Heritability of Clot Formation, Morphology, and Lysis: The EuroCLOT Study
OBJECTIVE—The relative balance between clot formation and fibrinolysis is considered to reflect thrombotic potential following vascular injury. The aims of the present study were to (1) to determine the contribution of genetic and environmental factors to variance in measures of clot structure/funct...
Saved in:
| Published in | Arteriosclerosis, thrombosis, and vascular biology Vol. 27; no. 12; pp. 2783 - 2789 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Philadelphia, PA
American Heart Association, Inc
01.12.2007
Hagerstown, MD Lippincott |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1079-5642 1524-4636 1524-4636 |
| DOI | 10.1161/ATVBAHA.107.153221 |
Cover
| Abstract | OBJECTIVE—The relative balance between clot formation and fibrinolysis is considered to reflect thrombotic potential following vascular injury. The aims of the present study were to (1) to determine the contribution of genetic and environmental factors to variance in measures of clot structure/function in the Leeds Family Study, and (2) to determine the relationship between measures of clot structure/function and cardiovascular risk.
METHODS AND RESULTS—Using high throughput turbidimetric assays, heritabilities of measures of clot formation, clot structure, and clot lysis were ≈0.30. Fibrinogen contributed to variance in all measures and plasminogen activator inhibitor-1 to variance in lysis variables. Subjects at increased cardiovascular risk due to the presence of the metabolic syndrome (MetS) had increased clot density (MaxAbsC0.358 [0.340, 0.375]au) and prolonged lysis times (LysT510 [6569, 7939]s) compared with those without MetS (MaxAbsC0.319 [0.310, 0.328]au, P=0.003; LysT7221 [4884, 5328]s, P<0.001). Furthermore, measures of clot structure/function increased progressively with increasing number of MetS components.
CONCLUSIONS—This study indicates that genetic factors contribute modestly to variance in clot structure/function and that clot structure/function is related to presence of the MetS and number of MetS components. Identification of the genetic and environmental factors influencing clot structure/function may further our understanding of the underlying factors predisposing to cardiovascular disease. |
|---|---|
| AbstractList | The relative balance between clot formation and fibrinolysis is considered to reflect thrombotic potential following vascular injury. The aims of the present study were to (1) to determine the contribution of genetic and environmental factors to variance in measures of clot structure/function in the Leeds Family Study, and (2) to determine the relationship between measures of clot structure/function and cardiovascular risk.
Using high throughput turbidimetric assays, heritabilities of measures of clot formation, clot structure, and clot lysis were approximately 0.30. Fibrinogen contributed to variance in all measures and plasminogen activator inhibitor-1 to variance in lysis variables. Subjects at increased cardiovascular risk due to the presence of the metabolic syndrome (MetS) had increased clot density (MaxAbs(C): 0.358 [0.340, 0.375]au) and prolonged lysis times (Lys(T): 510 [6569, 7939]s) compared with those without MetS (MaxAbs(C): 0.319 [0.310, 0.328]au, P=0.003; Lys(T): 7221 [4884, 5328]s, P<0.001). Furthermore, measures of clot structure/function increased progressively with increasing number of MetS components.
