AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Background

Mitral valve prolapse (MVP) is the most common valvular abnormality, affecting approximately 2-6% of the population in the United States. MVP usually results in a benign course. However, it occasionally leads to serious complications, including clinically significant mitral regurgitation, infective endocarditis, sudden cardiac death, and cerebrovascular ischemic events. MVP is also the most common cause of isolated mitral regurgitation in the United States, and it is the most common reason for mitral valve surgery.

Pathophysiology

Most patients with MVP are asymptomatic, and their natural history is benign. However, when large, floppy valves or ruptured chordae tendinea result in severe mitral regurgitation, mitral valve surgery or repair may be necessary. Myxomatous proliferation is the most common pathologic basis for MVP, and it can lead to myxomatous degeneration of the loose spongiosa and fragmentation of the collagen fibrils. Disruption of the endothelium may predispose patients to infectious endocarditis and thromboembolic complications. However, the vast majority of patients with MVP have only a minor derangement of the mitral valve structure that is usually clinically insignificant.

Frequency

United States

MVP is thought to be inherited with increased expression of the gene in female individuals (2:1). The most common form of inheritance is autosomal dominant, but X-linked inheritance has been described.

MVP commonly occurs with heritable connective tissue disorders, including Marfan syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta, and pseudoxanthoma elasticum. In fact, 90% of patients with Marfan syndrome have MVP due to the increased redundancy of the mitral leaflets and apparatus that occur as a result of myxomatous degeneration.

In the 1970s and 1980s, MVP was overdiagnosed because of the absence of rigorous echocardiographic criteria, with a reported prevalence of 5-15%. Subsequently, Levine et al reported that the 2-dimensional echocardiographic characterizations of prolapse, especially on the parasternal long-axis view, are most specific for the diagnosis of MVP.¹ Use of these criteria prevent overdiagnosis.

Data from the community-based Framingham study demonstrated that MVP syndrome occurred in only 2.4% of the population.

Mortality/Morbidity

Most patients with MVP are asymptomatic and have a benign prognosis, with survival rates similar to those of the general population. Nonetheless, high-risk patients (ie, those with moderate-to-severe mitral regurgitation) have increased cardiac morbidity and mortality rates, especially if reduced left ventricular systolic function is present.

See Complications.

Sex

MVP occurs more frequently in young women than in men. The most serious consequences of hemodynamically significant mitral regurgitation occur in men older than 50 years.

Age

MVP has been observed in all ages.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

History

Mitral valve prolapse (MVP) is often diagnosed from the physical examination, when the classic auscultatory finding of a mid-to-late systolic click and/or murmur is appreciated. Alternatively, it may be incidentally diagnosed during routine echocardiography or discovered when complications of MVP manifest.

Most patients are asymptomatic. Symptomatic patients with MVP are separated into 3 categories: (1) those with symptoms related to autonomic dysfunction; (2) those with symptoms related to the progression of mitral regurgitation; and (3) those with symptoms that occur as a result of an associated complication (ie, stroke, endocarditis, or arrhythmia).

• Symptoms related to autonomic dysfunction are usually associated with genetically inherited MVP and include the following:
• • Anxiety
  • Panic attacks
  • Arrhythmias
  • Exercise intolerance
  • Palpitations
  • Atypical chest pain
  • Fatigue
  • Orthostasis
  • Syncope or presyncope
  • Neuropsychiatric symptoms
• Symptoms related to progression of mitral regurgitation include the following:
• • Fatigue
  • Dyspnea
  • Exercise intolerance
  • Orthopnea
  • Paroxysmal nocturnal dyspnea (PND)
  • Progressive signs of congestive heart failure (CHF)
• ECG usually is normal, but can show nonspecific ST-segment and T wave abnormalities especially in leads II, III, aVF.
• MVP is also commonly seen in patients with inheritable connective tissue disorders.

Physical

Clinical characteristics are typically benign in young women, whereas men older than 50 years tend to have serious consequence of mitral regurgitation.

