Arteriosclerosis (Dallas, Tex.)最新文献

{"title":"Association of fasting insulin with blood pressure and lipids in young adults. The CARDIA study.","authors":"T A Manolio,&nbsp;P J Savage,&nbsp;G L Burke,&nbsp;K A Liu,&nbsp;L E Wagenknecht,&nbsp;S Sidney,&nbsp;D R Jacobs,&nbsp;J M Roseman,&nbsp;R P Donahue,&nbsp;A Oberman","doi":"10.1161/01.atv.10.3.430","DOIUrl":"https://doi.org/10.1161/01.atv.10.3.430","url":null,"abstract":"<p><p>The association of insulin with cardiovascular disease (CVD) may be mediated in part by the associations of insulin with CVD risk factors, particularly blood pressure and serum lipids. These associations were examined in 4576 black and white young adults in the CARDIA Study. Fasting insulin level was correlated in univariate analysis with systolic blood pressure (r = 0.16), diastolic blood pressure (r = 0.13), triglycerides (r = 0.27), total cholesterol (r = 0.10), high density lipoprotein (HDL) cholesterol (r = -0.25), and low density lipoprotein (LDL) cholesterol (r = 0.14), and with age, sex, race, glucose, body mass index, alcohol intake, cigarette use, physical activity, and treadmill duration (all p less than 0.0001). After adjustment for these covariates, insulin remained positively associated with blood pressure, triglycerides, total and LDL cholesterol, and apolipoprotein B and was negatively associated with HDL, HDL2 and HDL3 cholesterol, and apolipoprotein A-I in all four race-sex groups. Higher levels of fasting insulin are associated with unfavorable levels of CVD risk factors in young adults; these associations, though relatively small, can be expected to increase the risk of atherosclerosis. Demonstration of these relationships in a large, racially diverse, healthy population suggests that insulin may be an important intermediate risk factor for CVD in a broad segment of the U.S. population.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 3","pages":"430-6"},"PeriodicalIF":0.0,"publicationDate":"1990-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.3.430","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13341134","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":"Tumor necrosis factor induced release of endothelial cell lipoprotein lipase.","authors":"U Saxena,&nbsp;L D Witte,&nbsp;I J Goldberg","doi":"10.1161/01.atv.10.3.470","DOIUrl":"https://doi.org/10.1161/01.atv.10.3.470","url":null,"abstract":"<p><p>The major functional pool of lipoprotein lipase (LPL) that hydrolyzes triglycerides in circulating lipoproteins is located on the vascular endothelium. The macrophage-secreted cytokine tumor necrosis factor (TNF), a molecule known to affect endothelial cell functions, was used to test the hypothesis that alterations of endothelial cell metabolism regulate the binding of LPL to these cells. TNF addition induced rapid (maximum release at 45 minutes) dissociation of LPL protein and activity from its binding sites on cultured porcine aortic endothelial cells. LPL release by TNF required endothelial cell metabolic event(s) which involved cell secretion. In addition, LPL release was inhibited by pertussis toxin, suggesting the involvement of guanine nucleotide regulatory protein(s). Addition of arachidonic acid, a molecule known to be released by endothelial cells due to phospholipase A2 activation by TNF treatment, released LPL from the cell surface. Furthermore, direct modulation of cellular phospholipase A2 activity also led to changes in the release of LPL. Our studies demonstrate that alterations in the cellular metabolism of endothelial cells, for example, by TNF, may release functional pools of LPL from the vascular endothelium. This decrease in LPL on endothelial cell surfaces might be involved in the development of hypertriglyceridemia and redirection of energy flow during infections and inflammation.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 3","pages":"470-6"},"PeriodicalIF":0.0,"publicationDate":"1990-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.3.470","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13267044","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":"Roles of calcium, cyclic nucleotides, and protein kinase C in regulation of endothelial permeability.","authors":"Y Yamada,&nbsp;T Furumichi,&nbsp;H Furui,&nbsp;T Yokoi,&nbsp;T Ito,&nbsp;K Yamauchi,&nbsp;M Yokota,&nbsp;H Hayashi,&nbsp;H Saito","doi":"10.1161/01.atv.10.3.410","DOIUrl":"https://doi.org/10.1161/01.atv.10.3.410","url":null,"abstract":"<p><p>We studied the effects of calcium, cyclic nucleotides, and protein kinase C on albumin transfer, electrical resistance, and cytoskeletal actin filaments in cultured human umbilical vein endothelial cells. The endothelial monolayer grown on collagen-treated filters markedly restricted the transfer of albumin relative to its transfer across the filter alone. Both Ca++ ionophore A23187 and ethyleneglycol tetraacetic acid disrupted the integrity of the endothelial monolayer, thereby increasing endothelial albumin transfer and decreasing electrical resistance in a concentration-dependent manner. Neither W-7, a calmodulin antagonist, nor TMB-8, an intracellular Ca++ antagonist, influenced endothelial permeability. In contrast, increases in intracellular cyclic adenosine 5'-monophosphate (AMP) and/or cyclic guanosine 5'-monophosphate (GMP) induced by dibutyryl cyclic AMP, forskolin, 3-isobutyl-1-methylxanthine, 8-bromo cyclic GMP, dibutyryl cyclic GMP, or sodium nitroprusside significantly elevated endothelial electrical resistance and inhibited albumin transfer; similar effects resulted from activation of protein kinase C by phorbol-12-myristate-13-acetate or 1-oleoyl-2-acetyl-glycerol. These substances ruffled the dense peripheral bands of F-actin without compromising the integrity of endothelial monolayer. These results suggest that calcium, cyclic nucleotides, and protein kinase C play important roles in the regulation of endothelial permeability and the maintenance of endothelial integrity.