Procoagulatory changes induced by head-up tilt test in patients with syncope: observational study

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Abstract

Background

Orthostatic hypercoagulability is proposed as a mechanism promoting cardiovascular and thromboembolic events after awakening and during prolonged orthostasis.

We evaluated early changes in coagulation biomarkers induced by tilt testing among patients investigated for suspected syncope, aiming to test the hypothesis that orthostatic challenge evokes procoagulatory changes to a different degree according to diagnosis.

Methods

One-hundred-and-seventy-eight consecutive patients (age, 51 ± 21 years; 46% men) were analysed. Blood samples were collected during supine rest and after 3 min of 70° head-up tilt test (HUT) for determination of fibrinogen, von Willebrand factor antigen (VWF:Ag) and activity (VWF:GP1bA), factor VIII (FVIII:C), lupus anticoagulant (LA1), functional APC-resistance, and activated prothrombin time (APTT) with and without activated protein C (C+/−). Analyses were stratified according to age, sex and diagnosis.

Results

After 3 min in the upright position, VWF:Ag (1.28 ± 0.55 vs. 1.22 ± 0.54; p < 0.001) and fibrinogen (2.84 ± 0.60 vs. 2.75 ± 0.60, p < 0.001) increased, whereas APTT/C+/− (75.1 ± 18.8 vs. 84.3 ± 19.6 s; p < 0.001, and 30.8 ± 3.7 vs. 32.1 ± 3.8 s; p < 0.001, respectively) and APC-resistance (2.42 ± 0.43 vs. 2.60 ± 0.41, p < 0.001) decreased compared with supine values. Significant changes in fibrinogen were restricted to women ( p < 0.001) who also had lower LA1 during HUT ( p = 0.007), indicating increased coagulability. Diagnosis vasovagal syncope was associated with less increase in VWF:Ag during HUT compared to other diagnoses (0.01 ± 0.16 vs. 0.09 ± 0.17; p = 0.004).

Conclusions

Procoagulatory changes in haemostatic plasma components are observed early during orthostasis in patients with history of syncope, irrespective of syncope aetiology. These findings may contribute to the understanding of orthostatic hypercoagulability and chronobiology of cardiovascular disease.

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Most cited references 31

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Guidelines for the diagnosis and management of syncope (version 2009).

A. Moya, R. Sutton, F Ammirati … (2009)

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Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death.

J. Müller, I Schäfer, Nicola Rutherford … (1987)

We have previously reported that the frequencies of myocardial infarction and of sudden cardiac death are highest during the period from 6 a.m. to noon. Since platelet aggregation may have a role in triggering these disorders, we measured platelet activity at 3-hour intervals for 24 hours in 15 healthy men. In vitro platelet responsiveness to either adenosine diphosphate (ADP) or epinephrine was lower at 6 a.m. (before the subjects arose) than at 9 a.m. (60 minutes after they arose). The lowest concentration of these agents required to produce biphasic platelet aggregation decreased (i.e., aggregability increased) from a mean +/- SEM of 4.7 +/- 0.6 to 3.7 +/- 0.6 microM (P less than 0.01) for ADP and from 3.7 +/- 0.8 to 1.8 +/- 0.5 microM (P less than 0.01) for epinephrine. The period from 6 to 9 a.m. was the only interval in the 24-hour period during which platelet aggregability increased significantly. We subsequently studied 10 subjects on alternate mornings after they arose at the normal time and after delayed arising. The morning increase in platelet aggregability was not observed when the subjects remained supine and inactive. Thus, there is a temporal association between increased platelet aggregability in the morning and an increased frequency of myocardial infarction and of sudden cardiac death. Demonstration of this association does not establish a cause--effect relation, but together with other evidence linking platelets to these disorders, it may provide insight into the mechanisms precipitating myocardial infarction and sudden cardiac death and aid in the design of more effective preventive measures.

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Fibrinogen and risk of cardiovascular disease. The Framingham Study.

