Mitral regurgitation

Mitral regurgitation - failure of the mitral valve, leading to the emergence of flow from the left ventricle (LV) into the left atrium during systole. Symptoms of mitral regurgitation are palpitations, shortness of breath and holosistolic noise at the apex of the heart. The diagnosis of mitral regurgitation is established by physical examination and echocardiography. Patients with moderate, asymptomatic mitral regurgitation should be monitored, but progressive or symptomatic mitral regurgitation is an indication for the restoration or replacement of the mitral valve.

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Causes of the mitral regurgitation

Common causes include mitral valve prolapse, ischemic dysfunction of the papillary muscles, rheumatic fever and expansion of the mitral valve ring, secondary to systolic dysfunction and expansion of the left ventricle.

Mitral regurgitation may be acute or chronic. Causes of acute mitral regurgitation include ischemic dysfunction of papillary muscles or their rupture; infective endocarditis, acute rheumatic fever; spontaneous, traumatic or ischemic ruptures or tears of the cusps of the mitral valve or subvalvular apparatus; acute expansion of the left ventricle due to myocarditis or ischemia and mechanical failure of the prosthetic mitral valve.

Common causes of chronic mitral regurgitation are identical to the causes of acute mitral regurgitation, and also include mitral valve prolapse (MVP), extension of the mitral valve ring and non-ischemic papillary muscle dysfunction (for example, due to left ventricular dilatation). Rare causes of chronic mitral regurgitation include atrial myxoma, a congenital endocardial defect with splitting of the anterior valve leaflet, SLE, acromegaly, and calcification of the mitral ring (mainly in elderly women).

In newborns, the most likely causes of mitral regurgitation are papillary muscle dysfunction, endocardial fibroelastosis, acute myocarditis, split mitral valve with an endocardial base defect (or without it) and myxomatous degeneration of the mitral valve. Mitral regurgitation can be combined with mitral stenosis, if the thick valve leaflets do not close.

Acute mitral regurgitation can cause acute pulmonary edema and insufficiency of both ventricles with cardiogenic shock, respiratory arrest or sudden cardiac death. Complications of chronic mitral regurgitation include the gradual expansion of the left atrium (LP); dilatation and left ventricular hypertrophy, which initially compensates for the flow of regurgitation (keeping the stroke volume), but ultimately decompensation occurs (decrease in stroke volume); atrial fibrillation (AI) with thromboembolism and infective endocarditis.

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Symptoms of the mitral regurgitation

Acute mitral regurgitation causes the same symptoms as acute heart failure and cardiogenic shock. Most patients with chronic mitral regurgitation do not have symptoms at first, and clinical manifestations appear gradually, as the left atrium increases, pulmonary pressure increases and left ventricular remodeling occurs. Symptoms include shortness of breath, fatigue (due to heart failure) and palpitations (often due to atrial fibrillation). Sometimes patients develop endocarditis (fever, loss in body weight, embolism).

Symptoms appear when mitral regurgitation becomes moderate or severe. On examination and palpation, an intense pulsation in the projection area of the apex of the heart and pronounced movements of the left parasternal area can be detected due to an enlarged left atrium. Contractions of the left ventricle, which are strengthened, enlarged and shifted down and to the left, indicate hypertrophy and dilatation of the left ventricle. A diffuse precardial rise in the tissues of the chest occurs in severe mitral regurgitation due to an increase in the left atrium, which causes a displacement of the heart anteriorly. Noise of regurgitation (or tremor) can be felt in severe cases.

During auscultation I heart tone (S1) may be weakened or absent if the valve leaflets are rigid (for example, with combined mitral stenosis and mitral regurgitation against the background of rheumatic heart disease), but usually it is, if the valves are soft. Heart tone II (S2) can be split if severe pulmonary arterial hypertension has not developed. The III heart tone (S3), whose volume at the apex is proportional to the degree of mitral regurgitation, reflects a pronounced dilatation of the left ventricle. An IV heart tone (S4) is characteristic of a recent chord rupture, when the left ventricle did not have enough time for dilatation.

The main sign of mitral regurgitation is the holosystolic (pansystolic) noise, which is best heard at the apex of the heart through a stethoscope with a diaphragm, when the patient lies on the left side. With moderate mitral regurgitation, systolic murmur has a high frequency or blowing character, but as the flow increases, it becomes low or medium frequency. Noise begins with S1 under conditions that cause flaws during the entire systole (for example, destruction), but often begins after S (for example, when the expansion of the chamber to systole distorts the valve apparatus, and also when myocardial ischemia or fibrosis changes the dynamics). If noise begins after S2, it always continues to S3. Noise is carried forward to the left armpit; intensity can remain the same or change. If the intensity changes, the noise tends to increase in volume towards S2. The noise of mitral regurgitation increases with a handshake or squat, because peripheral vascular resistance increases, increasing the regurgitation in the left atrium. The intensity of the noise decreases when the patient is standing or during the Valsalva maneuver. A short indefinite average diastolic murmur arising from abundant mitral diastolic flow may immediately follow S2 or appear to be its continuation.

