Acquired Mitral Stenosis Workup

  • Author: M Silvana Horenstein, MD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Sep 1, 2010
 

Laboratory Studies

  • Rheumatic heart disease - Nonspecific, unless the patient is experiencing an acute attack of recurrent rheumatic fever, in which case, C-reactive protein, sedimentation rate, and antistreptolysin O (ASLO) antibodies are evident
  • Chronic rheumatic mitral valve disease - Persistence of elevated levels of antibody to the streptococcal group A carbohydrate in most patients with chronic rheumatic mitral valve disease
  • Systemic lupus erythematosus - Antinuclear antibodies, antibodies to double stranded DNA, and lupus erythematosus (LE) cells
  • Amyloidosis - Amyloid deposits in affected tissues
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Imaging Studies

  • Chest radiography
    • Left atrial enlargement
    • Pulmonic trunk and right ventricular and right atrial enlargement
    • Pulmonary venous congestion that results in redistribution of pulmonary blood flow with greater flow to the upper lobes and interstitial edema manifested by Kerley B lines
  • Echocardiography: Transthoracic and transesophageal echocardiography are the most important diagnostic tools for evaluating patients with mitral stenosis (MS). Transesophageal echocardiography is recommended when transthoracic examination is incomplete, especially if left atrial thrombus is suspected. It is also used in the operating room and catheterization laboratory to assess the effectiveness of intervention. Echocardiography provides the following:
    • Direct anatomic data is provided, including visualization of valve leaflet morphology and motility and measurement of valve orifice dimensions, as well as the degree of left atrial dilation.
    • Hemodynamic and physiologic data are provided, including the pressure gradient across the stenotic mitral valve, the presence and severity of mitral regurgitation, and the degree of pulmonary hypertension.
    • Spontaneous echo contrast is common in patients with MS, and its presence in the left atrium is associated with a higher risk of thromboembolism. One study postulated that platelet activation via increased sympathetic activity is responsible for this phenomenon.[6]
  • MRI: MRI is infrequently used; however, experience with this imaging modality is much less than with echocardiography.
  • CT scanning: Multislice CT scanning has been described as a new modality to assess the mitral valve area in patients with MS.[7]
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Other Tests

  • ECG findings are often within reference ranges in patients with mild MS.
  • In those with moderate-to-severe MS, ECG reveals left atrial enlargement, right ventricular hypertrophy, and, often, right atrial enlargement. It also reveals atrial dysrhythmia. A fragmented QRS (RSR', R or S wave notching in 2 contiguous leads) has been described in patients who have severe MS, lower ejection fraction, and increased pulmonary artery pressure.[8]
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Procedures

  • Cardiac catheterization can be used to obtain direct measurement of the pressure gradient across the mitral valve as well as pulmonary artery pressure and pulmonary vascular resistance.
  • The mitral valve area can be calculated using the Gorlin formula.
  • Currently, the diagnosis and hemodynamic assessment of patients with MS are performed noninvasively with echocardiography.
  • Cardiac catheterization may be needed to supplement the information obtained noninvasively. More commonly, it is performed to accomplish percutaneous balloon valvuloplasty.
  • Possible complications of cardiac catheterization include tachyarrhythmias, bradyarrhythmias, and vascular occlusion. Balloon valvuloplasty may result in significant mitral regurgitation.
  • Postcatheterization complications include hemorrhage, pain, nausea and vomiting, and arterial or venous obstruction from thrombosis or spasm.
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Histologic Findings

  • Cardiac involvement in rheumatic fever is characterized by inflammation of the endocardium and myocardium. Histologic changes are not observed during the early stage of myocarditis but become evident at later stages of the inflammatory process. The changes include tissue edema and a cellular infiltrate consisting of lymphocytes and plasma cells but few polymorphonuclear white blood cells.
  • Endocardial inflammation of the mitral valve produces essentially the same histologic changes observed in myocarditis.
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Contributor Information and Disclosures
Author

M Silvana Horenstein, MD  Assistant Professor, Department of Pediatrics, University of Texas Medical School at Houston; Medical Doctor Consultant, Legacy Department, Best Doctors, Inc

M Silvana Horenstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Michael Pettersen, MD  Director of Echocardiography, Division of Cardiology, Children's Hospital of Michigan; Associate Professor of Pediatrics, Wayne State University School of Medicine

Michael Pettersen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, and American Society of Echocardiography

Disclosure: Nothing to disclose.

Henry Walters III, MD  Associate Professor of Surgery, Wayne State University School of Medicine; Chief, Department of Surgery, Division of Cardiovascular Surgery, Children's Hospital of Michigan

Henry Walters III, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Thoracic Surgery, American Medical Association, International Society for Heart and Lung Transplantation, Phi Beta Kappa, and Society of Thoracic Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

Ira H Gessner, MD  Professor Emeritus, Pediatric Cardiology

Ira H Gessner, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

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.

References

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Hemodynamic changes in severe mitral valve stenosis (MS). MS causes an obstruction (in diastole) to blood flow from the left atrium (LA) to the left ventricle (LV). Increased LA pressures are transmitted retrograde to pulmonary veins and pulmonary capillaries, resulting in capillary leak with subsequent development of pulmonary edema. To overcome pulmonary edema, the arterioles constrict, increasing pulmonary pressures. Over time, capillaries develop intimal thickening, causing fixed (permanent) pulmonary hypertension. The right ventricle (RV) hypertrophies to generate enough pressure to overcome the increased afterload. Eventually, the RV fails, which manifests as hepatomegaly and/or ascites, edema of the extremities, and cardiomegaly on radiography.
 
 
 
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