eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Mitral Valve Prolapse

Author: Poothirikovil Venugopalan, MBBS, MD, FRCP (Glasg), FRCPCH, Consulting Staff, Department of Child Health, University Hospital of Hartlepool, UK
Contributor Information and Disclosures

Updated: Oct 8, 2008

Introduction

Background

Mitral valve prolapse (MVP), the most common anomaly of the mitral valve apparatus, occurs when one or both mitral valve leaflets excessively billows into the left atrium toward the end of systole. Mitral regurgitation (MR) develops in some patients with mitral valve prolapse, particularly those with more significant prolapse, when the valve edges fail to coapt. An extreme form of prolapse could include chordal rupture, in which the prolapsed mitral valve is flail. Mitral valves excised from patients with severe MR secondary to mitral valve prolapse have large leaflets and various histologic alterations.

Besides the symptoms attributable to the MR, various neuroendocrine and autonomic disturbances occur in some patients with mitral valve prolapse. In these patients, prolapse may be an epiphenomenon of the underlying autonomic or neurohumoral illness. The term mitral valve prolapse syndrome is often used to refer to the collection of these manifestations. However, in a significant proportion of patients, the mitral valve prolapse is trivial, and no such associated manifestations are present. In these patients, mitral valve prolapse constitutes an essentially benign condition.

Mitral valve prolapse syndrome was recognized as early as 1916, when Sir James MacKenzie described the soldier's heart in spare, thin young men with great vasomotor instability, easy fatigability, breathlessness, and pain over the region of the heart. Kerley first described the syndrome in 1920, and Lincoln described the syndrome in 1928. In 1963, Barlow and colleagues made the first clinical diagnosis of the syndrome as it is known today. The advent of echocardiography led to further advances and formed the basis of current knowledge.

Idiopathic mitral valve prolapse may be congenital in some patients, but recognition may be delayed until adolescence or adulthood. Associated complicating issues include cardiac arrhythmia, heart failure secondary to severe MR (rare), and, occasionally, thromboembolic events. Familial cases are known and occur in an autosomal dominant pattern with variable penetrance and expression (familial mitral valve prolapse).

Pathophysiology

Mitral valve prolapse is a heterogeneous disorder and may originate from various underlying causes affecting one or more portions of the mitral valve leaflets, chordae tendineae, papillary muscle, and/or valve annulus. The syndrome may occur in isolation or in association with generalized connective tissue abnormalities, such as Marfan syndrome and Ehlers-Danlos syndrome, in which specific enzymatic defects are found. Mitral valve prolapse may occur in the context of inflammatory disease such as rheumatic fever or endocarditis.

Isolated mitral valve prolapse can be sporadic or familial, demonstrating autosomal dominant and X-linked inheritance. Three different loci on chromosomes 16, 11, and 13 are linked to mitral valve prolapse, but no specific gene has been described. Another locus on chromosome X has also been found to cosegregate with a rare form of mitral valve prolapse called X-linked myxomatous valvular dystrophy.1

Isolated mitral valve prolapse has been independently associated with low body mass index; however, the reason for this association remains unexplained.2

Mitral valve prolapse may be secondary to rupture or dysfunction of the papillary muscles following myocardial infarction or ischemia, rupture of chordae tendineae due to infective endocarditis, or abnormal left ventricular wall motion in the setting of myocardial ischemia and/or primary myocardial disease. In these patients, the posterior leaflet in the floppy valve tends to have a significantly longer basal free-edge length and more frequent chordal rupture compared with patients with postinflammatory disease.

A connective tissue abnormality, possibly related to collagen metabolism, may underlie the idiopathic disorder. Abnormalities of collagen and elastic fibers have been documented in floppy mitral valves (FMV). Urokinase-plasminogen activator (PLAU), which is suggested in the pathogenesis of elastin and collagen degradation in arterial aneurysm, has also been implicated in mitral valve prolapse (PLAU T4065C TC genotype). A locus for autosomal dominant mitral valve prolapse has also been described on chromosome 11p15.4.

Electron microscopy of the affected valve leaflets shows a haphazard arrangement, disruption, and fragmentation of collagen fibrils. Myxomatous proliferation of the mitral valve, in which the middle spongiosa layer is predominantly involved, leads to the presence of unusually large amounts of myxomatous material and acid mucopolysaccharide. Degeneration of collagen within the central core of the chordae tendineae may lead to chordal rupture. Mitral valve prolapse can also follow rheumatic fever and myocardial infarction, in which case the prolapse is secondary to inflammatory or ischemic chordal rupture, respectively.

Metabolic and neuroendocrine abnormalities also occur in mitral valve prolapse and may separately result in prolapse unrelated to a connective tissue disorder. In such patients, increased norepinephrine and epinephrine may be found. Abnormalities in autonomic and neuroendocrine regulation have been demonstrated, including hyper-response to adrenergic stimulation, parasympathetic abnormalities (vagal withdrawal), altered baroreflex activity, renin-aldosterone regulation abnormalities, decreased intravascular volume, decreased left ventricular volume in upright posture, and atrial natriuretic factor secretion abnormalities.

