Arteriosclerosis (Dallas, Tex.)最新文献

{"title":"Changes in plasma factor VIII complex and serum lipid profile during atherogenesis in cynomolgus monkeys.","authors":"B W Baron,&nbsp;R T Lyon,&nbsp;C K Zarins,&nbsp;S Glagov,&nbsp;J M Baron","doi":"10.1161/01.atv.10.6.1074","DOIUrl":"https://doi.org/10.1161/01.atv.10.6.1074","url":null,"abstract":"<p><p>If endothelial injury plays a prominent role in early atherogenesis, the plasma levels of von Willebrand factor (VWF), which is made within and normally released from endothelial cells, might be expected to rise as a marker of the cellular damage. To evaluate this hypothesis, we measured plasma VWF (as VIIIR:Ag), factor VIII:C, and serum lipids serially up to 37 weeks in 29 adult male cynomolgus monkeys on an atherogenic diet. Factor VIII:C peaked at 113% above baseline by week 10 (p less than 0.0001), then fell and remained 53% below baseline (p less than 0.04) during weeks 20 to 37. However, the overall rise in VWF was not significant. In contrast, serum cholesterol continued to rise after week 21. Serum phospholipids (PL), triglycerides (TG), and free fatty acids (FFA) showed a temporal pattern similar to VIII:C. Significant positive correlations with VIII:C were noted for PL (r = 0.59, p = 0.0001) and TG (r = 0.36, p = 0.0096). At autopsy, small to moderately advanced atherosclerotic lesions were distributed throughout the aortas of the majority of the animals. We conclude that changes in plasma VIIIR:Ag do not correlate with atherogenesis in this model. However, the similar course of VIII:C, TG, and PL suggests that these substances may be involved and perhaps interrelated early in atherogenesis.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 6","pages":"1074-81"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.6.1074","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13278138","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":"Characterization of a Gla-containing protein from calcified human atherosclerotic plaques.","authors":"B L Gijsbers,&nbsp;L J van Haarlem,&nbsp;B A Soute,&nbsp;R H Ebberink,&nbsp;C Vermeer","doi":"10.1161/01.atv.10.6.991","DOIUrl":"https://doi.org/10.1161/01.atv.10.6.991","url":null,"abstract":"<p><p>In this article we describe the isolation of a 4-carboxyglutamic acid (Gla)-containing protein from calcified human atherosclerotic plaques. The protein was extracted from pulverized calcified plaques by demineralization with ethylenediaminetetraacetate and was subsequently purified by anion-exchange fast protein and high-performance liquid chromatography by using ion-exchange and gel-filtration columns. The protein was designated as plaque Gla protein (PGP) and has an apparent mass of 23 kD as estimated from sodium dodecyl sulfate-polyacrylamide gel analysis. By determining the sequence of its first six amino acid residues, the protein was unequivocally demonstrated to be not related to any other known protein. Moreover, no immunological relationship (as tested by Western blot analysis) was found between PGP and other known Gla-containing proteins.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 6","pages":"991-5"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.6.991","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13278141","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":"Effect of dietary fish oil on coronary artery and aortic atherosclerosis in African green monkeys.","authors":"J S Parks,&nbsp;J Kaduck-Sawyer,&nbsp;B C Bullock,&nbsp;L L Rudel","doi":"10.1161/01.atv.10.6.1102","DOIUrl":"https://doi.org/10.1161/01.atv.10.6.1102","url":null,"abstract":"<p><p>Studies were carried out for 2.5 to 3 years in adult male African green monkeys (grivet subspecies) fed diets containing 22% of calories as lard or fish oil with 40% of calories as fat and 0.75 mg cholesterol/Kcal to determine if isocaloric substitution of menhaden fish oil for lard affects coronary artery atherosclerosis. The average total plasma cholesterol concentrations during the experimental period were significantly lower for the fish-oil group (231 +/- 37 mg/dl) compared to the lard group (360 +/- 44 mg/dl), but this difference did not become apparent until after 5 months of experimental diet consumption. High density lipoprotein cholesterol concentrations were 30% lower (p less than 0.01) for the fish-oil group also (57 +/- 5 vs. 82 +/- 6 mg/dl). Plasma triglyceride concentrations were low for both groups, but after about 5 months of diet consumption, they were higher for the animals fed fish oil (25 +/- 2 mg/dl) compared to their lard-fed counterparts (15 +/- 1 mg/dl). Coronary artery intimal area (in this case a measure of early atherosclerotic lesion size) was low in all animals but was significantly less (p less than 0.03) for the fish oil vs. lard groups (0.01 +/- 0.002 vs. 0.03 +/- 0.009 mm2). More atherosclerosis was found in other arteries, and a trend