• Common general physical features associated with MVP include the following:
• • Asthenic body habitus
  • Low body weight or body mass index (BMI)
  • Straight-back syndrome
  • Scoliosis or kyphosis
  • Pectus excavatum
  • Hypermobility of the joints
  • Arm span greater than height (which may be indicative of Marfan syndrome)
• The classic auscultatory finding is a mid-to-late systolic click, which is present due to the leaflets prolapsing into the left atrium resulting in tensing of the mitral valve apparatus. It may or may not be followed by a high-pitched, mid-to-late systolic murmur at the cardiac apex.
• • The midsystolic click can vary in intensity and timing, primarily depending on left ventricular volume.
  • End-diastolic volume can be reduced by performing a Valsalva maneuver or by having the patient stand. These maneuvers result in an early click, which is close to the first heart sound, and a prolonged murmur. In the supine position, especially with the legs raised for increased venous return, left ventricular diastolic volume is increased, resulting in a click later in systole and a shortened murmur.
• Patients with MVP most frequently have symptoms of autonomic dysfunction, including easy fatigability, dizziness, and atypical chest pain. This pain is perhaps related to papillary muscle strain (ie, excessive pulling on the left ventricular wall with prolapsed leaflets in the left atrium).

Causes

MVP usually occurs as an isolated entity. As previously mentioned, it also commonly occurs with heritable disorders of connective tissue. MVP has also been described in association with a secundum atrial septal defect.

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Consider all inheritable connective tissue disorders mentioned previously, with emphasis on Marfan syndrome because of its increased frequency. All causes of mitral regurgitation should be considered. However, if only a mid-systolic click and/or a mid-to-late systolic murmur is present, the diagnosis is almost always MVP. If only a late systolic murmur without a click is present, papillary muscle dysfunction secondary to coronary artery disease is a possibility.

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Imaging Studies

• Echocardiography
• • Diagnostic criteria
  • • Perloff et al set the stage for accurately diagnosing mitral valve prolapse (MVP) by expanding the diagnostic standards to include clinical and echocardiographic criteria.^{2, 3}
    • In a Framingham Heart Study, Freed et al historically described echocardiographic criteria for MVP as classic versus nonclassic (see below).⁴
    • Use of the parasternal long-axis view reduce the over diagnosis of MVP.¹
  • Findings
  • • Classic MVP: The parasternal long-axis view shows > 2 mm superior displacement of the mitral leaflets into the left atrium during systole, with a leaflet thickness of at least 5 mm.
    • Nonclassic MVP: Displacement is > 2 mm, with a maximal leaflet thickness of < 5 mm.
    • Other: Other echocardiographic findings that should be considered as criteria are leaflet thickening, redundancy, annular dilatation, and chordal elongation.
• Contrast ventriculography: This study can also help in defining MVP with or without mitral regurgitation. However, with the advent of echocardiography, contrast ventriculography is rarely necessary.
• Chest radiography: Radiographs may demonstrate the progression from asymptomatic to chronic, severe mitral regurgitation with the development of cardiomegaly secondary to left atrial and left ventricular dilatation and evidence of heart failure. See Medscape's Heart Failure Resource Center.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Medical Care

• Asymptomatic patients with minimal disease
• • These patients should be strongly reassured of their benign prognosis.
  • They should undergo initial echocardiography for risk stratification. If no clinically significant mitral regurgitation and thin leaflets are observed, clinical examinations and echocardiographic studies can be scheduled every 3-5 years.
  • These patients are encouraged to pursue a normal, unrestricted lifestyle, including vigorous exercise.
• Patients with symptoms of autonomic dysfunction
• • A trial of beta-blockers for symptomatic relief can be recommended.
  • Abstinence from stimulants such as caffeine, alcohol, and cigarettes is also recommended. An ambulatory 24-hour monitor may be useful to detect supraventricular and/or ventricular arrhythmias.
• Patients with evidence of or progression to severe mitral regurgitation
• • Close follow-up and referral for surgical repair are indicated early, before left ventricular dilatation and systolic dysfunction develop.
  • Asymptomatic patients with moderate-to-severe mitral regurgitation and left ventricular enlargement, especially those with atrial fibrillation and/or pulmonary hypertension, should undergo surgery before left ventricular function deteriorates.
  • If the physician is unsure if the patient is asymptomatic, a treadmill stress test for exercise tolerance can be performed. That is, have the patient demonstrate that he or she can walk vigorously without symptoms.
• Patients with MVP and neurologic findings
• • After atrial fibrillation and left atrial thrombus are excluded, these patients should be given daily aspirin therapy at a dosage of 80-325 mg/d.
  • Cessation of smoking and oral contraceptive use to prevent a hypercoagulable state should be recommended.
  • Warfarin should be used when patients older than 65 years have atrial fibrillation, especially if they have associated risk factors of a previous stroke or TIA, clinically significant valvular heart disease, hypertension, diabetes, left atrial enlargement, or a history and/or findings of heart failure.
• Patients with a mid-systolic click and late-systolic mitral regurgitation murmur 
• • Consider antibiotic prophylaxis in these patients, including those with increased leaflet thickening or redundancy.
  • Antibiotic prophylaxis is not recommended for the patient with an isolated mid-to-late systolic click without a murmur, unless the echocardiogram demonstrates significant leaflet redundancy and/or thickness.