This study indicates that genetic factors contribute modestly to variance in clot structure/function and that clot structure/function is related to presence of the MetS and number of MetS components. Identification of the genetic and environmental factors influencing clot structure/function may further our understanding of the underlying factors predisposing to cardiovascular disease. The relative balance between clot formation and fibrinolysis is considered to reflect thrombotic potential following vascular injury. The aims of the present study were to (1) to determine the contribution of genetic and environmental factors to variance in measures of clot structure/function in the Leeds Family Study, and (2) to determine the relationship between measures of clot structure/function and cardiovascular risk.OBJECTIVEThe relative balance between clot formation and fibrinolysis is considered to reflect thrombotic potential following vascular injury. The aims of the present study were to (1) to determine the contribution of genetic and environmental factors to variance in measures of clot structure/function in the Leeds Family Study, and (2) to determine the relationship between measures of clot structure/function and cardiovascular risk.Using high throughput turbidimetric assays, heritabilities of measures of clot formation, clot structure, and clot lysis were approximately 0.30. Fibrinogen contributed to variance in all measures and plasminogen activator inhibitor-1 to variance in lysis variables. Subjects at increased cardiovascular risk due to the presence of the metabolic syndrome (MetS) had increased clot density (MaxAbs(C): 0.358 [0.340, 0.375]au) and prolonged lysis times (Lys(T): 510 [6569, 7939]s) compared with those without MetS (MaxAbs(C): 0.319 [0.310, 0.328]au, P=0.003; Lys(T): 7221 [4884, 5328]s, P<0.001). Furthermore, measures of clot structure/function increased progressively with increasing number of MetS components.METHODS AND RESULTSUsing high throughput turbidimetric assays, heritabilities of measures of clot formation, clot structure, and clot lysis were approximately 0.30. Fibrinogen contributed to variance in all measures and plasminogen activator inhibitor-1 to variance in lysis variables. Subjects at increased cardiovascular risk due to the presence of the metabolic syndrome (MetS) had increased clot density (MaxAbs(C): 0.358 [0.340, 0.375]au) and prolonged lysis times (Lys(T): 510 [6569, 7939]s) compared with those without MetS (MaxAbs(C): 0.319 [0.310, 0.328]au, P=0.003; Lys(T): 7221 [4884, 5328]s, P<0.001). Furthermore, measures of clot structure/function increased progressively with increasing number of MetS components.This study indicates that genetic factors contribute modestly to variance in clot structure/function and that clot structure/function is related to presence of the MetS and number of MetS components. Identification of the genetic and environmental factors influencing clot structure/function may further our understanding of the underlying factors predisposing to cardiovascular disease.CONCLUSIONSThis study indicates that genetic factors contribute modestly to variance in clot structure/function and that clot structure/function is related to presence of the MetS and number of MetS components. Identification of the genetic and environmental factors influencing clot structure/function may further our understanding of the underlying factors predisposing to cardiovascular disease. Objective— The relative balance