Secondary causes of MR include damage to the left ventricular myocardium through ischemia, infarction, or cardiomyopathy. Dilated cardiomyopathy can cause the mitral annulus to dilate, and hypertrophic cardiomyopathy can cause deformation of the mitral leaflets, chordae slack or displacement of the mitral apparatus. Other secondary causes of MR include collagen vascular diseases, trauma, carcinoid, and exposure to certain appetite suppressant drugs.
Clinical Phases
Symptoms of chronic MR include decreased exercise tolerance with dyspnea on exertion, orthopnea, palpitations, and tachycardia. These symptoms correlate with clinical phases of chronic mitral regurgitation. The clinical phases include the:
- Compensation Phase
- Transitional Phase
- Decompensation Phase
During the Compensation Phase, there is a gradual development of volume overload in the left atrium and left ventricle (LV) without diminished LV function. The myocardium compensates for the increased burden caused by MR and the individual can be asymptomatic for years or decades. Symptoms may not manifest until the Transitional Phase when the heart can no longer keep pace with the persistent and increasing volume overload. Symptoms progress during the Decompensation Phase as LV function is decreasing. Eventually symptoms of congestive heart failure appear.
Acute Mitral Regurgitation
Acute MR will rarely be part of an underwriting assessment. It is secondary to an extraordinarily sudden event, such as trauma or myocardial infarction, resulting in significant myocardial damage. Some portion of the valve structure gets damaged, deformed, distorted, or even severed, causing sudden dysfunction of the valve. Symptoms will be severe with abrupt onset. Other causes for acute MR include papillary muscle or chordae tendineae rupture leading to cardiogenic shock. Without immediate medical intervention, death could result.
Diagnosis
Auscultation with a stethoscope will reveal MR as a high-pitched holosystolic murmur at the apex radiating to the back or clavicular area. Loudness of the murmur does not correlate well with the severity of regurgitation. Also, a third heart sound is commonly heard. MVP with MR will be heard as a mid-systolic click with a late systolic murmur, heard best at the apex. It is characteristic for this murmur to be accentuated by standing or Valsalva maneuver and diminished with squatting.
Echocardiography is the preferred method for diagnosing, monitoring and quantifying MR. Echocardiography, in 2‑D and M‑Mode, reveals the anatomic basis for MR, such as mitral annular calcification or degenerative mitral leaflets. Findings of left atrial enlargement (LAE), left ventricular dilation, and left ventricular hyperkinesia, and evidence of pulmonary hypertension, help to determine the appropriate disease phase.
Additionally, more specific parameters that may be found on echocardiography reports include measurements for Color Flow Doppler regurgitant jet, Regurgitant Fraction (RF) and Effective Regurgitant Orifice area (ERO). These measurements can help to assess the degree of MR more accurately.
- Color Flow Doppler regurgitant jet measurements assess the area of regurgitant jet relative to size of the left atrium.
- Regurgitant Fraction (RF) measures the percentage of left ventricular stroke volume that regurgitates into the left atrium.
- Effective Regurgitant Orifice area (ERO) measures the area of regurgitant flow at the level of the mitral valve.
(See the table below showing how these measurements can be used to assess severity and clinical phases of MR.)
Cardiac catheterization is invasive but allows for more accurate assessment of MR, left ventricular function and pulmonary artery pressure.
Treatment
Patients with asymptomatic MR with normal heart and valve anatomy do not require treatment. Preventive antibiotic treatment for infective endocarditis before dental or surgical procedures was a common protocol in the past. These guidelines were updated in 2006. People with MR, who have not undergone heart valve surgery, no longer require preventative antibiotic treatment.
Mild to moderate MR in the elderly, caused by annular calcification, does not require surgical intervention. Symptomatic moderate-to-severe MR is treated with vasodilators, such as ACE inhibitors, over the short-term. These drugs act to reduce left ventricular volumes and improve symptoms.
Symptomatic moderate-to-severe MR with heart enlargement will require surgery to repair or replace the mitral valve. A bioprosthetic valve or mechanical valve may be used. A mechanical valve replacement will require long-term anticoagulation therapy.
Complications
Over time, chronic MR will cause changes to the heart muscle (myocardial remodeling) and the vascular system. Initially the heart can compensate for the gradual development of volume overload caused by MR. Left atrial enlargement is the first response to significant MR volume increase. Elevated ejection fraction (EF) occurs as an adaptive response to maintain adequate cardiac output, compensating for the volume loss by regurgitant flow into the left atrium. There usually are no symptoms during this Compensation Phase. These adaptive changes provide for normal left ventricular function with normal heart rhythm. Any remodeling changes at this stage are reversible.
Myocardial remodeling progresses during the Transitional Phase. As volume overload persists, dilation of the left ventricle will be seen in addition to the previous findings of LAE. EF decreases in the Transitional Phase. Since the EF is declining from the elevated EF found during the Compensation Phase, it may appear to be normal during the early Transitional Phase. Don’t be fooled! As LV function diminishes, the EF will drop further and become unmistakably low and abnormal. Symptoms likely to develop during this phase include decreased ability to exercise or be active, shortness of breath and palpitations. Also, as the left atrium enlarges, atrial fibrillation may develop. Not all people will experience symptoms. In the transitional phase, remodeling becomes irreversible. Surgical treatment may be considered at this point.
As mitral valve regurgitation worsens, myocardial remodeling increases, and proper LV function becomes severely inhibited. The heart muscle begins to fail. This is known as the Decompensation Phase or end-stage MR. During this phase, the left ventricle can no longer compensate for the regurgitation and its cascade of alterations. The EF declines to lower and lower levels during this phase. Both the left atrium and left ventricle become pathologically enlarged and heart function becomes inefficient. Abnormal heart rhythms can occur. Pulmonary hypertension develops due to flow reversal from the left atrium into the pulmonary veins. Over time all these irreversible changes lead to congestive heart failure (CHF).
Underwriting Mitral Regurgitation
Underwriting chronic mitral regurgitation requires the use of clinical criteria and measurable data to assess the severity of the valve disorder. Clinical criteria may include heart murmur and mid-systolic click heard on auscultation, chest pain, palpitations, arrhythmia, or an ECG with notched P‑waves (consistent with any atrial enlargement). Heart murmur intensity heard on auscultation correlates poorly with the severity of MR.
Measurable data concerning the severity of MR is obtained from echocardiography, cardiac MRI, and cardiac catheterization. The Echocardiogram with Doppler measurements is the most prevalent source of measurable data for MR and shows the anatomic basis for the disease. Measurable data includes left atrial and left ventricle dimensions, degree of regurgitation, left ventricular EF, Regurgitant Fraction (RF), Color Flow Doppler Regurgitant Jet, and Effective Regurgitant Orifice area (ERO).