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 3","pages":"410-20"},"PeriodicalIF":0.0,"publicationDate":"1990-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.3.410","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13341136","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":"Thrombogenicity of vascular cells. Comparison between endothelial cells isolated from different sources and smooth muscle cells and fibroblasts.","authors":"J J Zwaginga,&nbsp;H C de Boer,&nbsp;M J IJsseldijk,&nbsp;A Kerkhof,&nbsp;G Muller-Berghaus,&nbsp;J Gruhlichhenn,&nbsp;J J Sixma,&nbsp;P G de Groot","doi":"10.1161/01.atv.10.3.437","DOIUrl":"https://doi.org/10.1161/01.atv.10.3.437","url":null,"abstract":"<p><p>When the endothelial cell layer is damaged, a thrombotic reaction starts on the cells' subendothelium and on the connective tissue deposited by smooth muscle cells in the deeper layers. When more severe vascular damage occurs, hemostasis will involve the vessel adventitia in which fibroblasts are found. In this article, the influence of in vitro cultured endothelial cells, smooth muscle cells, and fibroblasts on the hemostatic balance was studied. To do so, perfusions were performed with low molecular weight heparin anticoagulated blood over the extracellular matrix of the cells. This method allowed the study of tissue factor-dependent thrombin generation and its influence on formation of fibrin and platelet aggregates. The experiments described in this article show that endothelial cells isolated from different human organs interfere differently in the hemostatic response. Endothelial cells isolated from umbilical veins are nonthrombogenic; they do not synthesize tissue factor under unstimulated conditions. On their extracellular matrix, only adherent platelets are found, but no aggregates and no fibrin. Endothelial cells isolated from omentum and atrium contain tissue factor activity under unstimulated conditions. As a consequence, thrombin is generated on their surfaces, and platelet aggregates and fibrin deposition are found on the extracellular matrices after perfusions with whole blood. The matrix of smooth muscle cells and fibroblasts behaved similarly. Increase in shear rate and perfusion time resulted in an increase in platelet aggregate formation. Polymerized fibrin deposition decreased when perfusions were performed at higher shear. Both platelet aggregation and fibrin deposition were tissue factor dependent and could be blocked more than 70% by an antibody against tissue factor. Based on these results, we conclude that endothelial cells isolated from umbilical veins form the best nonthrombogenic surface in vitro. Moreover, coagulation-dependent hemostasis should be included when thrombogenicity of subendothelium is discussed, especially when it concerns matrix derived from cells present in the deeper layer of the vessel wall.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 3","pages":"437-48"},"PeriodicalIF":0.0,"publicationDate":"1990-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.3.437","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13494077","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":"Inhibition of thrombus formation in vivo by novel antiplatelet agent.","authors":"U M Marzec,&nbsp;A B Kelly,&nbsp;S R Hanson,&nbsp;A Lasslo,&nbsp;L A Harker","doi":"10.1161/01.atv.10.3.367","DOIUrl":"https://doi.org/10.1161/01.atv.10.3.367","url":null,"abstract":"<p><p>The antithrombotic and antihemostatic effects of the novel antiplatelet compound, alpha, alpha'-bis[3-(N,N-diethylcarbamoyl)piperidino]-p-xylene dihydrobromide (GT-12), were investigated in a baboon model of platelet-dependent thrombosis under high flow conditions. In this model, segments of collagen-coated tubing and Dacron vascular graft were placed as thrombus-inducing extension devices in exteriorized femoral arteriovenous shunts. The deposition of 111In-labeled platelets was measured for each thrombogenic segment throughout 1 hour by using gamma camera imaging. In addition, the 125I-fibrin retained in the forming thrombus was measured. Intravenous infusion of GT-12 (100 mumol/kg, 63.3 mg/kg) over a 15-minute period before the insertion of the test segments prolonged the bleeding time from a baseline value of 4.4 +/- 0.4 min to 7.6 +/- 1.0 min (p = 0.036) and inhibited platelet aggregation ex vivo induced by adenosine diphosphate (ED50 4.7 +/- 0.9 to 10.3 +/- 2.2 microM; p less than 0.02) and collagen (ED50 2.0 +/- 0.4 to 8.0 +/- 2.4 micrograms/ml; p less than 0.05). Deposition of platelets and fibrin was decreased in concert by 30% (p less than 0.05) for vascular grafts and possibly collagen segments at the end of the 60-minute observation period. We conclude that GT-12 is antithrombotic for Dacron graft-induced thrombus formation in vivo.