Heart murmur pathophysiology: Difference between revisions
Jump to navigation
Jump to search
| (3 intermediate revisions by the same user not shown) | |||
| Line 4: | Line 4: | ||
==Overview== | ==Overview== | ||
Turbulent flow is responsible for most murmurs. Turbulent flow occurs when the velocity of blood flow becomes critically high because of a high volume of flow, the flow goes through an irregular or narrow area, the flow empties into a dilated vessel or chamber, or if the flow goes backward through an incompetent valve, septal defect, or [[patent ductus arteriosus]]. Frequently, a combination of these factors is operative. | [[Turbulent flow]] is responsible for most [[murmurs]]. [[Turbulent flow]] occurs when the [[velocity]] of [[blood]] flow becomes critically high because of a high volume of flow, the flow goes through an irregular or narrow area, the flow empties into a dilated [[vessel]] or chamber, or if the flow goes backward through an incompetent valve, [[septal defect]], or [[patent ductus arteriosus]]. Frequently, a combination of these factors is operative. | ||
The sounds most commonly originate from the abnormal movement of blood across valves and between cardiac chambers. When this occurs, turbulence results, which produces vibrations in the chambers of the heart or outflow vessels that are detected as Murmurs. | The sounds most commonly originate from the abnormal movement of [[blood]] across [[valves]] and between [[cardiac chambers]]. When this occurs, turbulence results, which produces vibrations in the chambers of the [[heart]] or outflow [[vessels]] that are detected as [[Murmurs]]. | ||
<br /> | <br /> | ||
== | ==Summery of pathophysiology for few causes of heart murmur== | ||
{| class="wikitable" | {| class="wikitable" | ||
|+ | |+ | ||
| Line 17: | Line 17: | ||
|[[aortic stenosis]] | |[[aortic stenosis]] | ||
| | | | ||
* | *Aortic stenosis is a progressive narrowing.<ref name="pmid27866029">{{cite journal| author=Galli D, Manuguerra R, Monaco R, Manotti L, Goldoni M, Becchi G et al.| title=Understanding the structural features of symptomatic calcific aortic valve stenosis: A broad-spectrum clinicopathologic study in 236 consecutive surgical cases. | journal=Int J Cardiol | year= 2016 | volume= 228 | issue= | pages= 364-374 | pmid=27866029 | doi=10.1016/j.ijcard.2016.11.180 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27866029 }} </ref> When the [[aortic valve]] area decreased by at least half, there will be a change in the antegrade velocity at the level of the [[aortic valve]] and also at the [[Subvalvular aortic stenosis|subvalvular]] ([[Subvalvular aortic stenosis|below the aortic valve]]) or [[Supravalvular aortic stenosis|supravalvular]] ([[Supravalvular aortic stenosis|above the aortic valve]]) levels. this will lead to chronic pressure overload in the [[left ventricle]].<ref name="pmid27810479">{{cite journal| author=Joseph J, Naqvi SY, Giri J, Goldberg S| title=Aortic stenosis: pathophysiology, diagnosis and therapy. | journal=Am J Med | year= 2016 | volume= | issue= | pages= | pmid=27810479 | doi=10.1016/j.amjmed.2016.10.005 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27810479 }} </ref> | ||
*chronic pressure caused by [[aortic stenosis]] lead to a slow compensatory mechanisms, the most prominent one is [[ventricular hypertrophy]] that leads to [[diastolic dysfunction]] and [[systolic dysfunction]].<ref name="pmid25140960">{{cite journal| author=Otto CM, Prendergast B| title=Aortic-valve stenosis--from patients at risk to severe valve obstruction. | journal=N Engl J Med | year= 2014 | volume= 371 | issue= 8 | pages= 744-56 | pmid=25140960 | doi=10.1056/NEJMra1313875 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25140960 }} </ref><ref name="pmid23062541">{{cite journal| author=Dweck MR, Boon NA, Newby DE| title=Calcific aortic stenosis: a disease of the valve and the myocardium. | journal=J Am Coll Cardiol | year= 2012 | volume= 60 | issue= 19 | pages= 1854-63 | pmid=23062541 | doi=10.1016/j.jacc.2012.02.093 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23062541 }} </ref> | *chronic pressure caused by [[aortic stenosis]] lead to a slow compensatory mechanisms, the most prominent one is [[ventricular hypertrophy]] that leads to [[diastolic dysfunction]] and [[systolic dysfunction]].<ref name="pmid25140960">{{cite journal| author=Otto CM, Prendergast B| title=Aortic-valve stenosis--from patients at risk to severe valve obstruction. | journal=N Engl J Med | year= 2014 | volume= 371 | issue= 8 | pages= 744-56 | pmid=25140960 | doi=10.1056/NEJMra1313875 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25140960 }} </ref><ref name="pmid23062541">{{cite journal| author=Dweck MR, Boon NA, Newby DE| title=Calcific aortic stenosis: a disease of the valve and the myocardium. | journal=J Am Coll Cardiol | year= 2012 | volume= 60 | issue= 19 | pages= 1854-63 | pmid=23062541 | doi=10.1016/j.jacc.2012.02.093 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23062541 }} </ref> | ||
