Mitral Valvuloplasty
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Historically, surgical commissurotomy was the standard treatment for relief of mitral stenosis. The first single-balloon valvuloplasty of the mitral valve was described by Inoue et al in 1984. [1] Percutaneous mitral balloon valvuloplasty (PMBV) has since become the treatment of choice for mitral stenosis. The Inoue balloon catheter remains the most commonly used technique for percutaneous mitral balloon valvuloplasty.
Rheumatic mitral valve stenosis occurs as a result of rheumatic fever, usually decades after the acute illness. Commissural fusion of the mitral valve leaflets leads to obstruction of blood flow from the left atrium to the left ventricle. This obstruction, in turn, leads to chronically elevated pulmonary arterial pressures and symptoms of heart failure, especially with exercise or other conditions associated with tachycardia.
Rheumatic heart disease remains uncommon in the United States today. It is much more prevalent in developing nations, where patients tend to present at a younger age. The prevalence of rheumatic heart disease has, however, seen small but significant increases in recent decades as increasing numbers of immigrants enter the United States from endemic areas. Small recent outbreaks of rheumatic fever have also been reported in the United States by new virulent strains of streptococci.
Rheumatic mitral valve disease, manifested by commissural leaflet fusion, is the most common cause of mitral stenosis. Nonrheumatic mitral stenosis is unusual, although calcific stenosis is now seen with increasing frequency in hemodialysis patients. Other rare causes of mitral stenosis include carcinoid syndrome, eosinophilic endomyocardial fibroelastosis, and congenital mitral stenosis. These are distinctly different processes from rheumatic mitral stenosis without commissural fusion. Though limited, experience with balloon valvuloplasty for congenital mitral stenosis suggests little benefit from a potentially dangerous procedure. Surgery is usually preferable in these patients who often have associated complex anatomy. These patients should, therefore, be evaluated by a multidisciplinary team at an experienced center.
Commisural fusion of the mitral valve leaflets results in loss of the mitral orifice size. This limits blood flow across the valve from the left atrium to the left ventricle. Additionally, there is a loss of valvular reserve, the ability of the valve to open wider for larger blood flows, to facilitate an increase in cardiac output. Left atrial pressure is determined by the transvalvular gradient, which is a function of both orifice area and diastolic filling time. With exercise, heart rate and cardiac output increase, leading to an increase in left atrial and pulmonary arterial pressures.
Mitral orifice size correlates with severity of mitral stenosis and usually correlates with symptoms. The normal mitral valve area (MVA) measures 4-6 cm2. Mild reduction, with MVA measuring 2.0-2.5 cm2, results in elevated left atrial pressures when blood flow or heart rate is increased. Moderate reduction, with MVA 1.5-2.0 cm2, results in mildly elevated left atrial pressures at rest and significantly increased pressures with exercise. Severe mitral stenosis, at valve areas less than 1.5 cm2, results in reduced cardiac output and dyspnea at rest.
See the list below:
The first complaints with mitral stenosis are usually of dyspnea on exertion.
Early symptoms may be very subtle, and a history of rheumatic fever is often difficult to elicit.
Patients are sometimes initially diagnosed with upper respiratory illness before re-evaluation prompts consideration for cardiovascular disease.
In selected patients, formal exercise testing can help to elicit exercise-induced symptoms.
Women with mitral stenosis frequently present during pregnancy when cardiac output and circulating intravascular volume increase.
Physical examination may demonstrate a diastolic rumble or an opening snap.
Chest radiography rarely shows pulmonary edema unless precipitated by an exacerbating illness; however, in advanced mitral stenosis, Kerley B lines from chronically elevated pulmonary venous pressures are sometimes visualized.
Left atrial enlargement is typically present on the lateral chest radiograph.
Left atrial enlargement is usually evident on the electrocardiogram.
Atrial fibrillation often occurs in mitral stenosis as a result of left atrial dilatation and chronically elevated left atrial wall stress.
Transthoracic echocardiography (TTE), the diagnostic test of choice, is usually necessary and sufficient to confirm the diagnosis of mitral stenosis.
