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| [[File:Siren.gif|30px|link=Mitral regurgitation resident survival guide]]|| <br> || <br>
| [[Mitral regurgitation resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']]
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{{Mitral regurgitation}}
{{Mitral regurgitation}}
{{CMG}}; {{AOEIC}} {{CZ}}; {{VK}}; {{LG}}; [[User:Mohammed Sbeih|Mohammed A. Sbeih, M.D.]] [mailto:msbeih@perfuse.org].
{{CMG}}; {{AE}} {{CZ}}; {{VK}}; {{LG}}; [[User:Mohammed Sbeih|Mohammed A. Sbeih, M.D.]] [mailto:msbeih@wikidoc.org]; {{Rim}}


==Overview==
==Overview==
'''Mitral regurgitation''' ('''MR'''), '''mitral insufficiency''' or '''mitral incompetence''' is  a disorder of the [[heart]] in which  the [[mitral valve]] does not close properly when the heart pumps out [[blood]].  It is the abnormal leaking of blood from the [[left ventricle]]through the mitral valve, and into the [[left atrium]], when the left ventricle contracts, i.e. there is [[Regurgitation (circulation)|regurgitation]] of blood back into the left atrium <ref>[http://www.mountsinai.org/Other/Diseases/Mitral%20valve%20regurgitation Mitral valve regurgitation] at [[Mount Sinai Hospital, New York|Mount Sinai Hospital]]</ref>. MR is the most common form of [[valvular heart disease]] <ref name='MedlineMitChron2008'>{{cite encyclopedia |last=Weinrauch |first=LA |author= |authorlink= |coauthors= |editor=|encyclopedia=Medline Plus Encyclopedia |title=Mitral regurgitation - chronic |url=http://www.nlm.nih.gov/medlineplus/ency/article/000176.htm |accessdate=2009-12-04 |edition=|date=2008-05-12 |year= |publisher=U.S. National Library of Medicine and National Institutes of Health |volume= |location= |id= |doi= |pages= |quote= }}</ref>.
Mitral regurgitation (MR) is  a disorder of the [[heart]] in which  the [[mitral valve]] does not close properly when the heart pumps out [[blood]].  MR is the abnormal leaking of blood from the [[left ventricle]] through the mitral valve, and into the [[left atrium]], when the left ventricle contracts. MR is the most common form of [[valvular heart disease]]. MR can be classified into either acute or chronic according to the acuity of the events leading to the valvular abnormality. Regardless of the underlying etiology of MR, a decrease in the coaptation between the leaflets of the valve commonly characterizes all cases of MR. The causes of MR depend on the acuity of the valvular abnormality and the underlying pathological mechanism. The blowing [[holosystolic murmur]] of mitral regurgitation must be distinguished from [[tricuspid regurgitation]] and a [[ventricular septal defect]]. MR is one of the most common [[valvular disease]]s in the general population, ranking first among valvular regurgitation abnormalities. The prevalence of MR of a severity equal to or worse than mild was reported in The Framingham Heart Study as 19.0% in men and 19.1% in women. The prevalence of MR increases with age. 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. The stage of MR can be estimated based on specific criteria for the valve anatomy, valve hemodynamics, associated cardiac findings, and symptoms.
Diseases that weaken or damage the valve or the heart tissue around the valve cause mitral regurgitation.
After age 55, some degree of mitral regurgitation is found in almost 20% of men and women who have an echocardiogram.
[[Image:Mitral Regurgitation.png|thumb|center|300px|'''Mitral regurgitation (schematic drawing)'''<br/>During systole, contraction of the left ventricle causes abnormal backflow (arrow) into the left atrium.<br/>1 [[Mitral valve]]<br/>2 [[Left Ventricle]]<br/>3 [[Left Atrium]]<br/>4 [[Aorta]]]]
<br clear="left"/>


==Anatomy==
==Classification==
The mitral valve is typically 4–6 cm² in area. It has two cusps, or leaflets (the anteromedial leaflet and the posterolateral leaflet).
MR can be classified into either acute or chronic according to the acuity of the events leading to the valvular abnormality. Chronic MR is further classified into primary or secondary based on the presence or absence of one or more abnormalities in the structures of the valves, respectively.


