冠状动脉钙化患者钙化积分与年龄、性别的关系探讨

目的：探讨冠状动脉钙化（CAC）患者钙化积分与年龄、性别的关系。方法回顾性分析行冠状动脉 CT成像（CTA）检查的患者共3597例,将 CS＞1分为检测阳性的患者1422例按年龄分组对 CAC 进行数据统计分析。结果≤44岁、45岁～54岁、≥75岁年龄组差异无统计学意义（ P ＞0．05）;55岁～64岁、64岁～74岁年龄组差异有统计学意义（ P ＜0．05）。结论 CAC 患者钙化积分和年龄呈正相关,男性高于女性。     

血钙血磷水平与冠状动脉狭窄积分关系的探讨

冠状动脉粥样硬化的特点是受累动脉的病变从内膜开始,先后有多种病变合并存在,包括局部有脂质和复合糖类积聚、纤维组织增生和钙质沉着,并有动脉中层的逐渐退变,继发性病变尚有斑块内出血、斑块破裂及局部血栓形成。而冠状动脉粥样硬化是冠状动脉粥样硬化性心脏病（冠心病）的基本病变。检出冠状动脉钙化即意味着粥样硬化的存在,对冠心病的确定有重大意义。     

维持性血液透析患者的血磷水平与冠状动脉钙化的关系研究

<正>近年来,随着慢性肾脏病（CKD）发病率不断增高,进展至终末期肾脏病（ESRD）的患者数量也逐年攀升。维持性血液透析（MHD）作为目前ESRD患者重要的肾脏替代治疗方法,可使ESRD患者远期生存率较以往得到很大提升^[1-2]。ESRD透析的患者中普遍存在血管钙化现象,由此引发的心脑血管并发症是导致透析患者死亡的主要原因。血管钙化已成为患者心脑血管并发症高发和心血管事件增加的独立危险因素^[3-4]。近年来,随着一些新的无创检测手段如电子束CT、多排螺旋CT等广泛应用于临床,其在定性、定量研究血管钙化方面逐渐深入^[5-6]。研究发现,影响CKD患者血管钙化的因素错综复杂,     

冠状动脉CT造影评估冠状动脉钙化进展及临床意义

冠状动脉粥样硬化是冠心病的病理学基础,而冠状动脉钙化是粥样硬化病变的重要标志。检测和评估冠状动脉钙化不仅对预测心血管事件有重要意义,还有助于了解疾病进展,从而更好地指导临床诊治。冠状动脉CT造影(CCTA)是对冠状动脉钙化斑块进行精确量化评估的无创检查手段,其对于定量冠状动脉钙化以及预后评估具有重要的临床价值。本文对冠状动脉钙化CCTA检测方法及其临床应用等进行综述。     

冠状动脉钙化的研究进展

冠状动脉钙化（CAC）是动脉粥样硬化的特异性标志,也是粥样斑块负荷程度的标志。冠脉钙化程度与冠脉管腔狭窄程度存在一定相关性,冠脉钙化对心血管疾病的发病率和死亡率具有独立影响。随着各种无创心血管检查技术的进步,冠状动脉钙化的检测和度量更为精确可靠,因此,对冠状动脉钙化的研究有利于早期针对亚临床动脉粥样硬化的干预。     

无创评价冠心病患者冠状动脉病变范围与钙化积分的关系

无创冠状动脉CT血管成像(CCTA)广泛用于临床评价冠状动脉粥样硬化性心脏病(冠心病),在显示冠状动脉管壁情况上是强项,它是检测冠状动脉钙化(CAC)的最敏感工具之一。CAC是冠状动脉粥样硬化发展过程中某阶段的产物〔1〕,研究认为CAC对评价中度危险冠心病有重要意义。本研究采用辐射剂量更低,且具备更宽探测器、更强数据处理能力的320排     

冠状动脉钙化积分与冠心病危险因素的相关性分析

目的 探讨冠状动脉钙化积分与冠心病危险因素之间的相关性。方法 选择2020年4月至12月于江苏省太湖干部疗养院接受胸部低剂量CT检查的冠心病患者150例,其中有钙化者97例,无钙化者53例,检查后应用Agatston积分计算冠状动脉钙化积分。数据分析首先对两组间的一般资料进行比较,然后再以冠状动脉钙化积分为因变量,进行多因素Logistic回归分析。结果 钙化阳性组的年龄、甘油三酯、胆固醇、L-DLC、血糖明显高于钙化阴性组,差异具有统计学意义(P<0.05)。多因素Logistic回归分析显示,年龄(OR=1.062,95%CI 1.021～1.105,P=0.003)、甘油三酯(OR=7.091,95%CI 2.888～17.415,P=0.000)、L-DLC(OR=1.927,95%CI 1.136～3.269,P=0.015)、血糖(OR=1.403,95%CI 1.057～1.863,P=0.019)与冠状动脉钙化显著相关。在钙化组中,广泛钙化和中度钙化者居多。结论 冠状动脉钙化积分与年龄、甘油三酯、L-DLC、血糖等危险因素有关,冠状动脉钙化积分可作为冠心病预测、早...     

