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Pediatric Mitral Valve Prolapse Clinical Presentation

  • Author: Poothirikovil Venugopalan, MBBS, MD, FRCPCH; Chief Editor: P Syamasundar Rao, MD  more...
Updated: Feb 21, 2014


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 and 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 are present in 7.4% of patients. The 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.


Panic attacks may occur. Nervousness, presyncope, and syncope occur in 0.9% of patients.

Thromboembolism, arrhythmia, or vasodepressor-vasovagal problems may be involved.


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


Apical midsystolic nonejection click and late systolic murmur are the hallmarks, but either may occur alone.

The 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


Heritable disorders of connective tissue include the following:

Skeletal abnormalities include the following:

Other diseases include the following:

Several reports suggest magnesium deficiency underlies the disease in some patients.

Contributor Information and Disclosures

Poothirikovil Venugopalan, MBBS, MD, FRCPCH Consultant Pediatrician with Cardiology Expertise, Department of Child Health, Brighton and Sussex University Hospitals, NHS Trust; Honorary Senior Clinical Lecturer, Brighton and Sussex Medical School, UK

Poothirikovil Venugopalan, MBBS, MD, FRCPCH is a member of the following medical societies: Royal College of Paediatrics and Child Health, Paediatrician with Cardiology Expertise Special Interest Group, British Congenital Cardiac Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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, American Autonomic Society, American Physiological Society

Disclosure: Received grant/research funds from Lundbeck Pharmaceuticals for none.

Chief Editor

P Syamasundar Rao, MD Professor of Pediatrics and Medicine, Division of Cardiology, Emeritus Chief of Pediatric Cardiology, University of Texas Medical School at Houston and Children's Memorial Hermann Hospital

P Syamasundar Rao, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, American College of Cardiology, American Heart Association, Society for Cardiovascular Angiography and Interventions, Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

Charles I Berul, MD Professor of Pediatrics and Integrative Systems Biology, George Washington University School of Medicine; Chief, Division of Cardiology, Children's National Medical Center

Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, Heart Rhythm Society, Cardiac Electrophysiology Society, Pediatric and Congenital Electrophysiology Society, American College of Cardiology, American Heart Association, Society for Pediatric Research

Disclosure: Received grant/research funds from Medtronic for consulting.

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Chest radiograph of 5-year-old girl with mitral valve prolapse (MVP) and mild mitral regurgitation. The radiograph shows cardiomegaly and normal pulmonary vasculature.
Two-lead electrocardiogram of a child with mitral valve prolapse (MVP) showing T-Wave inversion in leads III and aVF.
Two-dimensional echocardiographic picture taken from the parasternal long-axis view showing prolapse of both anterior and posterior mitral valve leaflets into the left atrium at systole.
Color-Doppler echocardiography of a child with mitral valve prolapse showing jet of mitral regurgitation.
M-mode echocardiographic picture of mitral valve prolapse showing pansystolic prolapse of both anterior and posterior mitral leaflets toward left atrium.
Plain radiograph of the left hand of a 10-year-old boy with marfanoid syndrome and mitral valve prolapse (MVP) showing the long thin metacarpals. The metacarpal index is longer than normal.
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