Svenja Wolf, B D’Agostino, W Castelli … (1987)

During the tenth biennial examination of the Framingham Study, 1315 participants who were free of cardiovascular disease had fibrinogen levels measured. During the ensuing 12 years, cardiovascular disease developed in 165 men and 147 women. For both sexes, the risk of cardiovascular disease was correlated positively to antecedent fibrinogen values higher than the 1.3 to 7.0 g/L (126 to 696 mg/dL) range. The magnitude of the risk diminished with advancing age in women but not in men. Risk for coronary heart disease also was significantly related to fibrinogen level. Here, the magnitude of risk displayed diminishing impact with age, again only in women. Risk of stroke increased progressively with fibrinogen level in men but not in women. The impact of fibrinogen value, considered as a separate variable, on cardiovascular disease was comparable with the major risk factors, such as blood pressure, hematocrit, adiposity, cigarette smoking, and diabetes. Fibrinogen values were also significantly related to these risk factors. Taking all these into account in a multivariate analysis, fibrinogen level was still significantly related to the incidence of cardiovascular disease in men and marginally significant in women. For coronary heart disease, the fibrinogen level was significant for both men and women. Elevated fibrinogen level is a predictor of cardiovascular disease that should be added to the cardiovascular risk factor profile.

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Author and article information

Contributors

Viktor Hamrefors:

ORCID: http://orcid.org/0000-0002-8475-0866

Viktor.hamrefors@med.lu.se

Artur Fedorowski: +46 40 33 10 00 , Artur.fedorowski@med.lu.se

Karin Strandberg: karin.strandberg@med.lu.se

Richard Sutton: r.sutton@imperial.ac.uk

Nazim Isma: nazim.isma@med.lu.se

Journal

Journal ID (nlm-ta): Thromb J

Journal ID (iso-abbrev): Thromb J

Title: Thrombosis Journal

Publisher: BioMed Central (London )

ISSN (Electronic): 1477-9560

Publication date (Electronic): 20 June 2017

Publication date PMC-release: 20 June 2017

Publication date Collection: 2017

Volume: 15

Electronic Location Identifier: 16

Affiliations

[1 ]ISNI 0000 0001 0930 2361, GRID grid.4514.4, Department of Clinical Sciences Malmö, , Lund University, ; SE 205-02 Malmö, Sweden

[2 ]ISNI 0000 0004 0623 9987, GRID grid.412650.4, Department of Internal Medicine, , Skåne University Hospital, ; SE 205-02 Malmö, Sweden

[3 ]ISNI 0000 0004 0623 9987, GRID grid.412650.4, Department of Medical Imaging and Physiology, , Skåne University Hospital, ; SE 205-02 Malmö, Sweden

[4 ]ISNI 0000 0004 0623 9987, GRID grid.412650.4, Department of Cardiology, , Skåne University Hospital, ; Inga Marie Nilssons gata 46, SE 205-02 Malmö, Sweden

[5 ]ISNI 0000 0004 0623 9987, GRID grid.412650.4, Centre for Thrombosis and Haemostasis, , Skåne University Hospital, ; SE 205-02 Malmö, Sweden

[6 ]ISNI 0000 0001 0705 4923, GRID grid.413629.b, National Heart and Lung Institute, Imperial College, , Hammersmith Hospital Campus, ; Ducane Road, London, W12 0NN UK

[7 ]GRID grid.411843.b, Department of Cardiology, , Skåne University Hospital, ; SE 221-85 Lund, Sweden

Author information

Viktor Hamrefors http://orcid.org/0000-0002-8475-0866

Article

Publisher ID: 139

DOI: 10.1186/s12959-017-0139-z

PMC ID: 5477734

SO-VID: dbca81b5-ba8f-405d-aadf-d5bac8c15622

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 30 March 2017

Date accepted : 13 June 2017

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100000781, European Research Council;

Award ID: StG 282225

Funded by: Swedish Medical Research Council

Funded by: FundRef http://dx.doi.org/10.13039/501100003793, Hjärt-Lungfonden;

Funded by: The Medical Faculty of Lund University

Funded by: The Crafoord Foundation

Funded by: The Ernhold Lundströms Research Foundation

Funded by: The Hulda and Conrad Mossfelt Foundation

Funded by: The Anna Lisa and Sven Erik Lundgrens Foundation

Funded by: The ALF Funds

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ScienceOpen disciplines: Cardiovascular Medicine

Keywords: orthostatic stress,hypercoagulability,coagulation factors,partial thromboplastin time,fibrinogen,von willebrand factor

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ScienceOpen disciplines: Cardiovascular Medicine

Keywords: orthostatic stress, hypercoagulability, coagulation factors, partial thromboplastin time, fibrinogen, von willebrand factor

Procoagulatory changes induced by head-up tilt test in patients with syncope: observational study

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Abstract

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Karger: Cardiovascular System

Most cited references 31

Guidelines for the diagnosis and management of syncope (version 2009).

Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden cardiac death.

Fibrinogen and risk of cardiovascular disease. The Framingham Study.

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