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{{Mitral regurgitation}}
{{CMG}}; {{AE}} {{CZ}}; [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S.; [[User:Mohammed Sbeih|Mohammed A. Sbeih, M.D.]] [mailto:msbeih@wikidoc.org]


{{CMG}}
==Overview==
The natural history of mitral regurgitation (MR) may follow one of two patterns, acute or chronic. Chronic MR can be either compensated or decompensated. The natural history and prognosis of MR depend on the underlying etiology and the degree of severity of the valvular abnormality.  Mild MR is associated with few if any complications. However, when severe, MR may lead to development of [[pulmonary edema]], [[pulmonary hypertension]], and [[right heart failure]].
==Natural History==
The natural history of MR may follow one of two patterns, acute or chronic. In acute MR, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature leading to sudden onset of [[dyspnea]], [[PND]], [[orthopnea]] and [[rales]].  Chronic MR can be either compensated or decompensated. During the chronic compensated phase of MR, compensatory changes in the [[left ventricle]] and [[left atrium]] maintain the forward cardiac output of the left ventricle, and minimize the signs and symptoms of pulmonary congestion that occur in the acute phase of the disease.  Individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerance.  An individual may remain in the compensated phase of mitral regurgitation for years, but will eventually develop left ventricular dysfunction, the hallmark for the chronic decompensated phase of mitral regurgitation.  Once the patient transitions into the decompensated phase, there may not be recovery of left ventricular funtion following operative repair or replacement of the [[mitral valve]].  The decompensated stage is defined on the basis of a decompensated ventricular function. At this stage, the patients are at risk for a poor results of valve replacement.


'''Associate Editor-In-Chief:''' [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S.
==Complications==
Mild MR is associated with few if any complications. However, when severe, MR may lead to development of (in alphabetical order):
*[[Atrial fibrillation]]
*[[Cardiogenic Shock]]
*[[Endocarditis]]
*[[Pulmonary edema]]
*[[Pulmonary hypertension]]
*[[Right heart failure]]
*[[Thromboembolism]]-[[Stroke]]


==Prognosis==
Patients with asymptomatic chronic severe MR have a high likelihood of developing symptoms or [[left ventricular dysfunction]] over the course of 6 to 10 years.<ref name="pmid8875918">{{cite journal |author=Ling LH, Enriquez-Sarano M, Seward JB, Tajik AJ, Schaff HV, Bailey KR, Frye RL |title=Clinical outcome of mitral regurgitation due to flail leaflet |journal=[[The New England Journal of Medicine]] |volume=335 |issue=19 |pages=1417–23 |year=1996 |month=November |pmid=8875918 |doi=10.1056/NEJM199611073351902|url=http://dx.doi.org/10.1056/NEJM199611073351902 |accessdate=2011-03-06}}</ref><ref name="pmid15745978">{{cite journal |author=Enriquez-Sarano M, Avierinos JF, Messika-Zeitoun D, Detaint D, Capps M, Nkomo V, Scott C, Schaff HV, Tajik AJ |title=Quantitative determinants of the outcome of asymptomatic mitral regurgitation |journal=[[The New England Journal of Medicine]] |volume=352 |issue=9 |pages=875–83 |year=2005 |month=March |pmid=15745978 |doi=10.1056/NEJMoa041451 |url=http://dx.doi.org/10.1056/NEJMoa041451|accessdate=2011-03-06}}</ref><ref name="pmid16651470">{{cite journal |author=Rosenhek R, Rader F, Klaar U, Gabriel H, Krejc M, Kalbeck D, Schemper M, Maurer G, Baumgartner H|title=Outcome of watchful waiting in asymptomatic severe mitral regurgitation |journal=[[Circulation]] |volume=113 |issue=18 |pages=2238–44 |year=2006 |month=May |pmid=16651470|doi=10.1161/CIRCULATIONAHA.105.599175 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=16651470 |accessdate=2011-03-06}}</ref> The incidence of [[sudden death]] in asymptomatic patients with normal [[left ventricular]] function varies widely among studies.


