高血压患者外周血白细胞端粒长度的变化

目的 探讨原发性高血压(EH)患者外周血白细胞端粒长度的变化及其与动脉弹性的关系.方法 应用实时荧光定量PCR方法检测163例EH患者和112健康对照者外周血白细胞相对端粒长度;应用彩色多普勒超声诊断仪测定颈总动脉断面膨胀系数(CSDC)和硬化参数(stiffness parameter)β作为动脉弹性指标.结果 高血压组相对端粒长度较对照组显著缩短(P＜0.01).两组端粒长度比值与年龄呈负相关(r=-0.345,P＜0.001),与CSDC呈正相关(r=0.286,P＜0.001),与硬化参数β呈负相关(r=-0.126,P=0.037).结论 高血压患者存在端粒长度过度损耗,其损耗程度与动脉硬化程度相关,端粒损耗参与高血压动脉粥样硬化发生发展的病理过程.     

急性冠状动脉综合征患者颈动脉斑块与血浆基质金属蛋白酶的相关性

目的研究急性冠状动脉综合征患者颈动脉斑块与血浆基质金属蛋白酶的相关性。方法采用高分辨率超声，测定30例急性冠状动脉综合征患者、29例稳定型心绞痛患者和17例正常对照者的颈动脉内膜中膜厚度及斑块积分，同时采用夹心酶联免疫分析法测定血浆基质金属蛋白酶9和组织型金属蛋白酶抑制因子1的变化。结果三组间的年龄、性别、总胆固醇、甘油三酯、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇无显著性差异。急性冠状动脉综合征组血浆基质金属蛋白酶9、组织型金属蛋白酶抑制剂、基质金属蛋白酶9，组织型金属蛋白酶抑制剂1及颈动脉内膜中膜厚度、总斑块积分、软斑块积分和硬斑块积分显著高于稳定型心绞痛组和正常对照组。基质金属蛋白酶9与颈动脉内膜中膜厚度、总斑块积分、软斑块积分呈正相关（r=0．468，P〈0．01；r=0．592，P〈0．01；r=0．677，P〈0．01）；组织型金属蛋白酶抑制剂与颈动脉内膜中膜厚度、总斑块积分、软斑块积分、硬斑块积分呈正相关（r=0．449，P〈0．01；r=0．493，P〈0．01；r=0．435，P〈0．01；r=0．227，P〈0.05）；基质金属蛋白酶9，组织型金属蛋白酶抑制剂1与颈动脉内膜中膜厚度、总斑块积分、软斑块积分呈正相关（r=0．253，P〈0．05；r=0．431，P〈0．01；r=0．547，P〈0．01）。去除年龄因素后，偏相关分析显示颈动脉内膜中膜厚度与基质金属蛋白酶9（r=0．461，P〈0．001）、组织型金属蛋白酶抑制剂1（r=0．441，P〈0.001）、基质金属蛋白酶9，组织型金属蛋白酶抑制剂1（r=0．241，P〈0．01）呈正相关关系。结论急性冠状动脉综合征患者血浆基质金属蛋白酶9、组织型金属蛋白酶抑制剂1、基质金属蛋白酶9，组织型金属蛋白酶抑制剂1及颈动脉内膜中膜厚度、总斑块积分、软斑块积分和硬斑块积分显著高于稳定型心绞痛患者和正常对照。血浆基质金属蛋白酶9、组织型金属蛋白酶抑制剂1、基质金属蛋白酶9，组织型金属蛋白酶抑制剂1与颈动脉内膜中膜厚度、总斑块积分、软斑块积分呈正相关关系。     

