Recurrent ST-Elevation Myocardial Infarction (STEMI) in Coronary Artery Aneurysm Secondary to Atherosclerosis.

We describe a rare case of coronary artery aneurysm (CAA) with recurrent ST-elevation myocardial infarction (STEMI) despite being on standard dual antiplatelet therapy (DAPT). A 47-year-old male presented with chest pain and was found to have inferior wall STEMI along with diffuse right coronary artery (RCA) ectasia and proximal RCA aneurysm, thrombotic occlusion, and dissection. He was managed with extensive thrombectomy, angioplasty, prolonged Heparinization, and DAPT. The patient went on to have a similar presentation nine months later with a recurrent inferior wall STEMI with proximal RCA aneurysm and thrombotic occlusion managed with thrombectomy and bare metal stent placement. He was placed on long-term anticoagulation and DAPT with no further recurrence of MI reported on follow-up.

European Stroke Organisation guidelines on treatment of patients with intracranial atherosclerotic disease.

The aim of the present European Stroke Organisation guideline is to provide clinically useful evidence-based recommendations on the management of patients with intracranial atherosclerotic disease (ICAD). The guidelines were prepared following the Standard Operational Procedure of the European Stroke Organisation guidelines and according to GRADE methodology. ICAD represents a major cause of ischemic stroke worldwide, and patients affected by this condition are exposed to a high risk for future strokes and other major cardiovascular events, despite best medical therapy available. We identified 11 relevant clinical problems affecting ICAD patients and formulated the corresponding Population Intervention Comparator Outcomes (PICO) questions. The first two questions refer to the asymptomatic stage of the disease, which is being increasingly detected thanks to the routine use of noninvasive vascular imaging. We were not able to provide evidence-based recommendations regarding the optimal detection strategy and management of asymptomatic ICAD, and further research in the field is encouraged as subclinical ICAD may represent a big opportunity to improve primary stroke prevention. The second block of PICOs (3-5) is dedicated to the management of acute large vessel occlusion (LVO) ischemic stroke caused by ICAD, a clinical presentation of this disease that is becoming increasingly relevant and problematic, since it is associated with more refractory endovascular reperfusion procedures. An operational definition of probable ICAD-related LVO is proposed in the guideline. Despite the challenging context, no dedicated randomized clinical trials (RCTs) were identified, and therefore the guideline can only provide with suggestions derived from observational studies and our expert consensus, such as the escalated use of glycoprotein IIb-IIIa inhibitors and angioplasty/stenting in cases of refractory thrombectomies due to underlying ICAD. The last block of PICOs is devoted to the secondary prevention of patients with symptomatic ICAD. Moderate-level evidence was found to recommend against the use of oral anticoagulation as preferred antithrombotic drug, in favor of antiplatelets. Low-level evidence based our recommendation in favor of double antiplatelet as the antithrombotic treatment of choice in symptomatic ICAD patients, which we suggest to maintain during 90 days as per our expert consensus. Endovascular therapy with intracranial angioplasty and or stenting is not recommended as a treatment of first choice in high-grade symptomatic ICAD (moderate-level evidence). Regarding neurosurgical interventions, the available evidence does not support their use as front line therapies in patients with high-grade ICAD. There is not enough evidence as to provide any specific recommendation regarding the use of remote ischemic conditioning in ICAD patients, and further RCTs are needed to shed light on the utility of this promising therapy. Finally, we dedicate the last PICO to the importance of aggressive vascular risk factor management in ICAD, although the evidence derived from RCTs specifically addressing this question is still scarce.

Association between parents' socioeconomic conditions and nutritional status during childhood and the risk of cardiovascular disease in their adult offspring: an intergenerational study in south India.

