Arteriosclerosis (Dallas, Tex.)最新文献

{"title":"Prevention of myocardial lesions in JCR:LA-corpulent rats by nifedipine.","authors":"J C Russell,&nbsp;D G Koeslag,&nbsp;P J Dolphin,&nbsp;R M Amy","doi":"10.1161/01.atv.10.4.658","DOIUrl":"https://doi.org/10.1161/01.atv.10.4.658","url":null,"abstract":"<p><p>Male rats of the JCR:LA-corpulent strain spontaneously develop atherosclerosis and myocardial lesions if corpulent. The corpulent rats exhibit a marked very low density hyperlipidemia and insulin resistance. The incidence of both vascular and myocardial lesions correlates strongly with the hyperinsulinemia, but not with the hyperlipidemia. Corpulent male rats were chronically treated with nifedipine or acetylsalicylic acid to explore the roles of smooth muscle spasm and platelet activity in induction of the myocardial lesions. Acetylsalicylic acid treatment was associated with no significant changes in fasting glucose, insulin, or lipid concentrations. Nifedipine caused no significant changes in glucose concentration but was associated with mildly increased insulin levels. Treatment with nifedipine resulted in significant decreases in serum triglyceride concentrations. The decreases were confined to longer-chain triacylglycerol molecular species with no change in the concentration of molecular species with 48 or 50 acyl carbon atoms. There was no effect on myocardial lesion frequency with acetylsalicylic acid treatment. In contrast, nifedipine prevented the development of old organized scarred lesions. This effect is similar to that seen with treatments that markedly reduce the insulin resistance. These findings suggest that platelet-initiated thrombus formation is not an important factor in lesion formation in the JCR:LA-cp rat, but that smooth muscle spasm is probably important.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 4","pages":"658-64"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.4.658","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13350085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dose- and shear rate-dependent effects of heparin on thrombogenesis induced by rabbit aorta subendothelium exposed to flowing human blood.","authors":"W Inauen,&nbsp;H R Baumgartner,&nbsp;T Bombeli,&nbsp;A Haeberli,&nbsp;P W Straub","doi":"10.1161/01.atv.10.4.607","DOIUrl":"https://doi.org/10.1161/01.atv.10.4.607","url":null,"abstract":"<p><p>The effect of heparin on thrombogenesis induced by the subendothelium of rabbit aorta was investigated in 24 healthy volunteers after intravenous injection of different doses (0, 1000, 2500, and 5000 IU). By using an ex vivo perfusion chamber system, the interaction between flowing blood and exposed subendothelium was measured at low (50 s-1), intermediate (650 s-1), and high (2600 s-1) wall shear rates. The low shear rate simulated blood flow in venous, the intermediate shear rate in arterial, and the high shear rate in small or stenosed arterial vessels. Deposition of fibrin, platelets, and platelet thrombi on vascular subendothelium (SE) was quantified by morphometrical and immunological techniques. Fibrin deposition prevailed at low shear rates and was only minimal at high shear rates (30 +/- 1% vs. 1 +/- 0.4% coverage of SE with fibrin, means +/- SEM, p less than 0.001). In contrast, the interaction of platelets with SE was more intense at high compared to low shear rates, as indicated by higher platelet adhesion (54 +/- 5% vs. 4 +/- 1% coverage of SE with platelets, p less than 0.001) and platelet thrombus volumes (4.8 +/- 1.3 vs. 0.5 +/- 0.1 microns 3/microns 2, p less than 0.001). Fibrin deposition on SE was inhibited by heparin in a dose-dependent manner and was abolished after high doses. In addition, high doses of heparin reduced the height and volume of platelet thrombi at low and intermediate wall shear rates, but no effect was found at the high shear rate. Our data show that heparin inhibits the formation of both fibrin and platelet thrombi on vascular subendothelium. The lack of effect of heparin on platelet thrombus formation at high shear rates indicates that thrombin modulates the growth rate and/or stability of platelet thrombi at low and intermediate shear rates, whereas additional factors may control platelet thrombus growth and stability at high shear conditions.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 4","pages":"607-15"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.4.607","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13519389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholesterol and coronary heart disease mortality. A 23-year follow-up study of 9902 men in Israel.","authors":"U Goldbourt,&nbsp;S Yaari","doi":"10.1161/01.atv.10.4.512","DOIUrl":"https://doi.org/10.1161/01.atv.10.4.512","url":null,"abstract":"<p><p>A 23-year follow-up study of 10,059 40- to 65-year-old participants in the Israeli Ischemic Heart Disease Study found that of 3473 deaths (34.5%), in 1098 (10.9%) coronary heart disease (CHD) was the underlying cause. Total serum cholesterol (TC) was measured in 9902 individuals. During the study, CHD mortality was elevated primarily in individuals in quintiles 4 and 5 (TC levels