between clot formation and fibrinolysis is considered to reflect thrombotic potential following vascular injury. The aims of the present study were to (1) to determine the contribution of genetic and environmental factors to variance in measures of clot structure/function in the Leeds Family Study, and (2) to determine the relationship between measures of clot structure/function and cardiovascular risk. Methods and Results— Using high throughput turbidimetric assays, heritabilities of measures of clot formation, clot structure, and clot lysis were ≈0.30. Fibrinogen contributed to variance in all measures and plasminogen activator inhibitor-1 to variance in lysis variables. Subjects at increased cardiovascular risk due to the presence of the metabolic syndrome (MetS) had increased clot density (MaxAbs C : 0.358 [0.340, 0.375]au) and prolonged lysis times (Lys T : 510 [6569, 7939]s) compared with those without MetS (MaxAbs C : 0.319 [0.310, 0.328]au, P =0.003; Lys T : 7221 [4884, 5328]s, P <0.001). Furthermore, measures of clot structure/function increased progressively with increasing number of MetS components. Conclusions— This study indicates that genetic factors contribute modestly to variance in clot structure/function and that clot structure/function is related to presence of the MetS and number of MetS components. Identification of the genetic and environmental factors influencing clot structure/function may further our understanding of the underlying factors predisposing to cardiovascular disease. Heritabilities of turbidimetric measures of structure/function were ≈0.30 in the Leeds Family Study. Clot structure/function was related to presence of the metabolic syndrome and number of metabolic syndrome components. Identification of the genetic and environmental factors influencing clot structure/function may further our understanding of factors predisposing to cardiovascular disease. OBJECTIVE—The relative balance between clot formation and fibrinolysis is considered to reflect thrombotic potential following vascular injury. The aims of the present study were to (1) to determine the contribution of genetic and environmental factors to variance in measures of clot structure/function in the Leeds Family Study, and (2) to determine the relationship between measures of clot structure/function and cardiovascular risk. METHODS AND RESULTS—Using high throughput turbidimetric assays, heritabilities of measures of clot formation, clot structure, and clot lysis were ≈0.30. Fibrinogen contributed to variance in all measures and plasminogen activator inhibitor-1 to variance in lysis variables. Subjects at increased cardiovascular risk due to the presence of the metabolic syndrome (MetS) had increased clot density (MaxAbsC0.358 [0.340, 0.375]au) and prolonged lysis times (LysT510 [6569, 7939]s) compared with those without MetS (MaxAbsC0.319 [0.310, 0.328]au, P=0.003; LysT7221 [4884, 5328]s, P<0.001). Furthermore, measures of clot structure/function increased progressively with increasing number of MetS components. CONCLUSIONS—This study indicates that genetic factors contribute modestly to variance in clot structure/function and that clot structure/function is related to presence of the MetS and number of MetS components. Identification of the genetic and environmental factors influencing clot structure/function may further our understanding of the underlying factors predisposing to cardiovascular disease. |