原发性高血压患者血清salusin-β水平与颈动脉病变关系

目的探究原发性高血压患者外周血中salusin-β水平与颈动脉病变关系。方法选取营口市中心医院2017年8月至2019年5月收治的140例原发性高血压患者作为观察组,用彩色多普勒超声观察颈动脉内膜厚度,分为颈动脉内膜正常组(55例)、颈动脉斑块组(35例)以及颈动脉内膜增厚组(50例)。选取同期在我院进行健康体检者40例作为对照组。检测患者外周血中salusin-β水平,比较各组salusin-β水平,并分析salusin-β与颈动脉斑块的关系。结果观察组外周血中salusin-β水平[(4.35±1.25)nmol/L]高于对照组[(3.37±0.91)nmol/L],差异有统计学意义(t=4.617,P <0.05)。颈动脉斑块组salusin-β水平[(4.88±1.36)nmol/L]高于颈动脉内膜正常组[(3.65±1.02)nmol/L]和颈动脉内膜增厚组[(4.23±1.18)nmol/L],差异有统计学意义(t=4.887、2.352,P <0.05)。观察组患者中,颈动脉斑块组高血压病程、高血脂、入院收缩压、salusin-β水平以及胆固醇水平高于无颈动脉斑块患者,差异有统计学意义(χ2/t=4.814、15.041、4.684、3.824、4.684,P <0.05)。多因素回归分析发现,合并高血脂、高血压病程、salusin-β是原发性高血压患者颈动脉斑块的独立危险因素(OR=1.102、1.312、1.671,P <0.05)。在高血压合并颈动脉斑块患者中,salusin-β水平与胆固醇、收缩压、舒张压呈正相关(r=3.651、3.251、3.013,P <0.05)。结论原发性高血压患者外周血salusin-β水平与颈动脉病变严重程度密切相关,salusin-β水平可能成为原发性高血压颈动脉斑块的有效生物学标记物。     

颈动脉粥样硬化患者外周血LDL-C水平、WBC计数变化及其相关性分析

目的观察颈动脉粥样硬化（CAs）患者外周血血清低密度脂蛋白胆固醇（LDL-C）水平、白细胞（WBC）计数变化及其相关性。方法用生化分析仪测定60例CAs患者（CAs组）和31例健康对照者（对照组）的外周血血清LDL-C,血细胞分析仪进行外周血WBC计数,彩色多普勒超声检测颈动脉内膜中层厚度（IMT）。结果 CAs组血清LDL-C水平、WBC计数较对照组升高（P均〈0.01）。CAs组颈动脉内膜斑块形成者血清LDL-C水平、WBC计数较颈动脉单纯内膜增厚者高（P均〈0.01）。CAs组血清LDL-C水平与WBC计数呈正相关（r=0.798,P〈0.01）。结论 CAs患者血清LDL-C水平、WBC计数升高,CAs程度重者血清LDL-C水平、WBC计数升高更明显,二者的升高是同步的。     

合并糖尿病的冠心病患者冠状动脉粥样硬化与颈动脉粥样硬化的关系

目的探讨合并糖尿病的冠心病患者颈动脉粥样硬化与冠状动脉粥样硬化的关系.方法通过对73例合并2型糖尿病的冠心病患者行冠状动脉造影明确冠状动脉病变,同时行颈动脉超声检查,检测颈动脉内膜-中膜厚度.结果不同支数冠状动脉病变者之间比较,颈动脉内膜-中膜厚度、颈动脉斑块积分和斑块发生率差异有显著性(分别为P＜0.001、P＜0.005、P＜0.01).冠状动脉病变支数与颈动脉内膜-中膜厚度和颈动脉斑块积分有明显的相关性,其相关系数分别为0.71和0.68(P＜0.001).冠状动脉造影积分与颈动脉内膜-中膜厚度及颈动脉斑块积分相关系数分别为0.69和0.66(P＜0.001).结论合并糖尿病冠心病患者颈动脉粥样硬化与冠状动脉粥样硬化存在显著的正相相关性,这类患者通过了解颈动脉病变可间接反映冠状动脉粥样硬化病变.     

白细胞端粒长度和颈动脉内膜中膜厚度的关系：Framingham心脏研究

患有心血管疾病的个体，白细胞端粒长度（LTL）较短。他们通过测量（Framingham后代）颈动脉内膜中膜厚度（IMT）测量，确定LTL和动脉粥样硬化之间的关系。方法和结果：选取1062参与者（496名男性，566名女性），年龄33～86岁。以末端限制性片断的平均数作为指标，用B超测定颈动脉IMT。     

