Cardiovascular diseases are a major global health concern, leading to high morbidity, mortality, and disability rates. Scaffold proteins, particularly A-kinase anchoring proteins (AKAPs), play a crucial role in signal transduction within the cardiovascular system. This review provides a comprehensive analysis of AKAPs’ involvement in the pathogenesis of cardiovascular diseases, emphasizing their key function in coordinating diverse signaling molecules, directing them to specific cellular microdomains, and minimizing signal interference. Disruptions in these interactions are linked to several cardiovascular disorders, such as cardiac hypertrophy, myocardial apoptosis, heart failure, arrhythmias, dysfunction in myocardial contraction and relaxation, and hypertension. Our goal was to explore the therapeutic potential of targeting the AKAP signaling pathway and offer new perspectives for the development and application of cardiovascular drugs that modulate AKAP signaling complexes.

Background and objectives:Atrial fibrillation (AF) and heart failure (HF) are common cardiovascular diseases associated with significant morbidity and mortality in patients with both conditions. The objective of this research is to enhance our understanding of the shared pathogenesis underlying the two diseases and to identify novel therapeutic targets. Materials and methods:Differentially expressed genes (DEGs) in heart failure and atrial fibrillation were obtained through the analysis and comparison of transcriptional expression profiles from the Gene Expression Omnibus (GEO) datasets. By integrating these datasets with the known ferroptosis-related genes (FRGs) from GeneCards and PubMed, we identified ferroptosis-related differentially expressed genes (FRDEGs). Functional enrichment and the construction of the PPI network for key genes were conducted. The mRNA-miRNA and mRNA-TF Regulatory Network were constructed via the ChIPBase and TarBase databases. Receiver operating characteristic (ROC) was utilized to screen out the FRDEGs and validate their diagnostic values. Gene expression levels were detected by qPCR in patient serum samples. Results:By analyzing the transcriptional expression profiles of the GEO datasets, TFRC, CP, SAT1, STEAP3, AKR1C1 and LPCAT3 were identified as FRDEGs in AF and HF, which were revealed to be involved in iron ion transport, homeostasis, and oxidoreductase activity. Further insights from Gene Set Enrichment Analysis (GSEA) indicated that FRDEGs are primarily enriched in the IL-12 signaling pathway in HF and significantly enriched in the collagen assembly pathway in AF. The diagnostic efficacy of six genes in AF validation sets was good (AUC:TFRC 0.940, CP 0.920, SAT1 1.000, STEAP3 0.960, AKR1C1 0.900, LPCAT3 0.960, as well as in the HF validation set (AUC: TFRC 0.842, CP 0.879, SAT1 0.865, STEAP3 0.787, AKR1C1 0.812, LPCAT3 0.696).Utilizing the GOSemSim package, we conducted a functional similarity analysis on the five hub genes and discovered their significant roles in disease, ranked as follows: STEAP3>TFRC>CP>SAT1>LPCAT3. qRT-PCR verified the expression differences of CP, STEAP3, and LPCAT3. Conclusion:Our findings provide a theoretical basis for the clinical diagnosis and treatment of AF and HF. These results provide valuable insights into potential biomarkers for diagnosis and targets for therapeutic intervention in AF and HF.

Objective: To investigate the effects of a drug-coated balloon (DCB) on inflammatory cytokines in patients with coronary artery calcification (CAC) after interventional therapy. Methods: This study included 58 patients with coronary heart disease who underwent coronary angiography (CAG) from October 2020 to September 2021. Patients were divided into CAC and non-CAC groups, and a DCB was used to intervene in the target lesions. Ten-milliliter preoperative and postoperative blood samples were drawn from the coronary lesions in both groups to detect the expression of serum interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecule-1 (ICAM-1). All patients were subjected to a 6-month follow-up to observe the incidence of major adverse cardiac events (MACEs). Results: No significant differences in baseline clinical data were found between the groups. Serum IL-6, TNF-alpha, and ICAM-1 expressions in coronary blood samples immediately before DCB were not significantly different from those after DCB in all patients. After DCB, serum TNF-alpha expression in the CAC group was significantly lower than that in the non-CAC group (p<0.05). In contrast, no significant difference in serum IL-6 and ICAM-1 expression was found between the groups. During the 6-month follow-up, no significant difference in the incidence of MACE was found between both groups. Conclusions: DCB reduced the expression of inflammatory cytokine TNF-alpha in CAC, which may be one of the key mechanisms underlying the treatment of CAC by DCB.