| Author | Grant, Peter J. Cymbalista, Charlotte M. Carter, Angela M. Spector, Tim D. |
| AuthorAffiliation | From the Academic Unit of Molecular Vascular Medicine (A.M.C., C.M.C., P.J.G.), The LIGHT Laboratories, University of Leeds, UK; and Twin Research & Genetic Epidemiology Unit (T.D.S.), King’s College London, London, UK |
| AuthorAffiliation_xml | – name: From the Academic Unit of Molecular Vascular Medicine (A.M.C., C.M.C., P.J.G.), The LIGHT Laboratories, University of Leeds, UK; and Twin Research & Genetic Epidemiology Unit (T.D.S.), King’s College London, London, UK |
| Author_xml | – sequence: 1 givenname: Angela surname: Carter middlename: M. fullname: Carter, Angela M. organization: From the Academic Unit of Molecular Vascular Medicine (A.M.C., C.M.C., P.J.G.), The LIGHT Laboratories, University of Leeds, UK; and Twin Research & Genetic Epidemiology Unit (T.D.S.), King’s College London, London, UK – sequence: 2 givenname: Charlotte surname: Cymbalista middlename: M. fullname: Cymbalista, Charlotte M. – sequence: 3 givenname: Tim surname: Spector middlename: D. fullname: Spector, Tim D. – sequence: 4 givenname: Peter surname: Grant middlename: J. fullname: Grant, Peter J. |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19872750$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/17932316$$D View this record in MEDLINE/PubMed |
| BookMark | eNp9kU2P0zAQhi20iP2AP8AB-QKnTfHYjp1wK9UuXaloDxSulhNPaMCNi-1olX9PVi0gcdjTzEjPM9LMe0nOhjAgIa-BLQAUvF9uv31crpcLYHoBpeAcnpELKLkspBLqbO6ZrotSSX5OLlP6wRiTnLMX5Bx0LbgAdUHu1hj7bJve93mioaMrHzK9DXFvcx-Ga_o5xMMu-PB9uqZ2cHQzpT59oNsd0psxhtXmfku_5NFNL8nzzvqEr071iny9vdmu1sXm_tPdarkpWgkCitoK11W1aMtWVYCWl0rLqkHnHLJOQKlrcAqwQuYaJplwrsKaN7IG1ilpxRV5d9x7iOHXiCmbfZ9a9N4OGMZkVFUKprWewTcncGz26Mwh9nsbJ_Pn-Bl4ewJsaq3voh3aPv3j6kpzXbKZq45cG0NKETvTzi97fE-OtvcGmHnMw5zymGdtjnnMKv9P_bv9KUkdpYfgM8b0048PGM0Orc-7p8TfB8mcjg |
| CODEN | ATVBFA |
| CitedBy_id | crossref_primary_10_1111_ijlh_14340 crossref_primary_10_3390_ijms26020746 crossref_primary_10_1017_thg_2019_75 crossref_primary_10_1253_circj_CJ_09_0835 crossref_primary_10_7759_cureus_33093 crossref_primary_10_1586_erc_13_20 crossref_primary_10_1016_j_thromres_2019_09_032 crossref_primary_10_6064_2012_402783 crossref_primary_10_1016_j_thromres_2015_11_008 crossref_primary_10_2337_dc11_1242 crossref_primary_10_1111_ijlh_14195 crossref_primary_10_2337_dc10_zb07 crossref_primary_10_1016_j_atherosclerosis_2022_01_011 crossref_primary_10_1016_j_numecd_2010_03_002 crossref_primary_10_1371_journal_pone_0048881 crossref_primary_10_3389_fendo_2019_00189 crossref_primary_10_1371_journal_pone_0035690 crossref_primary_10_3390_jcm10132999 crossref_primary_10_1093_cvr_cvad017 crossref_primary_10_1080_00365513_2024_2369993 crossref_primary_10_1186_s12933_019_0981_3 crossref_primary_10_1016_j_thromres_2014_12_030 crossref_primary_10_1111_hae_13961 crossref_primary_10_5551_jat_30676 crossref_primary_10_1177_1076029613486016 crossref_primary_10_1097_NCI_0b013e3181a0b5e8 crossref_primary_10_1371_journal_pone_0071150 crossref_primary_10_1055_s_0040_1713753 crossref_primary_10_2337_dc18_0050 crossref_primary_10_1586_epr_09_75 crossref_primary_10_1186_s12933_021_01427_y crossref_primary_10_1016_j_niox_2022_02_002 crossref_primary_10_1007_s11739_020_02375_3 crossref_primary_10_1016_j_rpth_2023_100043 crossref_primary_10_1186_s12878_017_0086_8 crossref_primary_10_1177_0271678X231214826 crossref_primary_10_1016_j_thromres_2020_04_040 crossref_primary_10_1038_s41598_024_60706_2 crossref_primary_10_1160_TH11_09_0662 