Pulmonic regurgitation pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
No edit summary
Line 5: Line 5:


==Overview==
==Overview==
The pathophysiologic mechanism of [[pulmonic regurgitation]] includes [[right ventricular overload]] resulting in right ventricular remodeling and progressive decline in function. The rate of decline in right ventricular [[systolic function]] is affected by associated conditions such as peripheral [[pulmonary artery stenosis]] and [[pulmonary hypertension]] which further increase the severity of [[pulmonary regurgitation]].
The pathophysiologic mechanism of [[pulmonic regurgitation]] includes [[right ventricular overload]] resulting in the right [[ventricular remodeling]] and progressive decline in function. The rate of decline in right ventricular [[systole|systolic function]] is affected by associated conditions such as peripheral [[pulmonary artery stenosis]] and [[pulmonary hypertension]] which further increase the severity of [[pulmonary regurgitation]].


==Pathophysiology==
==Pathophysiology==
The pulmonic regurgitation usually occurs by one of the following mechanisms:<ref>{{cite book | last = Khavandi | first = Ali | title = Essential revision notes for the cardiology KBA | publisher = Oxford University Press | location = Oxford | year = 2014 | isbn = 978-0199654901 }} </ref>
===Anatomy of and physiology of [[pulmonic valve]]===
===Pathogenesis===
The pulmonic regurgitation usually occurs by one of the following mechanisms:<ref>{{cite book | last = Khavandi | first = Ali | title = Essential revision notes for the cardiology KBA | publisher = Oxford University Press | location = Oxford | year = 2014 | isbn = 978-0199654901 }} </ref><ref>{{cite book | last = Khavandi | first = Ali | title = Essential revision notes for the cardiology KBA | publisher = Oxford University Press | location = Oxford | year = 2014 | isbn = 978-0199654901 }}</ref>


===Acquired alteration in the valvular leaflet morphology<ref name="CurtissMiller1983">{{cite journal|last1=Curtiss|first1=E I|last2=Miller|first2=T R|last3=Shapiro|first3=L S|title=Pulmonic regurgitation due to valvular tophi.|journal=Circulation|volume=67|issue=3|year=1983|pages=699–701|issn=0009-7322|doi=10.1161/01.CIR.67.3.699}}</ref>===  
====Acquired alteration in the valvular leaflet morphology<ref name="CurtissMiller1983">{{cite journal|last1=Curtiss|first1=E I|last2=Miller|first2=T R|last3=Shapiro|first3=L S|title=Pulmonic regurgitation due to valvular tophi.|journal=Circulation|volume=67|issue=3|year=1983|pages=699–701|issn=0009-7322|doi=10.1161/01.CIR.67.3.699}}</ref>====  
*The development of [[pulmonic regurgitation]] due to [[tophus]] valvular vegetations has been reported in a case. The patient reported had long-standing cyanotic [[congenital heart disease]] and developed [[hyperuricemia]] secondary to [[polycythemia]]. The possible mechanism of development of the [[vegetation]]s involved hemodynamic valvular trauma in the setting of sustained [[hyperuricemia]] and subsequent [[dystrophic calcification]] at primary [[tophus]] lesion.  
*The development of [[pulmonic regurgitation]] due to [[tophus]] valvular vegetations has been reported in a case. The patient reported had long-standing cyanotic [[congenital heart disease]] and developed [[hyperuricemia]] secondary to [[polycythemia]]. The possible mechanism of development of the vegetations involved hemodynamic [[valve|valvular]] trauma in the setting of sustained [[hyperuricemia]] and subsequent [[dystrophic calcification]] at primary [[tophus]] lesion.  
*On gross pathology vegetative lesions observed.
====Idiopathic dilatation of the pulmonary artery (IDPA)<ref name="pmid28228295">{{cite journal |vauthors=Malviya A, Jha PK, Kalita JP, Saikia MK, Mishra A |title=Idiopathic dilatation of pulmonary artery: A review |journal=Indian Heart J |volume=69 |issue=1 |pages=119–124 |date=2017 |pmid=28228295 |pmc=5319124 |doi=10.1016/j.ihj.2016.07.009 |url=}}</ref><ref name="pmid27891002">{{cite journal |vauthors=Sharma RK, Talwar D, Gupta SK, Bansal S |title=Idiopathic dilatation of pulmonary artery |journal=Lung India |volume=33 |issue=6 |pages=675–677 |date=2016 |pmid=27891002 |pmc=5112830 |doi=10.4103/0970-2113.192869 |url=}}</ref><ref name="SegallRitter1950">{{cite journal|last1=Segall|first1=S.|last2=Ritter|first2=I. I.|last3=Hwang|first3=W.|title=A Case of Marked Dilatation of the Pulmonary Arterial Tree Associated with Mitral Stenosis|journal=Circulation|volume=1|issue=4|year=1950|pages=777–781|issn=0009-7322|doi=10.1161/01.CIR.1.4.777}}</ref>====
*Polarized light microscopy of the material taken from the pulmonic valve demonstrated [[Gout diagnostic study of choice|negatively birefringent crystals]].
 
