Molecular Biology of Chronic Thromboembolic Pulmonary Hypertension

Richard S. Sacks, Carmelle V. Remillard, Negin Agange, William R. Auger, Patricia A. Thistlethwaite, Jason Yuan

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Recent efforts have seen major advances in elucidating the mechanisms underlying pulmonary arterial hypertension. However, chronic thromboembolic pulmonary hypertension (CTEPH) often has been excluded from these studies. Consequently, whereas the clinical, radiographic, and hemodynamic characteristics of CTEPH have been well described, there remains a deficit in our understanding of the cellular, molecular, and genetic mechanisms underlying CTEPH. Furthermore, although prior venous thromboembolism may act as the inciting event, it is still unclear what predisposes some patients to develop CTEPH. CTEPH has two major pathogenic components. The first is the primary obstruction of central pulmonary arteries by accumulation of thrombotic material. The second is characterized by severe pulmonary vascular remodeling, similar to that seen in idiopathic pulmonary arterial hypertension. Other articles in this series describe the pathological, surgical, and therapeutic aspects of CTEPH. Here, we review the potential molecular and cellular mechanisms that may contribute to the pathogenesis of CTEPH.

Original languageEnglish (US)
Pages (from-to)265-276
Number of pages12
JournalSeminars in Thoracic and Cardiovascular Surgery
Volume18
Issue number3
DOIs
StatePublished - 2006
Externally publishedYes

Fingerprint

Pulmonary Hypertension
Molecular Biology
Venous Thromboembolism
Pulmonary Artery
Hemodynamics
Lung

Keywords

  • pulmonary embolism
  • pulmonary hypertension
  • remodeling
  • thrombus

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Molecular Biology of Chronic Thromboembolic Pulmonary Hypertension. / Sacks, Richard S.; Remillard, Carmelle V.; Agange, Negin; Auger, William R.; Thistlethwaite, Patricia A.; Yuan, Jason.

In: Seminars in Thoracic and Cardiovascular Surgery, Vol. 18, No. 3, 2006, p. 265-276.

Research output: Contribution to journalArticle

Sacks, Richard S. ; Remillard, Carmelle V. ; Agange, Negin ; Auger, William R. ; Thistlethwaite, Patricia A. ; Yuan, Jason. / Molecular Biology of Chronic Thromboembolic Pulmonary Hypertension. In: Seminars in Thoracic and Cardiovascular Surgery. 2006 ; Vol. 18, No. 3. pp. 265-276.
@article{19fa6e27bad849efbedbdc1c49502760,
title = "Molecular Biology of Chronic Thromboembolic Pulmonary Hypertension",
abstract = "Recent efforts have seen major advances in elucidating the mechanisms underlying pulmonary arterial hypertension. However, chronic thromboembolic pulmonary hypertension (CTEPH) often has been excluded from these studies. Consequently, whereas the clinical, radiographic, and hemodynamic characteristics of CTEPH have been well described, there remains a deficit in our understanding of the cellular, molecular, and genetic mechanisms underlying CTEPH. Furthermore, although prior venous thromboembolism may act as the inciting event, it is still unclear what predisposes some patients to develop CTEPH. CTEPH has two major pathogenic components. The first is the primary obstruction of central pulmonary arteries by accumulation of thrombotic material. The second is characterized by severe pulmonary vascular remodeling, similar to that seen in idiopathic pulmonary arterial hypertension. Other articles in this series describe the pathological, surgical, and therapeutic aspects of CTEPH. Here, we review the potential molecular and cellular mechanisms that may contribute to the pathogenesis of CTEPH.",
keywords = "pulmonary embolism, pulmonary hypertension, remodeling, thrombus",
author = "Sacks, {Richard S.} and Remillard, {Carmelle V.} and Negin Agange and Auger, {William R.} and Thistlethwaite, {Patricia A.} and Jason Yuan",
year = "2006",
doi = "10.1053/j.semtcvs.2006.09.004",
language = "English (US)",
volume = "18",
pages = "265--276",
journal = "Seminars in Thoracic and Cardiovascular Surgery",
issn = "1043-0679",
publisher = "W.B. Saunders Ltd",
number = "3",

}

TY - JOUR

T1 - Molecular Biology of Chronic Thromboembolic Pulmonary Hypertension

AU - Sacks, Richard S.

AU - Remillard, Carmelle V.

AU - Agange, Negin

AU - Auger, William R.

AU - Thistlethwaite, Patricia A.

AU - Yuan, Jason

PY - 2006

Y1 - 2006

N2 - Recent efforts have seen major advances in elucidating the mechanisms underlying pulmonary arterial hypertension. However, chronic thromboembolic pulmonary hypertension (CTEPH) often has been excluded from these studies. Consequently, whereas the clinical, radiographic, and hemodynamic characteristics of CTEPH have been well described, there remains a deficit in our understanding of the cellular, molecular, and genetic mechanisms underlying CTEPH. Furthermore, although prior venous thromboembolism may act as the inciting event, it is still unclear what predisposes some patients to develop CTEPH. CTEPH has two major pathogenic components. The first is the primary obstruction of central pulmonary arteries by accumulation of thrombotic material. The second is characterized by severe pulmonary vascular remodeling, similar to that seen in idiopathic pulmonary arterial hypertension. Other articles in this series describe the pathological, surgical, and therapeutic aspects of CTEPH. Here, we review the potential molecular and cellular mechanisms that may contribute to the pathogenesis of CTEPH.

AB - Recent efforts have seen major advances in elucidating the mechanisms underlying pulmonary arterial hypertension. However, chronic thromboembolic pulmonary hypertension (CTEPH) often has been excluded from these studies. Consequently, whereas the clinical, radiographic, and hemodynamic characteristics of CTEPH have been well described, there remains a deficit in our understanding of the cellular, molecular, and genetic mechanisms underlying CTEPH. Furthermore, although prior venous thromboembolism may act as the inciting event, it is still unclear what predisposes some patients to develop CTEPH. CTEPH has two major pathogenic components. The first is the primary obstruction of central pulmonary arteries by accumulation of thrombotic material. The second is characterized by severe pulmonary vascular remodeling, similar to that seen in idiopathic pulmonary arterial hypertension. Other articles in this series describe the pathological, surgical, and therapeutic aspects of CTEPH. Here, we review the potential molecular and cellular mechanisms that may contribute to the pathogenesis of CTEPH.

KW - pulmonary embolism

KW - pulmonary hypertension

KW - remodeling

KW - thrombus

UR - http://www.scopus.com/inward/record.url?scp=33845476691&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33845476691&partnerID=8YFLogxK

U2 - 10.1053/j.semtcvs.2006.09.004

DO - 10.1053/j.semtcvs.2006.09.004

M3 - Article

C2 - 17185190

AN - SCOPUS:33845476691

VL - 18

SP - 265

EP - 276

JO - Seminars in Thoracic and Cardiovascular Surgery

JF - Seminars in Thoracic and Cardiovascular Surgery

SN - 1043-0679

IS - 3

ER -