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Mitral Regurgitation> >
Mitral regurgitation (MR) is incompetency of the mitral valve causing flow from the left ventricle (LV) into the left atrium during ventricular systole. MR can be primary (common causes are mitral valve prolapse and rheumatic fever) or secondary to LV dilation or infarction. Complications include progressive heart failure, arrhythmias, and endocarditis. Symptoms and signs include palpitations, dyspnea, and a holosystolic apical murmur. Diagnosis is by physical examination and echocardiography. Prognosis depends on LV function and etiology, severity, and duration of MR. Patients with mild, asymptomatic MR may be monitored, but progressive or symptomatic MR requires mitral valve repair or replacement.
MR may be acute or chronic.
Causes of acute MR include
Common causes of chronic MR are intrinsic valve pathology (primary MR) or distortion of a normal valve by dilatation and impairment of the left ventricle (secondary MR).
Primary MR pathology is most often mitral valve prolapse (see Mitral Valve Prolapse (MVP)) or rheumatic heart disease. Less common causes are connective tissue disorders, congenital cleft mitral valve, and radiation heart disease.
In secondary MR, ventricular impairment and dilation displace the papillary muscles, which tether the otherwise normal leaflets and prevent them from closing fully. The causes are MI (ischemic chronic secondary MR) or intrinsic myocardial disease (nonischemic chronic secondary MR).
In infants, the most likely causes of MR are papillary muscle dysfunction, endocardial fibroelastosis, acute myocarditis, cleft mitral valve with or without an endocardial cushion defect, and myxomatous degeneration of the mitral valve. MR may coexist with mitral stenosis when thickened valvular leaflets do not close.
Acute MR may cause acute pulmonary edema and cardiogenic shock or sudden cardiac death.
Complications of chronic MR include gradual enlargement of the left atrium (LA); LV enlargement and eccentric hypertrophy, which initially compensates for regurgitant flow (preserving forward stroke volume) but eventually decompensates (reducing forward stroke volume); atrial fibrillation (AF), which may be further complicated by thromboembolism; and infective endocarditis.
Acute MR causes the same symptoms and signs as acute heart failure and cardiogenic shock. Specific signs of mitral regurgitation may be absent (see Hypotension and cardiogenic shock). Most patients with chronic MR are initially asymptomatic and develop symptoms insidiously as the LA enlarges, pulmonary artery and venous pressure increases, and LV compensation fails. Symptoms include dyspnea, fatigue (due to heart failure), orthopnea, and palpitations (often due to AF). Rarely, patients present with endocarditis (eg, fever, weight loss, embolic phenomena).
Signs develop only when MR becomes moderate to severe. Inspection and palpation may detect a brisk apical impulse and sustained left parasternal movement due to systolic expansion of an enlarged LA. An LV impulse that is sustained, enlarged, and displaced downward and to the left suggests LV hypertrophy and dilation. A diffuse precordial lift occurs with severe MR because the LA enlarges, causing anterior cardiac displacement, and pulmonary hypertension causes right ventricular hypertrophy. A regurgitant murmur (or thrill) may also be palpable in severe cases.
On auscultation, the 1st heart sound (S 1 ) may be soft (or occasionally loud). A 3rd heart sound (S 3 ) at the apex reflects a dilated LV and important MR.
An S 3 that accompanies mitral regurgitation suggests a dilated left ventricle and progression to heart failure.
The cardinal sign of MR is a holosystolic (pansystolic) murmur, heard best at the apex with the diaphragm of the stethoscope when the patient is in the left lateral decubitus position. In mild MR, the systolic murmur may be abbreviated or occur late in systole. The murmur begins with S 1 in conditions causing leaflet incompetency throughout systole, but it often begins after S 1 (eg, when chamber dilation during systole distorts the valve apparatus or when myocardial ischemia or fibrosis alters dynamics). When the murmur begins after S 1 , it always continues to the 2nd heart sound (S 2 ). The murmur radiates toward the left axilla; intensity may remain the same or vary. If intensity varies, the murmur tends to crescendo in volume up to S 2 . MR murmurs increase in intensity with handgrip or squatting because peripheral vascular resistance to ventricular ejection increases, augmenting regurgitation into the LA; murmurs decrease in intensity with standing or the Valsalva maneuver. A short rumbling mid-diastolic inflow murmur due to torrential mitral diastolic flow may be heard following an S 3 . In patients with posterior leaflet prolapse, the murmur may be coarse and radiate to the upper sternum, mimicking aortic stenosis.
This holosystolic mitral regurgitation murmur maintains the same intensity throughout systole and extends from S 1 to S 2 .
MR murmurs may be confused with tricuspid regurgitation, which can be distinguished because tricuspid regurgitation murmur is augmented during inspiration.
Diagnosis is suspected clinically and confirmed by echocardiography. Doppler echocardiography is used to detect regurgitant flow and pulmonary hypertension. Two-dimensional or 3-dimensional echocardiography is used to determine the cause and severity of MR (see Table: Grading of Mitral Regurgitation), the presence and extent of annular calcification, and the size and function of the LV and LA and to detect pulmonary hypertension.
