Pediatric Mitral Valve Prolapse Clinical Presentation

  • Author: Poothirikovil Venugopalan, MBBS, MD, FRCP(Glasg), FRCPCH; Chief Editor: Stuart Berger, MD   more...
 
Updated: Mar 26, 2010
 

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
Next

Causes

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.

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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 North Tees and Hartlepool, UK

Poothirikovil Venugopalan, MBBS, MD, FRCP(Glasg), FRCPCH, is a member of the following medical societies: British Cardiac Society, Paediatrician with Cardiology Expertise Special Interest Group, Royal College of Paediatrics and Child Health, and Royal College of Physicians and Surgeons of Glasgow

Disclosure: Nothing to disclose.

Specialty Editor Board

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, American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, Pediatric and Congenital Electrophysiology Society, and Society for Pediatric Research

Disclosure: Johnson & Johnson Consulting fee Consulting

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

Disclosure: Nothing to disclose.

Gilbert Z Herzberg, MD  Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center

Gilbert Z 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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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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