吸烟与脑卒中高危人群颈动脉粥样硬化发生的相关性分析

目的探讨吸烟与脑卒中高危人群颈动脉硬化发生的相关性。方法选取2012年5月—2013年2月在北京市丰台区王佐卫生服务中心、蒲黄榆社区卫生服务中心、花乡社区卫生服务中心、方庄社区卫生服务中心筛查的脑卒中高危人群7 284例,将患者分为从未吸烟组和吸烟组进行颈动脉超声检查,观察两组患者颈动脉内膜中层厚度及斑块形成情况;根据吸烟指数将吸烟组患者分为轻度吸烟、中度吸烟及重度吸烟3个亚组,观察吸烟时间、吸烟量等因素下不同亚组间颈动脉内膜中层厚度及斑块形成情况。结果与未吸烟组相比,吸烟组颈动脉内膜增厚及斑块形成发生率明显增高(P0.01),颈动脉内膜增厚及斑块形成的发生率与吸烟呈正相关(Spearman相关系数分别为0.134、0.125,P0.05);在吸烟组各亚组间,颈动脉内膜增厚及斑块形成的发生率依次增高(P0.01),颈动脉内膜增厚及斑块形成发生率与吸烟指数呈正相关(Spearman相关系数分别为0.122、0.099,P0.05)。多因素Logistic回归分析显示,性别、年龄、高血压病史、糖尿病病史、吸烟指数、体育锻炼很少或轻体力劳动、明显超重等与颈动脉硬化相关。与不吸烟组相比,轻度吸烟组OR=1.549(P0.01),中度吸烟组OR=1.7 6 7(P0.01),重度吸烟组OR=2.147(P0.01)。结论在脑卒中高危人群中,吸烟是颈动脉硬化及斑块形成的独立危险因素,与颈动脉硬化及斑块形成的发生呈正相关,吸烟时间、吸烟量等因素与颈动脉硬化发生亦呈正相关,吸烟对颈动脉粥样硬化进程的影响是累积的。     

糖尿病病人颈动脉粥样硬化及相关性探讨

目的使用彩超检测2型糖尿病病人颈动脉粥样硬化,探讨二者之间的关系及相关性。方法对176例2型糖尿病和156例非糖尿病病人进行超声检查,观察双侧颈动脉内膜-中膜厚度（IMT）、斑块形成、狭窄程度变化。结果IMT随年龄增加而增厚（P〈0.01）,相同年龄段之间比较,糖尿病组较非糖尿病组增厚（P〈0.01）。颈动脉粥样硬化斑块糖尿病组发生率均显著高于非糖尿病组（P〈0.01）,狭窄程度≥40%的发生率糖尿病组显著高于对照组（P〈0.05）。结论通过观察颈动脉内膜-中膜厚度（IMT）和粥样斑块,可以判断2型糖尿病动脉硬化程度,预防并发症的发生。     

老年高血压患者颈动脉顺应性随增龄及脉压变化的研究

目的 研究老年高血压患者脉压和增龄与颈动脉顺应性及斑块形成的关系。方法 95例高血压患者分为非老年组50例和老年组45例，老年组按年龄分为60～69岁（1组）21例；70～74岁（2组）12例；≥75岁（3组）12例，并与正常对照组30例进行颈动脉超声检查。再根据颈动脉有无斑块情况分为斑块组30例，无斑块组65例，比较2组间的年龄及脉压分布有无统计学差异。结果 高血压组的颈动脉顺应性明显低于正常对照组，而老年组的颈动脉顺应性明显低于非老年组，并随年龄的增加而降低；老年组的颈总动脉内膜-中层厚度（IMT）及斑块发生率明显高于非老年组和正常对照组，并随年龄的增加而增加。结论 老年高血压患者颈动脉顺应性随增龄而降低；年龄增大，脉压增加，颈动脉斑块发生率增高。     

非冠心病患者白细胞端粒长度与阵发性心房颤动的相关性研究

目的探讨非冠心病患者白细胞端粒长度与阵发性心房颤动(房颤)的相关性。方法选择2014年5月~2016年1月在天津医科大学第二医院心脏科行冠状动脉造影术检查住院治疗的患者138例,根据诊断分为非房颤组88例和阵发性房颤组50例。抽取外周血并提取DNA,通过实时聚合酶链反应测量白细胞端粒长度,标化为端粒/单基因比值,记录并比较患者基线资料,采用非条件logistic回归分析二者相关性。结果与非房颤组比较,阵发性房颤组心力衰竭、体质量指数、D-二聚体、纤维蛋白原明显升高,他汀类药物使用比例明显降低,差异有统计学意义(P0.05,P0.010)。阵发性房颤组白细胞端粒较非房颤组更长,但差异无统计学意义[0.28(0.11,0.71)vs 0.20(0.06,0.46),P=0.100]。logistic回归分析显示,白细胞端粒长度与阵发性房颤无相关性(OR=1.498,95%CI:0.924~2.426,P=0.100),调整年龄、体质量指数、D-二聚体及纤维蛋白原等混杂变量后,白细胞端粒长度与阵发性房颤无相关性(OR=0.960,95%CI:0.124~7.404,P=0.970)。结论非冠心病患者白细胞端粒长度与阵发性房颤发病无相关性。     