===Idiopathic dilatation of the pulmonary artery (IDPA)<ref name="pmid28228295">{{cite journal |vauthors=Malviya A, Jha PK, Kalita JP, Saikia MK, Mishra A |title=Idiopathic dilatation of pulmonary artery: A review |journal=Indian Heart J |volume=69 |issue=1 |pages=119–124 |date=2017 |pmid=28228295 |pmc=5319124 |doi=10.1016/j.ihj.2016.07.009 |url=}}</ref><ref name="pmid27891002">{{cite journal |vauthors=Sharma RK, Talwar D, Gupta SK, Bansal S |title=Idiopathic dilatation of pulmonary artery |journal=Lung India |volume=33 |issue=6 |pages=675–677 |date=2016 |pmid=27891002 |pmc=5112830 |doi=10.4103/0970-2113.192869 |url=}}</ref><ref name="SegallRitter1950">{{cite journal|last1=Segall|first1=S.|last2=Ritter|first2=I. I.|last3=Hwang|first3=W.|title=A Case of Marked Dilatation of the Pulmonary Arterial Tree Associated with Mitral Stenosis|journal=Circulation|volume=1|issue=4|year=1950|pages=777–781|issn=0009-7322|doi=10.1161/01.CIR.1.4.777}}</ref>===
*The exact pathogenesis of dilatation of the [[pulmonary artery]] is not fully understood. The demonstration of the [[disease]] among [[child|pediatric population]] signals the [[congenital]] nature of the [[etiology]]. Main [[pulmonary artery]] and the origin of its right and left main pulmonary arteries are majorly affected. It is thought that [[pulmonary artery]] dilatation is mediated by the unequal division of truncus arteriosus communis. Other proposed mechanisms include maldevelopment of the whole [[pulmonary tree]] and the association of hypoplastic [[aorta]] with dilated.  
*The exact pathogenesis of dilatation of the [[pulmonary artery]] is not fully understood. The demonstration of the [[disease]] among [[child|pediatric population]] signals the [[congenital]] nature of the [[etiology]]. Main [[pulmonary artery]] and the origin of its right and left main pulmonary arteries are majorly affected. It is thought that [[pulmonary artery]] dilatation is mediated by the unequal division of truncus arteriosus communis. Other proposed mechanisms include maldevelopment of the whole [[pulmonary tree]] and the association of hypoplastic [[aorta]] with dilated.  
===[[Pulmonary artery]] aneurysm<ref name="pmid28228295">{{cite journal |vauthors=Malviya A, Jha PK, Kalita JP, Saikia MK, Mishra A |title=Idiopathic dilatation of pulmonary artery: A review |journal=Indian Heart J |volume=69 |issue=1 |pages=119–124 |date=2017 |pmid=28228295 |pmc=5319124 |doi=10.1016/j.ihj.2016.07.009 |url=}}</ref><ref name="pmid27891002">{{cite journal |vauthors=Sharma RK, Talwar D, Gupta SK, Bansal S |title=Idiopathic dilatation of pulmonary artery |journal=Lung India |volume=33 |issue=6 |pages=675–677 |date=2016 |pmid=27891002 |pmc=5112830 |doi=10.4103/0970-2113.192869 |url=}}</ref><ref name="pmid16181901">{{cite journal |vauthors=Deb SJ, Zehr KJ, Shields RC |title=Idiopathic pulmonary artery aneurysm |journal=Ann. Thorac. Surg. |volume=80 |issue=4 |pages=1500–2 |date=October 2005 |pmid=16181901 |doi=10.1016/j.athoracsur.2004.04.011 |url=}}</ref>===
[[Image:Quadricuspid pulmonary valve.jpg|thumb|left|Quadricuspid pulmonary valve (one of the congenital causes of [[PR]] - Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology http://www.peir.net]]
