代谢综合征颈动脉粥样硬化血管外膜重构的超声评价

目的 应用高频超声定量测定代谢综合征(MS)患者颈动脉血管外膜厚度(AT)变化,分析AT与颈动脉内-中膜厚度(IMT)的相关关系.方法 回顾分析2010年10月-2011年7月川北医学院附属医院代谢综合征患者161例和年龄性别匹配的健康对照组94例,将代谢综合征患者分为斑块组(MS-P,n=70)和无斑块组(MS-NP,n=91),采用高频超声获取颈动脉平均IMT、管壁厚度和AT进行分析比较和相关性评价.结果 MS-P组和MS-NP组患者的平均IMT和管壁厚度均显著高于健康对照组(P＜0.05),MS-P组平均AT[(0.77 ±0.13)mm]高于健康对照组[(0.66±0.11) mm,P＜0.01)]和MS-NP组[(0.69±0.13)mm,P＜0.01)],颈动脉平均AT与IMT在MS-P组、MS-NP组和健康对照组有一定的相关关系(分别为r=0.603,P＜0.01;r=0.325,P=0.005和r=0.344,P=0.004).结论 代谢综合征患者中AT出现增厚改变,AT与IMT在健康对照组和代谢综合征患者伴或不伴有斑块的患者中均有着较一致的变化,高频超声技术进行动脉外膜无创定量分析可提供评价血管外膜重构的信息.     

Quantitative analysis of carotid atherosclerotic lesions and high-sensitivity C-reactive protein in community-dwelling elderly 80 years or older

Aim:   To investigate the association between the carotid atherosclerotic lesions assessed by high-resolution ultrasonography and high-sensitivity C-reactive protein (hs-CRP) in the community-dwelling elderly aged 80 years or older.
Methods:   One hundred and seventy-nine community-dwelling elderly aged 65 years or older (78 ± 6 years, 69 men and 113 women) participated in this study. High-resolution B-mode ultrasonography was performed on the common carotid arteries. Intima-media thickness (IMT) was measured using automatic measuring system and compared with standardized examinations included blood pressure, body mass index, hemoglobin-A1c, cholesterol, creatinine, uric acid, fibrinogen and hs-CRP.
Results:   Subjects were divided into two age groups: young-old aged 65–79 years (113 subjects, 74 ± 3 years) and old-old aged 80 years or older (66 subjects, 84 ± 3 years). The maximum (max) IMT was significantly increased in the old-old compared to that of the young-old (1.7 ± 1.0 vs 1.4 ± 0.6 mm; P  = 0.02). Multivariate analysis showed that hs-CRP was the strongest predictor of thickened max IMT in the young-old ( P  = 0.022). However, it was not the predictor of thickened max IMT in the old-old.
Conclusions:   Depending on age, hs-CRP may have different meanings in the atherosclerotic process. In particular, the predictive power of hs-CRP as a marker of atherosclerotic process was less significant in subjects aged 80 years or older.     

Testosterone and Cardiovascular Health

There is an ongoing debate in the medical community regarding the effects of testosterone on cardiovascular (CV) health. For decades, there has been conflicting evidence regarding the association of endogenous testosterone levels and CV disease (CVD) events that has resulted in much debate and confusion among health care providers and patients alike. Testosterone therapy has become increasingly widespread, and after the emergence of studies that reported increased CVD events in patients receiving testosterone therapy, the US Food and Drug Administration (FDA) released a warning statement about testosterone and its potential risk regarding CV health. Some of these studies were later found to be critically flawed, and some experts, including the American Association of Clinical Endocrinologists and an expert panel regarding testosterone deficiency and its treatment, reported that some of the FDA statements regarding testosterone therapy were lacking scientific evidence. This article summarizes the current evidence regarding the relationship between testosterone (endogenous and supplemental) and CV health. A literature review was conducted via search using PubMed and specific journal databases, including the New England Journal of Medicine and the Journal of the American College of Cardiology. Key search terms included testosterone and cardiovascular health, coronary artery disease, heart failure, androgen deprivation therapy, intima-media thickness, and adrenal androgens. Initial study selection was limited to publications within the past 10 years (January 1, 2007, through December 31, 2016); however, key publications outside of this time frame were selected if they provided important quantitative data or historical perspectives for the review of this topic. The search was further supplemented by reviewing references in selected articles.     