超敏C反应蛋白与老年高血压患者合并颈动脉斑块稳定性的关系及其性别差异

目的观察血清超敏C反应蛋白(hsCRP)水平与老年高血压患者颈动脉斑块及其稳定性的相关性,以及是否有性别差异。方法 "老年高血压降压治疗长期随访研究"的研究对象中,172例70岁以上的高血压患者行颈动脉超声检查,以内膜中层厚度(IMT)1.3mm诊断动脉粥样斑块形成;根据有无斑块及斑块回声的特点分为无斑块组、稳定斑块组(扁平斑块和硬斑块)和易损斑块组(软斑块和溃疡型斑块)。同时测定hsCRP、血脂、血清肌酐、尿酸。结果颈动脉斑块组(n=131)血清hsCRP为(3.2±2.5)mg/L,显著高于无斑块组〔(2.0±1.8)mg/L,n=41,P=0.005〕。对危险因素进行logistic回归分析显示,只有血清hsCRP水平是发生颈动脉斑块的危险因素(RR=1.299,95%CI=1.052～1.604,P=0.015)。进一步分析显示易损斑块组血清hsCRP为(4.2±2.5)mg/L,显著高于稳定斑块组〔(2.5±2.2)mg/L〕和无斑块组(P0.001)。后两组之间血清hsCRP则无显著差异(P=0.278)。分别分析男性和女性血清hsCRP与颈动脉斑块的关系,易损斑块组的血清hsCRP均显著高于稳定斑块组和无斑块组(P0.05)。结论血清hsCRP水平与老年高血压患者颈动脉斑块的发生及其稳定性相关,易损斑块者的血清hsCRP显著高于无斑块者和稳定斑块者;并且这种相关性在70岁以上的男性和女性老年高血压患者中都存在,未观察到性别差异。     

原发性高血压患者血浆纤维蛋白原水平与颈动脉粥样硬化斑块的关系

目的探讨原发性高血压（EH）患者颈动脉粥样硬化斑块及性质与血浆纤维蛋白原（FIB）的关系。方法纳入EH患者404例,根据是否合并颈动脉硬化斑块分为斑块组（n=235）和无斑块组（n=169）,对两组受试者血浆纤维蛋白原（FIB）水平及斑块性质（分为软斑块、硬斑块、混合斑块）进行比较,并运用多因素回归分析对颈动脉粥样硬化斑块性质与血压、血脂、血糖、FIB关系进行研究。结果①斑块组FIB及低密度脂蛋白胆固醇（LDL-C）明显高于无斑块组[FIB：（3.92±2.82）g/L vs.（3.23±1.62）g/L,P=0.032;LDL-C：（3.23±0.91）mmol/L vs.（2.95±0.82）mmol/L,P=0.047],而HDL-C低于无斑块组[（1.17±0.31）mmol/L vs.（1.25±0.35）mmol/L,P=0.021）;②软斑块组患者血浆FIB水平高于混合斑块[（4.18±2.89）g/L vs.（3.84±2.16） g/L,P＜0.05]和硬斑块[（4.18±2.89）g/L vs.（3.69±2.21）g/L,P＜0.05],混合斑块与硬斑块患者之间无明显差异;③高FIB血症者颈动脉斑块检出率及软斑块比例均显著高于FIB正常者（74.7%vs.42.9%,P＜0.05;32.5%vs.8.1%,P＜0.05）;④多元回归分析发现血FIB水平、LDL-C与颈动脉斑块成正相关,HDL-C与颈动脉斑块成负相关。结论高血压患者血浆FIB水平与颈动脉斑块,尤其是软斑块密切相关。     

Detection of Chlamydia pneumoniae and Helicobacter pylori in atherosclerotic plaques of carotid artery by polymerase chain reaction.