crossref_primary_10_1186_s12933_021_01230_9 crossref_primary_10_1080_03008207_2016_1215443 crossref_primary_10_1111_j_1538_7836_2011_04343_x crossref_primary_10_1111_j_1538_7836_2010_03966_x crossref_primary_10_3390_jcm9062002 crossref_primary_10_1182_blood_2016_10_747915 crossref_primary_10_1016_j_thromres_2015_05_033 crossref_primary_10_1007_s10067_019_04629_8 crossref_primary_10_1177_1479164111432788 crossref_primary_10_1007_s13311_022_01203_0 crossref_primary_10_1016_j_trsl_2019_08_009 crossref_primary_10_1007_s00125_011_2301_7 crossref_primary_10_1016_j_numecd_2022_12_011 crossref_primary_10_1016_j_thromres_2014_07_013 crossref_primary_10_1182_blood_2013_01_481549 crossref_primary_10_1016_j_thromres_2014_03_039 crossref_primary_10_3390_antiox11040779 crossref_primary_10_1160_th14_05_0468 crossref_primary_10_1016_j_ahj_2024_11_012 crossref_primary_10_1016_j_rpth_2024_102361 crossref_primary_10_2478_ahem_2024_0011 crossref_primary_10_1080_09537104_2019_1572880 crossref_primary_10_1016_j_thromres_2011_08_022 crossref_primary_10_1160_TH11_01_0027 crossref_primary_10_1160_TH17_04_0259 crossref_primary_10_1016_j_thromres_2020_10_014 crossref_primary_10_1080_00207454_2018_1550400 crossref_primary_10_1111_sms_12836 crossref_primary_10_1111_tme_12989 crossref_primary_10_1093_clinchem_hvz015 crossref_primary_10_1182_blood_2009_05_222380 crossref_primary_10_1111_jth_12645 crossref_primary_10_3389_fimmu_2021_718845 crossref_primary_10_3109_10641963_2015_1013123 crossref_primary_10_1016_j_thromres_2013_12_016 crossref_primary_10_1111_ijlh_13183 crossref_primary_10_1016_j_thromres_2017_06_028 crossref_primary_10_1016_j_hrthm_2015_06_038 crossref_primary_10_1007_s11695_013_1100_2 crossref_primary_10_1186_s12933_021_01372_w crossref_primary_10_1681_ASN_2016030336 crossref_primary_10_1160_TH13_01_0075 crossref_primary_10_3324_haematol_2019_239558 crossref_primary_10_1097_MBC_0b013e32835a083c crossref_primary_10_1161_ATVBAHA_123_318286 crossref_primary_10_1016_j_jstrokecerebrovasdis_2024_107927 crossref_primary_10_3389_fendo_2018_00026 crossref_primary_10_3390_jcm12103471 crossref_primary_10_1093_eurheartj_ehy013 crossref_primary_10_1016_j_rpth_2023_100081 crossref_primary_10_1016_j_jacc_2019_07_030 crossref_primary_10_1182_bloodadvances_2024014235 crossref_primary_10_3390_life14050634 crossref_primary_10_1016_j_jstrokecerebrovasdis_2015_07_015 crossref_primary_10_1016_j_thromres_2014_02_023 crossref_primary_10_1160_TH15_12_0985 crossref_primary_10_1016_j_nano_2018_01_006 crossref_primary_10_1111_j_1538_7836_2012_04789_x crossref_primary_10_1160_th15_06_0467 crossref_primary_10_1093_bja_aev199 crossref_primary_10_1016_j_procbio_2013_03_017 crossref_primary_10_1016_j_atherosclerosis_2010_12_040 crossref_primary_10_1111_jth_14002 crossref_primary_10_3390_biom11091263 crossref_primary_10_1182_blood_2010_11_320325 crossref_primary_10_1016_j_freeradbiomed_2015_09_006 crossref_primary_10_1160_TH14_05_0404 crossref_primary_10_1097_MBC_0000000000000062 crossref_primary_10_3109_10715762_2014_960866 crossref_primary_10_1097_HJH_0000000000001316 crossref_primary_10_1016_j_freeradbiomed_2019_07_003 crossref_primary_10_1016_j_thromres_2014_08_018 crossref_primary_10_1007_s11239_011_0593_6 crossref_primary_10_1016_j_thromres_2012_11_010 crossref_primary_10_2337_dc13_1776 crossref_primary_10_1182_blood_2012_12_471482 crossref_primary_10_1371_journal_pone_0275956 crossref_primary_10_1177_1479164120920582 crossref_primary_10_1182_blood_2011_03_339572 crossref_primary_10_1016_j_thromres_2018_04_025 crossref_primary_10_1039_c4ib00173g crossref_primary_10_1111_jth_12872 crossref_primary_10_1002_ana_23838 crossref_primary_10_1177_17474930211067352 crossref_primary_10_1111_cen_12137 crossref_primary_10_1111_cen_12258 crossref_primary_10_1016_j_thromres_2018_01_004 |
