AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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INTRODUCTION

Section 2 of 11  

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• Introduction
• Clinical
• Differentials
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• Follow-up
• Miscellaneous
• Multimedia
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Background

Mitral valve prolapse (MVP) can occur in a multitude of disorders and, in most instances, it reflects a normal variant rather than a single disease process.

Despite years of research, the symptomatology and significance of MVP remain controversial. It was termed the disease of the decade in the 1980s, but now some consider it an interesting finding of dubious importance. Initial studies that reported associated symptoms of MVP as chest pain, dyspnea, anxiety, and panic, were probably flawed by recruitment bias. Recent studies imply that the incidence of MVP previously was overestimated by inaccurate echocardiographic diagnostic criteria and that associated symptoms, other than palpitations, are uncommon.

Despite this, patients with MVP are at risk for endocarditis, stroke, mitral regurgitation (MR), mitral valve replacement (MVR) surgery, and sudden death.

Pathophysiology

A myxomatous degeneration from collagen dissolution leads to excess mucopolysaccharides in the middle spongiosa layer of the mitral valve leaflets, resulting in stretching of the leaflets and the chordae tendineae.

MVP occurs when the left ventricular (LV) size is small in comparison to an enlarged mitral annulus, leaflets, or chordae tendineae, and it can be induced in healthy women with typical body habitus following dehydration that is reversed with rehydration. MVP resolves during pregnancy and following weight gain in anorexic patients.

Recent studies have shown that abnormalities of elastic fibers found in floppy mitral valves are related to genetic variants in fibrillin, one of the components of the microfibrils, as well as elastin and collagen I and II.

A constellation of abnormalities (eg, increased sensitivity to adrenergic stimuli, increased catecholamines, abnormal beta-receptors, increased atrial natriuretic factor, renin-aldosterone dysregulation, decreased intravascular volume, magnesium deficiency) has been thought to lead to chest pain, dyspnea, fatigue, dizziness, near-syncope symptoms, and anxiety in a subset of patients with MVP.

Cardiac manifestations include supraventricular arrhythmias, palpitations, mitral regurgitation, bacterial endocarditis, and sudden death. Chest pain may not be more common in patients with MVP than in the general population, and it may be attributed to myofascial syndromes, hyperventilation, coronary spasm, esophageal dysmotility, or gastroesophageal reflux.

MVP can result in cerebrovascular ischemia, which may be related to abnormal platelet activity or protein C or S deficiencies.

Frequency

United States

MVP can be identified by echocardiography in 3-4% of the general population, and it is identified in 7% of autopsies.

International

The worldwide incidence of MVP is similar to that in the United States.

Mortality/Morbidity

• In general, MVP is a benign disorder, but it may account for the majority of isolated cases of mitral regurgitation (MR), 90% of cases of ruptured chordae tendineae, 40% of strokes in young patients, and 10-15% of cases of endocarditis.
• Those with structural abnormalities (ie, thickened, deformed, or redundant mitral valve leaflets) are more likely to suffer complications (eg, progressive MR, endocarditis, sudden death).
• Cases of MVP with a murmur and not just an isolated click have a general mortality rate that is increased by 15-20%.

Race

Prevalence is similar among different ethnic groups.

Sex

• The female-to-male ratio is approximately 3:1.
• Men older than 45 years have twice the risk of MR and endocarditis.

Age

Age of onset is 10-16 years.

• MVP is uncommon before the adolescent growth spurt occurs. It usually is detected in young adulthood.
• Although MVP is considered congenital, echocardiographic findings typically are absent in newborns.

CLINICAL

Section 3 of 11  

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• Follow-up
• Miscellaneous
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History

• MVP usually is asymptomatic, nonprogressive, and benign.
• Palpitations occur in 40% of MVP cases. This percentage excludes palpitations due to withdrawal syndromes (eg, alcohol, sedatives), intoxications (eg, cocaine, amphetamine, phencyclidine), or medication exposures (eg, caffeine, sympathomimetic, anticholinergic).
• Chest pain and dyspnea previously were considered part of the MVP syndrome, but they are now felt to be no more common in cases of MVP than they are in the general population.
• Although controversial, anxiety and panic disorders may be more common in patients with MVP than the general population.
• Fatigue
• Syncope/presyncope
• Orthostasis