Surgical Care

See the surgical management discussion in Mitral Regurgitation.

FOLLOW-UP

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Further Outpatient Care

• Depending on its severity, patients with MVP may be monitored regularly with a careful history, physical examination, and echocardiography when indicated.
• If symptoms or physical findings change during outpatient care, echocardiography or other studies (ie, Holter monitor, radiography) may be indicated.

Complications

• Severe mitral regurgitation
• • This is the most common complication of MVP and leading cause of isolated mitral regurgitation requiring mitral valve surgery in the United States.
  • Severe mitral regurgitation is most frequently due to rupture of the chordae tendineae.
  • The risk increases with the following factors: patients older than 50 years, male sex, history of hypertension, increased BMI, increased mitral valve thickness or redundancy, and left atrial and left ventricular dilatation.
• Infective endocarditis
• • The main mechanism for increased risk is a turbulent flow state due to leaflet thickness or redundancy and mitral regurgitation.
  • The risk of endocarditis increases 3- to 8-fold with MVP.
  • The main predictors are age older than 50 years, male sex, history of hypertension, increased BMI, left atrial and ventricular enlargement, and increased mitral valve thickness or redundancy.
  • If an isolated mid-to-late systolic click is present (eg, no murmur), antibiotic prophylaxis is not usually recommended unless the echocardiogram demonstrates significant leaflet redundancy and/or thickness.
• Sudden cardiac death and cerebrovascular ischemic events
• • The association between sudden cardiac death and MVP is not well understood. Data suggest that MVP alone does result in excessive atrial or ventricular arrhythmias, which are most likely due to autonomic dysfunction. Patients with these findings have been said to have MVP syndrome.
  • The risk is increased when patients have evidence of left ventricular dilatation and dysfunction, severe mitral regurgitation, and increased mitral leaflet thickness or redundancy.
  • In the presence of QT prolongation and frequent ventricular ectopy, especially nonsustained ventricular or sustained ventricular tachycardia, an electrophysiologic study may be indicated to quantitate the risk of inducible ventricular tachycardia and/or ventricular fibrillation and sudden arrhythmic death.
  • In regard to cerebrovascular ischemic events, recent studies yielded mixed findings in terms of the association between the increased prevalence of cerebrovascular events and MVP in young patients without evidence of cerebrovascular disease.
  • • Gilon et al describes the lack of an association between MVP and stroke in young patients in a large case-control study.⁵
    • The hypothesized mechanism is the formation of platelet fibrin thrombi on the denuded, damaged myxomatous valves resulting in embolization. Data suggest that the prevalence of this mechanism is based on the degree of mitral regurgitation.
  • The major risk factors for cerebrovascular events include age older than 50 years, thickened mitral valve leaflets, atrial fibrillation, and a need for mitral valve surgery.

Prognosis

• Most patients with MVP are asymptomatic and have a benign course.
• Patients with high-risk characteristics and/or progressive mitral regurgitation are at increased risk for complications.
• See also the Mortality/Morbidity and Complications sections.

Patient Education

• Patients should receive education regarding their prognosis along with the signs and symptoms of disease progression.
• Of emphasis, most patients with MVP have a benign course, but the risk of ruptured chordae and/or clinically significant mitral regurgitation, infective endocarditis, embolic TIA or stroke, and rare sudden death must also be discussed.
• For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education article Mitral Valve Prolapse.

MISCELLANEOUS

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Strict diagnostic criteria should be used to prevent the overdiagnoses of MVP that occurred in the 1970s and 1980s.
• • Previous echocardiographic studies produced undue anxiety, particularly in asymptomatic patients.
  • Once again, the vast majority of patients with MVP should be strongly reassured of their benign prognosis.
• Failure to follow up patients with clinically significant MVP can be damaging.
• • When clinically significant MR develops or progresses, irreversible left ventricular dysfunction may occur in the absence of symptoms.
  • Also, endocarditis can be a subtle illness that makes prompt diagnosis difficult.

Special Concerns

• In many patients, MVP was diagnosed on the basis of imprecise echocardiographic criteria.
• In addition, being diagnosed with a heart condition can greatly affect patients' self-perceptions. Care should be taken to explain MVP syndrome in detail so that patients understand that the natural history of MVP is usually benign.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

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Article Last Updated: Jul 30, 2008