高龄患者冠状动脉钙化积分与慢性肾病的关系

目的 探讨高龄慢性肾病患者中冠状动脉钙化积分的严重程度.方法 采用多层螺旋计算机断层扫描进行冠脉钙化积分(CACS),入选研究对象158例,年龄(82.6±5.1)岁.结果 (1)在不调整其他心血管危险因素时,CACS分重度组与轻中度组比较,尿白蛋白/肌酐、估计肾小球滤过率(eGFR)水平均显著升高(P<0.05).(2)在调整心血管危险因素之后,CACS重度组eGFR水平仍低于对照组(P<0.001).(3)在调整心血管危险因素之后,慢性肾病eGFR≤60 ml·min-1·(1.73 m2)-1组CACS水平仍高于对照组(P=0.030).(4)CACS与eGFR呈负相关(r=-0.208.P<0.05).(5)eGFR每减少1个SD[30 ml·min-1·(1.73 m2)-1],发生严重CACS的危险增加1.03倍.而冠心病患者发生严重CACS的危险增加2.27倍.结论 冠脉重度钙化在高龄慢性肾病患者中较常见,并且与肾小球滤过率独立负相关.CACS严重程度是慢性肾病的独立危险因素.     

云南农村自然人群冠状动脉钙化情况的调查研究

目的 观察云南农村自然人群冠状动脉钙化及冠状动脉钙化积分情况.方法 对云南农村自然人群进行单纯随机抽样,采用16排螺旋CT对174例研究对象进行冠状动脉扫描,计算冠状动脉钙化,并应用Agatston积分法计算钙化积分,观察冠状动脉钙化及钙化积分的分布特征,按性别、年龄、种族进行分组,比较组间钙化率及钙化积分的差别.结果 174例入选研究对象中39例发现钙化(阳性率22.4％)及钙化积分≥l.51～60岁组、61～7l岁组钙化阳性率分别为15.5％、34.4％,钙化积分分别为11.2±52.4、38.0±82.0.钙化阳性率及钙化积分在不同年龄组间有显著性差异(P＜0.05),而在性别和种族之间无显著性差异.冠状动脉钙化阳性率为前降支＞回旋支=右冠状动脉＞左主干.结论 云南农村51～71岁自然人群中冠状动脉钙化及钙化积分存在年龄间的差异.钙化发生率最高在前降支,其次为回旋支和右冠状动脉.     

冠状动脉钙化积分与不稳定型心绞痛患者预后的关系

目的 探讨冠状动脉钙化积分(CCS)与不稳定型心绞痛(UA)患者冠状动脉病变严重程度的关系,以及CCS对经皮冠状动脉介入治疗(PCI)术后UA患者临床预后的预测价值.方法 回顾性分析2009年1月至2011年1月首次接受PCI术治疗的466例UA患者资料,入选患者均在术前接受心脏及冠状动脉320层螺旋CT检查并计算CCS.PCI术后对患者进行12个月的随访,记录术后有无死亡、非致命性心肌梗死、靶病变血运重建及再发心绞痛入院等主要心脏不良事件(MACE).结果 入选患者按CCS水平分为CCS≤100、100＜CCS≤400和CCS＞ 400组,CCS＞ 400组患者的冠状动脉多支病变比例、B2/C型病变比例及冠状动脉病变Gensini积分均显著高于另外两组患者(47.60％比29.70％比18.30％;45.00％比27.30％比15.70％;56.8±16.9比52.8±13.6比36.7±17.1;均为P＜0.05).随访12个月,Kaplan-Meier生存分析发现,CCS≤100、100＜ CCS≤400组和CCS＞ 400组患者累积无MACE事件生存率差异有统计学意义(88.2％比84.2％比77.2％,Logrank8.044,P=0.005),在校正了年龄后,多因素Cox回归分析显示CCS＞ 400是UA患者PCI术后MACE发生的独立预测因子.CCS ＞400组患者较CCS≤100组术后发生MACE的风险增加4.741倍(RR =4.741,P＜0.01).结论 UA患者CCS水平越高表明冠状动脉病变越严重,CCS升高是接受PCI治疗的UA患者临床预后不良的强有力预测因子.     