BACKGROUND: Some researchers have suggested that parents' exposure to poor socioeconomic conditions during childhood can increase their offspring's risk of cardiovascular disease, primarily through poor maternal nutrition and growth. However, epidemiological data on this association are limited. In an intergenerational cohort from rural India, we examined the association of parental childhood socioeconomic conditions and stature with offspring's cardiovascular risk, hypothesising an inverse association between the two. METHODS: We analysed data on 3175 adult offspring (aged 18-35 years, 58% men) and their parents from the third wave of the Andhra Pradesh Children and Parents' Study (2010-12). We used multilevel linear regression to estimate the association of parents' Standard of Living Index (SLI, an asset-based measure of socioeconomic conditions) in childhood, height and leg length with subclinical atherosclerosis and cardiovascular risk factors in their offspring. RESULTS: In multivariable models adjusted for offspring's socioeconomic conditions in childhood and adulthood, associations (beta coefficients and 95% CIs) of mother's and father's childhood SLI (per SD) were -0.00 mm (-0.01, 0.01) and 0.01 mm (-0.00, 0.02) for carotid intima media thickness, -0.17 mm Hg (-0.61, 0.27) and -0.30 mm Hg (-0.78, 0.20) for systolic blood pressure, -0.43 mg/dL (-2.00, 1.15) and -1.07 mg/dL (-2.79, 0.65) for total cholesterol and -0.00mU/L (-0.04, 0.03) and 0.01mU/L (-0.03, 0.04) for log fasting insulin. Results were of similar magnitude for parental height and leg length. CONCLUSIONS: Our findings do not support an inverse association between parental childhood socioeconomic conditions or stature and offspring's risk of cardiovascular disease. Intergenerational socioeconomic influences on cardiovascular risk may be of limited public health significance for this setting.

Data Processing Pipeline for Lipid Profiling of Carotid Atherosclerotic Plaque with Mass Spectrometry Imaging.

Atherosclerosis is a lipid and inflammation-driven disease of the arteries that is characterized by gradual buildup of plaques in the vascular wall. A so-called vulnerable plaque, consisting of a lipid-rich necrotic core contained by a thin fibrous cap, may rupture and trigger thrombus formation, which can lead to ischemia in the heart (heart attack) or in the brain (stroke). In this study, we present a protocol to investigate the lipid composition of advanced human carotid plaques using matrix-assisted laser desorption ionization (MALDI) mass spectrometry imaging (MSI), providing a framework that should enable the discrimination of vulnerable from stable plaques based on lipid composition. We optimized the tissue preparation and imaging methods by systematically analyzing data from three specimens: two human carotid endarterectomy samples (advanced plaque) and one autopsy sample (early stage plaque). We show a robust data reduction method and evaluate the variability of the endarterectomy samples. We found diacylglycerols to be more abundant in a thrombotic area compared to other plaque areas and could distinguish advanced plaque from early stage plaque based on cholesteryl ester composition. We plan to use this systematic approach to analyze a larger dataset of carotid atherosclerotic plaques.

Estimating the performance of three cardiovascular disease risk scores: the Estonian Biobank cohort study.

BACKGROUND: We aim to investigate the predictive ability of PCE (Pooled Cohort Equations), QRISK2 and SCORE (Systematic COronary Risk Estimation) scoring systems for atherosclerotic cardiovascular disease (ASCVD) risk prediction in Estonia, a country with one of the highest ASCVD event rates in Europe. METHODS: Seven-year risk estimates were calculated in risk score-specific subsets of the Estonian Biobank cohort. Calibration was assessed by standardised incidence ratios (SIRs) and discrimination by Harrell's C-statistics. In addition, a head-to-head comparison of the scores was performed in the intersection of the three score-specific subcohorts. RESULTS: PCE, QRISK2 and SCORE risk estimates were calculated for 4356, 7191 and 3987 eligible individuals, respectively. During the 7-year follow-up, 220 hard ASCVD events (PCE outcome), 671 ASCVD events (QRISK2 outcome) and 94 ASCVD deaths (SCORE outcome) occurred among the score-specific subsets of the cohort. While PCE (SIR 1.03, 95% CI 0.90 to 1.18) and SCORE (SIR 0.99, 95% CI 0.81 to 1.21) were calibrated well for the cohort, QRISK2 underestimated the risk by 48% (SIR 0.52, 95% CI 0.48 to 0.56). In terms of discrimination, PCE (C-statistic 0.778) was inferior to QRISK2 (C-statistic 0.812) and SCORE (C-statistic 0.865). All three risk scores performed at similar level in the head-to-head comparison. CONCLUSION: Of three widely used ASCVD risk scores, PCE and SCORE performed at acceptable level, while QRISK2 underestimated ASCVD risk markedly. These results highlight the need for evaluating the accuracy of ASCVD risk scores prior to use in high-risk populations.

