Causes (Etiology)
The valvular defect develops when any element of the valve apparatus is damaged: leaflets, chordae tendineae, papillary muscles, or the fibrous ring.
- Leaflet involvement: most commonly associated with rheumatic fever (tissues shrink and retract). The frequency of mitral valve prolapse as a cause of isolated regurgitation is increasing.
- Chordal involvement (rupture of tendinous cords): occurs due to rupture in chest trauma or destruction associated with infective endocarditis.
- Papillary muscle dysfunction: typical of coronary artery disease (CAD). In myocardial infarction, there is a high risk of their complete rupture.
- Changes in the fibrous ring and myocardium: left ventricular dilatation (in Marfan syndrome, dilated cardiomyopathy) leads to annular stretching and relative insufficiency. In elderly patients, calcification prevents normal contraction of the ring during systole.
Pathophysiology and hemodynamic changes
Normally, during left ventricular (LV) systole, all blood is ejected into the aorta. In valvular insufficiency, a portion of the blood rushes back into the left atrium (LA).
- Left atrial overload. The LA receives a double volume of blood: the normal inflow from the pulmonary veins is added to the regurgitant volume from the LV. This leads to marked atrial dilatation.
- Left ventricular overload. During diastole, this entire increased volume returns to the LV. To compensate for the volume overload and maintain adequate output into the aorta, tonogenic followed by myogenic dilatation develops, resulting in eccentric hypertrophy of the LV.
- Decompensation stage. When LV contractility weakens, pressure in the left atrium rises. This pressure is retrogradely transmitted to the pulmonary venous system, causing pulmonary hypertension and eventual right heart overload (a mechanism similar to mitral stenosis). In severe cases, the regurgitant volume may exceed the effective stroke volume, critically reducing cardiac output.
Clinical Presentation and Physical Status
Symptoms directly depend on the volume of reverse blood flow and the nature of the underlying disease.
- Complaints: mild regurgitation may be asymptomatic. With severe regurgitation (greater than 25% of stroke volume), pulmonary congestion develops. Patients complain of exertional dyspnea, palpitations, and a tendency toward orthopnoea (forced sitting position). With severe congestion, moist rales appear in the lungs, and occasionally attacks of cardiac asthma occur.
- General examination: appearance remains unremarkable for a long time. In late stages, cyanosis appears.
- Palpation and percussion: the apex beat is forceful, diffuse, displaced laterally (to the left) and downward. Percussion reveals leftward enlargement of cardiac dullness (signs of LV hypertrophy).
Auscultation (Physical examination)
Auscultation at the cardiac apex is the primary method for detecting clinical signs of the defect.
- Systolic murmur: in rheumatic heart disease, it is blowing, high-frequency, occupying the entire systole (pansystolic). It begins immediately after the first heart sound and lasts until the second heart sound. Typical radiation is to the axilla.
- Murmur of chordal rupture: becomes harsh, transmitted from the apex toward the sternum. Palpation may reveal a systolic thrill («cat's purr»).
- Changes in heart sounds: The first sound at the apex is diminished or absent (due to the absence of the closed-valve period and LV overfilling, the valvular and muscular components decrease). The second sound over the pulmonary artery is accentuated and split, indicating the development of pulmonary hypertension.
Instrumental diagnostics and treatment tactics
Diagnostic workup:
- Echocardiography: the gold standard. It reveals dilatation of the LA and LV cavities and hypertrophy of the LV walls. Color Doppler mapping visualizes the regurgitant jet and quantifies the orifice area and returning blood volume. Direct signs of leaflet defects are not always visible.
- ECG: signs of left atrial hypertrophy (P-mitrale), left ventricular hypertrophy, and in late stages, biventricular hypertrophy. Atrial fibrillation is frequently registered.
- Chest X-ray: dilatation of the LA and its appendage forms the "third" or "fourth" arch along the left cardiac contour. Cardiomegaly is characteristic of advanced stages.
- Angiocardiography (invasive): contrast administration via a catheter into the LV cavity for the most accurate quantitative assessment of regurgitation. Performed prior to surgery.
Treatment tactics: Medical therapy aims to treat the underlying cause and correct complications (heart failure, rhythm disorders). Surgical treatment (valvuloplasty with preservation of the native valve, or replacement) is indicated depending on the degree of regurgitation and clinical severity.
Briefly: answers to topical questions
What types of surgical treatment are used for mitral regurgitation?
For mitral regurgitation, valve repair and mitral valve replacement are used. Indications for surgery are determined by the degree of regurgitation and clinical presentation.
- Valvuloplasty — valve repair with preservation of the native valve. In severe primary mitral regurgitation with symptoms of chronic heart failure, mitral valve repair under cardiopulmonary bypass with reconstruction of subvalvular structures is preferred.
- Transcatheter mitral valve repair — used in severe primary mitral regurgitation with symptoms of chronic heart failure when surgery is contraindicated or the surgical risk is high.
- Mitral valve replacement — implantation of an artificial prosthesis.
Radiation of the murmur: in classical rheumatic regurgitation, the murmur "radiates" to the axilla, whereas in traumatic chordal rupture, it "projects" toward the sternum.
Class and exam questions
Why does the first heart sound weaken in mitral regurgitation?
Due to incomplete leaflet closure, the period of closed valves disappears, and the left ventricle is overfilled with blood. This leads to a sharp decrease in the valvular and muscular components of the first heart sound.
What happens in acute mitral regurgitation?
The acute form most frequently occurs in myocardial infarction with chordal rupture. It is characterized by the appearance of a harsh systolic murmur, rapid development of left ventricular failure, and pulmonary edema.
Which complications are most characteristic of this valvular defect?
Rhythm disorders (especially atrial fibrillation) and a high risk of thrombus formation with subsequent systemic and pulmonary thromboembolism.
What else to study on this topic
- Mechanisms of eccentric left ventricular hypertrophy formation
- Differences between tonogenic and myogenic myocardial dilatation
- Pathophysiology of pulmonary hypertension development in left heart disease
- ECG criteria for P-mitrale formation
- Indications for choosing between valvuloplasty and valve replacement
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