*Summary of the pathophysiology | *[[Aortic stenosis pathophysiology|Summary of the pathophysiology of aortic stenosis]]. | ||
|- | |- | ||
|[[aortic regurgitation]] | |[[aortic regurgitation]] | ||
| | | | ||
*[[Aortic regurgitation|Aortic insufficiency]] develop when the pressure in the [[left ventricle]] falls below the pressure in the [[aorta]],leading to volume overload of the [[left ventricle]].<ref name="pmid24939033">{{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 Thorac Cardiovasc Surg | year= 2014 | volume= 148 | issue= 1 | pages= e1-e132 | pmid=24939033 | doi=10.1016/j.jtcvs.2014.05.014 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24939033 }} </ref> <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> | |||
*In acute [[Aortic regurgitation|aortic insufficiency]]: | |||
**Sudden decrease in [[stroke volume]] and increase in left ventricular end diastolic volume causing decrease [[cardiac output]] and reflex [[tachycardia]], which eventually lead to profound [[hypotension]] and [[cardiogenic shock]]. | |||
**[[pulmonary edema]] develops in severe cases due to the rapidly rising in the left ventricular end diastolic pressure which equalizes with the aortic end-diastolic pressure leading to back flow of [[blood]].<ref name="pmid19564568">{{cite journal| author=Stout KK, Verrier ED| title=Acute valvular regurgitation. | journal=Circulation | year= 2009 | volume= 119 | issue= 25 | pages= 3232-41 | pmid=19564568 | doi=10.1161/CIRCULATIONAHA.108.782292 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19564568 }} </ref><ref name="pmid21423463">{{cite journal| author=Mokadam NA, Stout KK, Verrier ED| title=Management of acute regurgitation in left-sided cardiac valves. | journal=Tex Heart Inst J | year= 2011 | volume= 38 | issue= 1 | pages= 9-19 | pmid=21423463 | doi= | pmc=3060740 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21423463 }} </ref> | |||
In acute aortic insufficiency | |||
*In [[Aortic insufficiency|chronic aortic insufficiency]]: | |||
In chronic aortic insufficiency | **there is compensation for increased left ventricular end diastolic volume by progressive left ventricular dilatation and [[left ventricular hypertrophy]], which maintains normal wall stress. | ||
**Overtime, when the [[left ventricular hypertrophy]] fails to keep up with chronic volume overload, the [[left ventricle]] decompensate causing reduction in the left ventricular wall compliance with resultant [[congestive heart failure]].<ref name="pmid15470217">{{cite journal| author=Enriquez-Sarano M, Tajik AJ| title=Clinical practice. Aortic regurgitation. | journal=N Engl J Med | year= 2004 | volume= 351 | issue= 15 | pages= 1539-46 | pmid=15470217 | doi=10.1056/NEJMcp030912 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15470217 }} </ref><ref name="pmid10051296">{{cite journal| author=Devlin WH, Petrusha J, Briesmiester K, Montgomery D, Starling MR| title=Impact of vascular adaptation to chronic aortic regurgitation on left ventricular performance. | journal=Circulation | year= 1999 | volume= 99 | issue= 8 | pages= 1027-33 | pmid=10051296 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10051296 }} </ref> <ref name="Nishimura-2002">{{Cite journal | last1 = Nishimura | first1 = RA. | title = Cardiology patient pages. Aortic valve disease. | journal = Circulation | volume = 106 | issue = 7 | pages = 770-2 | month = Aug | year = 2002 | doi = | PMID = 12176943 }}</ref> | |||
|- | |- | ||
|[[mitral stenosis]] | |[[mitral stenosis]] | ||
| | | | ||
*Mitral stenosis ([[MS]]) is most commonly secondary to acute [[rheumatic fever]]. Generally, the initial [[valvulitis]] is associated with [[valvular]] [[regurgitation]] then over the years, the [[commissures]] fuse and the valves thicken and calcify.<ref name="pmid14879491">{{cite journal| author=BLAND EF, DUCKETT JONES T| title=Rheumatic fever and rheumatic heart disease; a twenty year report on 1000 patients followed since childhood. | journal=Circulation | year= 1951 | volume= 4 | issue= 6 | pages= 836-43 | pmid=14879491 | doi= | pmc= | url= }}</ref> | *Mitral stenosis ([[MS]]) is most commonly secondary to acute [[rheumatic fever]]. Generally, the initial [[valvulitis]] is associated with [[valvular]] [[regurgitation]] then over the years, the [[commissures]] fuse and the [[valves]] thicken and calcify.<ref name="pmid14879491">{{cite journal| author=BLAND EF, DUCKETT JONES T| title=Rheumatic fever and rheumatic heart disease; a twenty year report on 1000 patients followed since childhood. | journal=Circulation | year= 1951 | volume= 4 | issue= 6 | pages= 836-43 | pmid=14879491 | doi= | pmc= | url= }}</ref> | ||
