Mitral valve prolapse: causes, symptoms, diagnosis, treatment
Last reviewed: 23.04.2024
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The prolapse of the mitral valve is the deflection of the mitral valve flaps into the left atrium during systole. The most common cause is idiopathic myxomatous degeneration. Mitral valve prolapse is usually benign, but complications include mitral regurgitation, endocarditis, valve rupture, and possible thromboembolism.
Mitral valve prolapse usually proceeds asymptomatically, although some patients experience chest pain, dyspnea, and sympathicotonia (for example, palpitations, dizziness, presyncopal conditions, migraines, anxiety). Symptoms include a clear click in the middle of the systole, followed by a subsequent systolic murmur in the presence of regurgitation. Diagnosis is established by objective examination and echocardiography. The forecast is favorable. No specific treatment is required if there is no mitral regurgitation, although beta-adrenoblockers may be effective in patients with sympathicotonia symptoms.
The prolapse of the mitral valve is a frequent condition. Prevalence is 1-5% among healthy people. Women and men suffer equally often. The prolapse of the mitral valve usually develops after a youthful surge in growth.
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What causes mitral valve prolapse?
The prolapse of the mitral valve is most often caused by myxomatous degeneration of the mitral valve and tendon chords. Degeneration is usually idiopathic, although it can be inherited by an autosomal dominant type or (sometimes) by a recessive X-related type. Mikksomatous degeneration can also develop with connective tissue dysplasia (for example, Marfan or Ehlers-Danlo syndrome, adult kidney polycystosis, imperfect osteogenesis, elastic pseudocanthoma, SLE, nodular polyarteritis) and muscular dystrophy. Mitral valve prolapse is often detected in patients with Graves' disease (diffuse toxic goiter), hypomastia, von Willebrand syndrome, sickle cell anemia and rheumatic heart disease. Mikksomatous degeneration can also affect the aortic or tricuspid valve, leading to its prolapse; tricuspid regurgitation is rare.
The normal (that is, the non-myxomatous) valves of the mitral valve can prolapse if there is dysfunction of the papillary muscles or the mitral ring is dilated (eg, with dilated cardiomyopathy) or narrowed (eg, in hypertrophic cardiomyopathy or atrial septal defect). Transient prolapse of the mitral valve can occur with a marked decrease in the volume of circulating blood, for example, during severe dehydration or during pregnancy (when the woman lies, and the pregnant uterus squeezes the lower vena cava, reducing venous return).
Mitral regurgitation (MP) is the most common complication of mitral valve prolapse. Mitral regurgitation can be acute (due to rupture of tendon chords or dilated mitral valve flaps) or chronic. Complications of chronic mitral regurgitation include heart failure and atrial fibrillation (atrial fibrillation) with thromboembolism. It is unclear whether mitral valve prolapse leads to stroke regardless of mitral regurgitation or atrial fibrillation. In addition, mitral regurgitation increases the risk of infectious endocarditis, as well as thickened enlarged mitral valve flaps.
Symptoms of mitral valve prolapse
Most of the prolapse of the mitral valve is asymptomatic. Occasional indeterminate symptoms (for example, chest pain, shortness of breath, palpitations, dizziness, fainting, migraine, anxiety) are considered associated with poorly differentiated disorders in adrenergic impulse transmission and sensitivity, and not with the pathology of the mitral valve. In about a third of patients, emotional stress provokes heartbeats, which may be signs of benign arrhythmias (atrial extrasystoles, paroxysmal atrial tachycardia, ventricular extrasystoles, complicated ventricular ectopy).
In some patients, mitral regurgitation is detected, and endocarditis (fever, weight loss, thromboembolic complications) or stroke is less likely to be diagnosed. Sudden death occurs in less than 1% of cases, most often due to rupture of tendon chords and movable mitral valve flaps. Death due to fatal arrhythmia is rare.
As a rule, the prolapse of the mitral valve does not cause any visible cardiac symptoms. Isolated prolapse of the mitral valve results in an obvious click in the middle of the systole, which is heard best through the stethoscope with the diaphragm to the left of the apex, when the patient lies on the left side. When mitral valve prolapse with mitral regurgitation, a click is accompanied by a late systolic murmur of mitral regurgitation. The click becomes audible or moves closer to the I cardiac tone (S) and becomes louder for samples that decrease the size of the left ventricle (LV) (for example, squatting, rising, Valsalva test). The same samples lead to the appearance or strengthening and lengthening of the noise of mitral regurgitation. This is due to the fact that a decrease in the size of the left ventricle leads to the closing of papillary muscles and tendon chords closer to the center below the valve, which causes a more rapid pronounced prolapse with earlier significant regurgitation. Conversely, squatting and an isometric handshake lead to a decrease in the click of S and shorten the noise of mitral regurgitation. Systolic clicking can be confused with a click at congenital aortic stenosis; The difference between the latter is the appearance in a very early systole and the absence of changes in the change of the position of the body or changes in the volume of the left ventricle. Other findings include systolic jitter, presumably caused by vibration of valve flaps; these symptoms are usually transient and can change in different respiratory phases. The tone of the early diastolic opening, caused by the return of the prolapse valve to its normal position, is rarely heard.
Other physical findings associated with mitral valve prolapse, but not having diagnostic value, include hypomastia, dented chest, direct back syndrome and small anteroposterior diameter of the breast.
Diagnosis of mitral valve prolapse
The presumptive diagnosis is put clinically and is confirmed by two-dimensional echocardiography. A 3 mm or 3 mm lateral systolic displacement> 2 mm allows diagnosis in 95% of patients with mitral valve prolapse; this figure is slightly higher if echocardiography is performed when the patient is standing. It is believed that the thickened large valves of the mitral valve and a displacement of 5 mm indicate a more pronounced myxomatous degeneration and a greater risk of endocarditis and mitral regurgitation.
Holter monitoring and ECG in 12 leads can be useful for identifying and documenting arrhythmias in patients with palpitations.
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Prognosis and treatment of mitral valve prolapse
Mitral valve prolapse is usually benign, but severe myxomatous degeneration of the valve can lead to mitral regurgitation. In patients with severe mitral regurgitation, the incidence of left ventricular and left atrial enlargement, arrhythmias (eg, atrial fibrillation), infective endocarditis, stroke, the need for valve replacement and death is approximately 2-4% per year.
Mitral valve prolapse usually does not require treatment. You can prescribe b-adrenoblockers to reduce sympathicotonia (for example, palpitations, migraine headaches, dizziness) and the risk of dangerous tachycardia, although there is no evidence to support these effects. Typically, appoint atenolol 25-50 mg once a day or propranolol 20-40 mg 2 times a day. Atrial fibrillation may require additional treatment.
Treatment of mitral regurgitation depends on the severity and associated changes in the atrium and LV.
Prophylaxis of endocarditis with antibiotics is recommended before risky procedures only in the presence of mitral regurgitation or thickened enlarged valves. Anti-coagulants for the prevention of thromboembolism are recommended only for patients with atrial fibrillation, preceded by a transient ischemic attack or stroke.