{{EJ}}
The prognosis is poor in patients with severe symptomatic MR with an estimated eight year survival rate of only 33% in the absence of surgical intervention. [[Heart failure]] and [[sudden death]] due to ventricular arrhythmia are common causes of death.<ref name="pmid1936025">{{cite journal |author=Delahaye JP, Gare JP, Viguier E, Delahaye F, De Gevigney G, Milon H |title=Natural history of severe mitral regurgitation |journal=[[European Heart Journal]] |volume=12 Suppl B |issue= |pages=5–9 |year=1991 |month=July |pmid=1936025 |doi=|url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=1936025 |accessdate=2011-03-06}}</ref>


The pathophysiology of mitral regurgitation can be divided into three phases of the disease process:
Among subjects with severe MR due to a flail posterior mitral leaflet, 90% of patients are either dead or require mitral valve surgery by 10 years with a mortality rate of 6% to 7% per year. However, the risk of death is higher in those patients with a [[left ventricular ejection fraction]] <60% or with [[NYHA]] functional class III–IV symptoms.<ref name="pmid8875918">{{cite journal |author=Ling LH, Enriquez-Sarano M, Seward JB, Tajik AJ, Schaff HV, Bailey KR, Frye RL |title=Clinical outcome of mitral regurgitation due to flail leaflet |journal=[[The New England Journal of Medicine]] |volume=335 |issue=19 |pages=1417–23 |year=1996 |month=November |pmid=8875918|doi=10.1056/NEJM199611073351902 |url=http://dx.doi.org/10.1056/NEJM199611073351902 |accessdate=2011-03-06}}</ref><ref name="pmid9918527">{{cite journal |author=Tribouilloy CM, Enriquez-Sarano M, Schaff HV, Orszulak TA, Bailey KR, Tajik AJ, Frye RL |title=Impact of preoperative symptoms on survival after surgical correction of organic mitral regurgitation: rationale for optimizing surgical indications |journal=[[Circulation]] |volume=99 |issue=3 |pages=400–5 |year=1999 |month=January |pmid=9918527 |doi=|url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=9918527 |accessdate=2011-03-06}}</ref>


==Acute phase==
Severe symptoms are associated with a poor outcome after [[mitral valve]] repair or replacement.  Postoperative survival rates in patients with NYHA functional class III–IV symptoms at 5 and 10 years are 73 ± 3% and 48 ± 4% respectively, compared to 5 and 10 years survival rates of 90 ± 2% and 76 ± 5% respectively among patients with NYHA functional class I/II symptoms before surgery.<ref name="pmid9918527">{{cite journal |author=Tribouilloy CM, Enriquez-Sarano M, Schaff HV, Orszulak TA, Bailey KR, Tajik AJ, Frye RL |title=Impact of preoperative symptoms on survival after surgical correction of organic mitral regurgitation: rationale for optimizing surgical indications |journal=[[Circulation]] |volume=99 |issue=3|pages=400–5 |year=1999 |month=January |pmid=9918527 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=9918527 |accessdate=2011-03-06}}</ref>


Acute mitral regurgitation (as may occur due to the sudden rupture of a [[chordae tendineae]] or [[papillary muscle]]) causes a sudden volume overload of both the [[left atrium]] and the [[left ventricle]].
In a long-term retrospective study, 198 patients with an effective orifice area >40 mm² had a risk of cardiac death of 4% per year during a mean follow-up period of 2.7 years.<ref name="pmid15745978">{{cite journal |author=Enriquez-Sarano M, Avierinos JF, Messika-Zeitoun D, Detaint D, Capps M, Nkomo V, Scott C, Schaff HV, Tajik AJ |title=Quantitative determinants of the outcome of asymptomatic mitral regurgitation |journal=[[The New England Journal of Medicine]] |volume=352 |issue=9 |pages=875–83|year=2005 |month=March |pmid=15745978 |doi=10.1056/NEJMoa041451 |url=http://dx.doi.org/10.1056/NEJMoa041451 |accessdate=2011-03-06}}</ref>


The left ventricle develops volume overload because with every contraction it now has to pump out not only the volume of blood that goes into the [[aorta]] (the forward [[cardiac output]] or forward [[stroke volume]]), but also the blood that regurgitates into the [[left atrium]] (the regurgitant volume). 
Acute MR with [[cardiogenic shock]] is associated with an operative mortality of 80%.
 
The combination of the forward stroke volume and the regurgitant volume is known as the total stroke volume of the [[left ventricle]].
 
In the acute setting, the stroke volume of the left ventricle is increased (increased [[ejection fraction]]), but the forward cardiac output is decreased.  The mechanism by which the total stroke volume is increased is known as the [[Frank-Starling law of the heart|Frank-Starling mechanism]].
 
The regurgitant volume causes a volume overload and a pressure overload of the [[left atrium]].  The increased pressures in the left atrium inhibit drainage of blood from the lungs via the [[pulmonary vein]]s.  This causes [[congestive heart failure|pulmonary congestion]].
 