==Pathophysiology==
==Pathophysiology==
Mitral regurgitation is due to either perforation or prolapse of the leaflets, dilation of the mitral annulus or rupture of the papillary muscles or chordae tendineaeThere are several phases of mitral regurgitation (acute, chronic compensated, and chronic decompensated). In the acute phase, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature to cause an elevation of the [[pulomanry capillary wedge pressure]] which causes [[dyspnea]], [[PND]], [[orthopnea]] and [[rales]]. During the chronic compensated phase of mitral regurgitation, the left ventricle maintains forward [[cardiac output]] by filling with a larger volume of blood than usual to accomodate the fact that a portion of the blood will go backwards into the left atriumIn the decompensated phase, the left ventricle begins to dilate and fail. The markers of decompensation are as follows:
Regardless of the underlying etiology of MR, a decrease in the coaptation between the leaflets of the valve commonly characterizes all cases of MR.  Acute MR occurs when there is sudden disruption of one or more of the components of the [[mitral valve]], as occurs in leaflet perforation, rupture of a [[chordae tendineae]], or rupture of the [[papillary muscle]].  In the acute phase, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature to cause an elevation of the [[pulmonary capillary wedge pressure]], which causes [[dyspnea]], [[orthopnea]], and [[rales]]. In addition, there is decreased forward [[stroke volume]]. Chronic MR can be either primary or secondary. Chronic primary MR results from chronic disruption of one or more component of the [[mitral valve]] ([[papillary muscle]]s, [[chordae tendineae]], or valve leaflets), whereas chronic secondary MR results from the dysfunction and dilatation of the [[left ventricle]] rather than an intrinsic abnormality in one of the components of the [[mitral valve]]If the chronic MR develops slowly over months to years or if the acute phase is successfully managed with medical therapy, the patient enters the chronic compensated phase of MR that can eventually deteriorate into a decompensated phase as the [[left ventricular]] systolic function worsens. The markers of MR decompensation are as follows: [[left ventricular]] end-diastolic dimension greater than 70 mm, left ventricular end-systolic dimension greater than 45 to 47 mm, and left ventricular [[ejection fraction]] (LVEF) less than 50 to 55 percent.


# '''Left ventricular end-diastolic dimension greater than 70 mm'''
==Causes==
# '''Left ventricular end-systolic dimension greater than 45 to 47 mm'''
The causes of MR depend on the acuity of the valvular abnormality and the underlying pathological mechanism.  Acute MR occurs 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]]. The sudden disruption of the [[mitral valve]] can be caused by [[infective endocarditis]], degenerative mitral valve disease, or acute [[ST elevation myocardial infarction]].  Chronic primary MR is most commonly caused by [[mitral valve prolapse]]; other causes include [[rheumatic fever]] and [[Marfan's syndrome]].  Chronic secondary MR results from the dysfunction and dilatation of the left ventricle rather than an intrinsic abnormality in one of the components of the [[mitral valve]] and it can be caused by [[coronary artery disease]] (ischemic) or any disease causing [[left ventricular dysfunction]] and dilatation (functional).
# '''Left ventricular [[ejection fraction]] (LVEF) less than 50 to 55 percent'''
 
==Differential Diagnosis==
The blowing [[holosystolic murmur]] of mitral regurgitation must be distinguished from [[tricuspid regurgitation]] and a [[ventricular septal defect]].


==Epidemiology and Demographics==
==Epidemiology and Demographics==
The incidence of mitral regurgitation is approximately 2% in a modern Western population. In the past, rheumatic heart disease was the leading cause of mitral regurgitation in Western countries, but now [[mitral valve prolapse]] is the leading cause and accounts for 45% of cases in Western countriesIn Asia, North Africa, and the Middle East, and among some immagrant populations in the US, rheumatic heart disease remains the leading cause of mitral regurgitation.
MR is one of the most common [[valvular disease]]s in the general population, ranking first among valvular regurgitation abnormalities. The prevalence of MR of a severity equal to or worse than mild was reported in The Framingham Heart Study as 19.0% in men and 19.1% in womenThe prevalence of MR increases with age.


