炎性因子与颈动脉硬化斑块稳定性的相关性研究

目的 探讨炎性因子与动脉硬化斑块稳定性之间的关系.方法 选取颈动脉硬化斑块易损者40例为VP组,斑块稳定者40例为SP组,另选无斑块形成者40例为对照组,测定血清中IL-10、IL-18和MMP-9水平及斑块声学密度值(AD),对两组神经功能缺损评分.结果 SP组IL-18水平明显高于VP组(P＜0.05);SP组IL-10,MMP-9水平明显低于VP组(P＜0.05),表明VP组斑块不稳定;两组斑块声学密度值比较,SP组明显高于VP组(P＜0.05);两组神经功能缺损评分比较,SP组高于VP组(P＜0.05).结论 IL-10,IL-18,MMP-9和组织因子与颈动脉粥样硬化进展有相关性,对预测不稳定斑块破裂具有较高临床价值.     

In vitro evaluation of minimum inhibitory concentration of several antibacterial agents against Rickettsia japonica using a plaque reduction assay system

The study was conducted to determine the minimum inhibitory concentrations (MICs) of several antibacterial agents against Rickettsia japonica, which causes Japanese spotted fever. A plaque reduction assay as an in vitro culture method was conducted to determine the MICs of antibacterial agents (4 types of tetracyclines: tetracycline, doxycycline, minocycline, and tigecycline; 3 types of quinolones: ciprofloxacin, ofloxacin, and levofloxacin; and 2 types of macrolides: azithromycin and clarythromycin) against R. japonica. R. japonica was sensitive to the antibacterial agents tested with MICs similar to those against other spotted fever rickettsia determined in previously described plaque reduction assays.     

Intravascular evaluation of coronary atherosclerotic lesions among Egyptian diabetic patients with acute coronary syndromes

Background

Coronary artery disease is one of the main causes of death in diabetes mellitus (DM). Egypt was listed among the world top 10 countries regarding the number of diabetic patients by the International Diabetes Federation (IDF).

Carotid intima-media thickness is increased in subjects with ischemic heart disease having a familial incidence

OBJECTIVES: A family history of ischemic heart disease (IHD) is an independent risk factor for cardiovascular events. However, the mechanisms underlying this susceptibility have not been fully elucidated. The authors hypothesized that an important mediator of the familial incidence of IHD is subclinical atherosclerosis, which is detectable by noninvasive imaging. METHODS: One hundred forty-seven consecutive subjects (mean age 61.9 years, 57% men) were studied for one year using carotid ultra-sonogrophy for general medical screening, and familial IHD events were validated. Using a 7.5 MHz linear array transducer, carotid intima-media thickness (IMT) and carotid plaque were assessed. Subjects were subsequently divided into four groups based on the severity of IMT. RESULTS: The familial incidence of IHD and incidence of plaque were associated with the severity of IMT. No significant differences in risk factors were found between subjects with and without a family history of IHD. CONCLUSIONS: These findings suggest that subclinical atherosclerosis, as assessed in the carotid arteries, is more prevalent in individuals with a family history of IHD.     

冠脉斑块稳定性与肿瘤坏死因子相关研究

目的 探讨肿瘤坏死因子(Tumor necrosis fac-tor-alpha,TNF-α)与冠状动脉粥样硬化斑块稳定性的相关性。方法 以血管内超声(Intravascular Ultrasound,IVUS)检出冠状动脉粥样硬化斑块的软硬特性,通过临床是否为急性冠脉综合征患者,将具有软斑块特性,同时急性冠脉综合征者分为不稳定斑块组;而硬斑块特性,且不符合急性冠脉综合征者为稳定斑块组。测定两组间冠状窦及外周血血浆TNF-α浓度,结果与IVUS测定的斑块大小、斑块纤维帽厚度、脂核或无回声带大小、脂核或无回声带/斑块比及面积狭窄率进行相关性分析。结果 不稳定斑块组TNF-α值明显高于稳定斑块组[(o.11o±O.045)ng/mL vs(0.097±0.137)ng/mL,P<0.01和(0.111±0.037)ng/mL vs(0.042±0.022)ng/mL,P<0.05;将测得TNF-α与IVUS所测得纤维帽厚度、脂核或无回声带大小、斑块大小、脂核/斑块、面积狭窄率等进行相关分析,未见明显相关。结论TNF-α与斑块的稳定性有关,同时其在冠状循环与体循环中的量无差异,可望作为冠脉斑块不稳定性的判定指标。     