| Cites_doi | 10.1016/S0140-6736(03)13135-2 10.1055/s-0037-1612909 10.1160/TH06-09-0517 10.1161/01.atv.0000241589.52950.4c 10.1016/S0049-3848(99)00092-4 10.1016/S0140-6736(00)03541-8 10.1074/jbc.M212734200 10.1111/j.1538-7933.2003.00592.x 10.1160/TH04-01-0001 10.1161/atvb.22.3.506 10.1046/j.1464-5491.2002.00843.x 10.1086/316903 10.1055/s-0037-1615374 10.1007/s00277-004-0928-x 10.1016/0167-4838(89)90140-4 10.1016/j.jacc.2004.09.051 10.1161/atvb.20.5.1354 10.1055/s-0038-1650618 10.1161/01.cir.0000033221.73082.06 10.1016/0049-3848(94)90245-3 10.1353/hub.2005.0034 10.1182/blood-2003-07-2247 10.1111/j.1538-7836.2005.01778.x 10.1007/s00125-006-0197-4 10.1055/s-0037-1614250 10.1016/S0140-6736(05)67402-8 10.1375/136905203321536281 10.1111/j.1365-2796.2007.01781.x 10.1182/blood-2004-08-3253 10.1182/blood.V83.9.2541.2541 10.1016/S0140-6736(02)07813-3 10.1111/j.1538-7836.2006.01882.x |
| ContentType | Journal Article |
| Copyright | 2007 American Heart Association, Inc. 2008 INIST-CNRS |
| Copyright_xml | – notice: 2007 American Heart Association, Inc. – notice: 2008 INIST-CNRS |
| CorporateAuthor | EuroCLOT Investigators |
| CorporateAuthor_xml | – name: EuroCLOT Investigators |
| DBID | AAYXX CITATION IQODW CGR CUY CVF ECM EIF NPM 7X8 |
| DOI | 10.1161/ATVBAHA.107.153221 |
| DatabaseName | CrossRef Pascal-Francis Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE MEDLINE - Academic CrossRef |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 1524-4636 |
| EndPage | 2789 |
| ExternalDocumentID | 17932316 19872750 10_1161_ATVBAHA_107_153221 10.1161/ATVBAHA.107.153221 |
| Genre | Research Support, Non-U.S. Gov't Journal Article |
| GroupedDBID | --- .3C .55 .GJ .Z2 01R 0R~ 1J1 23N 2WC 3O- 40H 4Q1 4Q2 4Q3 53G 5GY 5RE 5VS 71W 77Y 7O~ AAAAV AAAXR AAGIX AAHPQ AAIQE AAMOA AAMTA AAQKA AARTV AASCR AASOK AAXQO ABASU ABBUW ABDIG ABJNI ABPXF ABQRW ABVCZ ABXVJ ABZAD ABZZY ACCJW ACDDN ACEWG ACGFS ACGOD ACILI ACLDA ACPRK ACWDW ACWRI ACXJB ACXNZ ACZKN ADBBV ADFPA ADGGA ADHPY ADNKB AE3 AE6 AEETU AENEX AFBFQ AFDTB AFFNX AFUWQ AGINI AHJKT AHMBA AHOMT AHQNM AHRYX AHVBC AIJEX AINUH AJCLO AJIOK AJNWD AJNYG AJZMW AKCTQ AKULP ALKUP ALMA_UNASSIGNED_HOLDINGS ALMTX AMJPA AMKUR AMNEI AOHHW AOQMC AYCSE BAWUL BOYCO BQLVK BS7 C1A C45 CS3 DIK DIWNM DUNZO E.X E3Z EBS EEVPB EJD ERAAH EX3 F2K F2L F2M F2N F5P FCALG FL- FRP FW0 GNXGY GQDEL GX1 H0~ H13 HLJTE HZ~ IKREB IKYAY IN~ IPNFZ J5H JF9 JG8 JK3 JK8 K8S KD2 KMI KQ8 L-C L7B N9A N~7 N~B N~M O9- OAG OAH OB2 OCUKA ODA OL1 OLG OLH OLU OLV OLY OLZ OPUJH ORVUJ OUVQU OVD OVDNE OVIDH OVLEI OWU OWV OWW OWX OWY OWZ OXXIT P-K P2P PQQKQ PZZ RAH RIG RLZ S4R S4S T8P TEORI TR2 TSPGW V2I VVN W3M W8F WOQ WOW X3V X3W X7M XXN XYM YFH ZGI ZZMQN AAYXX ADGHP CITATION IQODW CGR CUY CVF ECM EIF NPM 7X8 |
| ID | FETCH-LOGICAL-c4131-9a3df893c5c681ea256748beddde0f315791d61e8e0db0403dd8e92b4910f64a3 |
| ISSN | 1079-5642 1524-4636 |
| IngestDate | Fri Jul 11 09:05:32 EDT 2025 Mon Jul 21 05:36:01 EDT 2025 Mon Jul 21 09:11:37 EDT 2025 Tue Jul 01 02:21:25 EDT 2025 Thu Apr 24 23:10:13 EDT 2025 Fri May 16 03:46:46 EDT 2025 |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 12 |
| Keywords | Endocrinopathy Vascular disease Atherosclerosis Lysis Metabolic diseases Cardiovascular disease Metabolic syndrome Fibrinolysis coagulation Clot heritability |