OBJECTIVES: A possible role of some microorganisms has been proposed in the pathogenesis of atherosclerosis, but it is still an unresolved issue. We investigated the presence of Chlamydia pneumoniae and Helicobacter pylori DNA in carotid artery atherosclerotic plaques by using PCR. METHODS: One hundred and four patients with atherosclerotic diseases were included. The study group consisted of 52 atherosclerotic plaque specimens obtained from the carotid arteries of patients who had carotid endarterectomy and the control group consisted of 52 specimens obtained from the macroscopically healthy regions of ascending aorta in patients who had undergone coronary artery bypass grafting. The presence of C. pneumoniae and H. pylori DNA in endarterectomy specimens were demonstrated by PCR. RESULTS: C. pneumoniae DNA was detected in 16 of 52 (30.8%) atherosclerotic plaques and 1 of 52 (1.9%) macroscopically healthy ascending aorta wall specimens (P < 0.001). H. pylori DNA was detected in 9 of 52 (17.3%) atherosclerotic plaques and none of the controls (P = 0.003). CONCLUSIONS: The higher incidence of C. pneumoniae and H. pylori DNA in atherosclerotic plaques suggests that these microorganisms may play a role in the pathogenesis of atherogenesis.     

通心络胶囊联合辛伐他汀对颈动脉粥样斑块形成的干预作用研究

目的 观察通心络胶囊联合辛伐他汀对颈动脉粥样斑块形成的干预作用.方法 选择116例门诊颈动脉粥样斑块患者并随机分为3组.通心络胶囊组(39例)在常规治疗的基础上加通心络胶囊2粒,每日3次1辛伐他汀组(39例)在常规治疗基础上加辛伐他汀40 mg,每晚1次;联合治疗组(38例)在常规治疗基础上,应用通心络胶囊2粒,每日3次,辛伐他汀40 mg,每晚1次.患者均连续服药6个月,并均于服药前和服药后第6个月接受颈动脉超声检查,现察比较各组患者用药前后颈动脉粥样斑块的变化.结果 3组患者用药后颈动脉粥样硬化斑块明显减轻甚或消退.用药前后通心络胶囊组与辛伐他汀组之间无统计学意义(P＞0.05),但用药后与通心络胶囊组和辛伐他汀组相比,联合治疗组患者颈动脉粥样硬化斑块减轻更明显(P＜0.05).各组均未见明显的不良反应.结论 通心络胶囊和辛伐他汀对颈动脉粥样硬化斑块有明显的抑制作用,两药联合效果更佳,且患者无明显的不良反应.     

In vivo 18F-fluorodeoxyglucose positron emission tomography imaging provides a noninvasive measure of carotid plaque inflammation in patients.

OBJECTIVES: Given the importance of inflammation in atherosclerosis, we sought to determine if atherosclerotic plaque inflammation could be measured noninvasively in humans using positron emission tomography (PET). BACKGROUND: Earlier PET studies using fluorodeoxyglucose (FDG) demonstrated increased FDG uptake in atherosclerotic plaques. Here we tested the ability of FDG-PET to measure carotid plaque inflammation in patients who subsequently underwent carotid endarterectomy (CEA). METHODS: Seventeen patients with severe carotid stenoses underwent FDG-PET imaging 3 h after FDG administration (13 to 25 mCi), after which carotid plaque FDG uptake was determined as the ratio of plaque to blood activity (target to background ratio, TBR). Less than 1 month after imaging, subjects underwent CEA, after which carotid specimens were processed to identify macrophages (staining with anti-CD68 antibodies). RESULTS: There was a significant correlation between the PET signal from the carotid plaques and the macrophage staining from the corresponding histologic sections (r = 0.70; p < 0.0001). When mean FDG uptake (mean TBR) was compared with mean inflammation (mean percentage CD68 staining) for each of the 17 patients, the correlation was even stronger (r = 0.85; p < 0.0001). Fluorodeoxyglucose uptake did not correlate with plaque area, plaque thickness, or area of smooth muscle cell staining. CONCLUSIONS: We established that FDG-PET imaging can be used to assess the severity of inflammation in carotid plaques in patients. If subsequent natural history studies link increased FDG-PET activity in carotid arteries with clinical events, this noninvasive measure could be used to identify a subset of patients with carotid atherosclerosis in need of intensified medical therapy or carotid artery intervention to prevent stroke.     