Overall, mitral regurgitation affects both males and females equally <ref>[http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/mitral-valve-disease/ The Cleveland Clinic Center for Continuing Education > Mitral Valve Disease: Stenosis and Regurgitation] Authors:  Ronan J. Curtin and Brian P. Griffin. Retrieved September 2010</ref>. However, there are some minor imbalances when age is considered. In patients younger than 20 years, there is a male preponderance, and the severity of involvement is greater in males over the age of 50.
==Natural History, Complications, and Prognosis==
The natural history of 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]].


==Complications==
==Diagnosis==
Mild mitral regurgitation regurgitation is associated with few if any complications. However, when severe, mitral regurgitation may lead to development of (in alphabetical order):
===Stages===
*[[Atrial Fibrillation]]
The stage of MR can be estimated based on specific criteria for the valve anatomy, valve hemodynamics, associated cardiac findings, and symptoms. The stages of MR are the following: at risk of MR, progressive MR, asymptomatic severe MR, and symptomatic severe MR.
*[[Cardiogenic Shock]]
*[[Endocarditis]]
*[[Pulmonary Edema]]
*[[Pulmonary Hypertension]]
*[[Right Heart Failure]]
*[[Thromboembolism]]-[[Stroke]]
 
==Prognosis==
*Acute mitral regurgitation with [[cardiogenic shock]] is associated with an operative mortality of 80%.
*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 <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>. However, the incidence of [[sudden death]] in asymptomatic patients with normal LV function varies widely among these studies.
 
*The prognosis is poor in patients with severe symptomatic [[mitral regurgitation]] with an eight year survival rate of only 33% in the absence of surgical intervention. [[Heart failure]] being the common cause with [[sudden death]] attributing to ventricular arrhythmia <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>.
 
*In patients with severe mitral regurgitation due to a flail [[posterior mitral leaflet]], 90% of patients are either dead or require mitral valve surgery by 10 years with the mortality rate in patients with severe mitral regurgitation being 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>.
 
*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 <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>.
 
==Causes==
Mitral regurgitation is due to either perforation or prolapse of the leaflets, dilation of the mitral annulus or rupture of the [[papillary muscle rupture|papillary muscles]] or chordae tendineae.  There are several phases of mitral regurgitation (acute, chronic compensated, and chronic decompensated).
===Acute Mitral Regurgitation===
*[[Heart attack]] or [[acute MI]]: Dysfunction or injury to the mitral valve following a heart attack. [[Papillary muscle rupture]] or dysfunction that is associated with [[ST elevation myocardial infarction]].
*[[Endocarditis]]: The infaction may cause perforation of the leaflet, erosion of the surrounding structures, or a vagetation may not permit the leaflets to coapt.
*Trauma


===Chronic Mitral Regurgitation===
*[[Mitral valve prolapse]]:  This disorder now accounts for 45% of cases of mitral regurgitation in the Western world.
*[[Ischemic heart disease]] / [[Coronary artery disease]]:  This can be due to either papillary muscle dysfunction or left ventricular dilation and functional mitral regurgitation.  Ischemia is responsible for 3% to 25% of MR cases.
*[[Rheumatic heart disease]]:  In the past, this was the most common cause of MR in the Western world. In developing countries, [[rheumatic heart disease]] remains the most common cause.
==Differentiating Mitral Regurgitation From Other Diseases==
The blowing [[holosystolic murmur]] of mitral regurgitation must be distinguished from [[tricuspid regurgitation]] and a [[ventricular septal defect]].
==Diagnosis==
===History and Symptoms===
===History and Symptoms===
Acute and decompensated mitral insufficiency is associated with symptoms of congestive heart failure including [[dyspnea]], [[PND]], [[orthopnea]], and [[exercise intolerance]].  In chronic compensated mitral regurgitation there may be few symptoms.
Acute and decompensated MR is associated with symptoms of [[congestive heart failure]] including [[dyspnea]], [[paroxysmal nocturnal dyspnea]], [[orthopnea]], and [[exercise intolerance]].  Individuals with chronic compensated MR may be asymptomatic, with a [[Exercise stress testing|normal exercise tolerance]] and no evidence of [[heart failure]].