Association between short sleep duration and carotid atherosclerosis modified by age in a Chinese community population.

BACKGROUND AND AIM: Short sleep duration is a risk factor of cardiovascular disorder; however, the association between short sleep duration and carotid atherosclerosis has not been completely characterised. The aim of this study is to investigate the association between short sleep duration and carotid atherosclerosis. METHODS: We used the cross-sectional data collected between May 2014 and July 2014, which were based on a cardiovascular disease cohort study including 3798 participants aged 40 years and older who are residents of Beijing, China. We used logistic regression models to examine the associations between sleep duration and carotid atherosclerosis. RESULTS: After the adjustment of covariates, short sleep duration (less than 5 hours per night) was found to be associated with carotid atherosclerosis, and it also elevated the risk of, in both terms, the increment of prevalence (OR=1.31, P<0.05) and the quantity of carotid plaques (OR=1.28, P<0.05). When age was also taken into consideration, the largest association, in both terms of prevalence (OR=3.46, P<0.01) and the number of carotid plaques (OR=4.23, P<0.01), was found in subjects over the age of 60 with short sleep duration. CONCLUSION: In conclusion, sleep duration less than 5 hours per night is associated with a higher risk of carotid atherosclerosis compared with subjects who sleeps for 5 or over 5 hours per night, and the association may be modified by age.

Periodontitis is an independent risk indicator for atherosclerotic cardiovascular diseases among 60†174 participants in a large dental school in the Netherlands.

BACKGROUND: The association between periodontitis and atherosclerotic cardiovascular diseases (ACVD) has been established in some modestly sized studies (<10 000). Rarely, however, periodontitis has been studied directly; often tooth loss or self-reported periodontitis has been used as a proxy measure for periodontitis. Our aim is to investigate the adjusted association between periodontitis and ACVD among all individuals registered in a large dental school in the Netherlands (Academic Centre for Dentistry Amsterdam (ACTA)). METHODS: Anonymised data were extracted from the electronic health records for all registered patients aged >35 years (period 1998-2013). A participant was recorded as having periodontitis based on diagnostic and treatment codes. Any affirmative answer for cerebrovascular accidents, angina pectoris and/or myocardial infarction labelled a participant as having ACVD. Other risk factors for ACVD, notably age, sex, smoking, diabetes, hypertension, hypercholesterolaemia and social economic status, were also extracted. Logistic regression analyses were used to evaluate the adjusted associations between periodontitis and ACVD. RESULTS: 60 174 individuals were identified; 4.7% of the periodontitis participants (455/9730) and 1.9% of the non-periodontitis participants (962/50 444) reported ACVD; periodontitis showed a significant association with ACVD (OR 2.52; 95% CI 2.3 to 2.8). After adjustment for the confounders, periodontitis remained independently associated with ACVD (OR 1.59; 95% CI 1.39 to 1.81). With subsequent stratification for age and sex, periodontitis remained independently associated with ACVD. CONCLUSIONS: This cross-sectional analysis of a large cohort in the Netherlands of 60 174 participants shows the independent association of periodontitis with ACVD.

[Accelerated artherosclerosis in systemic lupus erythematosus patients and the role of some adipocytokines in this process].

The most severe forms of systemic lupus erythematosus (SLE) affect the kidneys, peripheral and central nervous system as well as heart and vessels. The underlying causes of heart and circulatory system disease are atherosclerosis, vasculitis and thromboembolic disorders; all these processes are interrelated. Premature atherosclerosis, the etiology of which remains incompletely accounted for, is of particular interest. Recently, some adipocytokines / adipokines have been indicated in the development of atherosclerosis, inflammatory and immune processes. It has been postulated that adipokines might regulate the immune response and hence also the atherogenic process.

