Pulmonic regurgitation pathophysiology: Difference between revisions

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==Overview==
==Overview==
[[Pulmonary valve]] is located at the junction of the [[Ventricular outflow tract|right ventricular outflow tract]] and [[pulmonary artery]]. Three equal-sized, semilunar cusps or leaflets make up the [[pulmonary valve]]. [[Pulmonary valve]] opens during right ventricular [[systole]] and closes during right ventricular [[diastole]]. [[PR|Pulmonary regurgitation]] (PR) may be caused by an acquired alteration in the valvular morphology, idiopathic dilatation of the pulmonary artery (IDPA), congenital absence or malformation of the pulmonary valve|valve]], and increasing regurgitation causing [[right ventricle|right ventricular]] volume overload. 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]]. Among [[patients]] with severe [[PR|pulmonary regurgitation]] (PR), the gene expression pattern of GRK2 and β2-[[Adrenergic receptor|adrenoceptor]] ( molecular markers of [[cardiac dysfunction]]) has been reported to be altered. Isolated [[PR]] is uncommon and is usually demonstrated with other [[valve|valvular]] abnormalities or in certain conditions. Conditions associated include [[TOF]], [[rheumatic heart disease]] and [[syphilis]]. On gross pathology vegetative lesions on the [[pulmonic valve]] leaflets may be observed among [[patient|patients]] with [[acquired]] alteration in the [[valve|valvular]] leaflet [[morphology]].
[[Pulmonary valve]] is located at the junction of the [[Ventricular outflow tract|right ventricular outflow tract]] and [[pulmonary artery]]. Three equal-sized, semilunar cusps or leaflets make up the [[pulmonary valve]]. [[Pulmonary valve]] opens during right ventricular [[systole]] and closes during right ventricular [[diastole]]. [[PR|Pulmonary regurgitation]] (PR) may be caused by an acquired alteration in the valvular [[morphology]], idiopathic dilatation of the [[pulmonary artery]] (IDPA), [[pulmonic valve]] ring dilatation,  congenital absence or malformation of the [[pulmonary valve|valve]], and increasing [[regurgitation]] causing [[right ventricle|right ventricular]] volume overload. 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]]. Among [[patients]] with severe [[PR]], the gene expression pattern of GRK2 and β2-[[Adrenergic receptor|adrenoceptor]] (molecular markers of [[cardiac dysfunction]]) has been reported to be altered. Isolated [[PR]] is uncommon and is usually demonstrated with other [[valve|valvular]] abnormalities or in certain conditions. Conditions associated include [[TOF]], [[rheumatic heart disease]] and [[syphilis]]. On gross pathology [[vegetation|vegetative lesions]] on the [[pulmonic valve]] leaflets may be observed among [[patient|patients]] with [[acquired]] alteration in the [[valve|valvular]] leaflet [[morphology]].