===Physical Examination===
===Physical Examination===
Chronic compensated mitral regurgitation causes a blowing [[holosystolic]] murmur which radiates to the axilla. The severity of the murmur is not associated with the volume of regurgitationA [[third heart sound]] ([[S3]]) may be present.  In patients with mitral regurgitation due to [[mitral valve prolapse]], a click may be present.
Chronic compensated MR causes a blowing holosystolic murmur which radiates to the left [[axilla]]. In acute severe MR, the murmur can be early systolic rather than the typical holosystolic murmur in chronic MR due to the abrupt elevation in the pressure in the [[left atrium]] and the equalization of pressures between the [[left atrium]] and the [[left ventricle]]. The intensity of the murmur decreases with [[valsalva maneuver]] and standing and becomes louder with hand grip, squatting, and leg raising.  The murmur might be short or absent in severe acute MRIn addition, [[S1]] is usually diminished and [[S2]] is commonly widely split.  The pulmonic component of the second heart sound ([[P2]]) is louder than the aortic component ([[A2]]) in the presence of severe [[pulmonary hypertension]], thus widening the [[splitting of S2]].


===Chest X-Ray===
===Chest X-Ray===
The chest [[x-ray]] in individuals with chronic [[mitral regurgitation]] is characterized by enlargement of the [[left atrium]] and the [[left ventricle]].  In acute mitral regurgitation, [[pulmonary edema]] is present, but the heart is not enlarged.
The [[chest X-ray]] in individuals with chronic [[mitral regurgitation]] (MR) is characterized by the presence of an enlargement of the [[left atrium]] and the [[left ventricle]].  In acute MR, [[pulmonary edema]] is present and the heart is not enlarged.
 
===Ventriculogram===
Echocardiography is the primary imaging modality that is used to diagnose and serially evaluate mitral regurgitation, but the ventriculogram can also be used to quantitate the magnitude of mitral regurgitation.


===Electrocardiogram===
===Electrocardiogram===
In severe cases of mitral regurgitation, [[left ventricular hypertrophy with strain]]; [[left atrial enlargement]], and signs of [[pulmonary hypertension]] may be observed on the resting EKG. Chronic mitral regurgitation is associated with an increased risk for [[atrial fibrillation]].
In severe cases of chronic MR, signs of [[left ventricular hypertrophy with strain]], [[left atrial enlargement]], and [[pulmonary hypertension]] may be observed on the resting [[electrocardiogram]] ([[ECG]]). Chronic mitral regurgitation is associated with an increased risk for [[atrial fibrillation]].  The ECG may reveal findings of [[coronary artery disease]] or other cardiac conditions that might have led to MR.


===Echocardiography===
===Echocardiography===
Transthoracic echocardiography should be performed in a patient with suspected mitral regurgitation to confirm the diagnosis and to establish the baseline severity of disease. It should then be performed to monitor the course of disease over time. Color doppler flow on the transthoracic echocardiogram (TTE) will reveal a jet of blood flowing from the left ventricle into the left atrium during [[ventricular systole]]. Echocardiographic features that suggest severe mitral regurgitation include systolic reversal of flow in the pulmonary veins and filling of the entire left atrial cavity by the regurgitant jet of MR.
[[Transthoracic echocardiography]] (TTE) should be performed in a patient with suspected MR to confirm the diagnosis and to establish the baseline severity of disease. It should then be performed to monitor the course of disease over time. Color doppler flow on the TTE will reveal a jet of blood flowing from the [[left ventricle]] into the [[left atrium]] during ventricular [[systole]]. Echocardiographic features that suggest severe MR include systolic reversal of flow in the [[pulmonary veins]] and filling of the entire left atrial cavity by the regurgitant jet of MR.
 
===Cardiac MRI===
[[Cardiac magnetic resonance]] ([[CMR]]) may be beneficial to evaluate the structure and function of the [[left atrium]] and [[left ventricle]] as well as the severity of the mitral regurgitation when [[echocardiography]] findings are inconclusive.