greater than or equal to 217 mg/dl). Although CHD mortality increased marginally with increasing TC at levels below 217 mg/dl, this was entirely explained by age and other correlated risk factors in a multivariate adjustment of the survival curves. The \"net\" 23-year survival in terms of CHD was 87% in quintile 5 (TC greater than 241) versus 93% in quintile 1 (TC less than 176 mg/dl). CHD mortality was inversely related to the percent of cholesterol in high density lipoprotein (PHDL). All-cause mortality increased only when TC was above 240 mg/dl and in the subjects with PHDL levels in the lowest 20%. Lipids appeared to be somewhat less effective in predicting subsequent CHD mortality than did hypertension and smoking and were clearly secondary in assessing risk of all-cause death. The results raise the question whether intensive treatment for hypercholesterolemia is indicated for men at \"borderline\" levels. We conclude that the association between serum cholesterol and long-term mortality partly reflects the role that levels of co-existing CHD risk factors play in prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 4","pages":"512-9"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.4.512","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13518111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelet secretory products increase low density lipoprotein oxidation, enhance its uptake by macrophages, and reduce its fluidity.","authors":"M Aviram,&nbsp;G Dankner,&nbsp;J G Brook","doi":"10.1161/01.atv.10.4.559","DOIUrl":"https://doi.org/10.1161/01.atv.10.4.559","url":null,"abstract":"<p><p>Oxidized low density lipoprotein (Ox-LDL) is considered to be involved in the atherogenic process. Factors influencing the formation of Ox-LDL are thus of importance. Oxidation of LDL in a cell-free system in the presence of copper ions was significantly increased (up to 60%) by the presence of platelet-conditioned medium, (PCM) obtained from collagen-activated platelets for the duration of the oxidation period. The effect was time- and dose-dependent and was related to hydrogen peroxide and superoxide production, since PCM-induced enhanced LDL oxidation was inhibited by catalase and by superoxide dismutase, but not by protease treatments. PCM also reduced the fluidity of oxidized LDL by 45%. Upon incubation with a J-774 macrophage-like cell line, PCM-treated Ox-LDL enhanced cellular cholesteryl ester synthesis by 47% and lipoprotein degradation by 41%. Thus platelet secretory products appeared to enhance LDL oxidation through the involvement of oxidative agents. The resulting Ox-LDL demonstrated increased atherogenic properties.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 4","pages":"559-63"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.4.559","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13518115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isolation and characterization of plasma lipoproteins of common marmoset monkey. Comparison of effects of control and atherogenic diets.","authors":"D Crook,&nbsp;K H Weisgraber,&nbsp;J K Boyles,&nbsp;R W Mahley","doi":"10.1161/01.atv.10.4.633","DOIUrl":"https://doi.org/10.1161/01.atv.10.4.633","url":null,"abstract":"<p><p>This study examines the potential of the common marmoset monkey (Callithrix jacchus) to serve as a model for human lipoprotein metabolism and atherosclerosis. The lipoproteins of animals fed a low-fat, low-cholesterol diet and a high-fat (12% wt/wt lard), high-cholesterol (0.34% wt/wt) diet were characterized by the combination of sequential ultracentrifugation and Pevikon block electrophoresis. Based on chemical and physical properties, equivalents of human very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL), including and HDL-with apolipoprotein E subclass, were demonstrated. In control animals, whose plasma cholesterol concentration was 140.1 +/- 20.2 mg/dl (means +/- SD), approximately 40% of the plasma cholesterol was transported by LDL as compared with approximately 70% in humans. The cholesterol-fed marmosets segregated into two groups: hypo- and hyper-responders. The hyper-responders had plasma cholesterol levels of 450 to 970 mg/ml. The hypercholesterolemia was associated with elevated concentrations of VLDL, intermediate density lipoproteins, and LDL; in addition, these lipoproteins were enriched in cholesteryl esters relative to lipoproteins isolated from control animals. The HDL (d greater than 1.09 g/ml) levels did not change in response to cholesterol feeding, although the HDL-with apolipoprotein E found in the d = 1.02 to 1.09 g/ml fraction increased approximately fivefold. Based on immunological characteristics and sialic acid content, the common marmoset appeared to lack a lipoprotein(a) equivalent. The results of a short-term feeding study (11 months) suggest that this monkey was susceptible to the development of diet-induced atherosclerosis. The hyper-responsive animals developed foam cell lesions and moderately proliferative intimal lesions, predominantly within the thoracic aorta. In summary, the results of our studies indicate that the common marmoset monkey potentially is a useful model for the study of both lipoprotein metabolism and diet-induced atherosclerosis.