Table 1. Mitral valve area and severity of mitral stenosis (Open Table in a new window)
MVA
Severity
Hemodynamic Effects
4-6 cm2
Normal
Normal LA pressure and cardiac output
2-2.5 cm2
Mild
LA pressure elevated only with increased blood flow or heart rate
1.5-2.0 cm2
Moderate
LA pressure mildly elevated at rest with significant increase during exercise
< 1.5 cm2
Severe
Reduced cardiac output and dyspnea at rest
American Heart Association (AHA)/American College of Cardiology (ACC) guideline recommendations are as follows: [2]
Perform PMBV for patients with severe mitral stenosis (MVA < 1.5 cm2), favorable valve morphology and absence of contraindications such as left atrial thrombus or significant mitral regurgitation (Class I).
Asymptomatic patients with MVA < 1.5 cm2, pulmonary hypertension (systolic pulmonary pressure >50 mm Hg at rest or >60 mm Hg with exercise), and favorable valve morphology should also be considered for PMBV (Class I).
Patients with calcific mitral stenosis who are at high risk for surgical commissurotomy should be considered for PMBV when advanced heart failure (NYHA Class III-IV) and severe mitral stenosis (MVA < 1.5 cm2) are present (Class IIa).
Similar patients who are at lower risk for surgical commissurotomy may also be considered for PMBV (Class IIb).
Symptomatic patients (NYHA class II-IV) with milder stenosis (MVA >1.5 cm2) and pulmonary hypertension may be considered for PMBV (Class IIb).
Asymptomatic patients with MVA less than 1.5 cm2 with new atrial fibrillation may also be considered for PMBV (Class IIb).
Similar recommendations have been made by the European Society of Cardiology. [3] Palliative treatment may be considered in patients who are not suitable candidates for surgery even when valve morphology is not ideal.
Table 2. Indications for percutaneous mitral balloon valvuloplasty – AHA/ACC guidelines (Open Table in a new window)
Class I
NYHA class II-IV with MVA < 1.5 cm2, favorable valve morphology, absence of LA thrombus, absence of mod-severe
Asymptomatic with MVA < 1.5 cm2 and PAP >50 mm Hg at rest or >60 mm Hg with exercise
Class IIa
NYHA Class III-IV, MVA < 1.5 cm2 calcified valve, high surgical risk
Class IIb
Asymptomatic with MVA < 1.5 cm2 new atrial fibrillation
NYHA Class II-IV MVA >1.5 cm2 and PAP >50 mm Hg at rest or >60 mm Hg with exercise
NYHA Class III-IV, MVA < 1.5 cm2 calcified valve, low surgical risk
The mitral valve apparatus consists of a fibrous mitral annulus and 2 mobile valve leaflets (anterior leaflet and posterior leaflet) tethered to the papillary muscles in the left ventricle by chordae tendineae. Blood flows across the valve from the left atrium into the ventricle during diastole. The normal mitral valve orifice size is 4-6 cm2. Commissural fusion of the mitral valve leaflets results in a decrease in mitral valve orifice size and an increase in left atrial pressures.
The anterior leaflet is located posterior to the aortic root and is also anchored to the aortic root, unlike the posterior leaflet. Accordingly, it is also known as the aortic, septal, greater, or anteromedial leaflet. The posterior leaflet is also known as the ventricular, mural, smaller, or posterolateral leaflet. The posterior leaflet is the section of the mitral valve that is located posterior to the 2 commissural areas. For more information about the relevant anatomy, see Mitral Valve Anatomy.
A transthoracic echocardiographic scoring system (see Imaging Studies section below) is used to evaluate the suitability of valve morphology for PMBV. Other anatomic considerations in evaluating patients prior to PMBV include exclusion of left atrial thrombus and severe mitral regurgitation, both of which are contraindications to the procedure (see Contraindications section below).