Physical

• Thin aesthetic body habitus with narrow anteroposterior diameter
• Skeletal abnormalities (ie, pectus excavatum, straight back, kyphoscoliosis)
• Supernumerary nipples in Asian Indians
• Resting bradycardia and orthostatic hypotension
• Cardiac auscultation
• • Apical, single or multiple, mid-to-late systolic clicks, which result from the tightening of the chordae tendineae or the redundant valve, can be heard.
  • An apical mid-to-late systolic murmur of crescendo, decrescendo, or constant nature can be heard, and the murmur continues to be heard in S₂.
  • The click and the murmur change as the position changes (closer to S₁ results in diminished LV volume; closer to S₂ results in increased LV volume)
  • In the supine position, the click is late (ie, close to S₂), and the murmur is brief.
  • In the standing position and during the Valsalva maneuver, the click is earlier (ie, close to S₁), and the murmur is longer. This may identify a murmur that previously was not noted.
  • In the squatting position, the click is later (ie, closer to S₂), and the murmur is shorter. The click and the murmur may even disappear.
  • The isometric handgrip exercise increases the intensity (ie, loudness) of the murmur without affecting the position.
  • The murmur should be distinguished from that of aortic stenosis (ie, early systolic, at base); pulmonic flow murmur (ie, short and early systolic, diminishes with Valsalva maneuver); hypertrophic cardiomyopathy (ie, diminishes with squatting and intensifies with standing and Valsalva maneuver); and mitral regurgitation (ie, holosystolic S₃, enlarged and displaced point of maximal intensity [PMI]).
• Mitral regurgitation
• Autonomic dysfunction - Decreased heart rate variability and parasympathetic tone
• Neuroendocrine dysfunction
• Ehlers-Danlos syndrome findings (eg, joint hypermobility, abnormal striae, bruising, distensibility of skin)
• Osteogenesis imperfecta findings (eg, blue sclera)
• Marfan syndrome findings (eg, scoliosis, straight back, pectus excavatum, arachnodactyly, arm span greater than body height)
• Stickler syndrome findings (eg, kyphosis, scoliosis, mandibular hypoplasia, retinal detachment). Whether Stickler syndrome is associated with MVP is debatable.

Causes

Most cases are primary, idiopathic in nature, and expressed as an autosomal dominant trait that exhibits both sex- and age-dependent penetrance.

• Connective tissue disorders
• • Marfan syndrome
  • Ehlers-Danlos syndrome (ie, types I, II, IV)
  • Osteogenesis imperfecta
  • Pseudoxanthoma elasticum
  • Polycystic kidney disease
  • Stickler syndrome
  • Systemic lupus erythematosus
  • Relapsing polychondritis
  • Polyarteritis nodosa
• Muscle disorders
• • Duchenne muscular dystrophy
  • Fragile X syndrome
  • Mucopolysaccharidoses
  • Myotonic dystrophy
• Congenital heart disease - Atrial septal defect (ASD)
• Ebstein anomaly
• Acquired heart disease
• • Papillary muscle dysfunction (eg, ischemia, myocarditis)
  • Cardiac trauma
  • Post mitral valve surgery
  • Rheumatic endocarditis
• Miscellaneous
• • Wolff-Parkinson-White syndrome
  • Von Willebrand disease

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Idiopathic hypertrophic subaortic stenosis (IHSS)
Tachyarrhythmias, narrow complex
Tachyarrhythmias, wide complex
Ventricular septal defect (VSD)
Stickler syndrome
Postural orthostatic tachycardia syndrome (POTS)
Benign joint hypermobility syndrome
Neurocardiogenic syncope

WORKUP

Section 5 of 11  

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Lab Studies

• Specific lab studies are not necessary to confirm MVP, although some may be indicated to exclude other diagnoses.
• • Arterial blood gas (ABG) analysis may be obtained to exclude the diagnosis of hyperventilation, hypoxemia, and metabolic acidosis in patients with tachypnea or dyspnea.
  • Serum electrolytes may be obtained to exclude the diagnosis of hypokalemia and acidosis in patients with dysrhythmias or palpitations.
  • Serum hemoglobin may be obtained to exclude the diagnosis of anemia in patients with fatigue or near-syncope.
  • Serum glucose may be obtained to exclude the diagnosis of hypoglycemia in patients with fatigue or near-syncope.
  • Cardiac enzymes may be obtained to exclude the diagnosis of an acute myocardial event in patients with chest pain.
  • A urine toxin screen may be obtained to exclude the diagnosis of an exposure to amphetamines, cocaine, or phencyclidine in patients with agitation, chest pain, dyspnea, and tachydysrhythmia.