==Pathophysiology==
==Pathophysiology==
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*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.
[[File:Dilatation of pulmonary artery-image reconstrust.jpg|thumb|400px|center|3-D reconstruction of chest CT demonstrating diffuse [[aneurysm|aneurysmal]] dilatation of the pulmonary outflow tract and main pulmonary artery (right and left) - <ref name="DebZehr2005">{{cite journal|last1=Deb|first1=Subrato J.|last2=Zehr|first2=Kenton J.|last3=Shields|first3=Raymond C.|title=Idiopathic Pulmonary Artery Aneurysm|journal=The Annals of Thoracic Surgery|volume=80|issue=4|year=2005|pages=1500–1502|issn=00034975|doi=10.1016/j.athoracsur.2004.04.011}}</ref>]]
[[File:Dilatation of pulmonary artery-image reconstrust.jpg|thumb|400px|center|3-D reconstruction of chest CT demonstrating diffuse [[aneurysm|aneurysmal]] dilatation of the pulmonary outflow tract and main pulmonary artery (right and left) - <ref name="DebZehr2005">{{cite journal|last1=Deb|first1=Subrato J.|last2=Zehr|first2=Kenton J.|last3=Shields|first3=Raymond C.|title=Idiopathic Pulmonary Artery Aneurysm|journal=The Annals of Thoracic Surgery|volume=80|issue=4|year=2005|pages=1500–1502|issn=00034975|doi=10.1016/j.athoracsur.2004.04.011}}</ref>]]
====[[Pulmonary valve]] ring dilatation<ref name="pmid3841897">{{cite journal |vauthors=Tsuneyoshi H, Hara K, Takeuchi H, Kashida M, Yamaguchi T, Toide H, Toda E, Machii K |title=[Pulmonary regurgitation with special reference to the shape of the pulmonary valve ring: a pulsed Doppler and angiographic study] |language=Japanese |journal=J Cardiogr |volume=15 |issue=4 |pages=1145–56 |date=December 1985 |pmid=3841897 |doi= |url=}}</ref>====
A study utilized pulsed [[doppler echocardiography]] and [[cineangiography]] to identify the significance of [[pulmonic valve]] ring dimensions in the development of [[PR]]. It reported the ratio of [[sagittal]] to the [[transverse]] diameter of the [[pulmonic valve]] ring to be greater among patients with [[PR]]. In [[patients]] with [[PAH]] the study also demonstrated greater dilatation of the [[sagittal]] diameter of the [[pulmonic valve]] ring than pulmonary sinus diameter. In the light of the results, the etiology of [[PR]] was attributed to the distortion of [[pulmonic valve]] ring.


====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>====
====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>====

Latest revision as of 16:40, 5 August 2020

Pulmonic regurgitation Microchapters

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Pathophysiology

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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], Javaria Anwer M.D.[4]

Overview

Pulmonary valve is located at the junction of the right ventricular outflow tract and pulmonary artery. Three equal-sized, semilunar cusps or leaflets make up the pulmonary valve. Pulmonary valve opens during right ventricular systole and closes during right ventricular diastole. Pulmonary regurgitation (PR) may be caused by an acquired alteration in the valvular morphology, idiopathic dilatation of the pulmonary artery (IDPA), pulmonic valve ring dilatation, congenital absence or malformation of the valve, and increasing regurgitation causing right ventricular volume overload. 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. Among patients with severe PR, the gene expression pattern of GRK2 and β2-adrenoceptor (molecular markers of cardiac dysfunction) has been reported to be altered. Isolated PR is uncommon and is usually demonstrated with other valvular abnormalities or in certain conditions. Conditions associated include TOF, rheumatic heart disease and syphilis. On gross pathology vegetative lesions on the pulmonic valve leaflets may be observed among patients with acquired alteration in the valvular leaflet morphology.

Pathophysiology

Anatomy of and physiology of pulmonic valve

Cadaveric specimen of heart demonstrating pulmonary valve location between right ventricular outflow tract and pulmonary artery - By Anatomist90 - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=20481209
  • Structure: Three equal sized, semilunar cusps or leaflets make up the pulmonary valve. Based on the corresponding aortic valve, the cusps are named right, left and anterior.[2] [2]
  • The three cusps are joined by commissures and the cusps are thinner when compared to the aortic valve, due to a low pressure in the right ventricle.[2]
  • Histologically, the pulmonary valve consists of stratified extracellular matrix compartments. The layers constitute fibrosa, spongiosa and ventricularis.[3]
  • The diameter of pulmonic valve is demonstrated to be closely related to the body size. For adult men (>17 years age) mean pulmonary valve diameter is 26.2 +/- 2.3 mm and 23.9 +/- 2.2 mm for adult women.[4]
  • Physiology: The right ventricle delivers the received blood entirely to the pulmonary circulation every beat, maintaining optimum pressure.[5] Pulmonary valve opens during right ventricular systole allowing the deoxygenated blood to be delivered to the lungs. [2] During the right ventricular diastole the pulmonary valves close completely to prevent regurgitation (back flow) of the blood into the right ventricle.[2]
  • The closure of the pulmonic valve contributes to the P2 component of the second heart sound (S2).

Pathogenesis

The pathogenesis of pulmonic regurgitation involves the following mechanisms:[6][7]

Dynamics of regurgitation

PR volume = regurgitant orifice area · constant · diastolic time · mean diastolic pressure difference between the MPA and RV.(P2−P1)0.5.