===Cardiac Catheterization===
===Cardiac Catheterization===
In patients with mitral regurgitation who have risk factors for Coronary artery disease, such as advanced age, hypercholesterolemia, and hypertension, or when there is a suspicion that mitral regurgitation is ischemic in origin, coronary angiography should be performed before surgery.
[[Cardiac catheterization]] is useful to evaluate mitral regurgitation when the results of the non-invasive testing are insufficient.  In addition, [[cardiac catheterization]] might be performed when there is lack of consistency between the clinical findings and the results of the non-invasive testing in order to rule out cardiac etiologies or [[pulmonary hypertension]] as the cause of the patient's symptoms. [[Coronary angiography]] should be considered prior to [[mitral regurgitation surgery|mitral valve surgery]] among patients with risk factors of [[coronary artery disease]] among whom the underlying etiology of mitral regurgitation is suspected to be of [[ischemia|ischemic]] origin.
 
===Assessment of Severity===
The severity of MR can be assessed by both clinical and echocardiographic criteria. Careful history is important to establish an estimate of baseline exercise tolerance of the patient.


The 2006 [[ACC]]/[[AHA]] guidelines included recommendations for echocardiographic monitoring in asymptomatic patients with chronic MR <ref name="pmid18820172">{{cite journal| author=Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD et al.| title=2008 Focused update incorporated into the ACC/AHA 2006 guidelines 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 (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. | journal=Circulation | year= 2008 | volume= 118 | issue= 15 | pages= e523-661 | pmid=18820172| doi=10.1161/CIRCULATIONAHA.108.190748 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18820172  }} </ref>. Echocardiography is performed to assess the left ventricular ejection fraction and end-systolic dimension.
<table border="1" cellpadding="5" cellspacing="0" align="left">
<caption>'''Determination of the degree of mitral regurgitation'''</caption>
<tr>
<th style="background:#efefef;">Degree of mitral regurgitation</th>
<th style="background:#efefef;">Regurgitant fraction</th>
<th style="background:#efefef;" width="100px">Regurgitant Orifice area</th>
</tr>
<tr><td>Mild mitral regurgitation</td><td>< 20 percent</td></tr>
<tr><td>Moderate mitral regurgitation</td><td>20 - 40 percent</td></tr>
<tr><td>Moderate to severe mitral regurgitation</td><td>40 - 60 percent</td></tr>
<tr><td>Severe mitral regurgitation</td><td>> 60 percent</td><td>> 0.3 cm<sup>2</sup></td></tr>
</table>
<br clear="left"/>
==Treatment==
==Treatment==
Vasodilator therapy with [[ACE inhibitors]] and [[hydralazine]] is the foundation of medical therapy and once the patient becomes symptomatic, mitral valve surgery is the definitive therapy. This chapter reviews general treatment measures for the patient with mitral regurgitation.
===Treatment Overview===
Vasodilator therapy with [[ACE inhibitors]] and [[hydralazine]] is the foundation of medical therapy; once the patient becomes symptomatic, mitral valve surgery is the definitive therapy. This chapter reviews general treatment measures for the patient with mitral regurgitation.


===Afterload Reduction===
===Acute Mitral Regurgitation Treatment===
* Afterload reduction should be instituted with the use of [[vasodilators]] such as [[ACE inhibitors]] and [[hydralazine]].
[[Mitral regurgitation surgery|Surgery]] is the main treatment of symptomatic acute severe primary MR and it should be performed urgently without any delay. Although some patients with moderate acute MR develop some compensatory mechanisms, surgery remains the treatment of choice for the majority of patients with acute MR. Medical therapy with vasodilators might be needed to  decrease the [[afterload]] and thereby decrease the regurgitant fraction until surgery can be performed. Prior to the surgical procedure, an [[intra-aortic balloon pump]] or percutaneous circulatory assist device might also be used to stabilize the patient.