Expression of JAK2/STAT3 signaling pathway in human umbilical vein endothelial cells exposed to the serum of type 2 diabetic macroangiopathy patients / 第二军医大学学报

Objective To investigate the role of Janus kinase 2/signal transducer and activator of transcription 3(JAK2/STAT3) signaling pathway in the pathogenesis of type 2 diabetic macroangiopathy. Methods The human umbilical vein endothelial cells (HUVECs) were incubated for 24 h with the serum of healthy volunteers, simple type 2 diabetic patients and patients with type 2 diabetic macroangiopathy. JAK2 specific inhibitor AG490 was used to block the JAK2/STAT3 signaling pathway. According to different treatments, the cells were divided into normal control group (NC group, n=30), simple diabetes mellitus group (DM group, n=30), type 2 diabetic macroangiopathy group (DV group, n=30), DM+AG490 group (DM+AG490 group, n=30) and DV+AG490 group (DV+AG490 group, n=30). Real-time quantitative PCR technique was used to detect the mRNA expression of JAK2, STAT3, vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor (FLT1) in each group. Western blotting analysis was used to detect the protein expression of JAK2, STAT3 and phosphorylated STAT3(p-STAT3). Results Compared with the NC group, the expression of JAK2, STAT3 mRNA and JAK2, and p-STAT3 protein were significantly up-regulated in DM and DV groups (P<0.05), and the expression of JAK2, STAT3 mRNA and JAK2, p-STAT3 protein in DV groups were significantly higher than those in DM group (P< 0.05). The expression of JAK2, STAT3 mRNA and JAK2, p-STAT3 protein in DM+AG490 group and DV+AG490 group were significantly lower than those in the DM group and DV group (P< 0.05). Compared with the NC and DM group, the expression of VEGF, FLT1 mRNA was significantly up-regulated in DV group(P<0.05). Compared with the DV group, the expression of VEGF and FLT1mRNA were significantly reduced in DV+AG490 group (P< 0.05). Conclusion JAK2/STAT3 signaling pathway may play a role in the pathogenesis of type 2 diabetic macroangiopathy.

Ambient air pollution and racial/ethnic differences in carotid intima-media thickness in the Multi-Ethnic Study of Atherosclerosis (MESA).

BACKGROUND: In the USA, ethnic disparities in atherosclerosis persist after accounting for known risk factors. Ambient air pollution is associated with increased levels of atherosclerosis and differs in the USA by race/ethnicity. We estimated the influence of ambient air pollution exposure to ethnic differences in common carotid intima-media thickness (IMT). METHODS: We cross-sectionally studied 6347 Caucasian-American, African-American, Hispanic and Chinese adults across 6 US cities in 2000-2002. Annual ambient air pollution concentrations (fine particulate matter [PM2.5] and oxides of nitrogen [NOX]) were estimated at each participant's residence. IMT was assessed by ultrasound. RESULTS: The mean IMT was 19.4 and 37.6 µm smaller for Hispanic women and men, 53.6 and 7.1 µm smaller for Chinese women and men, and 23.4 and 38.7 µm higher for African-American women and men compared with Caucasian-American women and men. After adjustment for PM2.5, the differences in IMT remained similar for Hispanic and African-American participants but was even more negative for Chinese participants (mean IMT difference of -58.4 µm for women and -15.7 µm for men) compared with Caucasian-American participants. The IMT difference in Chinese participants compared with Caucasian-American participants related to their higher PM2.5 exposures was 4.8 µm (95% CI 0.2 to 10.8) for women and 8.6 µm (95% CI 3.4 to 15.3) for men. NOX was not related to ethnic differences in IMT. CONCLUSIONS: The smaller carotid IMT levels in Chinese participants were even smaller after accounting for higher PM2.5 concentrations in Chinese participants compared with Caucasian-American participants. Air pollution was not related to IMT differences in African-American and Hispanic participants compared with Caucasian-American participants.