Frequency

United States

Mitral valve prolapse is the most prevalent cardiac valve disorder. Mitral valve prolapse is a common finding in otherwise healthy teenagers and young adults, particularly those patients who present with palpitations, chest pain, or dizziness. More than one third of cases in younger children are associated with other congenital heart defects. Reports vary, but 3-5% of pediatric patients likely have clinically significant mitral valve prolapse. However, a recent report from California places the prevalence at only 0.6%.3

International

Prevalence rates are 1-2% in children and 5-15% in adolescents and young adults. In a series of 278 surgically removed mitral valves with pure regurgitation, mitral valve prolapse was present in 43%.4

Mortality/Morbidity

When present, associated abnormalities dictate the risk. Presence of significant MR and prolonged QT interval on ECG may also influence outcome. QT prolongation is slightly more prevalent among patients with mitral valve prolapse and may be associated with repolarization abnormalities and arrhythmia vulnerability. When severe, MR can lead to heart failure.

Mortality is rare in children. Sudden death is also rare and occurs more often in young women with a history of recurrent syncope, sustained supraventricular tachycardia, or complex ventricular tachycardia. Family history of cardiac sudden death often is a risk-stratifying indicator.

Development of MR and the progression of mild or moderate MR to severe MR are important determinants to morbidity. One study showed that the prevalence of MR increased from 29% of patients to 43% of patients during 4.3 years of follow-up.5 Other possible complications include congestive cardiac failure, rupture of chordae tendineae, infective endocarditis (in 0.1-0.3 cases per 100 patient years), thromboembolic phenomena including cerebrovascular accidents, and sudden death. Cardiac arrhythmias such as ventricular tachycardia and ventricular fibrillation are more common in mitral valve prolapse.

Sex

Some studies show mitral valve prolapse is twice as frequent in females as in males.

Age

Although findings are more frequent in older children and adults, the defect is believed to be present at birth.

Clinical

Physical

Most patients are asymptomatic, and mitral valve prolapse (MVP) is an incidental auscultatory finding. Beta-blockers may markedly attenuate or abolish the symptoms, a fact that is important to remember while evaluating a patient who is receiving these agents. Findings are more marked when patients are examined in the outpatient department rather than in the inpatient setting, reflecting the contributory role of adrenergic state.

  • Chest pain
    • Chest pain occurs in 10% of patients diagnosed with mitral valve prolapse.
    • Chest pain may be caused by any of the following factors:
      • Excessive stretching of the chordae tendineae, leading to traction on papillary muscles
      • Coronary microembolism from platelet aggregates and fibrin deposits in the angle between the left atrium and the posterior mitral leaflet
      • Inappropriate tachycardia and excessive postural changes and physical and emotional stresses
      • Hyperadrenergic state, which increases myocardial oxygen demand
      • Coronary artery spasm
  • Palpitations
    • Palpitations are present in 7.4% of patients.
    • Occurrence may be related to cardiac arrhythmia, although this has not been conclusively proven.
  • Fatigability and dyspnea
    • These often develop upon exertion.
    • The cause may be alterations in centrally modulated breathing cycle control.
  • Neuropsychiatric
    • Panic attacks may occur.
    • Nervousness, presyncope, and syncope occur in 0.9% of patients.
    • Thromboembolism, arrhythmia, or vasodepressor-vasovagal problems may be involved.
  • Pulse
    • Findings are usually normal.
    • Pulse is occasionally irregular in the presence of premature contractions.
    • Exaggerated tachycardia (high-volume in severe mitral regurgitation [MR]) following exertion is not unusual.
  • Skeletal abnormalities
    • These are observed in two thirds of patients and do not fit into any of the recognized connective tissue disorders, although an occasional patient may have Marfan syndrome or other related syndromes.
    • Common findings are as follows:
      • Hypomastia
      • Thin children
      • Height-to-weight ratio greater than normal
      • Arm span greater than height (dolichostenomelia)
      • Arachnodactyly
      • Scoliosis
      • Narrow anteroposterior chest diameter (straight back)
      • Pectus excavatum or pectus carinatum
      • Cathedral palate
      • Crowding of teeth
      • Joint hypermobility
  • Auscultation
    • Apical midsystolic nonejection click and late systolic murmur are the hallmarks, but either may occur alone.
    • Heart sounds are usually normal, but the first heart sound (S1) may be accentuated when prolapse occurs early in systole because of the summation of S1 and mitral click.
    • Multiple clicks occur when prolapse of different leaflets occurs at different times during the systole and may resemble pericardial friction rub.
    • In patients with redundant floppy mitral valves and significant MR, the murmur may be holosystolic and the click may be absent.
    • In cases in which the posterior mitral valve leaflet is prolapsing, the murmur may radiate along the left sternal border to the aortic area, thus mimicking left ventricular outflow tract murmur. If the anterior leaflet prolapses, the murmur radiates to the axilla and the spine.
  • Dynamic auscultation
    • In the sitting or standing position in late systole, the click may appear earlier and the murmur may be more prominent. The systolic click moves toward S1 upon standing, often merging with S1 if marked postural tachycardia occurs, and new clicks may appear. If an exaggerated heart rate response occurs, the murmur becomes longer and often louder to holosystolic. Occasionally the murmur is present only in the upright posture.
    • When squatting from standing position, the click and murmur may move back to late systole. Continuous auscultation, while the patient is standing from squatting position, reveals the click and murmur moving back to early systole on a beat-to-beat basis as the heart rate accelerates.
    • A systolic precordial honk or whooping sound may occasionally be heard with the murmur. Often these are heard only in the sitting or standing position and may be limited to a few beats immediately after standing.
    • Dynamic auscultatory changes reflect alterations in the timing of the mitral valve prolapse, the timing and extent of the MR, the expected changes in left ventricular volume, myocardial contractility, and heart rate. In the upright posture, venous return decreases, as does the left ventricular volume. The reflex tachycardia that occurs in the upright position further reduces left ventricular volume. Timing and degree of the prolapse are determined by the position of the mitral leaflets at end diastole, which, in turn, is dependent on the distance from the mitral valve annulus to the attachment of the chordae to papillary muscles. Low left ventricular end-diastolic volume shortens the mitral annular papillary muscle distance, allowing the leaflets to prolapse earlier in systole.
    • Prompt squatting from standing position increases venous return and left ventricular volume; thus, the systolic click and murmur may become late systolic. Squatting, however, may also be associated with an increase in peripheral vascular resistance, which, in turn, increases the tension on the mitral valve apparatus, preferentially directing blood flow into the left atrium, rather than to the peripheral circulation. The late systolic click and murmur then become accentuated in the squatting position.
  • Other maneuvers
    • Other maneuvers are possible but none is as practical as a systematically performed postural dynamic auscultation.
    • These maneuvers include the following:
      • Leg elevation
      • Isometric hand grip exercise
      • Valsalva maneuver
      • Application of tourniquets to the extremities
      • Lower body negative pressure or amyl nitrate inhalation