2型糖尿病患者颈动脉粥样硬化斑块与骨密度的相关性分析

目的探讨住院2型糖尿病(T2DM)患者不同性别骨量减少(包括骨质疏松与低骨量)相关影响因素及其与颈动脉粥样硬化斑块之间的关系。方法回顾性分析720例T2DM患者的临床资料,将入选对象分为男性组和女性组,每组再分为骨量正常组和骨量减少组,颈动脉有斑块组和颈动脉无斑块组。结果在男性骨量减少组(77例)中,存在粥样斑块68例(88.31%),与骨量正常组(164例)比较,骨量减少组粥样斑块的发生率明显升高(P0.05);斑块形成组骨密度(BMD)明显减低(P0.05)。在女性骨量减少组(255例)中,存在粥样斑块191例(74.90%),与骨量正常组(224例)比较,骨量减少组粥样斑块的发生率明显升高(P0.05);斑块形成组骨密度明显减低(P0.05)。二元Logistic回归分析显示,男性骨量减少的影响因素有年龄(OR=1.059,P=0.002),体质指数(BMI)(OR=0.853,P=0.004),空腹血糖(FBG)(OR=1.138,P=0.044),有无颈动脉斑块(OR=2.514,P=0.035)。女性骨量减少的影响因素有年龄(OR=1.117,P=0.000),绝经年龄(OR=0.946,P=0.031),BMI(OR=0.910,P=0.003)。结论 T2DM患者颈动脉粥样硬化斑块与骨量减少密切相关。女性患者由于增龄等共同危险因素的存在,二者常相伴发生,然而在男性患者中,颈动脉粥样硬化斑块的形成是骨质疏松的危险因素,因此,颈动脉硬化的发展常伴有骨量变化,易发生骨质疏松。     

系统性红斑狼疮亚临床动脉粥样硬化危险因素研究

目的 评价系统性红斑狼疮(SLE)患者亚临床动脉粥样硬化的发生率、传统及非传统危险因素对动脉粥样硬化发生的影响.方法 选择58例确诊SLE同时既往无动脉粥样硬化疾病发生的患者作为研究对象.记录其传统危险因素、SLE临床及实验室指标、活动度评分、治疗情况.同时通过颈动脉彩色多普勒超声测量双侧颈动脉内中膜厚度(IMT)并观察有无动脉粥样硬化斑块.结果 58例患者中IMT增厚者22例(38%).有动脉粥样硬化斑块者10例(17%).有斑块者较无斑块者SLE病程更长,同时存在更多传统危险因素:年龄大、有高血压、糖尿病及已绝经者多,有更高的收缩压、总胆固醇及低密度脂蛋白水平.多因素分析显示,患者所具有的传统危险因素的数量及SLE病程是出现颈动脉粥样硬化斑块的独立危险因素.结论 传统危险因素在SLE患者动脉粥样硬化的发生中仍然发挥着重要作用,应该积极地予以控制.SLE病程是影响动脉粥样硬化发生的非传统独立危险因素,随着病程的延长,应该定期进行相关检查,尽早发现并治疗.     

Relationship of hypertensive retinopathy to thoracic aortic atherosclerosis in patients with severe arterial hypertension

Arterial hypertension complicated with atherosclerosis presents the most common cause of death in hypertensive patients. Eyes suffer vascular damage as a result of high blood pressure (BP) and these changes can be detected by funduscopy, although its role has recently been questioned. The aims of this study were to assess the prevalence of atherosclerotic plaques and other disorders of thoracic aorta by transesophageal echocardiography (TEE) in patients with severe arterial hypertension of at least 1 year duration and to analyze the association between aortic atherosclerotic plaques and hypertensive retinopathy. This was a prospective TEE study conducted on 56 hypertensive patients from September 2008 to January 2010. Mean patient age was 62.8 ± 8.2 years and 67.86% of them were women. Aortic atherosclerotic plaques were found on 96.4% of patients, whereas hypertensive retinopathy was present on 94.6% of them. The mean thickness of maximal atherosclerotic plaque found on each patient was 4.3 ± 1.9 mm and 28.6% of patients had ulcerative plaques, while descending aorta was the most common location of the lesions. Grade 1 and 2 hypertensive retinopathy was diagnosed in 14.3% and 80.3% of patients, respectively. Hypertensive retinopathy correlated highly with aortic atherosclerotic score (r = 0.76, p < 0.0001), as it correlated significantly with aortic plaque thickness (r = 0.69, p < 0.0001). Application of funduscopy should be encouraged since it is a noninvasive procedure that provides a good window of retinal arterioles. Hypertensive retinopathy, even in mild forms, should serve as a marker of atherosclerosis elsewhere in the organism.     