Imaging Studies

• Chest radiography is not specifically indicated except to exclude other causes of chest pain and dyspnea.
• • The chest radiograph may reveal an increased left atrial or pulmonary artery size, which is indicative of MR.
  • A lateral chest radiograph may reveal dorsal spine straightening and a narrow anteroposterior diameter.
• Outpatient echocardiography (echo) is indicated for those with a murmur.
• • Although screening subjects who are at a low risk for complications (ie, those without MR) is not indicated, 2-dimensional echo can detect the patients with more severe or unusual forms of MVP (eg, patients with significant MR, annular and leaflet thickening, chordal lengthening, atrial septal defect [ie, secundum], hypertrophic cardiomyopathy).
  • Two-dimensional echo is less sensitive than M-mode echo, detecting only 50% of patients with M-mode echo and auscultatory findings, but it is more specific for MVP than M-mode echo.
  • Diagnostic criteria include systolic billowing of one or both mitral leaflets. This systolic billowing occurs on the left atrial side, above the visualized annular plane, in the long-axis parasternal view.
• An M-mode echo gives many false-negative and false-positive results, but it can identify MVP with at least 2 mm of midsystolic prolapse or 3 mm of holosystolic or late-systolic movement of the leaflets, which are posterior to the line connecting the valve's opening and the closure points.
• Doppler echo is recommended every 2-3 years for patients with mild MR, and it is recommended yearly for those with significant MR.

Other Tests

• Electrocardiogram
• • Results usually are normal.
  • Minor QT prolongation (0.42 ± 0.52) may occur.
  • Nonspecific ST and T-wave changes were previously noted, but they may not be more frequent than in the general population.
• Holter monitor
• • Outpatient Holter monitoring or transtelephonic event recording should be considered in patients with palpitations that are associated with syncope or near-syncope.
  • Supraventricular tachydysrhythmias occur in 30% of patients with MVP, but the incidence of ventricular dysrhythmias is similar to that of the general population.
• Electrophysiologic testing is indicated for those with near-sudden death, symptomatic complex ventricular ectopy, Wolff-Parkinson-White syndrome, and recurrent unexplained syncope.
• Contrary to earlier studies that report a false-positive result 50% of the time on exercise stress ECGs and thallium imaging studies, recent reports have found stress test abnormalities no more likely in patients with MVP than in the general population.
• Single-photon emission computed tomographic myocardial perfusion imaging has excluded myocardial ischemia in patients with MVP and exercise-induced chest pain

TREATMENT

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Prehospital Care

The prehospital treatment of patients with chest pain, dyspnea, palpitations, a neurologic deficit, or syncope should include cardiac monitoring, supplemental oxygen, and intravenous catheter placement.

Emergency Department Care

• Patients with symptoms of chest pain, dyspnea, palpitations, a neurologic deficit, or syncope should be placed on oxygen, put in a supine or Fowler position, and monitored.
• • Pulse oximetry
  • Cardiac monitoring
  • Frequent vital signs, including one set of orthostatic vital signs when possible
• Anxious patients should be reassured regarding their status, and many may benefit from psychosocial intervention.

Consultations

• Consult a cardiologist in cases of diagnostic uncertainty, ventricular dysrhythmia, or risk of sudden death as well as when symptoms of severe MR are present.
• Consider consulting a cardiothoracic surgeon in patients with significant exertional dyspnea and congestive heart failure that is related to MR.

MEDICATION

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Medications generally are not necessary. Beta-blockers may be helpful if palpitations are severe.

Antiplatelet agents such as aspirin and/or clopidogrel (Plavix) are indicated for patients with transient ischemic attack or stroke. Some authors recommend prophylaxis with antiplatelet agents in all patients with MVP and murmur because of a small but significant increase in risk of stroke (10%).

Orthostatic hypotension and presyncope symptoms may be treated with sodium chloride tablets; however, if this treatment is not successful, fludrocortisone 0.05-0.10 mg/d PO may be used.

Magnesium supplementation may improve symptoms of the classic MVP syndrome.