[Assessment of progression and regression of coronary atherosclerosis by coronary angiography]. / Koronarangiographie zur Analyse einer Progression und Regression der koronaren Atherosklerose.

Quantitative coronary angiography (QCA) has been used for many years to study therapy effects. This became possible after a very high standardization of computer-assisted evaluation of coronary angiograms was introduced. The results of studies with various medications showed that the progression of coronary atherosclerosis could actually be inhibited. Reports on regression were rare and were in the range of 10 % of patients who showed such a response. In recent years only a few studies were carried out with QCA to test the effects of medications. Intravascular ultrasound is the new gold standard for recording coronary atherosclerosis. First rosuvastatin, later fluvastatin and simvastatin and recently rosuvastatin and atorvastatin were tested. Related to the progression and regression of coronary artery sclerosis, the data demonstrated that below a low-density lipoprotein (LDL) cholesterol threshold of 80 mg/dl patients developed regression and above this level progression was predominantly found. These results were similar to the studies using intravascular ultrasound; however, progression and regression are also related to the level of high density lipoprotein (HDL) cholesterol similar again to the level, which could be detected by intravascular ultrasound. Thus, not only intravascular ultrasound but also QCA should be used to study drug interactions with coronary atherosclerosis and particularly when new drugs are compared to statins.

Relationship between C-peptide and artherosclerosis in lower extremity in patients with type 2 diabetes / 实用医学杂志

Objective To investigate the relationship between C-peptide and artherosclerosis in lower ex-tremity in patients with type 2 diabetes. Methods Two hundred and fourteen type 2 diabetic patients were included in this retrospective study. They were divided into two groups:type 2 diabetes with artherosclerosis in lower extremi-ty in 123 cases and type 2 diabetes without artherosclerosis in lower extremity in 91 cases. Their medical history and the laboratory data were collected such as fasting serum C-peptide levels and postprandial serum C-peptide levels of 1 hour, 2 hours and 3 hours, glycated hemoglobin (HbA1c) and so on. Results Compared with artherosclerosis group in lower extremity, the age, duration of diabetes, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), glycated hemoglobin and smoking rate were significantly higher in type 2 diabetes without artherosclero-sis in lower extremity (P 0.05). Logistic regression analysis showed that fasting and postprandial (1 hour, 2 hours and 3 hours)serum C-pep-tide levels were all negatively related to artherosclerosis in lower extremity (OR 0.524,P = 0; OR 0.440, P = 0;OR 0.688, P=0;OR 0.795, P=0). Conclusions Serum C-peptide level may be an independent associated fac-tor with artherosclerosis in lower extremity in type 2 diabetes.

Blood viscosity in subcortical vascular mild cognitive impairment with versus without cerebral amyloid burden.

BACKGROUND: Subcortical vascular dementia (SVaD) is a common form of dementia, attributed to ischemic small-vessel disease. Blood viscosity (BV) may contribute to the pathophysiology of SVaD. However, SVaD patients with coexisting amyloid deposition may not show differences in BV because their small-vessel disease may result from amyloid angiopathy independently of BV. We, therefore, hypothesized that BV might show different changes compared with control subjects in subcortical vascular mild cognitive impairment (svMCI) that refers to the prodromal stage of SVaD according to cerebral amyloid burden detected by the [(11)C] Pittsburgh compound B (PiB) PET (positron emission tomography), and apolipoprotein 4 (ApoE4) genotype (a known risk factor for vascular and parenchymal amyloid). METHODS: Our subjects consisted of 33 healthy normal controls (NC), 28 patients with PiB(-) svMCI, and 12 with PiB(+) svMCI. They underwent scanning capillary tube viscometer measuring BV during systolic and diastolic phases. RESULTS: Compared with the NC group, the PiB(-) svMCI group showed increased diastolic blood viscosity (DBV) but no difference in systolic blood viscosity (SBV). By contrast, there was no significant difference in SBV and DBV between the NC and PiB(+) svMCI groups. Within the PiB(+) svMCI group, ApoE4(-) subgroup showed increased DBV compared with the ApoE4(+) subgroup. CONCLUSIONS: Increased DBV is an important contributor to the development of "pure" svMCI (ie, without cerebral amyloid deposition). The relationship between BV and PiB(+) svMCI differed according to ApoE genotype, suggesting that the pathogenesis of PiB(+) svMCI might also be heterogeneous.