==Chronic compensated phase==
 
If the mitral regurgitation develops slowly over months to years or if the acute phase can be managed with medical therapy, the individual will enter the chronic compensated phase of the disease. In this phase, the left ventricle develops eccentric hypertrophy in order to better manage the larger than normal stroke volume. 
 
The eccentric hypertrophy and the increased diastolic volume combine to increase the stroke volume (to levels well above normal) so that the forward stroke volume (forward cardiac output) approaches the normal levels.
 
In the left atrium, the volume overload causes enlargement of the chamber of the [[left atrium]], allowing the filling pressure in the left atrium to decrease.  This improves the drainage from the pulmonary veins, and signs and symptoms of pulmonary congestion will decrease.
 
These changes in the left ventricle and left atrium improve the low forward cardiac output state and the pulmonary congestion that occur in the acute phase of the disease.  Individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerances.
 
==Chronic decompensated phase==
 
An individual may be in the compensated phase of mitral regurgitation for years, but will eventually develop left ventricular dysfunction, the hallmark for the chronic decompensated phase of mitral regurgitation. It is currently unclear what causes an individual to enter the decompensated phase of this disease. However, the decompensated phase is characterized by calcium overload within the cardiac [[myocyte]]s.
 
In this phase, the ventricular myocardium is no longer able to contract adequately to compensate for the volume overload of mitral regurgitation, and the [[stroke volume]] of the left ventricle will decrease. The decreased stroke volume causes a decreased forward [[cardiac output]] and an increase in the [[systole|end-systolic]] volume. The increased end-systolic volume translates to increased filling pressures of the ventricular and increased pulmonary venous congestion. The individual may again have symptoms of [[congestive heart failure]].
 
The left ventricle begins to dilate during this phase.  This causes a dilatation of the [[mitral valve annulus]], which may worsen the degree of mitral regurgitation. The dilated left ventricle causes an increase in the wall stress of the cardiac chamber as well.
 
While the [[ejection fraction]] is less in the chronic decompensated phase than in the acute phase or the chronic compensated phase of mitral regurgitation, it may still be in the normal range (i.e: > 50 percent), and may not decrease until late in the disease course. A decreased ejection fraction in an individual with mitral regurgitation and no other cardiac abnormality should alert the physician that the disease may be in its decompensated phase.
 
===Summary: Distinguishing the Three Phases of Mitral Regurgitation===
<table border="1" cellpadding="5" cellspacing="0" align="center" style="float:center">
<caption>'''Comparison of acute and chronic mitral regurgitation'''</caption>
<tr>
<th style="background:#efefef;" width="100px"></th>
<th style="background:#efefef;" width="150px">Acute mitral regurgitation</th>
<th style="background:#efefef;" width="175px">Chronic mitral regurgitation</th>
</tr>
<tr><td>[[Electrocardiogram]]</td><td>Normal</td><td>P mitrale, [[atrial fibrillation]], [[left ventricular hypertrophy]]</td></tr>
<tr><td>Heart size</td><td>Normal</td><td>Cardiomegaly, left atrial enlargement</td></tr>
<tr><td>[[heart sounds|Systolic murmur]]</td><td>Heard at the base, radiates to the neck, spine, or top of head</td><td>Heard at the apex, radiates to the axilla</td></tr>
<tr><td>Apical thrill</td><td>May be absent</td><td>Present</td></tr>
<tr><td>[[jugular venous pressure|Jugular venous distension]]</td><td>Present</td><td>Absent</td></tr>
</table>


==References==
==References==
{{reflist|2}}
{{reflist|2}}


[[Category:cardiology]]
[[Category:Needs overview]]
 
[[Category:Valvular heart disease]]
[[Category:Cardiology]]
[[Category:Disease]]
[[Category:Cardiac surgery]]
[[Category:Surgery]]
[[Category:Overview complete]]


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Latest revision as of 18:20, 9 September 2014
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.; Mohammed A. Sbeih, M.D. [3]

Overview

The natural history of mitral regurgitation (MR) may follow one of two patterns, acute or chronic. Chronic MR can be either compensated or decompensated. The natural history and prognosis of MR depend on the underlying etiology and the degree of severity of the valvular abnormality. Mild MR is associated with few if any complications. However, when severe, MR may lead to development of pulmonary edema, pulmonary hypertension, and right heart failure.