The presence of left atrial thrombus is an absolute contraindication to PMBV because of the high risk for systemic embolism. Prior to proceeding with PMBV, all patients should be evaluated by transesophageal echocardiogram (TEE) with specific focus on the left atrial appendage to exclude thrombus. If left atrial thrombus is found, the patient should be treated with systemic anticoagulation for 3-6 months and undergo repeat TEE to confirm resolution of thrombus prior to PMBV. Patients with left atrial thrombus requiring more urgent therapy should be considered for surgical mitral valve replacement with ligation of the left atrial appendage.
Moderate to severe mitral regurgitation is also a contraindication to PMBV because of the risk of worsening regurgitation as a result of the procedure. Severe concomitant aortic valve disease, severe organic tricuspid stenosis, and severe functional tricuspid regurgitation with an enlarged annulus are also contraindications to PMBV.
Severe concomitant coronary artery disease requiring bypass surgery is a contraindication to PMBV. These patients should be considered for a combined coronary artery bypass and surgical mitral valve procedure.
Unfavorable valve morphology is a relative contraindication to PMBV, although in selected patients, especially in those who are high surgical risk or in cases of palliation, PMBV can be considered.
Inoue K, Owaki T, Nakamura T, Kitamura F, Miyamoto N. Clinical application of transvenous mitral commissurotomy by a new balloon catheter. J Thorac Cardiovasc Surg. 1984 Mar. 87(3):394-402. [Medline].
Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing Committee to Revise the 1998 guidelines for the management of patients with valvular heart disease) developed in collaboration with the Society of Cardiovascular Anesthesiologists endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. J Am Coll Cardiol. 2006 Aug 1. 48(3):e1-148. [Medline].
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MVA
Severity
Hemodynamic Effects
4-6 cm2
Normal
Normal LA pressure and cardiac output
2-2.5 cm2
Mild
LA pressure elevated only with increased blood flow or heart rate
1.5-2.0 cm2
Moderate
LA pressure mildly elevated at rest with significant increase during exercise
< 1.5 cm2
Severe
Reduced cardiac output and dyspnea at rest
Class I
NYHA class II-IV with MVA < 1.5 cm2, favorable valve morphology, absence of LA thrombus, absence of mod-severe
Asymptomatic with MVA < 1.5 cm2 and PAP >50 mm Hg at rest or >60 mm Hg with exercise
Class IIa
NYHA Class III-IV, MVA < 1.5 cm2 calcified valve, high surgical risk
Class IIb
Asymptomatic with MVA < 1.5 cm2 new atrial fibrillation
NYHA Class II-IV MVA >1.5 cm2 and PAP >50 mm Hg at rest or >60 mm Hg with exercise
NYHA Class III-IV, MVA < 1.5 cm2 calcified valve, low surgical risk
David H Adler, MD, FACC Assistant Professor of Medicine, Eastern Virginia Medical School; Cardiologist, Cardiovascular Associates, Ltd
David H Adler, MD, FACC is a member of the following medical societies: American College of Cardiology, American Heart Association
Disclosure: Nothing to disclose.
Robert N Piana, MD Associate Professor of Medicine, Director, Adult Congenital Interventional Program, Vanderbilt Heart and Vascular Institute, Vanderbilt University Medical Center
Robert N Piana, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Massachusetts Medical Society, Phi Beta Kappa
Disclosure: Nothing to disclose.
David XM Zhao, MD, FACC, FSCAI Associate Professor, Division of Cardiovascular Medicine, Department of Medicine, Director of Cardiac Catheterization Laboratories, Director of Interventional Cardiology, Director of Cardiac Catheterization Laboratory Research, Vanderbilt University Medical Center
David XM Zhao, MD, FACC, FSCAI is a member of the following medical societies: American College of Cardiology, American Heart Association, International Society for Heart and Lung Transplantation
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Karlheinz Peter, MD, PhD Professor of Medicine, Monash University; Head of Centre of Thrombosis and Myocardial Infarction, Head of Division of Atherothrombosis and Vascular Biology, Associate Director, Baker Heart Research Institute; Interventional Cardiologist, The Alfred Hospital, Australia
Karlheinz Peter, MD, PhD is a member of the following medical societies: American Heart Association, German Cardiac Society, Cardiac Society of Australia and New Zealand
Disclosure: Nothing to disclose.
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