Significant mitral regurgitation (MR) in the setting of hypertension (systolic blood pressure >140 mm Hg) may be improved with the use of angiotensin-converting enzyme inhibitors. No evidence exists as yet to support the use of these medications to halt the progression of MVP to MR.

Drug Category: Antibiotics

Antibiotic prophylaxis during surgical procedures (eg, contaminated wound repair, abscess incision and draining) is recommended for patients with a murmur, with evidence of nontrivial MR on an echo, or men older than 45 years with valve thickening. Antibiotic prophylaxis is recommended to prevent bacterial endocarditis. Prophylaxis is not suggested for patients who have an isolated click without a murmur or for patients with evidence of MR on an echo.

Patients who are allergic to penicillin and are undergoing dental, oral, respiratory tract, or esophageal procedures may be treated 1 hour before the procedure with clindamycin, 600 mg (20 mg/kg) PO, or azithromycin or clarithromycin, 500 mg (15 mg/kg) PO. Clindamycin, 600 mg (20 mg/kg) IV, may be administered 30 minutes before the procedure, as an alternative to the PO route.

For patients who are allergic to penicillin and are undergoing genitourinary or gastrointestinal procedures, the physician may decide to infuse vancomycin, 1 g (20 mg/kg) IV over 1-2 hours, with the infusion being completed 30 minutes before the procedure.

Drug Category: Beta-blockers

Blood pressure control may prevent chordal rupture and the progression of MVP to severe MR. Clonidine has been shown to diminish symptoms of the classic (disputed) MVP syndrome. Beta-blocking agents (eg, propranolol, atenolol, pindolol) may also be effective in those with neurocardiogenic syncope.

Drug Category: Antiarrhythmics

Digoxin has been effective in treating supraventricular tachycardia and in the prevention of symptoms of classic MVP syndrome (eg, chest pain, fatigue).

FOLLOW-UP

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Further Inpatient Care

• Patients with stroke, risk of sudden death, unstable ventricular dysrhythmias, severe symptomatic MR, or bacterial endocarditis may require inpatient management.

Further Outpatient Care

• Consultation by a cardiologist is recommended to confirm the diagnosis, to exclude other possible disorders from the diagnosis (eg, hypertrophic cardiomyopathy, atrial septal defect) and to further evaluate symptoms (eg, palpitations).
• Echocardiography may not be necessary for diagnosis in many cases because dynamic auscultation may be more reliable.
• Cognitive behavioral therapy and breathing retraining may diminish functional cardiac symptoms (eg, chest pain, dyspnea, dizziness).
• Follow-up care by a cardiothoracic surgeon is recommended for patients with hemodynamically significant MR. Surgical repair or replacement of the mitral valve is indicated for patients with exertional dyspnea, an ejection fraction below 50%, and a left ventricular end-systolic dimension approaching 45 mm.

Deterrence/Prevention

• Blood pressure control may diminish the risk of progression to MR.
• Exercise; biofeedback; meditation; and avoidance of smoking, alcohol, caffeine, and stimulants may prevent symptoms.

Complications

• For the following complications, the absolute risk (ie, annual incidence) and the odds ratios (OR), comparing patients with MVP to the general population, are as follows:
• • Sudden cardiac death - 0.06% annual incidence among patients with MVP and severe MR; OR of 50-100 with hemodynamically significant MR and depressed left ventricular function
  • Rupture of chordae tendineae (the most frequent serious complication of MVP)
  • Progressive MR - 0.06% annual incidence of requiring surgery; lifetime risk of surgery is 1.5% for women and 4-6% for men; OR of 30-40; increased risk in males, older than 75 years, elevated body weight, and high blood pressure.
  • Stroke - 0.02% annual incidence versus less than 0.02% in uncomplicated MVP; OR of 4-6
  • Infective endocarditis - 0.02% annual incidence; OR of 3-8; 1 in 1400 patients per year with MVP and murmur; increased risk in males older than 45 years
  • Atrial fibrillation can be persistent in 15% or paroxysmal in 13% when MR is severe enough to require mitral valve replacement (MVR) surgery. These rates are lower than seen with mitral stenosis requiring MVR.

Prognosis

• In most situations, the prognosis for patients with MVP is excellent.
• MR is the most significant risk factor for other complications (eg, sudden death, stroke, endocarditis).
• Patients whose echo shows abnormal valve anatomy, men, and those older than 45 years are at an increased risk of developing MR.
• Patients who are older, lack social support, have higher anxiety, and fail to exercise regularly are at risk for more symptoms.
• Cardiovascular mortality is predicted the most by moderate-to-severe MR and ejection fraction less than 50%, and less so by left atrial size greater than 40 mm, flail leaflet, atrial fibrillation, and age older than 50 years.