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 3","pages":"367-71"},"PeriodicalIF":0.0,"publicationDate":"1990-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.3.367","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13295502","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":"Different efflux pathways for high and low density lipoproteins from porcine aortic intima.","authors":"B G Nordestgaard,&nbsp;E Hjelms,&nbsp;S Stender,&nbsp;K Kjeldsen","doi":"10.1161/01.atv.10.3.477","DOIUrl":"https://doi.org/10.1161/01.atv.10.3.477","url":null,"abstract":"<p><p>To study the efflux of high (HDL) and low (LDL) density lipoproteins from the arterial wall in vivo, a surgical model in pigs was used. An isolated segment of the lesion-free thoracic aorta was pulse labeled from the lumen of the artery with 3H-cholesteryl ester labeled HDL and 14C-cholesteryl ester labeled LDL. Subsequently, the labeled aortic segment was exposed to cold chase in vivo. The transfer of HDL cholesteryl ester from plasma into intima expressed as intimal clearance was three to seven times greater than that of LDL cholesteryl ester. At least 50%, but possibly as much as 95%, of the HDL cholesteryl ester that entered the arterial intima during a period of 4 hours penetrated the arterial wall beyond the internal elastic lamina. In contrast, less than 15% of the LDL cholesteryl ester that entered the arterial intima in the same period penetrated beyond the luminal layer. After 24 hours of cold chase in vivo, more than 80% of both labeled HDL esterified cholesterol and labeled LDL esterified cholesterol had disappeared from the arterial wall. Transmural profiles after 9 hours of cold chase showed that labeled HDL was present throughout the entire arterial wall, whereas labeled LDL in quantitative amounts was present only in the luminal layer. The results suggest that the most important efflux route for HDL esterified cholesterol is through the vasa vasorum and lymphatics in the outer media and adventitia, whereas LDL esterified cholesterol predominantly leaves intima via the lumen of the artery.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 3","pages":"477-85"},"PeriodicalIF":0.0,"publicationDate":"1990-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.3.477","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13493306","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":"von Willebrand factor and occlusive arterial thrombosis. A study in normal and von Willebrand's disease pigs with diet-induced hypercholesterolemia and atherosclerosis.","authors":"T C Nichols,&nbsp;D A Bellinger,&nbsp;D A Tate,&nbsp;R L Reddick,&nbsp;M S Read,&nbsp;G G Koch,&nbsp;K M Brinkhous,&nbsp;T R Griggs","doi":"10.1161/01.atv.10.3.449","DOIUrl":"https://doi.org/10.1161/01.atv.10.3.449","url":null,"abstract":"<p><p>The thrombotic response of atherosclerotic arteries to stenosis and injury was studied in 14 pigs, eight normal and six with von Willebrand's disease (vWD). Atherosclerosis was produced by feeding a 1% to 2% cholesterol diet for 24 weeks. Both groups of pigs developed severe hypercholesterolemia, greater than five times baseline values. Coronary atherosclerosis was detected in all vWD pigs and in all but one normal pig and was not significantly different between groups. At sacrifice under general anesthesia, a Goldblatt clamp (GC) was positioned around the left anterior descending coronary (LAD) and carotid arteries to produce a stenotic segment, which was pinch-injured with needle holders. A 20 MHz Doppler velocity crystal was placed distal to the GC to detect cyclic flow reductions or permanent cessation of flow velocity indicative of occlusive thrombosis. In the phenotypically normal pigs with diet-induced atherosclerosis, occlusive thrombosis was detected in seven of seven LAD and seven of seven carotid arteries. In atherosclerotic vWD pigs, occlusive thrombosis failed to form in six LAD and 10 carotid arteries (p less than 0.003, Wilcoxon rank sum test). Scanning electron micrographs demonstrated platelet-fibrin microthrombi in both groups of pigs; only phenotypically normal pigs had occlusive thrombi. Von Willebrand factor is essential for the development of occlusive thrombosis and appears to support the progression of a mixed microthrombus to an occlusive thrombus.