Natural History

The natural history of MR may follow one of two patterns, acute or chronic. In acute MR, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature leading to sudden onset of dyspnea, PND, orthopnea and rales. Chronic MR can be either compensated or decompensated. During the chronic compensated phase of MR, compensatory changes in the left ventricle and left atrium maintain the forward cardiac output of the left ventricle, and minimize the signs and symptoms of pulmonary congestion that occur in the acute phase of the disease. Individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerance. An individual may remain in the compensated phase of mitral regurgitation for years, but will eventually develop left ventricular dysfunction, the hallmark for the chronic decompensated phase of mitral regurgitation. Once the patient transitions into the decompensated phase, there may not be recovery of left ventricular funtion following operative repair or replacement of the mitral valve. The decompensated stage is defined on the basis of a decompensated ventricular function. At this stage, the patients are at risk for a poor results of valve replacement.

Complications

Mild MR is associated with few if any complications. However, when severe, MR may lead to development of (in alphabetical order):

Prognosis

Patients with asymptomatic chronic severe MR have a high likelihood of developing symptoms or left ventricular dysfunction over the course of 6 to 10 years.[1][2][3] The incidence of sudden death in asymptomatic patients with normal left ventricular function varies widely among studies.

The prognosis is poor in patients with severe symptomatic MR with an estimated eight year survival rate of only 33% in the absence of surgical intervention. Heart failure and sudden death due to ventricular arrhythmia are common causes of death.[4]

Among subjects with severe MR due to a flail posterior mitral leaflet, 90% of patients are either dead or require mitral valve surgery by 10 years with a mortality rate of 6% to 7% per year. However, the risk of death is higher in those patients with a left ventricular ejection fraction <60% or with NYHA functional class III–IV symptoms.[1][5]

Severe symptoms are associated with a poor outcome after mitral valve repair or replacement. Postoperative survival rates in patients with NYHA functional class III–IV symptoms at 5 and 10 years are 73 ± 3% and 48 ± 4% respectively, compared to 5 and 10 years survival rates of 90 ± 2% and 76 ± 5% respectively among patients with NYHA functional class I/II symptoms before surgery.[5]

In a long-term retrospective study, 198 patients with an effective orifice area >40 mm² had a risk of cardiac death of 4% per year during a mean follow-up period of 2.7 years.[2]

Acute MR with cardiogenic shock is associated with an operative mortality of 80%.

References

  1. ↑ 1.0 1.1 Ling LH, Enriquez-Sarano M, Seward JB, Tajik AJ, Schaff HV, Bailey KR, Frye RL (1996). "Clinical outcome of mitral regurgitation due to flail leaflet". The New England Journal of Medicine. 335 (19): 1417–23. doi:10.1056/NEJM199611073351902. PMID 8875918. Retrieved 2011-03-06. Unknown parameter |month= ignored (help)
  2. ↑ 2.0 2.1 Enriquez-Sarano M, Avierinos JF, Messika-Zeitoun D, Detaint D, Capps M, Nkomo V, Scott C, Schaff HV, Tajik AJ (2005). "Quantitative determinants of the outcome of asymptomatic mitral regurgitation". The New England Journal of Medicine. 352 (9): 875–83. doi:10.1056/NEJMoa041451. PMID 15745978. Retrieved 2011-03-06. Unknown parameter |month= ignored (help)
  3. ↑ Rosenhek R, Rader F, Klaar U, Gabriel H, Krejc M, Kalbeck D, Schemper M, Maurer G, Baumgartner H (2006). "Outcome of watchful waiting in asymptomatic severe mitral regurgitation". Circulation. 113 (18): 2238–44. doi:10.1161/CIRCULATIONAHA.105.599175. PMID 16651470. Retrieved 2011-03-06. Unknown parameter |month= ignored (help)
  4. ↑ Delahaye JP, Gare JP, Viguier E, Delahaye F, De Gevigney G, Milon H (1991). "Natural history of severe mitral regurgitation". European Heart Journal. 12 Suppl B: 5–9. PMID 1936025. Retrieved 2011-03-06. Unknown parameter |month= ignored (help)
  5. ↑ 5.0 5.1 Tribouilloy CM, Enriquez-Sarano M, Schaff HV, Orszulak TA, Bailey KR, Tajik AJ, Frye RL (1999). "Impact of preoperative symptoms on survival after surgical correction of organic mitral regurgitation: rationale for optimizing surgical indications". Circulation. 99 (3): 400–5. PMID 9918527. Retrieved 2011-03-06. Unknown parameter |month= ignored (help)

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