New 3-Dimensional Volumetric Ultrasound Method for Accurate Quantification of Atherosclerotic Plaque Volume

BackgroundCarotid and femoral plaque burden is a recognized biomarker of cardiovascular disease risk. A new electronic-sweep 3-dimensional (3D)–matrix transducer method can improve the functionality and image quality of vascular ultrasound atherosclerosis imaging.ObjectivesThis study aimed to validate this method for plaque volume measurement in early and intermediate–advanced plaques in the carotid and femoral territories.MethodsPlaque volumes were measured ex vivo in pig carotid and femoral artery specimens by 3-dimensional vascular ultrasound (3DVUS) using a 3D-matrix (electronic-sweep) transducer and its associated 3D plaque quantification software, and were compared with gold-standard histology. To test the clinical feasibility and accuracy of the 3D-matrix transducer, an experiment was conducted in intermediate–high risk individuals with carotid and femoral atherosclerosis. The results were compared with those obtained using the previously validated mechanical-sweep 3D transducer and established 2-dimensional (2D)–based plaque quantification software.ResultsIn the ex vivo study, the authors assessed 19 atherosclerotic plaques (plaque volume, 0.76 µL-56.30 μL), finding strong agreement between measurements with the 3D-matrix transducer and the histological gold-standard (intraclass correlation coefficient [ICC]: 0.992; [95% CI: 0.978-0.997]). In the clinical analysis of 20 patients (mean age 74.6 ± 4.45 years; 40% men), the authors found 64 (36 carotid and 28 femoral) of 80 scanned territories with atherosclerosis (measured atherosclerotic volume, 10 μL-859 μL). There was strong agreement between measurements made from electronic-sweep and mechanical-sweep 3DVUS transducers (ICC: 0.997 [95% CI: 0.995-0.998]). Agreement was also high between plaque volumes estimated by the 2D and 3D plaque quantification software applications (ICC: 0.999 [95% CI: 0.998-0.999]). Analysis time was significantly shorter with the 3D plaque quantification software than with the 2D multislice approach with a mean time reduction of 46%.Conclusions3DVUS using new matrix transducer technology, together with improved 3D plaque quantification software, simplifies the accurate volume measurement of early (small) and intermediate–advanced plaques located in carotid and femoral arteries.     

Subclinical atherosclerosis in psoriatic arthritis: a case-control study

OBJECTIVE: To investigate the prevalence of subclinical atherosclerosis among patients with psoriatic arthritis (PsA). METHODS: Forty patients with PsA were enrolled. Controls were matched by age, sex, and atherosclerotic risk factors. All patients and controls underwent duplex scan of the carotid arteries. Carotid intima-media thickness (IMT) was evaluated and the presence of atherosclerotic plaques was recorded. The plaques were graded and carotid plaque index was calculated. RESULTS: Patients with PsA had a higher IMT (mean +/- standard deviation, 1.04 +/- 0.35 mm vs 0.88 +/- 0.29 mm in controls; p = 0.03), and had a higher carotid plaque index than did matched controls (2.3 +/- 2.6, compared to 1.12 +/- 2.09; p = 0.03). Multivariate analysis demonstrated that PsA status as well as age and triglyceride levels were associated with the presence of carotid plaque. Other traditional risk factors were more prevalent among patients with PsA; however, they were not statistically significant. CONCLUSION: Our study demonstrates that patients with PsA may have an increased prevalence of subclinical atherosclerosis. These findings may not be solely attributable to traditional risk factors alone. Special attention and strict control of atherosclerotic risk factors in patients with PsA is warranted.