*It is thought that the development of [[pulmonary artery]] aneurysm is mediated by either the congenital weakness or cystic [[tunica media|medial]] degeneration of the [[pulmonary artery]] walls. An association between cystic [[tunica media|medial]] degeneration and increased hemodynamic forces then leads to [[aneurysm]] formation. Pulmonary artery [[aneurysms]] have been associated with structural cardiac and vascular abnormalities, [[vasculitis]], and [[infection]] (such as [[syphilis]].
====Congenital absence or malformation of the valve<ref name="BouzasKilner2005">{{cite journal|last1=Bouzas|first1=Beatriz|last2=Kilner|first2=Philip J.|last3=Gatzoulis|first3=Michael A.|title=Pulmonary regurgitation: not a benign lesion|journal=European Heart Journal|volume=26|issue=5|year=2005|pages=433–439|issn=0195-668X|doi=10.1093/eurheartj/ehi091}}</ref><ref name="pmid28228295">{{cite journal |vauthors=Malviya A, Jha PK, Kalita JP, Saikia MK, Mishra A |title=Idiopathic dilatation of pulmonary artery: A review |journal=Indian Heart J |volume=69 |issue=1 |pages=119–124 |date=2017 |pmid=28228295 |pmc=5319124 |doi=10.1016/j.ihj.2016.07.009 |url=}}</ref><ref name="pmid27891002">{{cite journal |vauthors=Sharma RK, Talwar D, Gupta SK, Bansal S |title=Idiopathic dilatation of pulmonary artery |journal=Lung India |volume=33 |issue=6 |pages=675–677 |date=2016 |pmid=27891002 |pmc=5112830 |doi=10.4103/0970-2113.192869 |url=}}</ref><ref name="pmid16181901">{{cite journal |vauthors=Deb SJ, Zehr KJ, Shields RC |title=Idiopathic pulmonary artery aneurysm |journal=Ann. Thorac. Surg. |volume=80 |issue=4 |pages=1500–2 |date=October 2005 |pmid=16181901 |doi=10.1016/j.athoracsur.2004.04.011 |url=}}</ref>====
*Absent [[pulmonary valve]] syndrome (APVS) is rare and involves developmental abnormality and [[dysplasia]] or absolute absence of [[pulmonary valve]] cusps. A variable degree of dilatation/[[aneurysm]] of the main [[pulmonary artery]] always accompanies the disorder.
*It is thought that the development of [[pulmonary artery]] aneurysm is mediated by either the congenital weakness or cystic [[tunica media|medial]] degeneration of the [[pulmonary artery]] walls. An association between cystic [[tunica media|medial]] degeneration and increased hemodynamic forces then leads to [[aneurysm]] formation. Pulmonary artery [[aneurysms]] have been associated with structural cardiac and vascular abnormalities, [[vasculitis]], and [[infection]] (such as [[syphilis]]).
*The pathogenesis of Fallot type (APVS) involves either [[agenesis]] of [[ductus arteriosus]] or post pulmonary stenotic dilatation due to increased [[stroke volume]].
*Quuadricuspid [[pulmonary valve]] is rare but may cause [[PR]]. Thick [[valve|valvular]] leaflets with decreased mobility without complete closure during [[diastole]] may lead to the development of [[PR]].<ref name="pmid12094521">{{cite journal |vauthors=Kotani A, Nakagawa K, Yamamoto T, Hirano Y, Kimura H, Yamada S, Ikawa H, Ishikawa K |title=[Quadricuspid pulmonary valve with valvular stenosis and regurgitation identified by transthoracic echocardiography: a case report] |language=Japanese |journal=J Cardiol |volume=39 |issue=6 |pages=313–9 |date=June 2002 |pmid=12094521 |doi= |url=}}</ref>