| Language | English |
| License | CC BY 4.0 |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c4131-9a3df893c5c681ea256748beddde0f315791d61e8e0db0403dd8e92b4910f64a3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
| PMID | 17932316 |
| PQID | 68530777 |
| PQPubID | 23479 |
| PageCount | 7 |
| ParticipantIDs | proquest_miscellaneous_68530777 pubmed_primary_17932316 pascalfrancis_primary_19872750 crossref_citationtrail_10_1161_ATVBAHA_107_153221 crossref_primary_10_1161_ATVBAHA_107_153221 wolterskluwer_health_10_1161_ATVBAHA_107_153221 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2007-December |
| PublicationDateYYYYMMDD | 2007-12-01 |
| PublicationDate_xml | – month: 12 year: 2007 text: 2007-December |
| PublicationDecade | 2000 |
| PublicationPlace | Philadelphia, PA Hagerstown, MD |
| PublicationPlace_xml | – name: Philadelphia, PA – name: Hagerstown, MD – name: United States |
| PublicationTitle | Arteriosclerosis, thrombosis, and vascular biology |
| PublicationTitleAlternate | Arterioscler Thromb Vasc Biol |
| PublicationYear | 2007 |
| Publisher | American Heart Association, Inc Lippincott |
| Publisher_xml | – name: American Heart Association, Inc – name: Lippincott |
| References | e_1_3_3_17_2 e_1_3_3_16_2 e_1_3_3_19_2 e_1_3_3_18_2 e_1_3_3_13_2 e_1_3_3_12_2 e_1_3_3_15_2 e_1_3_3_34_2 e_1_3_3_14_2 (e_1_3_3_32_2) 2004; 29 e_1_3_3_33_2 e_1_3_3_11_2 e_1_3_3_30_2 e_1_3_3_10_2 e_1_3_3_31_2 e_1_3_3_6_2 e_1_3_3_5_2 e_1_3_3_8_2 e_1_3_3_7_2 e_1_3_3_28_2 e_1_3_3_9_2 e_1_3_3_27_2 e_1_3_3_29_2 e_1_3_3_24_2 e_1_3_3_23_2 e_1_3_3_26_2 e_1_3_3_25_2 e_1_3_3_2_2 e_1_3_3_20_2 e_1_3_3_1_2 e_1_3_3_4_2 e_1_3_3_22_2 e_1_3_3_3_2 e_1_3_3_21_2 |
| References_xml | – ident: e_1_3_3_29_2 doi: 10.1016/S0140-6736(03)13135-2 – ident: e_1_3_3_2_2 doi: 10.1055/s-0037-1612909 – ident: e_1_3_3_27_2 doi: 10.1160/TH06-09-0517 – ident: e_1_3_3_13_2 doi: 10.1161/01.atv.0000241589.52950.4c – ident: e_1_3_3_17_2 doi: 10.1016/S0049-3848(99)00092-4 – ident: e_1_3_3_3_2 doi: 10.1016/S0140-6736(00)03541-8 – ident: e_1_3_3_23_2 doi: 10.1074/jbc.M212734200 – ident: e_1_3_3_6_2 doi: 10.1111/j.1538-7933.2003.00592.x – ident: e_1_3_3_9_2 doi: 10.1160/TH04-01-0001 – ident: e_1_3_3_5_2 doi: 10.1161/atvb.22.3.506 – ident: e_1_3_3_15_2 doi: 10.1046/j.1464-5491.2002.00843.x – ident: e_1_3_3_1_2 doi: 10.1086/316903 – ident: e_1_3_3_30_2 doi: 10.1055/s-0037-1615374 – ident: e_1_3_3_19_2 doi: 10.1007/s00277-004-0928-x – ident: e_1_3_3_24_2 doi: 10.1016/0167-4838(89)90140-4 – ident: e_1_3_3_28_2 doi: 10.1016/j.jacc.2004.09.051 – ident: e_1_3_3_22_2 doi: 10.1161/atvb.20.5.1354 – ident: e_1_3_3_12_2 doi: 10.1055/s-0038-1650618 – ident: e_1_3_3_14_2 doi: 10.1161/01.cir.0000033221.73082.06 – ident: e_1_3_3_25_2 doi: 10.1016/0049-3848(94)90245-3 – ident: e_1_3_3_7_2 doi: 10.1353/hub.2005.0034 – ident: e_1_3_3_11_2 doi: 10.1182/blood-2003-07-2247 – ident: e_1_3_3_8_2 doi: 10.1111/j.1538-7836.2005.01778.x – ident: e_1_3_3_33_2 doi: 10.1007/s00125-006-0197-4 – ident: e_1_3_3_10_2 – ident: e_1_3_3_26_2 doi: 10.1055/s-0037-1614250 – ident: e_1_3_3_16_2 doi: 10.1016/S0140-6736(05)67402-8 – ident: e_1_3_3_31_2 doi: 10.1375/136905203321536281 – ident: e_1_3_3_21_2 doi: 10.1111/j.1365-2796.2007.01781.x – ident: e_1_3_3_34_2 doi: 10.1182/blood-2004-08-3253 – ident: e_1_3_3_20_2 doi: 10.1182/blood.V83.9.2541.2541 – ident: e_1_3_3_4_2 doi: 10.1016/S0140-6736(02)07813-3 – volume: 29 start-page: 470 year: 2004 ident: e_1_3_3_32_2 publication-title: Herz – ident: e_1_3_3_18_2 doi: 10.1111/j.1538-7836.2006.01882.x |