Ischemic bowel disease and risk of stroke: a one-year follow-up study.

BACKGROUND: Ischemic bowel disease and stroke have been noted to have shared pathomechanisms. However, data regarding the stroke occurrence following ischemic bowel disease are still lacking. AIM: The aim of this study is to explore the risk of stroke in patients with ischemic bowel disease during a one-year follow-up period in Taiwan. METHODS: Data used in this study were retrieved from the 'Longitudinal Health Insurance Database 2000. Five hundred sixty-nine patients hospitalized with ischemic bowel disease were included as the study group, and 3414 subjects, matched by age and gender, were randomly extracted as a comparison group. Cox proportional hazards regression analysis was performed to test the relationship of ischemic bowel disease and subsequent stroke during the one-year follow-up period. RESULTS: The incidence rate of stroke among the sampled subjects during the 30-day, 90-day, and 365-day follow-up period was 1·24, 0·76, and 0·43 per 10 person-years. The adjusted hazard ratio for stroke for those patients with ischemic bowel disease within 30-, 90-, and 365-day follow-up periods was found to be 3·71 (95% confidence interval = 1·89-7·27), 2·11 (95% confidence interval = 1·22-3·66), and 1·70 (95% confidence interval = 1·14-2·52) times that of matched comparisons, respectively. The adjusted hazard ratio of ischemic stroke for patients with ischemic bowel disease was found to be 5·29 during the 30-day follow-up period than comparisons. CONCLUSIONS: We found ischemic bowel disease to be significantly associated with stroke occurrence.

Clinical effect of amlodipine atorvastatin calcium in the treatment of hypertensive patients with dyslipidemia / 中国基层医药

Objective To investigate the treatment effect of amlodipine atorvastatin calcium for hypertensive patients with dyslipidemia.Methods The clinical data of 200 hypertensive patients with dyslipidemia were retrospectively studied.They were divided into the control group and the intervention group according to treatment method,100 cases in each group.The control group was given amlodipine besylate based on the conventional treatment,the intervention group was treated with amlodipine besylate and atorvastatin calcium tablets.The clinical effect was observed and compared between the two groups.Results After treatment,the systolic and diastolic blood pressure of the two groups were significantly lower than before treatment (t =4.57,5.32,4.72,4.61,all P ＜ 0.05) ; After treatment,IMT and plaque area of the two groups were obviously lower than before treatment(t =3.16,3.43,all P ＜ 0.05) ;After treatment,IMT and plaque area of the intervention group were (0.71 ± 0.29) mm and (1 t.13 ± 3.61) mm2,which were significantly lower than those of the control group [(0.82 ± 0.26) mm and (13.64 ± 2.86) mm2] (t =3.28,4.05,all P ＜ 0.05).Conclusion Amlodipine besylate and atorvastatin calcium tablets can effectively reduce hypertension,which has good synergistic effect and protective effect on blood vessels.

Effects of statin reloading before percutaneous coronary intervention on circulatory endothelial progenitor cells and inflammatory cytokines / 中国病理生理杂志