经过几十年的发展,经皮冠状动脉介入治疗(PCI)日益成熟,近年来PCI手术的开展趋于普及,手术量也日益上升.然而,对于慢性完全闭塞性病变、严重钙化病变、支架内再狭窄、支架膨胀不全等一些复杂病变,PCI仍面临诸多挑战.准分子激光冠状动脉斑块消融术是一项新兴的冠状动脉内病变处理技术,其在处理冠状动脉内复杂病变上有独特的优势.本文就准分子激光冠状动脉斑块消融术的技术原理、临床应用现状、安全性及有效性作一综述.

We reported that A-kinase anchoring protein 5 (AKAP5) played a role in cardiomyocyte apoptosis after hypoxia-reoxygenation (H/R). The role of AKAP5 in cardiomyocyte hypertrophy has not been fully elucidated. Herein we investigated whether AKAP5 regulates cardiomyocyte hypertrophy through calcium/calmodulin-dependent protein kinase II (CaMKII). After H/R, deficiency of AKAP5 in H9C2 cardiomyocytes and neonatal rat cardiac myocytes activated CaMKII and stimulated cardiomyocyte hypertrophy. AKAP5 upregulation limited this. Low expression of AKAP5 increased CaMKII interaction with histone deacetylases 4/5 (HDAC4/5) and increased nuclear export of HDAC4/5. In addition, AKAP5 interactions with protein kinase A (PKA) and phospholamban (PLN) were diminished. Moreover, the phosphorylation of PLN was decreased, and intracellular calcium increased. Interference of this process with St-Ht31 increased CaMKII signaling, decreased PLN phosphorylation and promoted post-H/R cell hypertrophy. And PKA-anchoring deficient AKAP5ΔPKA could not attenuate hypoxia-reoxygenation-induced cardiomyocyte hypertrophy, but AKAP5 could. Altogether, AKAP5 downregulation exacerbated H/R-induced hypertrophy in cardiomyocytes. This was due to, in part, to less in AKAP5-PKA interaction and the accumulation of intracellular Ca2+ with a subsequent increase in CaMKII activity.

OBJECTIVE:A-kinase anchoring protein 5 (AKAP5) is involved in ventricular remodeling in rats with heart failure after myocardial infarction; however, the specific mechanism is not clear. This study investigated whether AKAP5 anchors calcineurin (CaN) to regulate the remodeling of H9c2 cardiomyocytes. METHODS:H9c2 cells were subjected to hypoxia stress for 3 h and reoxygenation for 24 h to create a hypoxia-reoxygenation (H/R) model. These cells were divided into three groups: H/R (model), empty vector +H/R (NC), and siRNA-AKAP5+H/R (siRNA-AKAP5) groups. The non-H/R H9c2 cells were used as normal controls. Western blotting was used to detect cardiac hypertrophy-related protein expression in the cells, including atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), beta myosin heavy chain (β-MHC), and phosphorylated nuclear factor of activated T-cell 3 (p-NFATc3). Phalloidin staining was used to label the cytoskeleton and the cell area in different groups was measured. Immunofluorescence staining and coimmunoprecipitation were used to study the relationship between AKAP5 and CaN. H9c2 cells pretreated with the CaN inhibitor FK506 were used to further verify the relationship between AKAP5 and CaN. RESULTS:In the siRNA-AKAP5+H/R group, the expression level of cardiac hypertrophy-related proteins (ANP, BNP, and β-MHC) and CaN and the area of cardiomyocytes were significantly increased, while the p-NFATc3/NFATc3 ratio was decreased in H9c2H/R cells. AKAP5 and CaN proteins were colocalized and interacted in the cells. The CaN inhibitor significantly suppressed the expression of CaN, increased the p-NFATc3/NFATc3 ratio, and reduced the expression levels of ANP, BNP, and β-MHC proteins in the cells with low AKAP5 expression. CONCLUSIONS:AKAP5 downregulation aggravated the remodeling of cardiomyocytes after H/R. AKAP5 may anchor CaN to form a complex, which in turn activates NFATc3 dephosphorylation and expression of hypertrophy-related proteins.