Causes

More on Mitral Valve Prolapse

Overview: Mitral Valve Prolapse
Differential Diagnoses & Workup: Mitral Valve Prolapse
Treatment & Medication: Mitral Valve Prolapse
Follow-up: Mitral Valve Prolapse
Multimedia: Mitral Valve Prolapse
References
[ CLOSE WINDOW ]

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Further Reading

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Keywords

mitral valve prolapse, Barlow syndrome, billowing mitral valve syndrome, Da Costa syndrome, effort syndrome, familial MVP, floppy mitral valve syndrome, irritable heart syndrome, myxomatous mitral valve, neuro-circulatory asthenia, redundant cusp syndrome, soldier heart syndrome, systolic click-murmur syndrome, mitral regurgitation, heart failure, Marfan syndrome, Ehlers-Danlos syndrome, rheumatic fever, endocarditis, myocardial infarction, ischemia, syncope supraventricular tachycardia, ventricular tachycardia, ventricular fibrillation, cardiac arrhythmia, panic attacks, presyncope, Stickler syndrome

polycystic kidney disease, osteogenesis imperfecta, fragile X syndrome, Martin-Bell syndrome, pseudoxanthoma elasticum, periarteritis nodosa, asthenic habitus, straight back syndrome, pectus excavatum, pectus carinatum, atrial septal defect ostium secundum, tricuspid valve prolapse, aortic valve prolapse, Ebstein anomaly, Holt-Oram syndrome, hypertrophic cardiomyopathy, Graves disease, thyroiditis, sickle cell disease, muscular dystrophy, myotonic dystrophy, Von Willebrand disease, magnesium deficiency

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Contributor Information and Disclosures

Author

Poothirikovil Venugopalan, MBBS, MD, FRCP (Glasg), FRCPCH, Consulting Staff, Department of Child Health, University Hospital of Hartlepool, UK
Poothirikovil Venugopalan, MBBS, MD, FRCP (Glasg), FRCPCH is a member of the following medical societies: British Cardiac Society, Royal College of Paediatrics and Child Health, and Royal College of Physicians and Surgeons of Glasgow
Disclosure: Nothing to disclose.

Medical Editor

Charles I Berul, MD, Associate Professor of Pediatrics, Harvard Medical School; Senior Associate, Department of Cardiology, Children's Hospital of Boston
Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Heart Rhythm Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Julian M Stewart, MD, PhD, Associate Chairman of Pediatrics, Director, Center for Hypotension, Westchester Medical Center; Professor of Pediatrics and Physiology, New York Medical College
Julian M Stewart, MD, PhD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

CME Editor

Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College
Gilbert Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin
Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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