*Usually, the rate of decrement in the valve area is about 0.1 cm<sup>2</sup>/year once mitral stenosis is present.<ref name="pmid1552121">{{cite journal| author=Gordon SP, Douglas PS, Come PC, Manning WJ| title=Two-dimensional and Doppler echocardiographic determinants of the natural history of mitral valve narrowing in patients with rheumatic mitral stenosis: implications for follow-up. | journal=J Am Coll Cardiol | year= 1992 | volume= 19 | issue= 5 | pages= 968-73 | pmid=1552121 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1552121 }}</ref><ref name="pmid8800128">{{cite journal| author=Sagie A, Freitas N, Padial LR, Leavitt M, Morris E, Weyman AE et al.| title=Doppler echocardiographic assessment of long-term progression of mitral stenosis in 103 patients: valve area and right heart disease. | journal=J Am Coll Cardiol | year= 1996 | volume= 28 | issue= 2 | pages= 472-9 | pmid=8800128 | doi=10.1016/0735-1097(96)00153-2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8800128 }}</ref> | *Usually, the rate of decrement in the [[valve]] area is about 0.1 cm<sup>2</sup>/year once mitral stenosis is present.<ref name="pmid1552121">{{cite journal| author=Gordon SP, Douglas PS, Come PC, Manning WJ| title=Two-dimensional and Doppler echocardiographic determinants of the natural history of mitral valve narrowing in patients with rheumatic mitral stenosis: implications for follow-up. | journal=J Am Coll Cardiol | year= 1992 | volume= 19 | issue= 5 | pages= 968-73 | pmid=1552121 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1552121 }}</ref><ref name="pmid8800128">{{cite journal| author=Sagie A, Freitas N, Padial LR, Leavitt M, Morris E, Weyman AE et al.| title=Doppler echocardiographic assessment of long-term progression of mitral stenosis in 103 patients: valve area and right heart disease. | journal=J Am Coll Cardiol | year= 1996 | volume= 28 | issue= 2 | pages= 472-9 | pmid=8800128 | doi=10.1016/0735-1097(96)00153-2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8800128 }}</ref> | ||
*When the cross sectional area is about 2 cm<sup>2</sup> called | *When the cross sectional area is about 2 cm<sup>2</sup> called mild [[mitral stenosis]].<ref name="MS">Circulation http://circ.ahajournals.org/content/112/3/43November (2016) Accessed on November 22, 2016</ref> | ||
*When the cross sectional area goes below 2 cm<sup>2</sup>: | *When the cross sectional area goes below 2 cm<sup>2</sup>: | ||
**there will be impediment to the flow of blood into the left ventricle, creating a pressure gradient that increased by increases in the [[heart rate]] or [[cardiac output]]. | **there will be impediment to the [[flow]] of [[blood]] into the [[left ventricle]], creating a [[pressure]] [[gradient]] that increased by increases in the [[heart rate]] or [[cardiac output]]. | ||
**The [[atrial kick]] is required to fill the left ventricle with blood when the valve is so tight and the gradient is so high. | **The [[atrial kick]] is required to fill the [[left ventricle]] with [[blood]] when the valve is so tight and the gradient is so high. | ||
**When the heart rate goes above a certain point, the diastolic filling period is insufficient to fill the ventricle with blood and pressure builds up in the [[left atrium]], leading to [[pulmonary congestion]].<ref name="MS2">Circulation http://circ.ahajournals.org/content/112/3/43November (2016) Accessed on November 22, 2016</ref> | **When the [[heart rate]] goes above a certain point, the diastolic filling period is insufficient to fill the [[ventricle]] with [[blood]] and pressure builds up in the [[left atrium]], leading to [[pulmonary congestion]].<ref name="MS2">Circulation http://circ.ahajournals.org/content/112/3/43November (2016) Accessed on November 22, 2016</ref> | ||
*When the mitral valve area goes less than 1 cm<sup>2</sup>: | *When the mitral valve area goes less than 1 cm<sup>2</sup>: | ||
**the pressure gradient across the mitral valve will be 20 mm Hg and the left atrial pressure about 25 mm Hg. | **the pressure gradient across the mitral valve will be 20 mm Hg and the left atrial pressure about 25 mm Hg. | ||
| Line 53: | Line 51: | ||