The harm of heart failure mainly causes patients to develop dyspnea, fatigue, fluid retention, and other symptoms, which impair patients' activity tolerance and lead to a dramatic decrease in patients' quality of life. The purpose of this study was to verify whether metoprolol regulates AKAP5 expression and test the role of AKAP5 postinjury in mitigating cardiac infarction-associated tissue remodeling and fibrosis. Sprague-Dawley (SD) rats underwent coronary artery ligation (CAL), which was followed immediately with metoprolol daily. And western blot and coimmunoprecipitation experiments were performed to detect the expression of related proteins in the sham-operated group, model group, and drug-treated group. HW/BW ratio and cardiac expression of COL1 and COL3 were increased in rats following CAL compared with shams. Treatment with metoprolol postinjury was associated with a decrease in HW/BW ratio and COL1/COL3 expression compared to uncontrolled rats. CAL resulted in decreased cardiac AKAP5 expression compared to the control group, while metoprolol treatment restored levels compared to baseline shams. Cardiac expression levels of NFATc3/p-NFATc3 and GATA4 were modest at baseline and increased with injury, whereas metoprolol suppressed gene expression to below injury-associated changes. Immunoprecipitation indicated that AKAP5 could bind and regulate PP2B. In summary, we know that metoprolol alleviates ischemic cardiac remodeling and fibrosis, and the mechanism of alleviating remodeling may improve cardiac AKAP5 expression and AKAP5-PP2B interaction.

目的:探究自噬相关基因7(Atg7)介导Toll样受体4(TLR4)在脓毒症心肌自噬的可能机制.方法:通过盲肠结扎穿孔术(CLP)制备脓毒症小鼠模型,造模后于0、8、16、24 h分别眼球取血检测血白细胞和炎症因子的变化;采用Western blot法检测心肌组织TLR4、Atg7、p53、p53上调凋亡调节因子(Puma)蛋白的变化;HE和Masson染色观察小鼠心肌组织的变化.结果:随着时间推移,小鼠血清中炎症因子(IL-β、IL-6、TNF-α)含量逐渐上升,血白细胞浓度下降,表明脓毒症模型建立成功.心肌HE和Masson染色表现出心肌损伤逐渐加重.与0 h比较,8、16、24 h小鼠心肌组织中TLR4、Atg7、p53、Puma的蛋白表达明显增加(P<0.05);与8 h比较,16和24 h心肌组织中TLR4、Atg7、p53、Puma的蛋白表达也明显增加(P<0.05).结论:Atg7介导TLR4可能通过上调p53和Puma参与了脓毒症自噬引起的心肌损伤.

The A-kinase anchoring protein 5 (AKAP5) has a variety of biological activities. This study explored whether AKAP5 was involved in cardiomyocyte apoptosis induced by hypoxia and reoxygenation (H/R) and its possible mechanism. H9C2 cells were used to construct an H/R model in vitro, followed by AKAP5 overexpression. Flow cytometry was performed to determine the rate of cardiomyocyte apoptosis. Phosphorylation of phospholamban (PLN), sarcoplasmic/endoplasmic reticulum calcium ATPase 2a (SERCA2a), and apoptosis-related proteins was determined by western blotting. Immunofluorescence staining and immunoprecipitation were performed to detect the distribution and interaction between AKAP5, protein kinase A (PKA), and PLN. After H/R induction, H9C2 cells exhibited significantly reduced AKAP5 protein expression. Upregulation of AKAP5 promotes cell survival and significantly reduces lactate dehydrogenase (LDH) levels and apoptosis rates in H9C2 cells. In addition, the overexpression of AKAP5 was accompanied by the activation of the PLN/SERCA2a signaling pathway and a reduction in apoptosis. Immunofluorescence staining and immunoprecipitation revealed that AKAP5 co-localized and interacted with PLN and PKA. Interestingly, St-Ht31, an inhibitory peptide that disrupts AKAP interactions with regulatory subunits, inhibits the effect of AKAP5 overexpression on H/R-induced apoptosis in H9C2 cardiomyocytes. AKAP5 overexpression alleviated H/R-induced cardiomyocyte apoptosis possibly by anchoring PKA to mediate the PLN/SERCA pathway, suggesting that AKAP5 is a potential therapeutic target for the prevention and treatment of ischemia-reperfusion injury.