Acquired alteration in the valvular morphology[11][10]

Regurgitation is avoided despite large regurgitation orifice due to Torricelli principle. Progressively, an increased size and capacitance of central pulmonary ateries and right ventricular dilatation occurs due to increased RV stroke volume. The changes described progress with age accompanied by a longer duration of diastole and decreased heart rate. This progressively leads to an increase in the degree of PR.

A few factors influencing the progression of pulmonary regurgitation (PR) after TOF repair - [10]

Idiopathic dilatation of the pulmonary artery (IDPA)[12][13][14]

3-D reconstruction of chest CT demonstrating diffuse aneurysmal dilatation of the pulmonary outflow tract and main pulmonary artery (right and left) - [15]

Pulmonary valve ring dilatation[16]

A study utilized pulsed doppler echocardiography and cineangiography to identify the significance of pulmonic valve ring dimensions in the development of PR. It reported the ratio of sagittal to the transverse diameter of the pulmonic valve ring to be greater among patients with PR. In patients with PAH the study also demonstrated greater dilatation of the sagittal diameter of the pulmonic valve ring than pulmonary sinus diameter. In the light of the results, the etiology of PR was attributed to the distortion of pulmonic valve ring.

Congenital absence or malformation of the valve[17][12][13][18]

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

Increasing regurgitation causing right ventricular volume overload[9]