Longitudinal Relationships among Coronary Artery Calcification,Serum Phosphorus,and Kidney Function

Background and objectives: Coronary artery calcification (CAC) is common in advanced chronic kidney disease (CKD), yet its onset and time course are uncertain. The study objective was to assess longitudinal relationships among CAC, kidney function, and traditional and putative cardiovascular disease (CVD) risk factors.Design, setting, participants, & measurements: This is a prospective cohort analysis from the Spokane Heart Study, a long-term observational study of community-dwelling adults who were assessed every 2 yr for CAC (electron-beam computed tomography), CVD risk factors, and laboratory testing. Estimated GFR (eGFR) was determined by the reexpressed Modification of Diet in Renal Disease equation.Results: CAC was present in 28% (245 of 883) at baseline. After 6 yr, new-onset CAC developed in 33% (122 of 371); severity increased from a median CAC score of 38 to 152 in those with baseline CAC. Neither eGFR (101 ± 34 versus 104 ± 31 ml/min per 1.73 m², respectively) nor serum phosphorus (3.25 ± 0.49 versus 3.29 ± 0.48 mg/dl, respectively) differed by CAC presence or absence at baseline; however, multivariate models (generalized estimating equations for incidence and prevalence) revealed that independent predictors of CAC over time were greater baseline CAC scores, higher serum phosphorus levels, lower eGFR levels, and traditional CVD risk factors. Each 1-mg/dl increase in phosphorus imparted odds ratios for CAC of 1.61 (incidence) and 1.54 (prevalence), risks comparable to traditional CVD risk factors.Conclusions: CAC becomes more frequent and severe over time. Higher levels of serum phosphorus and reduced kidney function independently predicted CAC.When kidney function declines, death from cardiovascular disease (CVD) predominates over progression of chronic kidney disease (CKD) (1–3). Excess CVD risk even in early-stage CKD is not fully explained by traditional, Framingham-type CVD risk factors. In ESRD, coronary artery calcification (CAC) is a common finding associated with clinical CVD (4). In ESRD, the extent of CAC is related to serum phosphorus and the calcium-phosphorus product along with traditional CVD risk factors (4,5). Many years ago, a meticulous autopsy study of hemodialysis patients described a distinctive coronary artery pathology characterized by medial calcification (6). Vascular pathology was similar in nondialysis patients with CKD, but arterial calcification was less frequent and severe (6). Although CAC appears before ESRD, its onset and time course in relation to decreased kidney function are unknown.Experimental models point to hyperphosphatemia, a hallmark of bone and mineral metabolism disorders in CKD, as a potential causal link to vascular calcification. Uremic rodents are protected from developing aortic calcification and/or atherosclerotic lesions by treatment with noncalcemic phosphate binders (7,8). In gene knockout models for phosphorus-regulating factors, fibroblast growth factor 23, or Klotho, nonuremic mice develop elevated serum phosphorus levels and vascular calcification (9,10). Observational studies of people with and without clinically apparent kidney disease also show that higher serum phosphorus levels within the “normal” range are associated with clinical CVD and CAC (11–14). The study objective was to assess longitudinal relationships among CAC, kidney function, and traditional and putative CVD risk factors, including serum phosphorus, among participants in the Spokane Heart Study, a long-term observational study of adults in the community.     

Association of Serum Alkaline Phosphatase with Coronary Artery Calcification in Maintenance Hemodialysis Patients

Background and objectives: Recent in vitro studies have shown a link between alkaline phosphatase and vascular calcification in patients with chronic kidney disease (CKD). High serum levels of alkaline phosphatase are associated with increased death risk in epidemiologic studies of maintenance hemodialysis (MHD) patients. We hypothesized that coronary artery calcification is independently associated with increased serum alkaline phosphatase levels in MHD patients.Design, setting, participants, & measurements: We examined the association of coronary artery calcification score (CACS) and alkaline phosphatase in 137 randomly selected MHD patients for whom markers of malnutrition, inflammation, and bone and mineral disorders were also measured.Results: Serum alkaline phosphatase was the only measure with significant and robust association with CACS (P < 0.003), whereas either other biochemical markers had no association with CACS or their association was eliminated after controlling for case-mix variables. Serum alkaline phosphatase >120 IU/L was a robust predictor of higher CACS and was particularly associated with the likelihood of CACS >400 (multivariate odds ratio 5.0 95% confidence interval 1.6 to 16.3; P = 0.007). Serum alkaline phosphatase of approximately 85 IU/L seemed to be associated with the lowest likelihood of severe coronary artery calcification, but in the lowest tertile of alkaline phosphatase, the CACS predictability was not statistically significant.Conclusions: An association between serum alkaline phosphatase level and CACS exists in MHD patients. Given the high burden of vascular calcification in patients with CKD, examining potential therapeutic interventions to modulate the alkaline phosphatase pathway may be warranted.Vascular calcification is common in individuals with chronic kidney disease (CKD) and is a significant correlate of the high cardiovascular death risk (1–3). Both intimal and medial calcification are observed frequently in patients with CKD (4–7). Several mechanisms have been implicated for the high prevalence of vascular calcification in CKD, including the high burden of conventional cardiovascular risks such as diabetes, hypertension, and dyslipidemia; bone and mineral disorders such as calcium load and secondary hyperparathyroidism (SHPT); chronic inflammation such as high level of proinflammatory cytokines; and deficiency of anticalcemic factors such as fetuin (8,9). Lomashvili et al. (5) reported that vascular damage can induce expression of tissue-nonspecific alkaline phosphatase (AlkPhos), which per se hydrolyzes and inactivates inorganic pyrophosphates, a process that can enhance vascular calcification. We recently showed that higher serum AlkPhos levels in maintenance hemodialysis (MHD) patients were independently associated with increased all-cause and cardiovascular mortality in approximately 74,000 MHD patients, even after adjustment for surrogates of nutrition, inflammation, minerals, serum parathyroid hormone (PTH), and liver enzymes (10). Nevertheless, the pathophysiologic link between increased AlkPhos level and mortality in MHD patients is not clear. Given the recent in vitro findings about the link between AlkPhos and vascular calcification via the pyrophosphate pathway, we hypothesized that the increased cardiovascular and all-cause death risk observed in the setting of high serum AlkPhos level may be related to vascular calcification in MHD patients (6,11). To test this hypothesis, we examined the association of serum AlkPhos and coronary artery calcification in a cohort of MHD patients for whom other risk factors of cardiovascular disease including inflammatory markers were also examined.     