PAS疗法对颈动脉硬化不稳定斑块的影响

目的研究与分析阿司匹林、普罗布考和阿托伐他汀钙三药联用治疗颈动脉硬化患者的不稳定斑块的作用。方法对我院2010年3月至2012年5月间126例颈动脉硬化患者随机分为PAS组与AS组各63例,AS组患者给予阿司匹林100mg／日和阿托伐他汀钙20mg／日,PAS组在As组基础上加用普罗布考500mg／次,2次／日,在治疗后6个月进行颈动脉超声检测。比较与分析颈动脉斑块的面积和性质的变化。结果治疗后6个月,两组患者不稳定斑块面积均有减小,PAS组不稳定斑块的面积减小程度大于As组,差异具有统计学意义（P＜0．05）,PAS组不稳定斑块数目减少程度大于AS组。结论PAS疗法对消除颈动脉粥样硬化斑块具有显著作用,普罗布考在降血脂及抗血小板的基础上可进一步减轻和消退颈动脉不稳定斑块．延缓动脉粥样硬化的形成和发展．此疗法具有显著优势．在临床更具应用价值．     

Comprehensive analysis of intravascular ultrasound and angiographic morphology of culprit lesions between ST-segment elevation myocardial infarction and non-ST-segment elevation acute coronary syndrome

Background

Some plaques lead to ST-segment elevation myocardial infarction (STEMI), whereas others cause non-ST-segment elevation acute coronary syndrome (NSTEACS). We used angiography and intravascular ultrasound (IVUS) to investigate the difference of culprit lesion morphologies in ACS.

Methods

Consecutive 158 ACS patients whose culprit lesions were imaged by preintervention IVUS were enrolled (STEMI = 81; NSTEACS = 77). IVUS and angiographic findings of the culprit lesions, and clinical characteristics were compared between the groups.

Results

There were no significant differences in patients' characteristics except for lower rate of statin use in patients with STEMI (20% vs 44%, p = 0.001). Although angiographic complex culprit morphology (Ambrose classification) and thrombus were more common in STEMI than in NSTEACS (84% vs 62%, p = 0.002; 51% vs 5%, p < 0.0001, respectively), SYNTAX score was lower in STEMI (8.6 ± 5.4 vs 11.5 ± 7.1, p = 0.01). In patients with STEMI, culprit echogenicity was more hypoechoic (64% vs 40%, p = 0.01), and the incidence of plaque rupture, attenuation and “microcalcification” were significantly higher (56% vs 17%, p < 0.0001; 85% vs 69%, p = 0.01; 77% vs 61%, p = 0.04, respectively). Furthermore, the maximum area of ruptured cavity, echolucent zone and arc of microcalcification were significantly greater in STEMI compared with NSTEACS (1.80 ± 0.99 mm² vs 1.13 ± 0.86 mm², p = 0.006; 1.52 ± 0.74 mm² vs 1.21 ± 0.81 mm², p = 0.004; 99.9 ± 54.6° vs 77.4 ± 51.2°, p = 0.01, respectively). Quantitative IVUS analysis showed that vessel and plaque area were significantly larger at minimum lumen area site (16.6 ± 5.4 mm² vs 14.2 ± 5.5 mm², p = 0.003; 13.9 ± 5.1 mm² vs 11.6 ± 5.2 mm², p = 0.003, respectively).

Conclusion

Morphological feature (outward vessel remodeling, plaque buildup and IVUS vulnerability of culprit lesions) might relate to clinical presentation in patients with ACS.     

The carotid plaque as paradigmatic case of site-specific acceleration of aging process: The microRNAs and the inflammaging contribution

Atherosclerosis is considered a chronic inflammatory disease of arteries associated with the aging process. Many risk factors have been identified and they are mainly related to life-styles, gene-environment interactions and socioeconomic status. Carotid and coronary artery diseases are the two major atherosclerotic conditions, being the primary cause of stroke and heart attack, respectively. Nevertheless, carotid plaque assumes particular aspects not only for the specific molecular mechanisms, but also for the types of atheroma which may be associated with a better or a worst prognosis. The identification of circulating blood biomarkers able to distinguish carotid plaque types (stable or vulnerable) is a crucial step for the improvement of adequate therapeutic approaches avoiding or delaying endarterectomy in the oldest old individuals (> 80 years), a population predicted to growth in the next years. The review highlights the most recent knowledge on carotid plaque molecular mechanisms, focusing on microRNAs (miRs), as a site-specific accelerated aging within the conceptual framework of Geroscience for new affordable therapies.