AIM:To investigate the effects of atorvastatin reloading in pre-percutaneous coronary intervention ( PCI) period on endothelial progenitor cell ( EPC) count and inflammatory cytokine expression in the stable angina pectoris patients who had previously received long-term statin treatment.METHODS:The patients with stable angina pectoris that had received long-term statin therapy and planned to accept PCI were randomized into 3 groups:80 mg atorvastatin 12 h and 40 mg 2 h before coronary angioplasty (80 mg reloading), pre-operatively with 40 mg/d atorvastatin for 7 d (40 mg re-loading) , and without atorvastatin reloading ( no reloading ) .CD45 -/CD133+/CD34 +, CD45 -/CD34 +/KDR+ and CD45 -/CD144 +/KDR+EPCs in 100 μL peripheral blood were determined by flow cytometry 1 h prior to PCI and 1 h, 6 h and 24 h after PCI.The serum concentrations of soluble intercellular adhesion molecule 1 ( sICAM-1) , C-reactive protein ( CRP) and troponin I ( TnI) were analyzed immediately prior to and 24 h after PCI.RESULTS:(1) In 80 mg reloading group, the numbers of circulating CD45 -/CD133 +/CD34 +and CD45 -/CD34 +/KDR+early differentiation stage EPCs 1 h and 6 h after coronary angioplasty was significantly elevated compared with those before PCI (P<0.05).(2) In control group, the serum concentrations of sICAM-1 and CRP 24 h after PCI were significantly elevated ( P<0.05) compared with preoperative values.(3) The rise in serum TnI concentration from pre-to post-operation in 80 mg reloading group was lowerthan that in control group.CONCLUSION: The method of atorvastatin reload before PCI affects the number of EPCs inperi-operative period.High dose of atorvastatin application before PCI triggers early EPC circulation.The serum levels ofpost-operative inflammatory cytokine sICAM-1 as well as CRP are reduced by atorvastatin reloading before PCI.

Factores de riesgo de la cardiopatía isquémica / Risk factors in ischemic heart disease

Introducción: la enfermedad arterial coronaria es una de las principales causas de mortalidad en todo el mundo. En su fisiopatología juega un papel importante el desarrollo y la progresión de la aterosclerosis coronaria, la cual está íntimamente relacionada con determinados hábitos de vida y ciertas características personales que se conocen como factores de riesgo. Objetivo: actualizar a los profesionales de la Atención Primaria de Salud sobre los factores de riesgo de la Cardiopatía Isquémica. Métodos: se realizó una revisión bibliográfica en libros de Medicina y artículos científicos disponibles en revistas digitales, a través de buscadores de información. Se accedió a diferentes fuentes de información como bases de datos, libros electrónicos, revistas electrónicas, etcétera, de infomed e internet. Luego se hizo un análisis crítico sobre el tema, avalado por la en contrado en la literatura consultada. Desarrollo: la situación de las enfermedades cardiovascularesen el mundo ha pasado por distintas fases, en correspondencia con el desarrollo socioeconómico de los países y el aumento en la incidencia de los distintos factores de riesgo, los cuales influyen de manera diferente en la aparición de la Cardiopatía Isquémica. Conclusiones: es importante conocer la influencia de cada factor de riesgo cardiovascular en la aparición de la Cardiopatía Isquémica para tomar estrategias encaminadas al control de los mismos y evitar llegar a la enfermedad...

Introduction: coronary artery disease is one of the main causes of mortality worldwide. An important role in the physiopathology of this disease is played by the development and progression of coronary artherosclerosis which is closely related to certain life habits and individual characteristics known as risk factors. Objective: to provide the primary health care professionals with an updating on the risk factors of ischemic heart disease. Method: a literature review including medical books and scientific articles from on line journals was made through the use of information searchers. It was possible to have access to several sources of information such as databases, electronic books, electronic journals, etc from Infomed and Internet. Finally, a critical analysis of the topic, supported on the findings of this literature, was made. Discussion: the situation of cardiovascular diseases worldwide has undergone several phases according to the social and economic development of the nations and the increase of the incidence of a number of factors affecting in different ways the occurrence of ischemic heart disease. Conclusions: it is important to know about the influence of each cardiovascular risk factor over the occurrence of ischemic heart disease in order to draw strategies for their control and to prevent the disease...

The urotensin II receptor antagonist, urantide, protects against atherosclerosis in rats.