The role of tissue factor pathway inhibitor in atherosclerosis and arterial thrombosis

Tissue factor pathway inhibitor (TFPI) is the main inhibitor of tissue factor (TF)-mediated coagulation. In atherosclerotic plaques TFPI co-localizes with TF, where it is believed to play an important role in attenuating TF activity. Findings in animal models such as TFPI knockout models and gene transfer models are consistent on the role of TFPI in arterial thrombosis as they reveal an active role for TFPI in attenuating arterial thrombus formation. In addition, ample experimental evidence exists indicating that TFPI has inhibitory effects on both smooth muscle cell migration and proliferation, both which are recognized as important pathological features in atherosclerosis development. Nonetheless, the clinical relevance of these antithrombotic and atheroprotective effects remains unclear. Paradoxically, the majority of clinical studies find increased instead of decreased TFPI antigen and activity levels in atherothrombotic disease, particularly in atherosclerosis and coronary artery disease (CAD). Increased TFPI levels in cardiovascular disease might result from complex interactions with established cardiovascular risk factors, such as hypercholesterolemia, diabetes and smoking. Moreover, it is postulated that increased TFPI levels reflect either the amount of endothelial perturbation and platelet activation, or a compensatory mechanism for the increased procoagulant state observed in cardiovascular disease. In all, the prognostic value of plasma TFPI in cardiovascular disease remains to be established. The current review focuses on TFPI in clinical studies of asymptomatic and symptomatic atherosclerosis, coronary artery disease and ischemic stroke, and discusses potential atheroprotective actions of TFPI.     

超声检测颈动脉粥样硬化、肱动脉舒张功能与脑梗死相关性探讨

目的探讨老年高血压病患者颈动脉粥样硬化、肱动脉内皮依赖性血管舒张功能与脑梗死发生的关系。方法100例患者分为高血压组(EH组)、脑梗死组(CI组)各50例,并与正常对照组(对照组)50例进行比较,分析血压、血脂、颈动脉内膜-中层厚度(IMT)、肱动脉内皮依赖性血管舒张(FMD)功能等变化。结果CI组表现为老年性高血压,舒张压降低明显,脉压增大;空腹血糖较对照组升高明显,但与EH组尚无显著差异;TG显著升高;CI组IMT显著增厚,斑块数及发生率显著增高,FMD下降明显。三组IMT与FMD均呈显著负相关,FMD与年龄呈负相关。结论CI组颈动脉粥样硬化程度显著增加,推测脉压增大、高TG是导致CI组患者斑块数增加引发脑梗死的直接重要危险因素。颈动脉粥样硬化、肱动脉FMD下降与脑梗死发生有密切相关性,IMT与FMD检查对预测脑梗死的发生并且对临床预防和治疗脑梗死提供重要依据。     

阿托伐他汀对原发性高血压患者血压及内-中膜厚度的影响

目的探讨阿托伐他汀对原发性高血压（essential hypertension,EH）患者血压、血脂及内-中膜厚度（intima—media thick—ness,IMT）的影响。方法1、2级原发性高血压（EH）78例,分为正常胆固醇组（NC）和高胆固醇组（HC）组,各39例。NC组和HC组再按随机数字表分别分为他汀治疗组（NCS,HCS）和对照组（NCC,HCC）,他汀治疗组每天予氨氯地平5mg＋阿托伐他汀20mg;对照组每天予氨氯地平5mg,均为12周。20例正常健康者为正常对照组。患者于基线及治疗12周后检测血压、血脂及IMT。结果EH各组患者经12周治疗后血压较前明显降低（P〈0．05）,以他汀治疗组下降幅度更加明显（P〈0．05）;NCC、HCC组血脂改变不明显（P〉0．05）,NCS和HCS组,TC、TG、LDL—C下降明显,HDL—C明显增高（P〈0．05）;EH组内血压、IMT、IMT／D及颈动脉斑块明显高于健康对照组（P〈0．05）;治疗后IMT及IMT／D均下降（P〈0．05）,治疗后各亚组内他汀治疗组与对照组比较下降有统计学意义（P〈0．05）;治疗后颈动脉斑块较对照组斑块改善不明显（P〉0．05）,但治疗组中位数较对照组有下降趋势。结论阿托伐他汀与氨氯地平等降压药物合用使降压效果更明显,有辅助降压作用;有效调脂的同时,可以使IMT／D改善明显,但短期内颈动脉斑块未见明显改善。