===Diuretics===
===Chronic Mitral Regurgitation Treatment===
*Diuretics are useful in reducing left ventricular volumes to improve functional mitral regurgitation and to improve [[pulmonary edema]].
The distinction between [[mitral regurgitation classification|primary]] and [[mitral regurgitation classification|secondary]] MR is of the utmost importance when determining the appropriate treatment strategies for patients with chronic MR.  Primary and secondary MR have different underlying pathophysiology and, therefore, have different indications for [[mitral regurgitation surgery|surgery]] and medical therapy. [[Mitral regurgitation surgery|Surgery]] is generally the treatment of choice among patients with chronic primary MR and [[left ventricular systolic dysfunction]]; nevertheless, medical therapy is warranted when surgery is delayed or not planned.  The cornerstone of the treatment of patients with chronic secondary MR with decreased [[ejection fraction]] is the standard regimen for the treatment of [[heart failure]], which includes one or more of the following: [[beta blocker]]s, [[angiotensin converting enzyme inhibitor]]s, [[angiotensin receptor blocker]]s, or [[aldosterone antagonist]]s.  [[Mitral regurgitation surgery|Mitral valve surgery]] is indicated in some circumstances among patients with chronic severe secondary MR, particularly those undergoing [[coronary artery bypass graft]] or patients with [[New york heart association functional classification|NYHA class III/IV]] heart failure symptoms.


===Digitalis===
===Follow Up===
*[[Digitalis]] may be used to strengthen contractility, and potentially reduce hospitalization in patients with congestive heart failure.
Regular follow up is recommended among patients with asymptomatic MR and preserved [[left ventricular ejection fraction]].


===Diet===
==References==
*A low-sodium diet may be helpful.
{{Reflist|2}}


===Activity===
[[Category:Cardiology]]
*Most patients with chronic compensated mitral regurgitation have no symptoms; but if a person develops symptoms, activity should be restricted.


===Beta Blockers===
[[Beta blockers]] are generally not recommended as they would slow the compensatory tachycardia and would allow greater time over which the regurgitation could occur and increase the regurgitant volume.


===Calcium Channel Blockers===
* In the presence of [[atrial fibrillation]], a [[calcium channel blocker]] or [[digoxin]] can be administered to slow the heart rate down and improve left ventricular filling.
===Cardioversion===
Cardioversion should be considered in the patient with atrial fibrillation or flutter who is hemodynamically unstable.
===Anticoagulation===
* Anti-coagulation therapy should be considered in patients with [[atrial fibrillation]] and in patients with prosthetic [[mitral valve replacement]] surgery.
===Antibiotic Prophylaxis===
* Prophylactic antibiotics prior to a periodontal procedure which involves manipulation of gingival tissue, the periapical region of a tooth, or perforation of oral mucosa is recommended in patients with previous [[infective endocarditis]], patients who have a prosthetic mitral valve implanted and in those with congentital heart disease.<ref name="pmid17446442">{{cite journal |author=Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, Bolger A, Cabell CH, Takahashi M, Baltimore RS, Newburger JW, Strom BL, Tani LY, Gerber M, Bonow RO, Pallasch T, Shulman ST, Rowley AH, Burns JC, Ferrieri P, Gardner T, Goff D, Durack DT |title=Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group |journal=[[Circulation]] |volume=116 |issue=15 |pages=1736–54 |year=2007 |month=October |pmid=17446442 |doi=10.1161/CIRCULATIONAHA.106.183095 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=17446442 |accessdate=2011-03-16}}</ref>
===Surgery===
Vasodilator theray with [[ACE inhibitor]]s and [[hydralazine]] is the mainstay of therapy in patient with chronic compensated mitral regurgitation. Acute mitral regurgitation requires urgent [[mitral valve repair]] or [[mitral valve replacement]].  MV surgery is beneficial for patients with chronic severe MR and NYHA functional class II, III, or IV symptoms in the absence of severe LV dysfunction (severe LV dysfunction is defined as ejection fraction less than 0.30) and/or end-systolic dimension greater than 55 mm.  MV surgery is beneficial for asymptomatic patients with chronic severe MR and mild to moderate LV dysfunction, ejection fraction 0.30 to 0.60, and/or end-systolic dimension greater than or equal to 40 mm. MV repair is recommended over MV replacement in the majority of patients with severe chronic MR who require surgery, and patients should be referred to surgical centers experienced in MV repair.
==References==
{{Reflist|2}}
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Latest revision as of 14:50, 19 August 2020



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Acute Mitral Regurgitation Treatment

Chronic Mitral Regurgitation Treatment

Surgery

Follow Up

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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. [3]; Lakshmi Gopalakrishnan, M.B.B.S. [4]; Mohammed A. Sbeih, M.D. [5]; Rim Halaby, M.D. [6]