|[[mitral regurgitation]] | |[[mitral regurgitation]] | ||
| | | | ||
* Acute [[Mitral regurgitation|Mitral Regurgitation]] <ref name="pmid37425242">{{cite journal| author=Kusiak V, Brest AN| title=Acute mitral regurgitation: pathophysiology and management. | journal=Cardiovasc Clin | year= 1986 | volume= 16 | issue= 2 | pages= 257-80 | pmid=3742524 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3742524 }}</ref> | *Acute [[Mitral regurgitation|Mitral Regurgitation]] <ref name="pmid37425242">{{cite journal| author=Kusiak V, Brest AN| title=Acute mitral regurgitation: pathophysiology and management. | journal=Cardiovasc Clin | year= 1986 | volume= 16 | issue= 2 | pages= 257-80 | pmid=3742524 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3742524 }}</ref> | ||
** Develop when there is sudden disruption of one or more of the components of the [[mitral valve]], such as leaflet perforation, rupture of a [[chordae tendineae]], or rupture of the [[papillary muscle]]. | **Develop when there is sudden disruption of one or more of the components of the [[mitral valve]], such as leaflet perforation, rupture of a [[chordae tendineae]], or rupture of the [[papillary muscle]]. | ||
** In the acute setting, the total stroke volume is increased, but the forward cardiac output into the [[aorta]] is decreased because a proportion of the blood is going backward into the [[left atrium]]. | **In the acute setting, the total stroke volume is increased, but the forward cardiac output into the [[aorta]] is decreased because a proportion of the blood is going backward into the [[left atrium]]. | ||
** [[Pulmonary congestion]] and [[hypoxia]] occur in acute [[Mitral regurgitation|MR]] causes a sudden volume overload of both the [[left atrium]] and the [[left ventricle]]. | **[[Pulmonary congestion]] and [[hypoxia]] occur in acute [[Mitral regurgitation|MR]] causes a sudden volume overload of both the [[left atrium]] and the [[left ventricle]]. | ||
*Chronic Compensated [[mitral regurgitation]]: <ref name="pmid24603192">{{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: executive summary: 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= 2438-88 | pmid=24603192 | doi=10.1016/j.jacc.2014.02.537 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24603192 }}</ref> | *Chronic Compensated [[mitral regurgitation]]: <ref name="pmid24603192">{{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: executive summary: 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= 2438-88 | pmid=24603192 | doi=10.1016/j.jacc.2014.02.537 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24603192 }}</ref> | ||
**Develops slowly and the [[left ventricle]] develops eccentric hypertrophy to reduce the wall stress associated with the rise in total [[stroke volume]]. | **Develops slowly and the [[left ventricle]] develops eccentric hypertrophy to reduce the wall stress associated with the rise in total [[stroke volume]]. | ||
Latest revision as of 17:40, 31 January 2021
|
Heart murmur Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Heart murmur pathophysiology On the Web |
|
American Roentgen Ray Society Images of Heart murmur pathophysiology |
|
Risk calculators and risk factors for Heart murmur pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Nuha Al-Howthi, MD[2]
Overview
Turbulent flow is responsible for most murmurs. Turbulent flow occurs when the velocity of blood flow becomes critically high because of a high volume of flow, the flow goes through an irregular or narrow area, the flow empties into a dilated vessel or chamber, or if the flow goes backward through an incompetent valve, septal defect, or patent ductus arteriosus. Frequently, a combination of these factors is operative. The sounds most commonly originate from the abnormal movement of blood across valves and between cardiac chambers. When this occurs, turbulence results, which produces vibrations in the chambers of the heart or outflow vessels that are detected as Murmurs.
Summery of pathophysiology for few causes of heart murmur
| pathophysiology | |
|---|---|
| aortic stenosis |
|
| aortic regurgitation |
|
| mitral stenosis |
|
| mitral regurgitation |
|
References
- ↑ Galli D, Manuguerra R, Monaco R, Manotti L, Goldoni M, Becchi G; et al. (2016). "Understanding the structural features of symptomatic calcific aortic valve stenosis: A broad-spectrum clinicopathologic study in 236 consecutive surgical cases". Int J Cardiol. 228: 364–374. doi:10.1016/j.ijcard.2016.11.180. PMID 27866029.