| SSID | ssj0004220 |
| Score | 2.3263304 |
| Snippet | OBJECTIVE—The relative balance between clot formation and fibrinolysis is considered to reflect thrombotic potential following vascular injury. The aims of the... Objective— The relative balance between clot formation and fibrinolysis is considered to reflect thrombotic potential following vascular injury. The aims of... The relative balance between clot formation and fibrinolysis is considered to reflect thrombotic potential following vascular injury. The aims of the present... |
| SourceID | proquest pubmed pascalfrancis crossref wolterskluwer |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 2783 |
| SubjectTerms | Adult Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Blood Coagulation - genetics Blood Coagulation Tests - methods Cardiology. Vascular system Cardiovascular Diseases - blood Cardiovascular Diseases - genetics Cardiovascular system Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Europe Female Fibrinogen - metabolism Fibrinolysis - genetics Genetic Predisposition to Disease Genetic Variation Gynecology. Andrology. Obstetrics Humans Male Mammary gland diseases Medical sciences Metabolic Syndrome - blood Metabolic Syndrome - complications Metabolic Syndrome - genetics Middle Aged Nephelometry and Turbidimetry Pedigree Pharmacology. Drug treatments Plasminogen Activator Inhibitor 1 - blood Risk Factors Thrombosis - blood Thrombosis - complications Thrombosis - genetics Time Factors Tumors Vasodilator agents. Cerebral vasodilators |
| Title | Heritability of Clot Formation, Morphology, and Lysis: The EuroCLOT Study |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/17932316 https://www.proquest.com/docview/68530777 |
| Volume | 27 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Zj9MwELbKIiGkFeImHEseeMsmG-ewk8dwLNWKIiG6aN-ixLElRLeptqlW8GP4rczEzlEoK5aXqE1iy_VM5_DMfEPIKyUSX4Av60qeCBfRUdzUl4mLyOCBojKNEywUnn1k09Po5Cw-m0x-jrKWNk3piR8760r-h6pwD-iKVbLXoGw_KdyAz0BfuAKF4fpPNJ5KdO3b9FadV7GoG-e4K0dszzpr2Me-IAUPyT8gBMnYJM0wqfNrvYa5QWNqyAFsnnBedt9wWJ-xalCbhtjFhWntkWF6bOHMvP7R9_MS4RW1fdrG9eumkaM3Pq9MzKDlGedt_-A9aNAhfdg58bYOJ_go0UPLU5-nbsw0gJYnjYwNIhdxysZCWAMEdMwWjEUq151ujHrGyt3dop-h6M_mX15n08yjeHAWg7Sig6Lrgvu_6b8-K7H1hxjNzRw5zJHrOW6QmwEH2wyD_p9GaPRBoNEuzI_sirIYPfpzHVuGz_4KqFYslG6essu7gXcua0yYWH9r6yVGVs_8Lrlj3BU707x3j0zk8j65NTMJGQ9IPGZBu1Y2sqDds-ChPTDgoQ18ZLfs95CcHr-bv5m6phOHK8DIoW5ahJUCy1bEgiVUFmAn8ygpZQXK0VchjXlKK0ZlIv2qBLUQVlUi06CMwBhVLCrCR2RvWS_lE2JHUqmkEtg-MYwCKlKwJ-OUCXCro7JMC4vQbptyYWDqsVvKIv87eSzi9GNWGqTlyrcPtnZ_GAIyC9sdWORlR44chC1G0IqlrDfrnIFx63POLfJYU2kYC3oOXCVmkaMtsuW6nPmK5Ty91uKfkdvD_-w52WsuNvIFmMVNedDy5i9AeK4U |
| linkProvider | Colorado Alliance of Research Libraries |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Heritability+of+Clot+Formation%2C+Morphology%2C+and+Lysis&rft.jtitle=Arteriosclerosis%2C+thrombosis%2C+and+vascular+biology&rft.au=Carter%2C+Angela+M.&rft.au=Cymbalista%2C+Charlotte+M.&rft.au=Spector%2C+Tim+D.&rft.au=Grant%2C+Peter+J.&rft.date=2007-12-01&rft.issn=1079-5642&rft.eissn=1524-4636&rft.volume=27&rft.issue=12&rft.spage=2783&rft.epage=2789&rft_id=info:doi/10.1161%2FATVBAHA.107.153221&rft.externalDBID=n%2Fa&rft.externalDocID=10_1161_ATVBAHA_107_153221 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1079-5642&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1079-5642&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1079-5642&client=summon |