===Congenital absence or malformation of the valve===
====Increasing regurgitation causing [[right ventricle|right ventricular]] volume overload<ref name="pmid26430501">{{cite journal| author=Bigdelian H, Mardani D, Sedighi M| title=The Effect of Pulmonary Valve Replacement (PVR) Surgery on Hemodynamics of Patients Who Underwent Repair of Tetralogy of Fallot (TOF). | journal=J Cardiovasc Thorac Res | year= 2015 | volume= 7 | issue= 3 | pages= 122-5 | pmid=26430501 | doi=10.15171/jcvtr.2015.26 | pmc=4586599 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26430501  }} </ref>====
===Increasing regurgitation causing [[right ventricle|right ventricular]] volume overload<ref name="pmid26430501">{{cite journal| author=Bigdelian H, Mardani D, Sedighi M| title=The Effect of Pulmonary Valve Replacement (PVR) Surgery on Hemodynamics of Patients Who Underwent Repair of Tetralogy of Fallot (TOF). | journal=J Cardiovasc Thorac Res | year= 2015 | volume= 7 | issue= 3 | pages= 122-5 | pmid=26430501 | doi=10.15171/jcvtr.2015.26 | pmc=4586599 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26430501  }} </ref>===
* Patients with [[pulmonic regurgitation]] develop chronic [[right ventricle|right ventricular]] overload resulting in right [[Ventricular remodeling|ventricular remodeling]] and progressive decline in function. The rate of decline in right ventricular [[systole|systolic function]] is affected by associated conditions such as peripheral [[pulmonary artery stenosis]] and [[pulmonary hypertension]] which further increase the severity of pulmonary regurgitation. Among patients with increased [[pulmonary artery pressure]] from dysfunction of [[left ventricle]] or residual [[pulmonary artery stenosis]] increases the severity of [[pulmonary regurgitation]]. Progressive dilation of the [[right ventricle]] results in functional [[tricuspid regurgitation]] and increases the risk of developing [[arrhythmias]].
* Patients with [[pulmonic regurgitation]] develop chronic [[right ventricular overload]] resulting in right [[ventricular remodelling]] and progressive decline in function. The rate of decline in right ventricular [[systolic function]] is affected by associated conditions such as peripheral [[pulmonary artery stenosis]] and [[pulmonary hypertension]] which further increase the severity of pulmonary regurgitation. Among patients with increased [[pulmonary artery pressure]] from dysfunction of [[left ventricle]] or residual [[pulmonary artery stenosis]] increases the severity of [[pulmonary regurgitation]]. Progressive dilation of the [[right ventricle]] results in functional [[tricuspid regurgitation]] and increases the risk of developing [[arrhythmias]].
*The [[Diastolic blood pressure|diastolic pressure]] difference between [[right ventricle]] and [[pulmonary artery]] is usually very small and steers the pulmonic valve regurgitation. The right ventricular stiffness due to [[right ventricular hypertrophy]] (such as in [[Tetralogy of Fallot]]) and [[fibrosis]], increases the ventricular [[diastolic pressure]], decreasing the gradient thus causing regurge. A slight increase in the intrathoracic pressure (such as among [[ventilated]] patients) can accentuate the pulmonary regurgitation considerably.<ref name="pmid17569817">{{cite journal| author=Chaturvedi RR, Redington AN| title=Pulmonary regurgitation in congenital heart disease. | journal=Heart | year= 2007 | volume= 93 | issue= 7 | pages= 880-9 | pmid=17569817 | doi=10.1136/hrt.2005.075234 | pmc=1994453 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17569817  }} </ref>
*The [[Diastolic blood pressure|diastolic pressure]] difference between [[right ventricle]] and [[pulmonary artery]] is usually very small and steers the pulmonic valve regurgitation. The right ventricular stiffness due to [[right ventricular hypertrophy]] (such as in [[Tetralogy of Fallot]]) and [[fibrosis]], increases the ventricular [[diastolic pressure]], decreasing the gradient thus causing regurge. A slight increase in the intrathoracic pressure (such as among [[ventilated]] patients) can accentuate the pulmonary regurgitation considerably.<ref name="pmid17569817">{{cite journal| author=Chaturvedi RR, Redington AN| title=Pulmonary regurgitation in congenital heart disease. | journal=Heart | year= 2007 | volume= 93 | issue= 7 | pages= 880-9 | pmid=17569817 | doi=10.1136/hrt.2005.075234 | pmc=1994453 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17569817  }} </ref>
*The severity of [[regurgitant jet]] is dependent on:<ref name="pmid26430501">{{cite journal| author=Bigdelian H, Mardani D, Sedighi M| title=The Effect of Pulmonary Valve Replacement (PVR) Surgery on Hemodynamics of Patients Who Underwent Repair of Tetralogy of Fallot (TOF). | journal=J Cardiovasc Thorac Res | year= 2015 | volume= 7 | issue= 3 | pages= 122-5 | pmid=26430501 | doi=10.15171/jcvtr.2015.26 | pmc=4586599 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26430501  }} </ref>
*The severity of [[regurgitant jet]] is dependent on:<ref name="pmid26430501">{{cite journal| author=Bigdelian H, Mardani D, Sedighi M| title=The Effect of Pulmonary Valve Replacement (PVR) Surgery on Hemodynamics of Patients Who Underwent Repair of Tetralogy of Fallot (TOF). | journal=J Cardiovasc Thorac Res | year= 2015 | volume= 7 | issue= 3 | pages= 122-5 | pmid=26430501 | doi=10.15171/jcvtr.2015.26 | pmc=4586599 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26430501  }} </ref>
Line 29: Line 31:
**[[Right ventricle]] [[diastolic]] [[compliance]]
**[[Right ventricle]] [[diastolic]] [[compliance]]
**Duration of [[right ventricular]] [[diastole]]
**Duration of [[right ventricular]] [[diastole]]
==== According to 2014, ACC/AHA valvular heart disease guidelines the stages of severe pulmonary regurgitation are described as follows:<ref name="pmid24603191">{{cite journal| author=Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA et al.| title=2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. | journal=J Am Coll Cardiol | year= 2014 | volume= 63 | issue= 22 | pages= e57-185 | pmid=24603191 | doi=10.1016/j.jacc.2014.02.536 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24603191  }} </ref> ====
 