was seen of less atherosclerosis in the thoracic aorta and common carotid arteries of the fish-oil group. The size of lesions in the abdominal aorta was similar between diet groups, but microscopic examination of arteries of the lard group revealed relatively more cholesterol monohydrate crystals compared to the arteries of the fish-oil group. Chemical analysis showed that there was less esterified cholesterol (1.46 +/- 0.71 vs. 3.43 +/- 0.74 mg/g, p = 0.04) and free cholesterol (3.7 +/- 2.15 vs. 7.05 +/- 1.68 mg/g, p = 0.08) in the abdominal aortas taken from the animals fed fish oil. There was a significant correlation between low density lipoprotein (LDL) cholesteryl ester (CE) fatty acid ratio (i.e., saturated + monounsaturated/polyunsaturated species) and the amount of esterified (r = 0.59) and free (r = 0.63) cholesterol in the abdominal aortas. Compared to the lard group, animals fed fish oil had significantly lower LDL CE melting temperatures (26 +/- 1 vs. 38 +/- 1 degree C) and significantly smaller LDL particles (2.68 +/- 0.10 vs. 3.25 +/- 0.38 g/mumol). Therefore, the potentially antiatherogenic effects of dietary fish oil include its ability to decrease the concentration, size, CE content, and CE melting temperature of plasma LDL.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 6","pages":"1102-12"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.6.1102","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13396604","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":"Secretion of plasminogen activator inhibitor-1 from cultured human umbilical vein endothelial cells is induced by very low density lipoprotein.","authors":"A Stiko-Rahm,&nbsp;B Wiman,&nbsp;A Hamsten,&nbsp;J Nilsson","doi":"10.1161/01.atv.10.6.1067","DOIUrl":"https://doi.org/10.1161/01.atv.10.6.1067","url":null,"abstract":"<p><p>Clinical studies have demonstrated an impaired fibrinolytic function in patients with angiographically ascertained coronary artery disease or previous myocardial infarction. This decreased fibrinolytic function is to a major extent explained by the presence of high plasma levels of plasminogen activator inhibitor-1 (PAI-1) and is most common in patients with hyperlipoproteinemias type IIB and IV. To further investigate the association between hypertriglyceridemia and elevated plasma levels of PAI-1, cultured human umbilical vein endothelial cells were exposed to purified lipoproteins isolated from normo- and hypertriglyceridemic (NTG and HTG) individuals. We found that very low density lipoprotein (VLDL) from both NTG and HTG subjects stimulated the secretion of PAI-1 from endothelial cells in a dose-dependent manner. HTG-VLDL at a concentration of 100 micrograms/ml gave rise to a 73% increase in PAI-1 secretion as compared to control cultures, whereas NTG-VLDL only gave rise to a 30% increase (p less than 0.05), indicating that HTG-VLDL is a more potent stimulus to PAI-1 secretion than is NTG-VLDL. Experiments in which endothelial cells were exposed to VLDL subfractions indicated that large VLDL particles, in particular, induce PAI-1 release. Binding experiments demonstrated a specific cellular binding of both NTG- and HTG-VLDL to the cells, but HTG-VLDL bound about four times more effectively than NTG-VLDL. Exposure of the endothelial cells to an LDL receptor antibody was found to block 75% (p less than 0.005) of the VLDL-induced secretion of PAI-1 from the cells.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 6","pages":"1067-73"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.6.1067","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13396602","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":"Dysregulation of lipid metabolism in Tangier monocyte-derived macrophages.","authors":"G Schmitz,&nbsp;H Fischer,&nbsp;M Beuck,&nbsp;K P Hoecker,&nbsp;H Robenek","doi":"10.1161/01.atv.10.6.1010","DOIUrl":"https://doi.org/10.1161/01.atv.10.6.1010","url":null,"abstract":"<p><p>The cellular defect in Tangier mononuclear phagocytes (MNP) was shown to be associated with significant abnormalities in cellular phospholipid, triglyceride, and cholesteryl ester metabolism by using various radiolabeled precursors (32Pi, 3H-serine, 3H-choline, 14C-acetate, and 14C-oleic acid). Tangier MNP expressed increased rates of synthesis for phospholipids (twofold), triglycerides (fivefold), and cholesteryl esters (threefold) as compared to normal MNP when incubated in McCoy's medium containing 0.2% human serum albumin. The turnover rate of cellular phospholipids was also enhanced, while the turnover rates for triglycerides and cholesteryl esters were normal, thus leading to the accumulation of a larger pool of labeled triglycerides and cholesteryl esters in Tangier MNP. The individual phospholipid classes, phosphatidylcholine, sphingomyelin, phosphatidylethanolamine, and phosphatidylserine were similarly affected. Cholesterol loading led