目的 本研究评估血管内超声(Intravascular ultrasound,IVUS)指导对冠状动脉左主干病变患者经皮冠状动脉介入治疗(Percutaneous coronary intervention,PCI)临床预后的影响.方法 选择皖南医学院第一附属医院2012年1月1日至2016年1月1日间共76例冠状动脉左主干病变并接受PCI治疗的患者.分为两组:IVUS组:29例患者术中使用IVUS指导;造影组:47例患者使用常规造影指导.通过虚拟组织学超声(Virtual histology intravascular ultrasound,VH-IVUS)识别的易损斑块又将IVUS组患者又分为两个亚组:"易损斑块组(12例)"和"非易损斑块组(17例)".随访的主要终点事件为主要心血管不良事件(Major adverse cardiac events,MACE),包括:心源性死亡、心肌梗死和靶血管血运重建.结果 IVUS组患者术后最小支架直径(Minimum stent diameter,MSD)和最小支架横截面积(Minimum stent area,MSA)均大于冠脉造影组患者,有统计学差异[(3.9±0.3)mm vs(3.7±0.3)mm,P=0.004)]、[(12.2±2.1)mm2 vs(10.9±1.6)mm2,P=0.003)].IVUS组患者与冠脉造影组相比术后1年的MACE事件发生率有降低趋势(6.9％vs 19.1％,log-rank P=0.072).易损斑块组和非易损斑块组术后1年的MACE事件发生率相似(8.3％vs 5.9％,log-rank P=0.702).结论 IVUS指导与冠脉造影指导相比有减少左主干病变患者PCI术后1年的MACE事件发生率的趋势,值得临床推广.与非易损斑块组相比,IVUS指导未增加易损斑块组患者PCI术后1年MACE事件的发生风险.

目的观察PHD2、HIF-1α在心肌梗死后心衰时表达量的变化, 探讨β肾上腺受体(β-AR)调控PHD2/HIF-1α通路对心肌梗死后心衰发生影响。方法采用冠状动脉左前降支结扎法制备大鼠急性心梗模型, 实验分为3组:假手术组、模型组、普萘洛尔组。记录冠脉结扎前后心电图变化, 12周后利用心脏超声检测心功能变化, PCR和Western Blot检测PHD2、HIF-1α的mRNA及蛋白表达的变化。结果结扎冠脉后心电图示ST段显著抬高。结扎12周后心脏射血分数(Ejection fraction, EF )从假手术组的(79.45±2.86)%下降到模型组的(61.10±2.78)%(P <0.05 ), 普萘洛尔组则高于模型组为(67.33±2.66)% (P <0.05 )。PHD2的mRNA及蛋白表达在模型组显著下降(P <0.05), 而普萘洛尔组较模型组明显上升(P <0.05)。HIF-1α的mRNA及蛋白表达在模型组显著上升(P <0.05), 而普萘洛尔组较模型组明显下降(P <0.05)。结论 PHD2/HIF-1α通路在大鼠心梗后心衰的发生过程中可能具有重要作用;而心肌梗死后β-肾上腺系统激活, 可能通过对PHD2/HIF-1α通路的调节进而促进心衰的发生。

2019新型冠状病毒(SARS-CoV-2)是新型冠状病毒肺炎(coronavirus disease 2019,COVID-19)的病原体,具有较强的传染性,目前已在全世界范围内流行.虽然大量药物已经应用于COVID-19患者的治疗中,但目前仍然没有针对其使用的特异性药物和预防性疫苗.虽然该传染性疾病主要表现为呼吸道等相关症状,但大量研究表明COVID-19与高血压病有着密切相关性,因此,了解二者之间的关系对指导临床医师诊治该类疾病具有重要意义.本文主要就COVID-19对高血压病的相关影响机理及治疗方案进行综述,以期提高临床医师对COVID-19与高血压病的进一步认识.

Abstract Background Postcardiac injury syndrome (PCIS) is an inflammatory response syndrome characterized by pericardial effusion with or without pleural effusion; however, serious PCIS with peripheral hematoma of the ascending aorta and acute cerebral infarction after percutaneous coronary intervention (PCI) have not been reported. Case presentation This article reports a very rare case of a 40-year-old patient who developed acute pericardial and pleural effusions (both bloody), acute respiratory distress, peripheral hematoma of the ascending aorta, and acute cerebral infarction after PCI. The patient’s ECG showed bow-back downward ST elevation in leads I, II, III, and V4–V6. A blood test showed significant increases in eukaryotic-cell count, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP). Echocardiography and pulmonary artery computed tomography angiography (CTA) showed a large amount of pericardial effusion and pleural effusion. CTA of the thoracic and abdominal aorta showed a peripheral hematoma of the ascending aorta. A cranial computed tomography (CT) showed cerebral infarction anterior to the anterior horn of the right ventricle. After tracheal intubation, ventilator breathing support, pericardial and pleural drainage, and adrenocortical steroid (prednisone) treatment, he gradually recovered and was discharged 20 days later. Conclusion We report the management of a case of serious PCIS with peripheral hematoma of the ascending aorta and acute cerebral infarction after PCI. Early diagnosis, early differential diagnosis, and early use of steroid therapy are the key in treating PCIS.