{| class="wikitable"
===Genetics===
!Stage
*25% cases of absent [[pulmonary valve]] syndrome (APVS) are associated with [[Chromosome abnormality|chromosomal anomalies]] such as [[Trisomy 21]], [[Trisomy 13]], [[chromosome]] 6 and 7 deletions.<ref name="pmid24843213">{{cite journal |vauthors=Grewal DS, Chamoli SC, Saxena S |title=Absent pulmonary valve syndrome - Antenatal diagnosis |journal=Med J Armed Forces India |volume=70 |issue=2 |pages=198–200 |date=April 2014 |pmid=24843213 |pmc=4017172 |doi=10.1016/j.mjafi.2013.07.002 |url=}}</ref>
!Definition
*22q11 microdeletion has been shown to be associated with 25% cases of APVS.<ref name="pmid15386602">{{cite journal |vauthors=Volpe P, Paladini D, Marasini M, Buonadonna AL, Russo MG, Caruso G, Marzullo A, Arciprete P, Martinelli P, Gentile M |title=Characteristics, associations and outcome of absent pulmonary valve syndrome in the fetus |journal=Ultrasound Obstet Gynecol |volume=24 |issue=6 |pages=623–8 |date=November 2004 |pmid=15386602 |doi=10.1002/uog.1729 |url=}}</ref>
!Pulmonary Valve
 