to approximately 30% down-regulation of phospholipid synthesis in normal cells, but Tangier MNP showed a smaller response. When nonloaded normal MNP were exposed to high density lipoprotein3 (HDL3), they diminished cellular cholesterol esterification mediated by acyl-CoA:cholesterol acyltransferase (ACAT); in Tangier MNP, ACAT activity increased in the presence of HDL3. When cholesterol-loaded normal and Tangier MNP were treated with HDL3, an up-regulation of phospholipid synthesis was observed in both cell types, but Tangier MNP showed a smaller response. We conclude that the defect in Tangier disease, which we recently described as a \"disorder of intracellular traffic\" (Schmitz et al. Proc Natl Acad Sci USA 1985;82:6305-6309), is associated with a dysregulation of cellular lipid metabolism, leading to an overproduction of triglycerides and esterified cholesterol and to enhanced synthesis and catabolism of phospholipids.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 6","pages":"1010-9"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.6.1010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13396616","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":"Regulation of differentiated properties and proliferation of arterial smooth muscle cells.","authors":"J Thyberg,&nbsp;U Hedin,&nbsp;M Sjölund,&nbsp;L Palmberg,&nbsp;B A Bottger","doi":"10.1161/01.atv.10.6.966","DOIUrl":"https://doi.org/10.1161/01.atv.10.6.966","url":null,"abstract":"","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 6","pages":"966-90"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.6.966","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13398505","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":"High density lipoprotein cholesterol. A 16-year longitudinal study in aging male twins.","authors":"J C Christian,&nbsp;D Carmelli,&nbsp;W P Castelli,&nbsp;R Fabsitz,&nbsp;C E Grim,&nbsp;F J Meaney,&nbsp;J A Norton,&nbsp;T Reed,&nbsp;C J Williams,&nbsp;P D Wood","doi":"10.1161/01.atv.10.6.1020","DOIUrl":"https://doi.org/10.1161/01.atv.10.6.1020","url":null,"abstract":"<p><p>The National Heart, Lung, and Blood Institute Twin Study is a collaborative, longitudinal study of white, male twins who were veterans of World War II and were born between 1917 and 1927. The twins were selected from the National Academy of Sciences/National Research Council Twin Panel and were examined three times (1969-73, 1981-82, and 1986-87). At all three exams, the dizygotic (DZ) twins were found to have a greater total variance for high density lipoprotein cholesterol (HDL-C) than the monozygotic (MZ) twins (p less than 0.05). DZ variance estimates were also larger than the variance of singletons from the second National Health and Nutrition Examination Survey. At the third exam, HDL-C was divided by precipitation into HDL2 and HDL3 fractions, and HDL2 was found to be the primary cause of the greater DZ total variance (DZ/MZ HDL2 variance = 2.22). The DZ/MZ variance ratio decreased 9% after adjustment of HDL2 for correlations with plasma triglycerides, alcohol consumption, smoking, exercise, and body mass index measured at the third exam. Postulated causes of the difference between MZ and DZ total variances include World War II induction screening, environmental influences unique to one zygosity, and genetic factors related to twinning. Further understanding of the etiology of this striking difference between MZ and DZ twin variance for HDL-C fractions could lead to more effective methods of decreasing the complications of arteriosclerosis.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 6","pages":"1020-5"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.6.1020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13396617","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":"Characterization in vitro of interaction of human apolipoprotein E-free high density lipoprotein with human hepatocytes.","authors":"D Schouten,&nbsp;M F Kleinherenbrink-Stins,&nbsp;A Brouwer,&nbsp;D L Knook,&nbsp;J A Kamps,&nbsp;J Kuiper,&nbsp;T J van Berkel","doi":"10.1161/01.atv.10.6.1127","DOIUrl":"https://doi.org/10.1161/01.atv.10.6.1127","url":null,"abstract":"<p><p>Characterization of the interaction of iodinated apolipoprotein (apo) E-free high density lipoprotein (HDL) with cultured human hepatocytes provides evidence for a saturable, Ca2(+)-independent, high affinity binding site with an apparent km value of 20 micrograms/ml of apolipoprotein. Nitrated HDL and low density lipoprotein (LDL) did not compete for the binding of HDL, in contrast to very low density lipoprotein (VLDL). It is suggested that VLDL competition is exerted by the presence of apo Cs. Degradation of HDL was relatively low and in some cases not detectable. In cases where degradation was found, inhibitors of the lysosomal pathway of protein degradation had no effect, while LDL degradation was inhibited