When it is acute, severe MR may not be apparent on color Doppler echocardiography, but suspicion is raised when acute heart failure is accompanied by hyperdynamic LV systolic function.
Grading of Mitral Regurgitation
If endocarditis or valvular thrombi are suspected, transesophageal echocardiography (TEE) can provide a more detailed view of the mitral valve and LA. TEE is also indicated when mitral valve repair instead of replacement is being considered to evaluate the mechanism of MR in more detail.
An ECG and chest x-ray are usually obtained initially. ECG may show LA enlargement and LV hypertrophy with or without ischemia. Sinus rhythm is usually present when MR is acute because the atria have not had time to stretch and remodel.
Chest x-ray in acute MR may show pulmonary edema; abnormalities in cardiac silhouette are not evident unless an underlying chronic disorder is also present. Chest x-ray in chronic MR may show LA and LV enlargement. It may also show pulmonary vascular congestion and pulmonary edema with heart failure.
Cardiac catheterization is done before surgery, mainly to determine whether coronary artery disease (CAD) is present. A prominent systolic c-v wave is seen on pulmonary artery occlusion pressure (pulmonary capillary wedge pressure) tracings during ventricular systole. Ventriculography can be used to quantify MR. Cardiac MRI can accurately measure regurgitant fraction and determine the cause of dilated myopathy with MR.
Periodic exercise testing (stress ECG ) is often done to detect any decrease in effort tolerance, which would prompt consideration of surgical intervention. Periodic echocardiography is done to detect progression of MR.
ACE inhibitors and other vasodilators do not delay LV dilation or MR progression and so have no role in asymptomatic MR with preserved LV function. However, if LV dilation or dysfunction is present, vasodilators, spironolactone, and vasodilating β-blockers (eg, carvedilol) are indicated. If the ECG shows left bundle branch block, then biventricular pacing may be beneficial for secondary MR. Loop diuretics such as furosemide are helpful in patients with exertional or nocturnal dyspnea. Digoxin may reduce symptoms in patients with AF or those in whom valve surgery is not appropriate.
Antibiotic prophylaxis is no longer recommended except for patients who have had valve replacement (see Table: Recommended Endocarditis Prophylaxis During Oral-Dental or Respiratory Tract Procedures*).
Anticoagulants are used to prevent thromboemboli (see Pulmonary Embolism (PE) : Prevention of Pulmonary Embolism) in patients with AF.
Acute MR requires emergency mitral valve repair or replacement with concomitant coronary revascularization as necessary. Pending surgery, nitroprusside or nitroglycerin infusion and an intra-aortic ballon pump may be used to reduce afterload, thus improving forward stroke volume and reducing ventricular and regurgitant volume.
Chronic primary MR that is severe needs intervention at the onset of symptoms or LV decompensation (LV EF < 60% or LV end-systolic diameter > 40 mm). Even in the absence of these triggers, intervention may be beneficial when valve morphology suggests a high likelihood of successful repair, particularly if there is new onset AF or resting pulmonary systolic pressure is > 50 mm Hg. When the EF falls < 30%, surgical risk is high, necessitating a careful weighing of risk and benefit.
Chronic secondary MR has much fewer indications for intervention. Because the primary pathology involves the LV muscle, correction of the MR is not as likely to be beneficial. Additionally, there is no durable way to repair secondary MR and valve replacement may further worsen LV function. Unlike primary MR, a recent randomized trial found no benefit of repair over replacement.
For patients undergoing cardiac surgery for other indications, concomitant mitral valve surgery should be considered for a repairable valve with MR that is moderate or severe. If the valve is not repairable, then replacement is usually done only when the MR is severe.
The closer the mitral valve intervention mimics the native valve, the better for LV preservation and mortality. Hence, repair is preferred over replacement with chordal preservation, which is preferred over replacement with removal of chordae. Mechanical prostheses are preferred because tissue valves have reduced longevity in the mitral position. Repair of secondary MR with an annuloplasty ring often provides only temporary relief of MR but is usually done at the time of coronary artery bypass grafting if the MR is moderate or greater. New percutaneous procedures that tailor the mitral leaflets are being studied in both primary and secondary MR. In some patients, these new procedures reduce regurgitation enough to improve symptoms and reduce hospitalizations. Percutaneous procedures to place artificial valves are being developed.
In about 50% of decompensated patients, prosthetic valve implantation markedly depresses ejection fraction because in such patients, ventricular function has become dependent on the afterload reduction of MR.
Selected patients with AF may benefit from concomitant ablation therapy, although this therapy increases operative morbidity.
Common causes include mitral valve prolapse, rheumatic fever, and LV dilation or infarction.
Acute MR may cause acute pulmonary edema and cardiogenic shock or sudden cardiac death.
Chronic MR causes slowly progressive symptoms of heart failure and, if AF develops, palpitations.
Typical heart sounds are a holosystolic murmur that is heard best at the apex, radiates toward the left axilla, increases in intensity with handgrip or squatting, and decreases in intensity with standing or the Valsalva maneuver.
Symptomatic patients and those meeting certain echocardiographic criteria benefit from valve replacement or repair.
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