The aim of this study was to explore the use of urantide as an antagonist of the urotensin II (UII) receptor, G protein-coupled receptor 14 (GPR14), to protect against atherosclerosis (AS) in rats. The AS rat model was induced by an intraperitoneal injection of vitamin D3 (VD3) into rats fed with a high-fat diet for four weeks. Urantide was then injected into the rats. Immunohistochemical staining, serum biochemical assay, reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to investigate the expression of UII and its receptor GPR14 in the AS rat model. Four weeks after induction, pathological changes typical of AS were observed in the AS rat model. In the plaques of the aortic tunica intima and tunica media, expression of UII and GPR14 was observed. The protein and gene expression levels of UII and GPR14 in the model group were significantly increased compared with those in the normal group (P<0.01). Urantide ameliorated the pathological changes of AS in the rat model and reduced the gene and protein expression levels of UII and GPR14 (P<0.05 or P<0.01). UII is associated with AS and the UII receptor GPR14-specific antagonist, urantide, demonstrates the ability to protect against AS. Thus, this study provides new insight and experimental theories for the clinical application of urantide to treat AS.

Human cytomegalovirus infection concerned with carotid atherosclerosis / 中国综合临床

Objective To study the correlation of human cytomegalovirus infection with carotid atherosclerosis.Methods A total of 120 patients with carotid atherosclerosis and 140 healthy control patients were recruited for HCMV-PP65 antigen detection and Ultrasound examination.Results In carotid atherosclerosis and healthy patients,58.20％(71 cases)and 6.43％(9 cases)of the subjects were positive for HCMV-PP65 antigen(x2 =32.98,P ＜ 0.05).In carotid atherosclerosis group,69.01％(49 cases)of the patients with positive HCMV-PP65 antigen had instable plaques,while it was 47.06％(24 cases)in the patients with negative HCMV-PP65 antigen.The difference in the positivity of HCMV-PP65 between the two groups were significant(x2 =8.22,P ＜ 0.05).Conclusion Active infection of HCMV may be associated with Carotid Atherosclerosis and the plaques will be more instable.

Effects of rosiglitazone on the expression of nuclear factor-κB P65 and metalloproteinase-9 mRNA in peripheral blood monocyte-derived macrophages in patients with coronary artery disease / 中华急诊医学杂志

Objective To investigate the effects and mechanisms of rosiglitazone on the expressions of nuclear factor-κB and matrix metalloprotease (MMP-9) in peripheral blood monocyte-derived macrophages (MDMs) in patients with coronary heart disease. Method This was a clinical case-control study. Forty-eight actue coronary symdrome (ACS) patients (ACS group), and 20 patients with stable angina (SA) (control group) were collected. They were performed coronary arteriography in the Department of Cardiology of the Second Xiangya Hospital from March to April in 2007. Exclusion criteria included acute infection, trauma or surgery patients within four weeks, cerebral vascular accident, liver and kidney dysfunction, cancer, and so on. The peripheral blood mononuclear cells were isolated and transformed into MDMs with macrophage colony-stimulating factor treatment. The transformed MDMs were randomly assigned into subgrougs and incubated with 0 /μmol/L, 1 μmol/L, 10 μmol/L, 20 μmol/L of rosiglitazone respectively. The expressions of PPAR-γ mRNA, MMP-9 mRNA were determined by RT-PCR and nuclear factor-κB P65 (NF-KB P65) expression by immunohistochemistry. Multiple comparisons were examined for significant differences using analysis of variance (ANOVA). Results The basal expression of PPAR-y mRNA was lower, in contrast, the levels of NF-KB P65 and MMP-9 mRNA were higher in ACS group than control group. PPAR-γ mRNA expression were significantly upregulated in both ACS and control groups with rosiglitazone treatment. PPAR-γ mRNA expression was positive correlation, while the expressions of MMP-9 mRNA were negative correlation with the rosiglitazone concentration in the ACS group. Rosiglitazone inhibited the expression of NF-KB in a concentration-independent manner in ACS and control groups. Conclusions The expression of PPAR-y mRNA is inhibited, while the activity of NF-KB and expression of MMP-9 mRNA are enhanced in MDMs of ACS cases. Rosiglitazone intervention may inhibit NF-KB activity and MMP-9 expression by upregulation of PPAR-y expression in MDMS of patiens with ACS.