Anatomy
===Associated conditions===
!Valve Hemodynamics
Isolated [[PR]] is uncommon and is usually demonstrated with other [[valve|valvular]] abnormalities or in certain conditions. The most important conditions/[[diseases]] associated with [[PR]] include:
!Hemodynamic Consequences
*[[TOF]]: Surgical repair of [[pulmonic stenosis]] associated with [[TOF]] may lead to [[PR]]. Post [[TOF]] repair, [[PR]] is a common complication.
!Symptoms
*[[Marfan syndrome]]
|-
*[[Rheumatic heart disease]]
|C,D
*[[Syphilis]]
|Severe [[PR]]
*[[Carcinoid syndrome|Carcinoid heart disease]]
|
 
*Distorted or absent leaflets
===Gross pathology===
*Annular dilation
*On gross pathology vegetative lesions on the [[pulmonic valve]] leaflets may be observed in a [[patient]] with [[acquired]] alteration in the [[valve|valvular]] leaflet [[morphology]].<ref name="CurtissMiller1983">{{cite journal|last1=Curtiss|first1=E I|last2=Miller|first2=T R|last3=Shapiro|first3=L S|title=Pulmonic regurgitation due to valvular tophi.|journal=Circulation|volume=67|issue=3|year=1983|pages=699–701|issn=0009-7322|doi=10.1161/01.CIR.67.3.699}}</ref>
|
===Microscopic pathology===
*Color jet fills [[right ventricular outlet tract]]
*In polarized light microscopy of the material taken from the [[pulmonic valve]], [[Gout diagnostic study of choice|negatively birefringent crystals]] may be observed in [[acquired]] alteration in the [[valve|valvular]] leaflet [[morphology]].<ref name="CurtissMiller1983">{{cite journal|last1=Curtiss|first1=E I|last2=Miller|first2=T R|last3=Shapiro|first3=L S|title=Pulmonic regurgitation due to valvular tophi.|journal=Circulation|volume=67|issue=3|year=1983|pages=699–701|issn=0009-7322|doi=10.1161/01.CIR.67.3.699}}</ref>
*CW jet density and contour: dense laminar flow with steep deceleration slope; may terminate abruptly
 
|
*Paradoxical [[Interventricular septum|septal]] motion (volume overload pattern)
*Right ventricular enlargement
|None or variable and dependent on the cause of [[PR]] and [[right ventricle|right ventricular]] function
|}


==References==
==References==
{{Reflist}}
{{Reflist|2}}


==See Also==
==See Also==

Revision as of 20:13, 3 August 2020

Pulmonic regurgitation Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differential diagnosis

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Electrocardiogram

Chest X-Ray

Echocardiography

Cardiac MRI

Severity Assessment

Treatment

Medical Therapy

Surgical therapy

Follow up

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2], Aysha Anwar, M.B.B.S[3]

Overview

The pathophysiologic mechanism of pulmonic regurgitation includes right ventricular overload resulting in the right ventricular remodeling and progressive decline in function. The rate of decline in right ventricular systolic function is affected by associated conditions such as peripheral pulmonary artery stenosis and pulmonary hypertension which further increase the severity of pulmonary regurgitation.

Pathophysiology

Anatomy of and physiology of pulmonic valve

Pathogenesis

The pulmonic regurgitation usually occurs by one of the following mechanisms:[1][2]

Acquired alteration in the valvular leaflet morphology[3]

Idiopathic dilatation of the pulmonary artery (IDPA)[4][5][6]

Quadricuspid pulmonary valve (one of the congenital causes of PR - Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology http://www.peir.net

Congenital absence or malformation of the valve[7][4][5][8]

Increasing regurgitation causing right ventricular volume overload[10]

Genetics

Associated conditions

Isolated PR is uncommon and is usually demonstrated with other valvular abnormalities or in certain conditions. The most important conditions/diseases associated with PR include:

Gross pathology

Microscopic pathology


References

  1. ↑ Khavandi, Ali (2014). Essential revision notes for the cardiology KBA. Oxford: Oxford University Press. ISBN 978-0199654901.
  2. ↑ Khavandi, Ali (2014). Essential revision notes for the cardiology KBA. Oxford: Oxford University Press. ISBN 978-0199654901.
  3. ↑ 3.0 3.1 3.2 Curtiss, E I; Miller, T R; Shapiro, L S (1983). "Pulmonic regurgitation due to valvular tophi". Circulation. 67 (3): 699–701. doi:10.1161/01.CIR.67.3.699. ISSN 0009-7322.
  4. ↑ 4.0 4.1 Malviya A, Jha PK, Kalita JP, Saikia MK, Mishra A (2017). "Idiopathic dilatation of pulmonary artery: A review". Indian Heart J. 69 (1): 119–124. doi:10.1016/j.ihj.2016.07.009. PMC 5319124. PMID 28228295.
  5. ↑ 5.0 5.1 Sharma RK, Talwar D, Gupta SK, Bansal S (2016). "Idiopathic dilatation of pulmonary artery". Lung India. 33 (6): 675–677. doi:10.4103/0970-2113.192869. PMC 5112830. PMID 27891002.
  6. ↑ Segall, S.; Ritter, I. I.; Hwang, W. (1950). "A Case of Marked Dilatation of the Pulmonary Arterial Tree Associated with Mitral Stenosis". Circulation. 1 (4): 777–781. doi:10.1161/01.CIR.1.4.777. ISSN 0009-7322.
  7. ↑ Bouzas, Beatriz; Kilner, Philip J.; Gatzoulis, Michael A. (2005). "Pulmonary regurgitation: not a benign lesion". European Heart Journal. 26 (5): 433–439. doi:10.1093/eurheartj/ehi091. ISSN 0195-668X.
  8. ↑ Deb SJ, Zehr KJ, Shields RC (October 2005). "Idiopathic pulmonary artery aneurysm". Ann. Thorac. Surg. 80 (4): 1500–2. doi:10.1016/j.athoracsur.2004.04.011. PMID 16181901.
  9. ↑ Kotani A, Nakagawa K, Yamamoto T, Hirano Y, Kimura H, Yamada S, Ikawa H, Ishikawa K (June 2002). "[Quadricuspid pulmonary valve with valvular stenosis and regurgitation identified by transthoracic echocardiography: a case report]". J Cardiol (in Japanese). 39 (6): 313–9. PMID 12094521.
  10. ↑ 10.0 10.1 Bigdelian H, Mardani D, Sedighi M (2015). "The Effect of Pulmonary Valve Replacement (PVR) Surgery on Hemodynamics of Patients Who Underwent Repair of Tetralogy of Fallot (TOF)". J Cardiovasc Thorac Res. 7 (3): 122–5. doi:10.15171/jcvtr.2015.26. PMC 4586599. PMID 26430501.
  11. ↑ Chaturvedi RR, Redington AN (2007). "Pulmonary regurgitation in congenital heart disease". Heart. 93 (7): 880–9. doi:10.1136/hrt.2005.075234. PMC 1994453. PMID 17569817.
  12. ↑ Grewal DS, Chamoli SC, Saxena S (April 2014). "Absent pulmonary valve syndrome - Antenatal diagnosis". Med J Armed Forces India. 70 (2): 198–200. doi:10.1016/j.mjafi.2013.07.002. PMC 4017172. PMID 24843213.
  13. ↑ Volpe P, Paladini D, Marasini M, Buonadonna AL, Russo MG, Caruso G, Marzullo A, Arciprete P, Martinelli P, Gentile M (November 2004). "Characteristics, associations and outcome of absent pulmonary valve syndrome in the fetus". Ultrasound Obstet Gynecol. 24 (6): 623–8. doi:10.1002/uog.1729. PMID 15386602.

See Also

Template:WikiDoc Sources

Retrieved from "https://www.wikidoc.org/index.php?title=Pulmonic_regurgitation_pathophysiology&oldid=1646881"