Patient Education

• Patients with a murmur, patients who have echo evidence of nontrivial MR, or men older than 45 years who have valve thickening should inform their dentist and surgeon of their health complications so that they can receive antibiotic prophylaxis prior to any procedures.
• Patients with palpitations should avoid caffeine, alcohol, stimulants, and smoking.
• Symptoms of the classic MVP syndrome may improve with exercise, meditation, and biofeedback.
• For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education articles Mitral Valve Prolapse, Chest Pain, and Palpitations.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Evidence of MVP should not be an excuse to terminate further diagnostic evaluation of patients with symptoms such as chest pain, palpitations, dyspnea, or syncope.

Special Concerns

• MVP does not predispose women to any increased risk during pregnancy.
• Aviators with MVP may develop MR under positive-G force and may be at risk for dysrhythmia or syncope.
• MVP should be considered in the differential diagnosis of patients with unexplained cerebral ischemia.
• Patients with MVP and a murmur should avoid high-intensity competitive sports if they have syncope associated with dysrhythmia, a family history of sudden death associated with MVP, significant supraventricular or ventricular dysrhythmias, or moderate-to-severe MR. Those who have had a previous embolic event also should avoid high-intensity competitive sports.
• MVP is the third most common cause of sudden death in athletes, following congenital coronary artery anomalies and hypertrophic cardiomyopathy.

MULTIMEDIA

Section 10 of 11  

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Media file 1:  Mitral valve prolapse. A patient with straight back syndrome.
	View Full Size Image
Media type:  X-RAY

