Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Pulmonary Embolism I: Introduction01:19

Pulmonary Embolism I: Introduction

A blood clot, or thrombus, is a semi-solid mass composed of fibrin, platelets, and red blood cells. When it forms within a vessel, it can obstruct blood flow, known as thrombosis. If part of the clot detaches, it becomes an embolus that can travel and block distant vessels. When this occurs in the pulmonary arteries, it causes a condition known as pulmonary embolism (PE).Origin and ImpactMost often, the embolus originates from a thrombus in the deep veins of the lower limbs, a condition called...
Pulmonary Embolism I: Introduction01:29

Pulmonary Embolism I: Introduction

Pulmonary embolism (PE) occurs when a thrombus, fat or air embolus, amniotic fluid, or tumor tissue blocks one or more pulmonary arteries. These blockages originate in the venous system or the right side of the heart.EtiologyPE primarily arises from deep vein thrombosis (DVT) and other hypercoagulable states, such as inherited thrombophilias. Additional etiological factors include venous stasis, commonly seen in obesity, and endothelial injury from surgery and trauma. Less common causes include...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
Chronic Obstructive Pulmonary Disease I: Introduction01:23

Chronic Obstructive Pulmonary Disease I: Introduction

Chronic obstructive pulmonary disease is a common, preventable, and treatable respiratory disorder characterized by persistent symptoms and progressive airflow limitation. This limitation results from a combination of small-airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), both driven by chronic inflammation from exposure to harmful particles or gases.The disease includes two main pathological entities: emphysema, marked by destruction of alveolar walls and...
Chronic Obstructive Pulmonary Disease-I: Introduction01:20

Chronic Obstructive Pulmonary Disease-I: Introduction

Chronic Obstructive Pulmonary Disease (COPD) is a long-lasting respiratory condition requiring continuous attention and care. It is a progressive lung disease that leads to breathing challenges due to airflow obstruction. It manifests as persistent respiratory symptoms and restricted airflow resulting from abnormalities in the airways and alveoli, usually due to long-term exposure to harmful particles or gases. COPD mainly consists of two primary conditions: emphysema and chronic bronchitis.
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Kardiologia Polska at the end of 2021: The pandemic and beyond.

Kardiologia polska·2021
Same author

Towards Personalized Therapy of Aortic Stenosis.

Journal of personalized medicine·2021
Same author

Challenges for Polish Archives of Internal Medicine in 2021: what is new in 2022?

Polish archives of internal medicine·2021
Same author

Direct oral anticoagulants in patients with atrial fibrillation following bariatric surgery: A single center experience.

Kardiologia polska·2021
Same author

[Teaching Evidence Based Medicine EBM in medical faculties in Poland].

Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego·2021
Same author

Fibrinogen β chain and FXIII polymorphisms affect fibrin clot properties in acute pulmonary embolism.

European journal of clinical investigation·2021

Related Experiment Video

Updated: Jun 1, 2026

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
08:01

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well

Published on: February 27, 2026

Thrombin generation in chronic obstructive pulmonary disease: dependence on plasma factor composition.

Anetta Undas1, Milosz Jankowski, Przemysław Kaczmarek

  • 1Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland. mmundas@cyf-kr.edu.pl

Thrombosis Research
|June 1, 2011
PubMed
Summary

Chronic obstructive pulmonary disease (COPD) patients exhibit a prothrombotic state due to elevated prothrombin and clotting factors VIII and IX, and reduced tissue factor pathway inhibitor. These alterations enhance thrombin generation, increasing thromboembolic risk.

More Related Videos

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
13:08

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization
06:28

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization

Published on: June 4, 2020

Related Experiment Videos

Last Updated: Jun 1, 2026

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
08:01

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well

Published on: February 27, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
13:08

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization
06:28

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization

Published on: June 4, 2020

Area of Science:

  • Coagulation science
  • Pulmonary medicine
  • Thrombosis research

Background:

  • Chronic obstructive pulmonary disease (COPD) is linked to a higher incidence of thromboembolic events.
  • Understanding the hemostatic balance in COPD is crucial for risk stratification and management.

Purpose of the Study:

  • To investigate thrombin generation profiles in COPD patients.
  • To determine the influence of plasma coagulation factor and inhibitor levels on thrombin generation in COPD.

Main Methods:

  • Compared coagulation factors (II, V, VII, VIII, IX, X), antithrombin, protein C, and free tissue factor pathway inhibitor (fTFPI) in 60 COPD patients and 43 controls.
  • Assessed tissue factor-initiated thrombin generation computationally using individual plasma coagulation protein compositions.
  • Excluded patients receiving anticoagulation.

Main Results:

  • COPD patients showed higher levels of prothrombin (fII), factors V, VII, VIII, and IX, and lower fTFPI compared to controls.
  • Computational analysis revealed significantly higher maximum thrombin levels, rates, and total thrombin formation in COPD patients.
  • The initiation phase and time to maximum thrombin generation were shorter in COPD patients.

Conclusions:

  • The prothrombotic phenotype in COPD is primarily driven by increased prothrombin, factors VIII and IX, and decreased fTFPI.
  • These hemostatic alterations contribute to the heightened risk of thromboembolic events in COPD.
  • Thrombin generation profiles in COPD can potentially be normalized by correcting specific factor levels.