The noise of mitral regurgitation can be confused with tricuspid regurgitation, but at the last one the noise increases during inhalation.

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Complications and consequences

Complications include progressive heart failure, arrhythmias and endocarditis.

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Diagnostics of the mitral regurgitation

A preliminary diagnosis is made clinically and confirmed by echocardiography. Doppler echocardiography is used to detect the flow of regurgitation and assess its severity. Two-dimensional echocardiography is used to identify the causes of mitral regurgitation and the detection of pulmonary arterial hypertension.

If endocarditis or valve thrombus is suspected, transesophageal echocardiography (TEE) can provide more detailed visualization of the mitral valve and the left atrium. Also, TEE is prescribed in cases where the mitral valve plasty is planned instead of replacing it, since the study confirms the absence of severe fibrosis and calcification.

Initially, ECG and chest radiography are usually performed. An ECG can reveal dilation of the left atrium and left ventricular hypertrophy with or without ischemia. A sinus rhythm is usually present if mitral regurgitation is acute, since there was no time for atrial stretching and remodeling.

Chest X-ray in acute mitral regurgitation may demonstrate pulmonary edema. Changes in the shadow of the heart is not detected if there is no concomitant chronic pathology. Chest X-ray in chronic mitral regurgitation may show enlargement of the left atrium and left ventricle. Vascular congestion and pulmonary edema are also possible with heart failure. Vascular congestion in the lungs is limited to the right upper lobe of approximately 10% of patients. Probably, this option is associated with the expansion of the right upper lobe and central pulmonary veins due to selective regurgitation into these veins.

Before surgery, cardiac catheterization is performed, mainly to detect coronary artery disease. A pronounced atrial systolic wave is detected when determining the pressure of the pulmonary artery occlusion (wedge pressure in the pulmonary capillaries) during ventricular systole. Ventriculography can be used to quantify mitral regurgitation.

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Treatment of the mitral regurgitation

Acute mitral regurgitation is an indication for emergency mitral valve repair or replacement. Patients with ischemic papillary muscle tearing may also require coronary revascularization. Before performing a surgical procedure, sodium nitroprusside or nitroglycerin can be administered to reduce the afterload, thus improving stroke volume and reducing ventricular volume and severity of regurgitation.

Radical treatment of chronic mitral regurgitation is plastic or prosthetic mitral valve, but in patients with asymptomatic or moderate chronic mitral regurgitation and the absence of pulmonary arterial hypertension or MA can be limited to periodic monitoring.

At present, the ideal time for surgery is not determined, but performing an operation before ventricular decompensation develops (final diastolic diameter determined during echocardiography> 7 cm, final systolic diameter> 4.5 cm, ejection fraction <60%) improves the results and reduces the likelihood deterioration of the functions of the left ventricle. After the development of decompensation, the functioning of the ventricle depends on a decrease in the afterload with mitral regurgitation, and in approximately 50% of patients with decompensation, valve replacement leads to a noticeable decrease in the ejection fraction. In patients with moderate mitral regurgitation and significantly severe coronary artery disease, perioperative mortality is 1.5% with isolated aorto-coronary bypass and 25% with simultaneous valve replacement. If there is a technical possibility, it is preferable to plastic the valve instead of prosthetics; perioperative mortality is 2–4% (compared to 5–10% for prosthetics), and the long-term prognosis is quite good (80–94% survival for 5–10 years compared to 40–60% for prosthetics).

Antibiotic prophylaxis is indicated before procedures that can cause bacteremia. In case of rheumatic mitral regurgitation, which is moderately severe, penicillin preparations are recommended continuously until reaching approximately 30 years of age for the prevention of recurrent acute rheumatic fever. In most Western countries, rheumatism is extremely rare after 30 years, which limits the duration of the necessary prevention. Since long-term antibiotic therapy can lead to the development of the resistance of microorganisms that can cause endocarditis, patients who are constantly receiving penicillin drugs can additionally be given other antibiotics to prevent endocarditis.

To prevent thromboembolism, anticoagulants are used in patients with heart failure or MA. Although severe mitral regurgitation tends to separate atrial thrombi and thus to some extent prevent thrombosis, most cardiologists recommend the use of anticoagulants.

Forecast

The prognosis depends on the functions of the left ventricle, the severity and duration of mitral regurgitation, and the severity and cause of mitral regurgitation. As soon as mitral regurgitation becomes pronounced, every year after that approximately 10% of patients develop clinical manifestations of mitral regurgitation. Approximately 10% of patients with chronic mitral regurgitation caused by mitral valve prolapse require surgical intervention.

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