Mitral regurgitation overview: Difference between revisions
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| [[Mitral regurgitation resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] | | [[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@wikidoc.org] | {{CMG}}; {{AOEIC}} {{CZ}}; {{VK}}; {{LG}}; [[User:Mohammed Sbeih|Mohammed A. Sbeih, M.D.]] [mailto:msbeih@wikidoc.org]; {{Rim}} | ||
==Overview== | ==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]].<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> | |||
== | ==Classification== | ||
Mitral regurgitation (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.<ref name="pmid24589852">{{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=Circulation | year= 2014 | volume= 129 | issue= 23 | pages= 2440-92 | pmid=24589852 | doi=10.1161/CIR.0000000000000029 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24589852 }} </ref> Secondary MR can be either ischemic or functional.<ref name="pmid21586426">{{cite journal| author=Ciarka A, Van de Veire N| title=Secondary mitral regurgitation: pathophysiology, diagnosis, and treatment. | journal=Heart | year= 2011 | volume= 97 | issue= 12 | pages= 1012-23 | pmid=21586426 | doi=10.1136/hrt.2010.219170 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21586426 }} </ref> | |||
==Pathophysiology== | ==Pathophysiology== | ||
Regardless of the underlying etiology of mitral regurgitation (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. | |||
==Causes== | |||
The causes of mitral regurgitation (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]].<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 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).<ref name="pmid21586426">{{cite journal| author=Ciarka A, Van de Veire N| title=Secondary mitral regurgitation: pathophysiology, diagnosis, and treatment. | journal=Heart | year= 2011 | volume= 97 | issue= 12 | pages= 1012-23 | pmid=21586426 | doi=10.1136/hrt.2010.219170 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21586426 }} </ref> | |||
==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== | ||
Mitral regurgitation (MR) is one of the most common [[valvular disease]]s in the general population, ranking first among valvular regurgitation abnormailities. The prevalence of MR of a severity equal to or more 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.<ref name="pmid10190406">{{cite journal| author=Singh JP, Evans JC, Levy D, Larson MG, Freed LA, Fuller DL et al.| title=Prevalence and clinical determinants of mitral, tricuspid, and aortic regurgitation (the Framingham Heart Study) | journal=Am J Cardiol | year= 1999 | volume= 83 | issue= 6 | pages= 897-902 | pmid=10190406 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10190406 }} </ref> | |||
==Natural history, Complications and Prognosis== | |||
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]]. | |||
==Complications | |||
==Diagnosis== | ==Diagnosis== | ||
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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.[1]
Classification
Mitral regurgitation (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.[2] Secondary MR can be either ischemic or functional.[3]
Pathophysiology
Regardless of the underlying etiology of mitral regurgitation (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 mitral regurgitation (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.[4] 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).[3]
Differential Diagnosis
The blowing holosystolic murmur of mitral regurgitation must be distinguished from tricuspid regurgitation and a ventricular septal defect.
Epidemiology and Demographics
Mitral regurgitation (MR) is one of the most common valvular diseases in the general population, ranking first among valvular regurgitation abnormailities. The prevalence of MR of a severity equal to or more 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.[5]
Natural history, Complications and Prognosis
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.
Diagnosis
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.
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 regurgitation. A third heart sound (S3) may be present. In patients with mitral regurgitation due to mitral valve prolapse, a click may be present.
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.
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
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.
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.
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.
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 [6]. Echocardiography is performed to assess the left ventricular ejection fraction and end-systolic dimension.
| Degree of mitral regurgitation | Regurgitant fraction | Regurgitant Orifice area |
|---|---|---|
| Mild mitral regurgitation | < 20 percent | |
| Moderate mitral regurgitation | 20 - 40 percent | |
| Moderate to severe mitral regurgitation | 40 - 60 percent | |
| Severe mitral regurgitation | > 60 percent | > 0.3 cm2 |
Treatment
Unlike mitral stenosis or aortic stenosis where one waits on symptoms as an indication for valve replacement, mitral valve repair or replacement is preferably undertaken before the development of symptoms.
- 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.
Afterload Reduction
- Afterload reduction should be instituted with the use of vasodilators such as ACE inhibitors and hydralazine.
Diuretics
- Diuretics are useful in reducing left ventricular volumes to improve functional mitral regurgitation and to improve pulmonary edema.
Digitalis
- Digitalis may be used to strengthen contractility, and potentially reduce hospitalization in patients with congestive heart failure.
Diet
- A low-sodium diet may be helpful.
Activity
- 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.[7]
Surgery
Vasodilator theray with ACE inhibitors 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
- ↑ Weinrauch, LA (2008-05-12). "Mitral regurgitation - chronic". Medline Plus Encyclopedia. U.S. National Library of Medicine and National Institutes of Health. Retrieved 2009-12-04.
- ↑ 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". Circulation. 129 (23): 2440–92. doi:10.1161/CIR.0000000000000029. PMID 24589852.
- ↑ 3.0 3.1 Ciarka A, Van de Veire N (2011). "Secondary mitral regurgitation: pathophysiology, diagnosis, and treatment". Heart. 97 (12): 1012–23. doi:10.1136/hrt.2010.219170. PMID 21586426.
- ↑ 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.
- ↑ Singh JP, Evans JC, Levy D, Larson MG, Freed LA, Fuller DL; et al. (1999). "Prevalence and clinical determinants of mitral, tricuspid, and aortic regurgitation (the Framingham Heart Study)". Am J Cardiol. 83 (6): 897–902. PMID 10190406.
- ↑ Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD; et al. (2008). "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". Circulation. 118 (15): e523–661. doi:10.1161/CIRCULATIONAHA.108.190748. PMID 18820172.
- ↑ 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 (2007). "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". Circulation. 116 (15): 1736–54. doi:10.1161/CIRCULATIONAHA.106.183095. PMID 17446442. Retrieved 2011-03-16. Unknown parameter
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