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 4","pages":"633-47"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.4.633","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13270236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Albumin and Cr-EDTA uptake by systemic arteries, veins, and pulmonary artery of rabbit.","authors":"M J Lever,&nbsp;M T Jay","doi":"10.1161/01.atv.10.4.551","DOIUrl":"https://doi.org/10.1161/01.atv.10.4.551","url":null,"abstract":"<p><p>Experiments have been performed both in vivo and in vitro to measure the steady-state uptake of labeled albumin and Cr-ethylenediaminetetraacetate by various blood vessels of the rabbit: the ascending and descending portions of the thoracic aorta, the carotid artery, the pulmonary artery, and the inferior vena cava. The in vitro experiments indicated that the wall tissues of the pulmonary artery and the vena cava have much greater distribution volumes for albumin than do the systemic arteries. This may in part explain the differences in wall tissue concentrations in vivo and, in turn, the differences between vessels in their susceptibility to atherosclerosis.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 4","pages":"551-8"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.4.551","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13270309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polyclonal antibodies against formaldehyde-modified apolipoprotein A-I. An approach to circumventing fixation-induced loss of antigenicity in immunocytochemistry.","authors":"B Harrach,&nbsp;H Robenek","doi":"10.1161/01.atv.10.4.564","DOIUrl":"https://doi.org/10.1161/01.atv.10.4.564","url":null,"abstract":"<p><p>A central requirement for the subcellular localization of synthesized and/or endocytozed lipoproteins is the availability of antibodies against the antigen to be localized. The preparation of cells for electron microscopy, in particular the fixation and embedding routine, influences the antigenicity, often resulting in a markedly reduced labeling intensity. To ameliorate fixation-induced changes in antigenicity, we produced antibodies against pre-fixed human apolipoprotein (apo) A-I. Purified apo A-I was fixed with 4% formaldehyde and was used to raise polyclonal antibodies in rabbits. The antiserum was purified by protein A-Sepharose followed by affinity chromatography with the fixed antigen coupled to vinylsulfone-activated agarose. The specificity of the antibodies was ascertained by enzyme-linked immunosorbent assay (ELISA) and Western blot analysis against different fixed and unfixed lipoproteins. Nonspecific binding to unfixed or to fixed apolipoproteins was not observed. Thus, the antibodies reacted specifically with apo A-I and recognized the fixed as well as the unfixed protein. In ELISA, the reaction of the antibodies was markedly enhanced with the fixed antigen, indicating that the antibodies were directed against epitopes characteristically modified by the fixation. The efficacy of the antibodies for light and electron microscopy was tested on HepG2 cells and on human liver cells which are known to synthesize apo A-I. When HepG2 cells were exposed to anti-apo A-I antibodies followed by a secondary fluorescein isothiocyante-labeled antibody, fluorescence was found intracellularly in distinct regions. Electron microscopy revealed that the endoplasmic reticulum, and in particular the trans elements of the Golgi complexes, were the main compartments stained for apo A-I both in HepG2 cells, as shown by the immunoperoxidase technique, and in human hepatocytes, as shown by the protein A-gold technique on ultrathin cryosections. Furthermore, we were able to localize apo A-I in foam cells of the human aortic plaque by postembedding immunolabeling techniques. These findings demonstrate the potential of antibodies to fixed lipoproteins in impaired localization at the light microscopic and electron microscopic levels.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 4","pages":"564-76"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.4.564","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12859922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Familial defective apolipoprotein B-100. Comparison with familial hypercholesterolemia in 18 cases detected in Munich.","authors":"H Schuster,&nbsp;G Rauh,&nbsp;B Kormann,&nbsp;T Hepp,&nbsp;S Humphries,&nbsp;C Keller,&nbsp;G Wolfram,&nbsp;N Zöllner","doi":"10.1161/01.atv.10.4.577","DOIUrl":"https://doi.org/10.1161/01.atv.10.4.577","url":null,"abstract":"<p><p>It has recently been suggested that a substitution of glutamine for arginine at residue 3500 of apolipoprotein (apo) B-100 causes familial defective apo B-100 (FDB), an autosomal, dominantly inherited disorder, which leads to increased serum cholesterol levels. From a sample of 243 patients from Munich with type IIa hyperlipoproteinemia (HL), we have identified eight individuals with the apo B-100 arginine(3500)----glutamine mutation. In a group of 57 subjects with defective low density lipoprotein receptor (LDLR), no mutant apo B alleles were detected. The frequency of FDB in patients with type IIa HL was estimated to be 3%. In the kindreds of three of the probands, 10 additional carriers of the apo B mutation were identified. Clinical and biochemical data reveal a striking similarity between patients with FDB and those with a defect in the LDLR gene. Our data support previous findings that FDB is a serious disorder causing premature atherosclerosis.