The activation of the beta-adrenergic receptor (beta-AR) regulates the human ether a-go-go-related gene (HERG) channel via protein kinase A (PKA), which in turn induces lethal arrhythmia in patients with long QT syndromes (LQTS). However, the role of A-kinase anchoring proteins (AKAPs) in PKA's regulation of the HERG channel and its molecular mechanism are not clear. Here, HEK293 cells were transfected with the HERG gene alone or co-transfected with HERG and AKAP5 using Lipofectamine 2000. Western blotting was performed to determine HERG protein expression, and immunofluorescence and immunoprecipitation were used to assess the binding and cellular colocalization of HERG, AKAP5, and PKA. The HEK293-HERG and HEK293-HERG + AKAP5 cells were treated with forskolin at different concentrations and different time. HERG protein expression significantly increased under all treatment conditions (P < 0.001). The level of HERG protein expression in HEK293-HERG + AKAP5 cells was higher than that observed in HEK293-HERG cells (P < 0.001). Immunofluorescence and immunoprecipitation indicated that HERG bound to PKA and AKAP5 and was colocalized at the cell membrane. The HERG channel protein, AKAP5, and PKA interacted with each other and appeared to form intracellular complexes. These results provide evidence for a novel mechanism which AKAP5 anchors PKA to upregulate the HERG channel protein.

目的 系统分析愈风宁心(葛根)辅助治疗冠心病的疗效.方法 检索中文数据库(中国知网、万方、重庆维普、中国生物医学文献数据库),英文数据库(PubMed、Embase、Cochrane library),时间截止至2019年3月.检索愈风宁心辅助治疗冠心病的临床随机对照实验研究.筛选检索的文章并提取基本信息和相关数据,在RevMan5.1.5软件上进行Meta分析.结果 在选择的6篇研究中,共有682例患者.Meta分析结果显示:在愈风宁心辅助治疗下,冠心病缓解总有效率优于常规治疗(P<0.00001);同时治疗组的显效率也显著高于对照组(P=0.0004);治疗组在纤维蛋白原降低方面较对照组要明显(P<0.0001).结论 愈风宁心辅助治疗冠心病具备更好的有效性.

Objective: To investigate the effects of dual education system on the postgraduates majoring in cardiology in their specialization program. Methods:The academic results were retrospectively analyzed in the postgraduates receiving training under dual education system in the cardiology depart-ment from September of 2012 to 2016.The candidates were divided into standardized training group and non-standardized training group to analyze the effects on the achievement in basic theories,clinical skills as well as the number and quality of the published research papers in postgraduates received standardized training for professional degree.Results:The two groups were not significantly different in scores in basic academic theories and the number of research papers published in journals at levelⅢ or under( P>0.05) ,yet the candidates that received standardized training had better achievement in clini-cal skills and ability of case analysis as well as lower number of papers published in journals at levelⅡ or above than those free of standardized training (P<0.05).Conclusion:Dual education system may improve the clinical skills of postgraduates majoring in cardiology in their master training.However,this training mode model can counteract the ability of the candidates in writing academic papers,which should be taken into consideration in following program for standardized training of the postgraduates.

低密度脂蛋白胆固醇(LDL-C)血浆水平升高是动脉粥样硬化性心血管疾病(ASCVD)的主要危险因素.目前临床上最常用的他汀类药物可有效减少血脂异常,但仅对50％的患者有预防心血管事件发生的作用.在家族性高胆固醇血症患者中,这些药物无法达到降低LDL-C和心血管疾病发生风险的目的.此外,许多患者甚至对他汀类药物产生耐药性和(或)不耐受.大量研究表明前蛋白转化酶枯草溶菌素9 (PCSK9)与血浆LDL-C紧密相关,抑制PCSK9可以显著降低LDL-C水平及ASCVD发生率.本文主要对PCSK9与ASCVD的关联性及其机制,以及临床可用的PCSK9抑制剂的新研究进展作一综述.