more than 80%. In the presence of 10 microM of monensin, the cell-association of HDL was unaffected, but the degradation was inhibited by 30%. Under similar conditions, LDL association was inhibited by 40% and LDL degradation, by 90%. Incubation of human hepatocytes with fluorescently labeled HDL (Dil-HDL) revealed (in contrast to Dil-LDL) mainly strong membrane-bound fluorescence and hardly any labeling of small intracellular vesicles. It is concluded that human hepatocytes possess a specific high affinity site for human HDL with recognition properties similar to those described earlier on rat hepatocytes. No evidence that the binding of HDL is actively coupled to uptake and lysosomal degradation could be obtained, indicating that binding of LDL and HDL to human hepatocytes is coupled differently to intracellular pathways.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 6","pages":"1127-35"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.6.1127","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13396606","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":"Hemostatic variables in homozygous familial hypercholesterolemia. Effect of regular plasma cholesterol removal by low density lipoprotein apheresis.","authors":"G Di Minno,&nbsp;A M Cerbone,&nbsp;F Cirillo,&nbsp;A Postiglione,&nbsp;M Colucci,&nbsp;N Semeraro,&nbsp;N Scarpato,&nbsp;A Gnasso,&nbsp;M Margaglione,&nbsp;G Gallotta","doi":"10.1161/01.atv.10.6.1119","DOIUrl":"https://doi.org/10.1161/01.atv.10.6.1119","url":null,"abstract":"<p><p>Plasma levels of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) and the in vitro ability of platelets to aggregate and of monocytes to express procoagulant (tissue factor) activity (PCA) were evaluated in five patients who are homozygous for familial hypercholesterolemia (FH) before and after a single and a regular 5-month cholesterol removal by low density lipoprotein (LDL) apheresis. The biweekly procedure resulted in a 25% to 30% reduction (approximately 150 mg/dl) in total and LDL cholesterol (both were greater than 550 mg/dl at the beginning of the study). The basal levels of t-PA antigen and fibrinolytic activity before and after 10 minutes of venous stasis, basal PAI activity, and PAI-1 antigen were comparable to controls and were not affected by LDL apheresis. Likewise, regardless of the cholesterol removal, the PCA of freshly isolated monocytes and that of monocytes incubated with lipopolysaccharide did not differ from control values. Finally, the pre-apheresis sensitivity of platelets to adenosine diphosphate, arachidonic acid, and collagen was 1.5 to 2 times the normal value. This ratio was unchanged throughout the 5-month procedure. We conclude that fibrinolysis and monocyte PCA are normal in FH patients, whereas platelet aggregation is abnormally high, and none of these parameters is significantly affected by a 25% to 30% reduction in total and LDL cholesterol by LDL apheresis. Furthermore, our data suggest that removal of cholesterol from plasma by LDL apheresis is important for gaining insight into the mechanisms involved in the ischemic complications of arteriosclerosis in FH patients.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 6","pages":"1119-26"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.6.1119","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13278143","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":"Relationship between high density lipoprotein subfractions and coronary risk factors in a rural white population.","authors":"H J Steenkamp,&nbsp;P L Jooste,&nbsp;A J Benadé,&nbsp;M L Langenhoven,&nbsp;J E Rossouw","doi":"10.1161/01.atv.10.6.1026","DOIUrl":"https://doi.org/10.1161/01.atv.10.6.1026","url":null,"abstract":"<p><p>The relationship of serum high density lipoprotein cholesterol (HDL-C) levels and of the HDL2-C and HDL3-C subfractions to several factors associated with coronary risk was examined in a cross-sectional study, which included 655 men and 731 women ages 20 to 64 years. Participants with coronary heart disease (CHD) had lower levels of HDL-C, HDL2-C, and HDL3-C; however, only HDL-C in women was significant. Maleness, body mass index, triglyceride levels, tobacco use, and carbohydrate intake (in men) were significantly inversely related to total HDL-C, while alcohol intake was significantly positively related to HDL-C. The associations were stronger for HDL2-C than for HDL3-C, except that alcohol intake in men was more strongly related to HDL3-C. The findings of this study suggest that several factors that influence CHD risk do so in part through modifying HDL2-C levels.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 6","pages":"1026-31"},"PeriodicalIF":0.0,"publicationDate":"1990-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.6.1026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13396618","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}