- ↑ Joseph J, Naqvi SY, Giri J, Goldberg S (2016). "Aortic stenosis: pathophysiology, diagnosis and therapy". Am J Med. doi:10.1016/j.amjmed.2016.10.005. PMID 27810479.
- ↑ Otto CM, Prendergast B (2014). "Aortic-valve stenosis--from patients at risk to severe valve obstruction". N Engl J Med. 371 (8): 744–56. doi:10.1056/NEJMra1313875. PMID 25140960.
- ↑ Dweck MR, Boon NA, Newby DE (2012). "Calcific aortic stenosis: a disease of the valve and the myocardium". J Am Coll Cardiol. 60 (19): 1854–63. doi:10.1016/j.jacc.2012.02.093. PMID 23062541.
- ↑ Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA; et al. (2014). "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". J Thorac Cardiovasc Surg. 148 (1): e1–e132. doi:10.1016/j.jtcvs.2014.05.014. PMID 24939033.
- ↑ Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA; et al. (2014). "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". J Am Coll Cardiol. 63 (22): e57–185. doi:10.1016/j.jacc.2014.02.536. PMID 24603191.
- ↑ Stout KK, Verrier ED (2009). "Acute valvular regurgitation". Circulation. 119 (25): 3232–41. doi:10.1161/CIRCULATIONAHA.108.782292. PMID 19564568.
- ↑ Mokadam NA, Stout KK, Verrier ED (2011). "Management of acute regurgitation in left-sided cardiac valves". Tex Heart Inst J. 38 (1): 9–19. PMC 3060740. PMID 21423463.
- ↑ Enriquez-Sarano M, Tajik AJ (2004). "Clinical practice. Aortic regurgitation". N Engl J Med. 351 (15): 1539–46. doi:10.1056/NEJMcp030912. PMID 15470217.
- ↑ Devlin WH, Petrusha J, Briesmiester K, Montgomery D, Starling MR (1999). "Impact of vascular adaptation to chronic aortic regurgitation on left ventricular performance". Circulation. 99 (8): 1027–33. PMID 10051296.
- ↑ Nishimura, RA. (2002). "Cardiology patient pages. Aortic valve disease". Circulation. 106 (7): 770–2. PMID 12176943. Unknown parameter
|month=ignored (help) - ↑ BLAND EF, DUCKETT JONES T (1951). "Rheumatic fever and rheumatic heart disease; a twenty year report on 1000 patients followed since childhood". Circulation. 4 (6): 836–43. PMID 14879491.
- ↑ Gordon SP, Douglas PS, Come PC, Manning WJ (1992). "Two-dimensional and Doppler echocardiographic determinants of the natural history of mitral valve narrowing in patients with rheumatic mitral stenosis: implications for follow-up". J Am Coll Cardiol. 19 (5): 968–73. PMID 1552121.
- ↑ Sagie A, Freitas N, Padial LR, Leavitt M, Morris E, Weyman AE; et al. (1996). "Doppler echocardiographic assessment of long-term progression of mitral stenosis in 103 patients: valve area and right heart disease". J Am Coll Cardiol. 28 (2): 472–9. doi:10.1016/0735-1097(96)00153-2. PMID 8800128.
- ↑ Circulation http://circ.ahajournals.org/content/112/3/43November (2016) Accessed on November 22, 2016
- ↑ Circulation http://circ.ahajournals.org/content/112/3/43November (2016) Accessed on November 22, 2016
- ↑ Marcus RH, Sareli P, Pocock WA, Barlow JB (1994). "The spectrum of severe rheumatic mitral valve disease in a developing country. Correlations among clinical presentation, surgical pathologic findings, and hemodynamic sequelae". Ann Intern Med. 120 (3): 177–83. PMID 8043061.
- ↑ Circulation http://circ.ahajournals.org/content/112/3/43November (2016) Accessed on November 22, 2016
- ↑ Kusiak V, Brest AN (1986). "Acute mitral regurgitation: pathophysiology and management". Cardiovasc Clin. 16 (2): 257–80. PMID 3742524.
- ↑ Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA; et al. (2014). "2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". J Am Coll Cardiol. 63 (22): 2438–88. doi:10.1016/j.jacc.2014.02.537. PMID 24603192.
- ↑ Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA; et al. (2014). "2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". J Am Coll Cardiol. 63 (22): 2438–88. doi:10.1016/j.jacc.2014.02.537. PMID 24603192.