% CI, 0.46-1.03) were also less likely than users of protease inhibitor-based HAART to have moderate-to-high CHD risk, although 95% CIs overlapped the null. Low income was associated with increased likelihood of moderate-to-high CHD risk (for annual income < $10,000 vs. > $40,000: OR, 2.32; 95% CI, 1.51-3.56 ). Elevated body mass index (calculated as weight in kilograms divided by the square of height in meters) predicted increased likelihood of moderate-to-high CHD risk (for BMI of 18.5-24.9 vs. BMI of 25-30: OR, 1.41 [95% CI, 1.03-1.93]; for BMI of 18.5-24.9 vs. BMI > or = 30: OR, 1.79 [95% CI, 1.25-2.56]). CONCLUSIONS: Among HIV-infected adults, in addition to antiretroviral drug exposures, being overweight and having a low income level were associated with increased predicted CHD risk. This suggests a need to target HIV-infected men and women with these characteristics for vascular risk factor screening.     

Interaction of apolipoprotein E genotype with smoking and physical inactivity on coronary heart disease risk in men and women

ObjectiveApolipoprotein E genotype (APOE) polymorphism affects lipid levels and coronary heart disease (CHD) risk. However, these associations may be modified by lifestyle factors. Therefore, we studied whether smoking, physical inactivity or overweight interact with APOE on cholesterol levels and CHD risk.MethodsCombining two Swedish case-control studies yielded 1735 CHD cases and 4654 population controls (3747 men, 2642 women). Self-reported questionnaire lifestyle data included smoking (ever [current or former regular] or never) and physical inactivity (mainly sitting leisure time). We obtained LDL cholesterol levels and APOE genotypes. CHD risk was modelled using logistic regression to obtain odds ratios (ORs) and 95% confidence intervals (CIs), adjusted for relevant covariates.ResultsSmoking interacted with APOE on CHD risk; adjusted ORs for ever versus never smoking were 1.45 (95% CI 1.00–2.10) in ?2 carriers, 2.25 (95% CI 1.90–2.68) in ?3 homozygotes and 2.37 (95% CI 1.85–3.04) in ?4 carriers. Female ?4 carriers had OR 3.62 (95% CI 2.32–5.63). The adjusted ORs for physical inactivity were 1.09 (95% CI 0.73–1.61), 1.34 (95% CI 1.12–1.61), and 1.79 (95% CI 1.38–2.30) in ?2, ?3?3 and ?4 groups, respectively. No interaction was seen between overweight and APOE for CHD risk, or between any lifestyle factor and APOE for LDL cholesterol levels.ConclusionThe APOE ?2 allele counteracted CHD risk from smoking in both genders, while the ?4 allele was seen to potentiate this risk mainly in women. Similar ?2 protection and ?4 potentiation was suggested for CHD risk from physical inactivity.     

冠状动脉慢血流与肾小球滤过率降低有关联

目的:观察和分析冠脉慢血流与肾小球滤过率的关系。方法: 入选50例冠脉造影为慢血流患者组以及51例正常对照组，运用简化肾脏病膳食改良试验评估肾功能。结果: 冠脉慢血流组的肾小球滤过率显著降低，尿酸水平较高。经回归分析，尿酸（OR 1.007，95%CI 1.0-1.013，P=0.038）、肾小球滤过率（OR 0.968，95%CI 0.938-0.999，P=0.045）和吸烟（OR 3.513，95%CI 1.135-10.869，P=0.029）为冠脉慢血流独立相关因子。结论: 冠脉慢血流与肾小球滤过率有关联。     

Predictors of on-duty coronary events in male firefighters in the United States

Coronary heart disease (CHD) accounts for 39% of "on-duty" deaths in firefighters in the United States. No studies have examined the factors that distinguish fatal from nonfatal work-associated CHD events. Male firefighters experiencing on-duty CHD events were retrospectively investigated to identify cardiovascular risk factors predictive of case fatality; 87 fatalities (death within 24 hours of the event) were compared with 113 survivors who retired with disability pensions for heart disease after on-duty nonfatal events. Cardiovascular risk factors were then examined for associations with case fatality. Predictors of CHD death in multivariate analyses were a previous diagnosis of CHD (or peripheral/cerebrovascular disease) (odds ratio [OR] 4.09, 95% confidence intervals [CI] 1.58 to 10.58), current smoking (OR 3.68, 95% CI 1.61 to 8.45), and hypertension (OR 4.15, 95% CI 1.83 to 9.44). Age < or =45 years, diabetes mellitus, and serum cholesterol level were not significant predictors of case fatality. In conclusion, previous CHD, current smoking, and hypertension are strong predictors of fatality in male firefighters experiencing on-duty CHD events. Accordingly, prevention efforts should include early detection and control of hypertension, smoking cessation/prohibition, and the restriction of most firefighters with significant CHD from strenuous duties.