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{{Mitral regurgitation}}
{{Mitral regurgitation}}
{{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}}; [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S.
{{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}}; [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S.
==Overview==


The pathophysiology of mitral regurgitation can be divided into three phases of the disease process:
The pathophysiology of mitral regurgitation can be divided into three phases of the disease process:


==Acute phase==
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]]. 
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). 
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>


==Complications of Mitral Regurgitation==
==Complications of Mitral Regurgitation==

Revision as of 13:58, 15 September 2011

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.

Overview

The pathophysiology of mitral regurgitation can be divided into three phases of the disease process:


Complications of Mitral Regurgitation

Mitral Regurgitation when mild almost never cause any complications. However, when severe, it may lead to development of:

Prognosis

  • Patients with asymptomatic chronic severe mitral regurgitation have a high likelihood of developing symptoms or LV dysfunction over the course of 6 to 10 years [1] [2] [3]. However, the incidence of sudden death in asymptomatic patients with normal LV function varies widely among these studies.
  • Clinical outcome is poor in patients with severe symptomatic mitral regurgitation with eight year survival rate of 33% without surgical intervention. Heart failure being the common cause with sudden death attributing to ventricular arrhythmia.[4]
  • In patients with severe mitral regurgitation due to a flail posterior mitral leaflet, 90% of patients are dead or require MV operation at 10 years with the mortality rate in patients with severe mitral regurgitation being 6% to 7% per year. However, the risk of death are predominantly in patients with a left ventricular ejection fraction <60% or with NYHA functional class III–IV symptoms [1] [5].
  • Severe symptoms also predict 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. While in patients with NYHA functional class I/II symptoms before surgery survival rates at 5 and 10 years are 90 ± 2% and 76 ± 5%, respectively[5].
  • In a long-term retrospective study [2], 198 patients with an effective orifice area >40 mm² had a risk of cardiac death at 4% per year during a mean follow-up period of 2.7 years. However, in the another study where 132 patients were followed up prospectively for 5 years, indications for surgery were development of symptoms, LV dysfunction (EF <60%), LV dilatation (LV end-systolic diameter >45 mm), atrial fibrillation, orpulmonary hypertension and there was only 1 cardiac death in an asymptomatic patient, but this patient had refused surgery though it was indicated by development of LV dilation[3]. This suggests good prognosis with valve surgery.
  • In 80% of patients with atrial fibrillation greater than or equal to 3 months duration during the pre-operative period had persistence of atrial fibrillation after surgery. Hence, mitral valve repair should be done before or soon after the onset of atrial fibrillation to maximize the chance of postoperative sinus rhythm and avoid long-term anticoagulation with warfarin [6].

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. 3.0 3.1 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)
  6. Chua YL, Schaff HV, Orszulak TA, Morris JJ (1994). "Outcome of mitral valve repair in patients with preoperative atrial fibrillation. Should the maze procedure be combined with mitral valvuloplasty?". The Journal of Thoracic and Cardiovascular Surgery. 107 (2): 408–15. PMID 8302059. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)

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