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 4","pages":"577-81"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.4.577","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13317418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of atherosclerosis susceptibility in mice with genetic defects in platelet function.","authors":"B Paigen,&nbsp;P A Holmes,&nbsp;E K Novak,&nbsp;R T Swank","doi":"10.1161/01.atv.10.4.648","DOIUrl":"https://doi.org/10.1161/01.atv.10.4.648","url":null,"abstract":"<p><p>To determine whether platelets contribute to the development of atherosclerosis, we compared the severity of atherosclerosis in susceptible C57BL/6 mice carrying either a normal or a variant phenotype for platelet function. Five genetically distinct mutants with increased bleeding times and abnormal dense granules were used: maroon (ru-2mr), light ear (le), ruby eye (ru), beige (bg1), and pale ear (ep). After a 14-week consumption of an atherogenic diet, three mutants had significantly less disease involvement than the control: light ear, maroon, and ruby eye. In contrast, pale ear ahd lesions similar to control animals. After 48 weeks, the two mutants with the least degree of atherosclerosis at 14 weeks, light ear and ruby eye, showed greater than 50% survival. In contrast, no animals from the beige, pale ear, or the normal C57BL/6 strains survived. To determine whether a specific biochemical component of platelet function is related to atherosclerosis, we measured serotonin found in dense granules. Serotonin showed no correlation with each mutant's atherosclerosis susceptibility. These results indicate that some particular component of platelet function affects atherosclerosis. That component is intact in pale ear, moderately affected in beige and maroon, and severely affected in light ear and ruby eye. The identity of that component remains an interesting question whose answer may provide further insight into the atherosclerotic disease process.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 4","pages":"648-52"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.4.648","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13519390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inheritance of low density lipoprotein subclass patterns in familial combined hyperlipidemia.","authors":"M A Austin,&nbsp;J D Brunzell,&nbsp;W L Fitch,&nbsp;R M Krauss","doi":"10.1161/01.atv.10.4.520","DOIUrl":"https://doi.org/10.1161/01.atv.10.4.520","url":null,"abstract":"<p><p>The inheritance of low density lipoprotein (LDL) subclass patterns was investigated in 234 members of seven large kindreds with familial combined hyperlipidemia (FCHL), a disorder characterized by elevated LDL cholesterol and/or triglyceride and increased coronary disease risk in families. Analysis of LDL subclasses by nondenaturing gradient gel electrophoresis showed a predominance of large, buoyant LDL particles (pattern A) in 71% of the family members and a predominance of small, dense LDL particles (pattern B) in 29% of family members. Based on complex segregation analysis, pattern B appeared to be inherited as an autosomal trait with either a dominant or an additive mode of inheritance and a small, but significant, multifactorial inheritance component. The proposed allele for pattern B was common (frequency = 0.3), and reduced penetrance was observed among men under age 20 and among women under age 50. These results in these FCHL families are consistent with those from a previously reported population-based sample of families, in which pattern B showed an apparent dominant mode of inheritance. In that study, reduced penetrance was observed for men under age 20 and for premenopausal women, but a somewhat lower allele frequency was found for pattern B (0.25). In the FCHL family members, LDL subclass pattern B was associated with significantly increased plasma levels of apolipoprotein B and triglyceride and decreased high density lipoprotein cholesterol. In comparison with a group of controls, the FCHL family members with pattern A had similar mean triglyceride levels, but higher mean apolipoprotein B. Thus, in families with FCHL, a predominance of small, dense LDL particles appears to be inherited as a common, single-gene trait, which is closely associated with the higher plasma triglyceride levels found in these families. The increased plasma apolipoprotein B levels found in FCHL cannot, however, be accounted for by this proposed locus.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 4","pages":"520-30"},"PeriodicalIF":0.0,"publicationDate":"1990-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.4.520","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13518112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}