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 3","pages":"449-61"},"PeriodicalIF":0.0,"publicationDate":"1990-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.3.449","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13494078","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":"An alpha 1/beta 1-like integrin receptor on rat aortic smooth muscle cells mediates adhesion to laminin and collagen types I and IV.","authors":"R I Clyman,&nbsp;D C Turner,&nbsp;R H Kramer","doi":"10.1161/01.atv.10.3.402","DOIUrl":"https://doi.org/10.1161/01.atv.10.3.402","url":null,"abstract":"<p><p>Extracellular matrix receptors on vascular smooth muscle cells may enable the cells to migrate through both interstitial and basement membrane matrices during vascular remodelling after injury. Rat aortic smooth muscle cells attach to surfaces coated with fibronectin, laminin, and collagen types I and IV. Members of the beta 1 family of integrin receptors appear to mediate attachment to these extracellular matrix components. We used a monoclonal antibody, 3A3, to identify a 185/120 kD, alpha 1/beta 1-like, heterodimeric integrin receptor that mediates rat aortic smooth muscle cell adhesion to collagen types I and IV as well as to laminin. This receptor appears to be the only beta 1 integrin receptor mediating adhesion to type IV collagen. On the other hand, the smooth muscle cells have several other beta 1 integrin receptors in addition to the 185/120 kD receptor that bind to laminin- and to collagen type I-Sepharose affinity columns. By using 3A3 to inhibit only the 185/120 kD receptor, we suggest that these other receptors also can be used by rat aortic smooth muscle cells to attach to laminin and collagen type I.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 3","pages":"402-9"},"PeriodicalIF":0.0,"publicationDate":"1990-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.3.402","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13314345","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":"Carotid artery atherosclerosis in cholesterol-fed female cynomolgus monkeys. Effects of oral contraceptive treatment, social factors, and regional adiposity.","authors":"C A Shively,&nbsp;J R Kaplan,&nbsp;T B Clarkson","doi":"10.1161/01.atv.10.3.358","DOIUrl":"https://doi.org/10.1161/01.atv.10.3.358","url":null,"abstract":"<p><p>Female cynomolgus monkeys, a previously established model of carotid and coronary artery atherosclerosis, were used to study the relationships between potential risk factors and carotid artery atherosclerosis. Over a 24-month treatment period, one-third of the monkeys (n = 25) were given the oral contraceptive Ovral, one-third of the monkeys (n = 26) were given the oral contraceptive Demulen, and the remaining monkeys constituted a control group (n = 26). At necropsy, the atherosclerosis extent was measured in the left and right common carotid arteries and the left and right carotid bifurcations. Plasma lipid concentrations, regional adiposity, and social status were related to carotid artery atherosclerosis extent. The relationships between regional adiposity and social status and carotid artery atherosclerosis were accounted for, at least in part, by plasma lipid concentrations. Oral contraceptives had an adverse effect on plasma cholesterol concentrations and a protective effect against carotid artery atherosclerosis after adjusting for their effect on plasma lipids. The net result of these effects was little or no change in atherosclerosis extent in the carotid arteries due to oral contraceptive treatment.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 3","pages":"358-66"},"PeriodicalIF":0.0,"publicationDate":"1990-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.3.358","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13494072","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 adhesion to vascular cells. The role of exogenous von Willebrand factor in platelet adhesion.","authors":"P F Nievelstein,&nbsp;P G de Groot,&nbsp;P D'Alessio,&nbsp;H F Heijnen,&nbsp;E Orlando,&nbsp;J J Sixma","doi":"10.1161/01.atv.10.3.462","DOIUrl":"https://doi.org/10.1161/01.atv.10.3.462","url":null,"abstract":"<p><p>Platelet deposition on cultured fibroblasts and on their extracellular matrix (FBM) was investigated in a flow system with citrated blood and was compared with platelet deposition on cultured endothelial cells, smooth muscle cells, and their extracellular matrices. Platelet deposition was present at all surfaces except on intact endothelial cells. Deposition on FBM consisted of contact platelets, spread platelets, and a few small aggregates. On intact fibroblasts cells, the surface coverage was lower, and platelets formed aggregates. Factors involved in primary hemostasis, particularly the wall shear rate, von Willebrand factor (vWF), and fibronectin, were investigated on FBM. The reactivity of FBM was determined by the passage number of the cultured cells. The vWF was involved in platelet adhesion on FBM at only the high shear rate (greater than 800 s-1). Platelet deposition was independent of plasma fibronectin at all shear rates tested. Matrix-associated fibronectin was involved in adhesion at low and high wall shear rates. We conclude that FBM can be used as a platelet adhesive surface especially to study the contribution of exogenous vWF to platelet adhesion because FBM does not contain vWF.</p>","PeriodicalId":77492,"journal":{"name":"Arteriosclerosis (Dallas, Tex.)","volume":"10 3","pages":"462-9"},"PeriodicalIF":0.0,"publicationDate":"1990-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1161/01.atv.10.3.462","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13493304","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}