Overview

Mitral regurgitation (MR) is a disorder of the heart in which the mitral valve does not close properly when the heart pumps out blood. MR is the abnormal leaking of blood from the left ventricle through the mitral valve, and into the left atrium, when the left ventricle contracts. MR is the most common form of valvular heart disease. MR can be classified into either acute or chronic according to the acuity of the events leading to the valvular abnormality. Regardless of the underlying etiology of MR, a decrease in the coaptation between the leaflets of the valve commonly characterizes all cases of MR. The causes of MR depend on the acuity of the valvular abnormality and the underlying pathological mechanism. The blowing holosystolic murmur of mitral regurgitation must be distinguished from tricuspid regurgitation and a ventricular septal defect. MR is one of the most common valvular diseases in the general population, ranking first among valvular regurgitation abnormalities. The prevalence of MR of a severity equal to or worse than mild was reported in The Framingham Heart Study as 19.0% in men and 19.1% in women. The prevalence of MR increases with age. 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. The stage of MR can be estimated based on specific criteria for the valve anatomy, valve hemodynamics, associated cardiac findings, and symptoms.

Classification

MR can be classified into either acute or chronic according to the acuity of the events leading to the valvular abnormality. Chronic MR is further classified into primary or secondary based on the presence or absence of one or more abnormalities in the structures of the valves, respectively.

Pathophysiology

Regardless of the underlying etiology of MR, a decrease in the coaptation between the leaflets of the valve commonly characterizes all cases of MR. Acute MR occurs when there is sudden disruption of one or more of the components of the mitral valve, as occurs in leaflet perforation, rupture of a chordae tendineae, or rupture of the papillary muscle. In the acute phase, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature to cause an elevation of the pulmonary capillary wedge pressure, which causes dyspnea, orthopnea, and rales. In addition, there is decreased forward stroke volume. Chronic MR can be either primary or secondary. Chronic primary MR results from chronic disruption of one or more component of the mitral valve (papillary muscles, chordae tendineae, or valve leaflets), whereas chronic secondary MR results from the dysfunction and dilatation of the left ventricle rather than an intrinsic abnormality in one of the components of the mitral valve. If the chronic MR develops slowly over months to years or if the acute phase is successfully managed with medical therapy, the patient enters the chronic compensated phase of MR that can eventually deteriorate into a decompensated phase as the left ventricular systolic function worsens. The markers of MR decompensation are as follows: left ventricular end-diastolic dimension greater than 70 mm, left ventricular end-systolic dimension greater than 45 to 47 mm, and left ventricular ejection fraction (LVEF) less than 50 to 55 percent.

Causes

The causes of MR depend on the acuity of the valvular abnormality and the underlying pathological mechanism. Acute MR occurs 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. The sudden disruption of the mitral valve can be caused by infective endocarditis, degenerative mitral valve disease, or acute ST elevation myocardial infarction. Chronic primary MR is most commonly caused by mitral valve prolapse; other causes include rheumatic fever and Marfan's syndrome. Chronic secondary MR results from the dysfunction and dilatation of the left ventricle rather than an intrinsic abnormality in one of the components of the mitral valve and it can be caused by coronary artery disease (ischemic) or any disease causing left ventricular dysfunction and dilatation (functional).

Differential Diagnosis

The blowing holosystolic murmur of mitral regurgitation must be distinguished from tricuspid regurgitation and a ventricular septal defect.

Epidemiology and Demographics

MR is one of the most common valvular diseases in the general population, ranking first among valvular regurgitation abnormalities. The prevalence of MR of a severity equal to or worse than mild was reported in The Framingham Heart Study as 19.0% in men and 19.1% in women. The prevalence of MR increases with age.

Natural History, Complications, and Prognosis

The natural history of 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.

Diagnosis

Stages

The stage of MR can be estimated based on specific criteria for the valve anatomy, valve hemodynamics, associated cardiac findings, and symptoms. The stages of MR are the following: at risk of MR, progressive MR, asymptomatic severe MR, and symptomatic severe MR.

History and Symptoms

Acute and decompensated MR is associated with symptoms of congestive heart failure including dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and exercise intolerance. Individuals with chronic compensated MR may be asymptomatic, with a normal exercise tolerance and no evidence of heart failure.