Coronary Artery Calcification

Coronary artery calcification (CAC) is an established marker of subclinical atherosclerosis and an independent predictor of future coronary heart disease in the asymptomatic primary prevention population, particularly in the intermediate risk cohort. CAC also helps in reclassifying those patients and their risk of cardiovascular events into higher or lower risk categories. MESA (Multi-Ethnic Study of Atherosclerosis) is a National Heart, Lung, and Blood Institute–sponsored population-based medical research study involving 6,814 men and women from 6 U.S. communities without a medical history of clinical cardiovascular disease. The evidence from this population cohort revealed that CAC scoring was independently predictive and highly effective at risk stratification of major adverse cardiac events. This review provides available data based on MESA. We focus on the utility of CAC for cardiovascular disease risk stratification of individuals, and we describe its diagnostic value in identifying patients at risk.     

冠状动脉钙化研究进展

冠状动脉钙化越来越受到重视,发现钙化即意味着亚临床动脉粥样硬化的存在,而动脉硬化不一定都有钙化。通常钙化越严重,冠脉管腔狭窄程度也就越高。但有时二者却缺乏很好的相关性。现就冠脉钙化的发生机制,冠脉钙化及积分与冠心病及其严重程度的关系,冠脉钙化检测方法及积分,血管重构在严重的冠脉钙化却没有明显的管腔狭窄中的作用等方面做一综述。     

冠状动脉钙化研究进展

冠状动脉钙化(CAC)是导致一般人群和冠状动脉性心脏病患者不良结局的危险因素。CAC的发病机制和骨形成有共同的途径,目前已经确定了一些导致CAC发生和发展的危险因素。用药物治疗控制CAC的努力没有取得成功,而冠状动脉钙化的患者经皮冠脉介入术和冠状动脉搭桥术后的无事件生存率也较低。虽然应用药物洗脱支架和斑块修饰装置对钙化血管的预后有一定改善,但不良事件发生率仍然很高。在未来,仍需创新的药物和器械治疗来改善CAC患者的不良预后。     

Serum Uric Acid Is Associated With Coronary Artery Calcification

Uric acid (UA) is associated with atherosclerosis, and coronary artery calcium (CAC) is a marker of atherosclerosis. The authors studied the association between UA and CAC. A total of 663 asymptomatic patients (564 men; mean age, 55±7 years) were evaluated for the presence of CAC. The study population was divided into three tertiles according to their UA levels, and the prevalence of CAC was compared between the tertiles. CAC was detected in 349 (53%) patients. Levels of UA were significantly higher in those with CAC than in those without CAC (5.6+1.2 vs 5.3+1.3; P=.003). The odds ratio for the presence of CAC in the highest vs lowest UA tertile was 1.72 (95% confidence interval, 1.17–2.51). The highest UA tertile remained associated with the presence of CAC after adjustment for known cardiovascular risk factors. The results show that high serum UA levels are associated with the presence of CAC.     

Association Between Nonalcoholic Fatty Liver Disease and Coronary Artery Calcification

Background  

Both nonalcoholic fatty liver disease (NAFLD) and coronary artery disease (CAD) are closely related to many metabolic disorders. Multislice computed tomography (MSCT) is a reliable noninvasive method in demonstrating coronary plaque. However, the association between coronary artery calcium (CAC) score and NAFLD remains controversial.