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. ↑ Maganti K, Rigolin VH, Sarano ME, Bonow RO (2010). "Valvular heart disease: diagnosis and management". Mayo Clin Proc. 85 (5): 483–500. doi:10.4065/mcp.2009.0706. PMC 2861980. PMID 20435842.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 Schmoldt A, Benthe HF, Haberland G, Felt V, Nedvídková J, Hynie S, Mosinger B, Vavrinková M, Järvisalo J, Saris NE (September 1975). "Digitoxin metabolism by rat liver microsomes". Biochem. Pharmacol. 24 (17): 1639–41. doi:10.1016/0006-2952(75)90009-x. PMC 5922622. PMID 10.
  3. ↑ Combs MD, Yutzey KE (August 2009). "Heart valve development: regulatory networks in development and disease". Circ. Res. 105 (5): 408–21. doi:10.1161/CIRCRESAHA.109.201566. PMC 2777683. PMID 19713546.
  4. ↑ Capps SB, Elkins RC, Fronk DM (May 2000). "Body surface area as a predictor of aortic and pulmonary valve diameter". J. Thorac. Cardiovasc. Surg. 119 (5): 975–82. doi:10.1016/S0022-5223(00)70092-4. PMID 10788818.
  5. ↑ Pinsky MR (September 2016). "The right ventricle: interaction with the pulmonary circulation". Crit Care. 20: 266. doi:10.1186/s13054-016-1440-0. PMC 5018168. PMID 27613549.
  6. ↑ Khavandi, Ali (2014). Essential revision notes for the cardiology KBA. Oxford: Oxford University Press. ISBN 978-0199654901.
  7. ↑ Khavandi, Ali (2014). Essential revision notes for the cardiology KBA. Oxford: Oxford University Press. ISBN 978-0199654901.
  8. ↑ 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.
  9. ↑ 9.0 9.1 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.
  10. ↑ 10.0 10.1 10.2 10.3 Geva T (January 2011). "Repaired tetralogy of Fallot: the roles of cardiovascular magnetic resonance in evaluating pathophysiology and for pulmonary valve replacement decision support". J Cardiovasc Magn Reson. 13: 9. doi:10.1186/1532-429X-13-9. PMC 3036629. PMID 21251297.
  11. ↑ 11.0 11.1 11.2 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.
  12. ↑ 12.0 12.1 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.
  13. ↑ 13.0 13.1 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.
  14. ↑ 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.
  15. ↑ Deb, Subrato J.; Zehr, Kenton J.; Shields, Raymond C. (2005). "Idiopathic Pulmonary Artery Aneurysm". The Annals of Thoracic Surgery. 80 (4): 1500–1502. doi:10.1016/j.athoracsur.2004.04.011. ISSN 0003-4975.
  16. ↑ Tsuneyoshi H, Hara K, Takeuchi H, Kashida M, Yamaguchi T, Toide H, Toda E, Machii K (December 1985). "[Pulmonary regurgitation with special reference to the shape of the pulmonary valve ring: a pulsed Doppler and angiographic study]". J Cardiogr (in Japanese). 15 (4): 1145–56. PMID 3841897.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 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.
  20. ↑ Wünnemann, Florian; Ta-Shma, Asaf; Preuss, Christoph; Leclerc, Severine; van Vliet, Patrick Piet; Oneglia, Andrea; Thibeault, Maryse; Nordquist, Emily; Lincoln, Joy; Scharfenberg, Franka; Becker-Pauly, Christoph; Hofmann, Philipp; Hoff, Kirstin; Audain, Enrique; Kramer, Hans-Heiner; Makalowski, Wojciech; Nir, Amiram; Gerety, Sebastian S.; Hurles, Matthew; Comes, Johanna; Fournier, Anne; Osinska, Hanna; Robins, Jeffrey; Pucéat, Michel; Elpeleg, Orly; Hitz, Marc-Phillip; Andelfinger, Gregor (2019). "Loss of ADAMTS19 causes progressive non-syndromic heart valve disease". Nature Genetics. 52 (1): 40–47. doi:10.1038/s41588-019-0536-2. ISSN 1061-4036.
  21. ↑ Massadeh, Salam; Alhashem, Amal; Laar, Ingrid M.B.H.; Alhabshan, Fahad; Ordonez, Natalia; Alawbathani, Salem; Khan, Suliman; Kabbani, Mohamed S.; Chaikhouni, Farah; Sheereen, Atia; Almohammed, Iman; Alghamdi, Bader; Frohn‐Mulder, Ingrid; Ahmad, Salim; Beetz, Christian; Bauer, Peter; Wessels, Marja W.; Alaamery, Manal; Bertoli‐Avella, Aida M. (2020). "ADAMTS19 ‐associated heart valve defects: Novel genetic variants consolidating a recognizable cardiac phenotype". Clinical Genetics. 98 (1): 56–63. doi:10.1111/cge.13760. ISSN 0009-9163. line feed character in |title= at position 9 (help)
  22. ↑ Rodríguez-Serrano M, Rueda Soriano J, Buendía Fuentes F, Osa Sáez AM, Montó Guillot F, D'Ocon Navaza P, Aguero J, Oliver E, Serrano F, Martínez-Dolz L (July 2019). "Changes in Adrenoceptor and GRK Expression in Patients With Chronic Pulmonary Regurgitation". Rev Esp Cardiol (Engl Ed). 72 (7): 569–576. doi:10.1016/j.rec.2018.05.030. PMID 30104167.
  23. ↑ 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.
  24. ↑ 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.
  25. ↑ Nollen GJ, van Schijndel KE, Timmermans J, Groenink M, Barentsz JO, van der Wall EE, Stoker J, Mulder BJ (May 2002). "Pulmonary artery root dilatation in Marfan syndrome: quantitative assessment of an unknown criterion". Heart. 87 (5): 470–1. doi:10.1136/heart.87.5.470. PMC 1767105. PMID 11997425.
  26. ↑ Eisenberg MJ (January 1993). "Rheumatic heart disease in the developing world: prevalence, prevention, and control". Eur. Heart J. 14 (1): 122–8. doi:10.1093/eurheartj/14.1.122. PMID 8432279.
  27. ↑ prasad, Arun; Kumar, Sanjeev; Kr Singh, Birendra; Kumari, Neelam (2017). "Mortality Due to Rheumatic Heart Disease in Developing World: A Preventable Problem". Journal of Clinical & Experimental Cardiology. 08 (03). doi:10.4172/2155-9880.1000503. ISSN 2155-9880.
  28. ↑ Raymond TE, Khabbaza JE, Yadav R, Tonelli AR (December 2014). "Significance of main pulmonary artery dilation on imaging studies". Ann Am Thorac Soc. 11 (10): 1623–32. doi:10.1513/AnnalsATS.201406-253PP. PMC 4298979. PMID 25406836.

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