Previous studies have found decreased functional capacity of the sodium pump (Na+-K+-ATPase) alpha and beta subunits and recovery of Na+-K+-ATPase activity significantly decreased myocyte apoptosis in myocardial ischemia-reperfusion (I/R) injury. However, the potential role of the Na+-K+-ATPase α-2 subunit (ATP1A2) in cardiomyocyte anoxia-reoxygenation (A/R) injury has not been elucidated. Rat myocardial cells were subjected to siRNA transfection followed by A/R injury. Apoptosis and expression of endoplasmic reticulum (ER) stress proteins CHOP, GRP78, and caspase-12 were detected in 4 groups of cells: ATP1A2 siRNA + A/R, control siRNA + A/R, control, and A/R injury model. We found that apoptosis was significantly elevated in the ATP1A2 siRNA + A/R group as compared with control siRNA + A/R, control, and A/R injury model groups (p < 0.05, p < 0.01, and p < 0.05). Furthermore, expression of CHOP, GRP78, and caspase-12 were significantly elevated in the ATP1A2 siRNA + A/R group as compared with control siRNA + A/R, control, and A/R injury model groups (p < 0.05, p < 0.01, and p < 0.05). Our findings suggest that cardiomyocyte ATP1A2 is a target of A/R injury, and its cardioprotective function may be mediated via inhibiting the ER-stress-related apoptosis.

OBJECTIVE:To observe the changes of rapidly activated delayed rectifier potassium channel (IKr) and slowly activated delayed rectifier potassium channel (IKs) in cardiac hypertrophy and to evaluate the effects of IKr and IKs blocker on the incidence of ventricular arrhythmias in guinea pigs with left ventricular hypertrophy (LVH).
 Methods: Guinea pigs were divided into a sham operation group and a left ventricular hypertrophy (LVH) group. LVH model was prepared. Whole cell patch-clamp technique was used to record IKr and IKs tail currents in a guinea pig model with LVH. The changes of QTc and the incidence rate of ventricular arrhythmias in LVH guinea pigs were observed by using the IKr and IKs blockers.
 Results: Compared with cardiac cells in the control group, the interventricular septal thickness at end systole (IVSs), left ventricular posterior wall thickness at end systole (LVPWs), QTc interval and cell capacitance in guinea pigs with LVH were significantly increased (P<0.05); while IKs densities were significantly reduced [+60 mV: (0.36±0.03) pA/pF vs (0.58±0.05) pA/pF, P<0.01]. However, LVH exerted no significant effect on IKr densities. IKr blocker markedly prolonged the QTc interval (P<0.01) and increased the incidence of ventricular arrhythmias in guinea pigs with LVH compared with the control guinea pigs. In contrast, IKs blocker produced modest increase in QTc interval in guinea pigs of control group with no increase in LVH animals. IKs blocker did not induce ventricular arrhythmias incidence in either control or LVH animals.
 Conclusion: The cardiac hypertrophy-induced arrhythmogenesis is due to the down-regulation 
of IKs.

Objective: To investigate the risk factors of coronary artery disease (CAD) in the young-middle-aged and elderly patients in southern Anhui areas. Methods: 337 inpatients of CAD confirmed by coronary angiography in our hospital were included, and allocated to the young-middle-aged group (＜ 60 years) and elderly group (≥60 years). The differences were analyzed between groups regarding the gender ratio, history of hypertension, diabetes and smoking as well as family history of CAD and blood lipid level. Results: Elderly patients had higher proportion of smoking and history of hypertension than the young-middle-aged (P ＜ 0.05), yet the young-middle-aged group had higher levels of Body Mass Index (BMI), triglyceride (TG) and low density lipoprotein-cholesterol (LDL-C) (P ＜ 0.05). By gender, males in the young-middle-aged group had higher BMI and TG levels and lower high density lipoprotein-cholesterol (HDL-C) level (P ＜ 0.05), and elderly males had higher proportion of history of hypertension and smoking. Females in the young-middle-aged group had higher LDL-C levels than the elderly females, who had higher proportion of history of hypertension (P ＜ 0.05). Conclusion: The risk factors of CAD in the young-middle-aged population are associated with BMI and blood fat level, whereas in the elderly with cigarette smoking and hypertension.