Evidence map›Paper›PMID 37561240›Full record

ReviewCurrent hypertension reports2023

Irregularities of Coagulation in Hypertension.

Saira Rafaqat, Amber Khalid, Saira Riaz, Sana Rafaqat

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hypertension reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. D-dimer levels and outcomes in heart failure with mildly reduced ejection fraction.International journal of cardiology. Heart & vasculature · 2026
    Article
  2. Article
  3. β-Antithrombin Levels in Patients with Venous Thromboembolism.International journal of molecular sciences · 2025
    Article
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  5. Article
  6. Review
  7. Article
  8. Article
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  11. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Saira RafaqatDepartment of Zoology (Molecular Physiology), Lahore College for Women University, Lahore, Punjab, Pakistan. saera.rafaqat@gmail.com.ORCID 0000-0001-7177-5602
Amber KhalidDepartment of Zoology, Lahore College for Women University, Lahore, Punjab, Pakistan.
Saira RiazDepartment of Environmental Science, Lahore College for Women University, Lahore, Punjab, Pakistan.
Sana RafaqatDepartment of Biotechnology (Human Genetics), Lahore College for Women University, Lahore, Punjab, Pakistan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewThis review article summarizes the role of coagulation in the pathogenesis of hypertension. It specifically focuses on significant factors and markers associated with coagulation, including D-dimer, fibrinogen and fibrin, prothrombin, P-selectin, soluble urokinase plasminogen activator receptor, thrombomodulin, tissue factor, tissue plasminogen activator, von Willebrand factor, β-thromboglobulin, and Stuart-Prower factor. RECENT

findingsD-dimer levels were elevated in hypertensive individuals compared to healthy controls, and the levels increased with the severity of hypertension. These findings indicate that increased coagulation activity of fibrin plays a role in the development of thromboembolic complications in hypertensive patients. Additionally, both fibrinogen levels and D-dimer levels displayed a positive correlation with the duration of hypertension, suggesting that these biomarkers were positively associated with the length of time an individual had been hypertensive. Increased systolic and diastolic blood pressures have been linked to higher levels of prothrombin time and activated partial thromboplastin time in individuals with hypertension as well as those with normal blood pressure. Also, the presence of P-selectin, produced by activated platelets and endothelial cells during angiotensin II stimulation, played a role in the development of cardiac inflammation and fibrosis associated with hypertension. Moreover, the change in systolic blood pressure was associated with baseline soluble urokinase plasminogen activator receptor (suPAR) in hypertensive participants, and the change in suPAR levels was associated with the development of hypertension. Moreover, it was observed a decrease in thrombomodulin expression in the placenta of preeclamptic patients, suggesting its potential involvement in placental dysfunction, possibly driven by an imbalance in angiogenic factors. Tissue factors and autophagy might have significant implications in the pathogenesis of chronic thromboembolic pulmonary hypertension, particularly in the context of vascular remodelling. Likewise, ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) might be a promising biomarker for the early detection of pulmonary arterial hypertension and the von Willebrand factor is a candidate prognostic biomarker. The arterial β-thromboglobulin levels were significantly lower than venous levels. This article concludes that D-dimer, fibrinogen and fibrin, prothrombin, P-selectin, soluble urokinase plasminogen activator receptor, thrombomodulin, tissue factor, tissue plasminogen activator, von Willebrand factor, and β-thromboglobulin are important factors involved in the pathogenesis of hypertension.

Indexed as

HypertensionTissue Plasminogen Activatorbeta-ThromboglobulinBiomarkersEndothelial CellsFemaleFibrinogenHumansPlacentaPregnancyProthrombinP-SelectinReceptors, Urokinase Plasminogen ActivatorThrombomodulinThromboplastinvon Willebrand Factorbeta-ThromboglobulinBiomarkersFibrinogenProthrombinP-SelectinReceptors, Urokinase Plasminogen ActivatorThrombomodulinThromboplastinTissue Plasminogen Activatorvon Willebrand FactorCoagulationCoagulation factorsCoagulation markersHypertensionPathogenesis

Identifiers

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.