REFERENCES

Section 11 of 11

• Authors and Editors
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• Clinical
• Differentials
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• Follow-up
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• Avierinos JF, Brown RD, Foley DA. Cerebral ischemic events after diagnosis of mitral valve prolapse: a community-based study of incidence and predictive factors. Stroke. Jun 2003;34(6):1339-44. [Medline].
• Avierinos JF, Gersh BJ, Melton LJ. Natural history of asymptomatic mitral valve prolapse in the community. Circulation. Sep 10 2002;106(11):1355-61. [Medline].
• Berbarie RF, Roberts WC. Frequency of atrial fibrillation in patients having mitral valve repair or replacement for pure mitral regurgitation secondary to mitral valve prolapse. Am J Cardiol. Apr 1 2006;97(7):1039-44. [Medline].
• Bobkowski W, Siwinska A, Zachwieja J. A prospective study to determine the significance of ventricular late potentials in children with mitral valvar prolapse. Cardiol Young. Jul 2002;12(4):333-8. [Medline].
• Bonow RO, Carabello B, de Leon AC, et al. ACC/AHA Guidelines 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 (Committee on Management of Patients With Val. J Heart Valve Dis. Nov 1998;7(6):672-707. [Medline].
• Chou HT, Shi YR, Hsu Y. Association between fibrillin-1 gene exon 15 and 27 polymorphisms and risk of mitral valve prolapse. J Heart Valve Dis. Jul 2003;12(4):475-81. [Medline].
• Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association. JAMA. Jun 11 1997;277(22):1794-801. [Medline].
• Devereux RB, Kramer-Fox R, Kligfield P. Mitral valve prolapse: causes, clinical manifestations, and management. Ann Intern Med. Aug 15 1989;111(4):305-17. [Medline].
• Etchells E, Bell C, Robb K. Does this patient have an abnormal systolic murmur?. JAMA. Feb 19 1997;277(7):564-71. [Medline].
• Fontana ME, Sparks EA, Boudoulas H, Wooley CF. Mitral valve prolapse and the mitral valve prolapse syndrome. Curr Probl Cardiol. May 1991;16(5):309-75. [Medline].
• Freed LA, Levy D, Levine RA, et al. Prevalence and clinical outcome of mitral-valve prolapse. N Engl J Med. Jul 1 1999;341(1):1-7. [Medline].
• Freed LA, Acierno JS, Dai D. A locus for autosomal dominant mitral valve prolapse on chromosome 11p15.4. Am J Hum Genet. Jun 2003;72(6):1551-9. [Medline].
• Freed LA, Benjamin EJ, Levy D. Mitral valve prolapse in the general population: the benign nature of echocardiographic features in the Framingham Heart Study. J Am Coll Cardiol. Oct 2 2002;40(7):1298-304. [Medline].
• Gilon D, Buonanno FS, Joffe MM, et al. Lack of evidence of an association between mitral-valve prolapse and stroke in young patients. N Engl J Med. Jul 1 1999;341(1):8-13. [Medline].
• Gould FK, Elliott TS, Foweraker J. Guidelines for the prevention of endocarditis: report of the Working Party of the British Society for Antimicrobial Chemotherapy. J Antimicrob Chemother. Jun 2006;57(6):1035-42. [Medline].
• Han L, Ho TF, Yip WC, Chan KY. Heart rate variability of children with mitral valve prolapse. J Electrocardiol. Jul 2000;33(3):219-24. [Medline].
• Kao CH, Tsai SC, Hsieh JF, et al. Radionuclide esophageal transit test to detect esophageal disorders in patients with mitral valve prolapse. Nuklearmedizin. 2000;39(4):92-6. [Medline].
• Karakurum B, Topçu S, Yildirim T. Silent cerebral infarct in patients with mitral valve prolapse. Int J Neurosci. Nov 2005;115(11):1527-37. [Medline].
• Kitlinski M, Stepniewski M, Nessler J. Is magnesium deficit in lymphocytes a part of the mitral valve prolapse syndrome?. Magnes Res. Mar 2004;17(1):39-45. [Medline].
• Kochiadakis GE, Parthenakis FI, Zuridakis EG, et al. Is there increased sympathetic activity in patients with mitral valve prolapse?. Pacing Clin Electrophysiol. Nov 1996;19(11 Pt 2):1872-6. [Medline].
• La Vecchia L, Ometto R, Centofante P, et al. Arrhythmic profile, ventricular function, and histomorphometric findings in patients with idiopathic ventricular tachycardia and mitral valve prolapse: clinical and prognostic evaluation. Clin Cardiol. Oct 1998;21(10):731-5. [Medline].
• Leung DY, Dawson IG, Thomas JD, Marwick TH. Accuracy and cost-effectiveness of exercise echocardiography for detection of coronary artery disease in patients with mitral valve prolapse. Am Heart J. Dec 1997;134(6):1052-7. [Medline].
• Lichodziejewska B, Klos J, Rezler J, et al. Clinical symptoms of mitral valve prolapse are related to hypomagnesemia and attenuated by magnesium supplementation. Am J Cardiol. Mar 15 1997;79(6):768-72. [Medline].
• O''Farrell DA, Cannon DP, Nunley JA. Digital ischemia associated with a thrombosed aneurysm of the dorsal interosseous artery. A case report. J Bone Joint Surg Am. Mar 1997;79(3):441-3. [Medline].
• Ozkan M, Kaymaz C, Dinckal H, et al. Single-photon emission computed tomographic myocardial perfusion imaging in patients with mitral valve prolapse. Am J Cardiol. Feb 15 2000;85(4):516-8, A11. [Medline].
• Raggi P, Callister TQ, Lippolis NJ, Russo DJ. Is mitral valve prolapse due to cardiac entrapment in the chest Cavity? A CT view. Chest. Mar 2000;117(3):636-42. [Medline].
• Scordo KA. Mitral valve prolapse syndrome: interventions for symptom control. Dimens Crit Care Nurs. Jul-Aug 1998;17(4):177-86. [Medline].
• Singh RG, Cappucci R, Kramer-Fox R, et al. Severe mitral regurgitation due to mitral valve prolapse: risk factors for development, progression, and need for mitral valve surgery. Am J Cardiol. Jan 15 2000;85(2):193-8. [Medline].
• Tamam L, Ozpoyraz N, San M, Bozkurt A. Association between idiopathic mitral valve prolapse and panic disorder. Croat Med J. Dec 2000;41(4):410-6. [Medline].
• Taubert KA, Dajani AS. Preventing bacterial endocarditis: American Heart Association guidelines. Am Fam Physician. Feb 1 1998;57(3):457-68. [Medline].
• Theal M, Sleik K, Anand S. Prevalence of mitral valve prolapse in ethnic groups. Can J Cardiol. Apr 2004;20(5):511-5. [Medline].

Article Last Updated: Jun 14, 2006