Physical Examination

Chronic compensated MR causes a blowing holosystolic murmur which radiates to the left axilla. In acute severe MR, the murmur can be early systolic rather than the typical holosystolic murmur in chronic MR due to the abrupt elevation in the pressure in the left atrium and the equalization of pressures between the left atrium and the left ventricle. The intensity of the murmur decreases with valsalva maneuver and standing and becomes louder with hand grip, squatting, and leg raising. The murmur might be short or absent in severe acute MR. In addition, S1 is usually diminished and S2 is commonly widely split. The pulmonic component of the second heart sound (P2) is louder than the aortic component (A2) in the presence of severe pulmonary hypertension, thus widening the splitting of S2.

Chest X-Ray

The chest X-ray in individuals with chronic mitral regurgitation (MR) is characterized by the presence of an enlargement of the left atrium and the left ventricle. In acute MR, pulmonary edema is present and the heart is not enlarged.

Electrocardiogram

In severe cases of chronic MR, signs of left ventricular hypertrophy with strain, left atrial enlargement, and pulmonary hypertension may be observed on the resting electrocardiogram (ECG). Chronic mitral regurgitation is associated with an increased risk for atrial fibrillation. The ECG may reveal findings of coronary artery disease or other cardiac conditions that might have led to MR.

Echocardiography

Transthoracic echocardiography (TTE) should be performed in a patient with suspected MR to confirm the diagnosis and to establish the baseline severity of disease. It should then be performed to monitor the course of disease over time. Color doppler flow on the TTE will reveal a jet of blood flowing from the left ventricle into the left atrium during ventricular systole. Echocardiographic features that suggest severe MR include systolic reversal of flow in the pulmonary veins and filling of the entire left atrial cavity by the regurgitant jet of MR.

Cardiac MRI

Cardiac magnetic resonance (CMR) may be beneficial to evaluate the structure and function of the left atrium and left ventricle as well as the severity of the mitral regurgitation when echocardiography findings are inconclusive.

Cardiac Catheterization

Cardiac catheterization is useful to evaluate mitral regurgitation when the results of the non-invasive testing are insufficient. In addition, cardiac catheterization might be performed when there is lack of consistency between the clinical findings and the results of the non-invasive testing in order to rule out cardiac etiologies or pulmonary hypertension as the cause of the patient's symptoms. Coronary angiography should be considered prior to mitral valve surgery among patients with risk factors of coronary artery disease among whom the underlying etiology of mitral regurgitation is suspected to be of ischemic origin.

Treatment

Treatment Overview

Vasodilator therapy with ACE inhibitors and hydralazine is the foundation of medical therapy; once the patient becomes symptomatic, mitral valve surgery is the definitive therapy. This chapter reviews general treatment measures for the patient with mitral regurgitation.

Acute Mitral Regurgitation Treatment

Surgery is the main treatment of symptomatic acute severe primary MR and it should be performed urgently without any delay. Although some patients with moderate acute MR develop some compensatory mechanisms, surgery remains the treatment of choice for the majority of patients with acute MR. Medical therapy with vasodilators might be needed to decrease the afterload and thereby decrease the regurgitant fraction until surgery can be performed. Prior to the surgical procedure, an intra-aortic balloon pump or percutaneous circulatory assist device might also be used to stabilize the patient.

Chronic Mitral Regurgitation Treatment

The distinction between primary and secondary MR is of the utmost importance when determining the appropriate treatment strategies for patients with chronic MR. Primary and secondary MR have different underlying pathophysiology and, therefore, have different indications for surgery and medical therapy. Surgery is generally the treatment of choice among patients with chronic primary MR and left ventricular systolic dysfunction; nevertheless, medical therapy is warranted when surgery is delayed or not planned. The cornerstone of the treatment of patients with chronic secondary MR with decreased ejection fraction is the standard regimen for the treatment of heart failure, which includes one or more of the following: beta blockers, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, or aldosterone antagonists. Mitral valve surgery is indicated in some circumstances among patients with chronic severe secondary MR, particularly those undergoing coronary artery bypass graft or patients with NYHA class III/IV heart failure symptoms.

Follow Up

Regular follow up is recommended among patients with asymptomatic MR and preserved left ventricular ejection fraction.

References


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