It is recommended to take medicine under the guidance of a doctor after a detailed examination. The cause of mitral regurgitation is streptococcal infection. Colds can aggravate the condition. Pay attention to preventing colds and injecting flu vaccines.

Related information:

Name

Chinese name: Mitral regurgitation English name: mitral insufficiency

Disease overview

The mitral valve consists of four components: leaflets, annulus, chordae tendineae and papillary muscles. Structural abnormality or dysfunction in any one of them can lead to mitral insufficiency.

Cause

The main pathophysiological change of mitral regurgitation is that mitral regurgitation increases the left atrial load and left ventricular diastolic load. When the left ventricle contracts, blood flows from the left ventricle into the aorta and the left atrium, which has less resistance. The regurgitant flow into the left atrium can reach more than 50% of the left ventricular blood output. In addition to receiving blood from the pulmonary veins, the left atrium also receives blood from the left ventricle. Therefore, the increase in left atrial pressure can cause an increase in the pressure of the pulmonary veins and pulmonary capillaries, followed by dilation and congestion. At the same time, the diastolic volume load of the left ventricle increases and the left ventricle enlarges. In chronic patients, through compensation in the early stage, the stroke volume and ejection fraction increase, but the end-diastolic volume and pressure of the left ventricle may not increase, and there may be no clinical symptoms at this time; during decompensation, the stroke volume and ejection fraction decrease, and the left ventricular diastolic volume and pressure may not increase. At the end of the period, the volume and pressure increased significantly, and clinical manifestations of left heart failure such as pulmonary congestion and hypoperfusion of the systemic circulation appeared. Pulmonary hypertension and total heart failure may occur in the late stages.

Rheumatic heart disease

It is the most common cause in my country and is more common in men. Often accompanied by mitral valve stenosis and aortic valve damage.

Mitral valve prolapse

Part of it is one of the manifestations of other inherited connective tissue diseases (such as Marfan syndrome).

Coronary heart disease

Due to chronic ischemia or post-infarction fibrosis of the left ventricular papillary muscles or basal left ventricular myocardium, papillary muscle dysfunction occurs.

Rupture of the chordae tendineae

Most of the causes are unknown (idiopathic), occasionally secondary to mitral valve prolapse, and the posterior lobe chordae tendineae are more common.

Calcification of the mitral valve annulus and lower part of the annulus

is a degenerative change in the elderly.

Infectious endocarditis

The vegetations destroy the edges of the valve leaflets, perforate the valve leaflets, or contract the valve leaflets after inflammation heals.

Significant enlargement of the left ventricle

Caused by valve annulus expansion and lateral displacement of the papillary muscles.

Other rare causes

Congenital malformations, systemic lupus erythematosus, rheumatoid arthritis, hypertrophic obstructive cardiomyopathy, endocardial fibrosis and left atrial myxoma wait.

Pathological changes

Among chronic patients, valve leaflet damage caused by rheumatic fever is the most common, accounting for 1/3 of all patients with mitral regurgitation, and many Seen in men. The pathological changes are mainly inflammation and fibrosis, which cause the valve leaflets to harden, shorten, deform, adhesion and fusion, and chordae tendineae to fuse and shorten. About 50% of patients have mitral valve stenosis. Mitral regurgitation can also be seen in: ① Coronary atherosclerotic heart disease (coronary heart disease): After myocardial infarction and chronic myocardial ischemia, the papillary muscles and adjacent ventricular wall myocardium are involved, causing papillary muscle fibrosis and dysfunction. ②Congenital malformations: mitral valve cleft, most commonly caused by endocardial cushion defect or corrected transposition of the heart; endocardial fibroelastosis; parachute-type mitral valve deformity. ③Mitral annular calcification: It is an idiopathic degenerative disease and is more common in elderly female patients. In addition, patients with hypertension, Marfan syndrome, chronic renal failure and secondary hyperthyroidism are also prone to mitral annular calcification. ④ Left ventricular enlargement: Obvious left ventricular enlargement caused by any cause can dilate the mitral valve annulus and shift the papillary muscles laterally, affecting the closure of the valve leaflets, thus leading to mitral valve insufficiency. ⑤ Mitral valve prolapse syndrome. ⑥ Other rare causes: connective tissue diseases such as systemic lupus erythematosus, rheumatoid arthritis, etc.; hypertrophic obstructive cardiomyopathy; ankylosing sclerosing spondylitis. Acute mitral regurgitation is mostly caused by chordae tendineae rupture, valve damage or rupture, papillary muscle necrosis or rupture, and cracking after artificial valve replacement. It can be seen in infective endocarditis, acute myocardial infarction, perforating or closed mitral valve insufficiency. Thoracic trauma and spontaneous chordae tendineae rupture.

Clinical diagnosis

Clinical diagnosis is mainly based on the typical blowing systolic murmur in the apical area and the enlargement of the left atrium and left ventricle. The diagnosis can be confirmed by echocardiography.

Clinical manifestations

(1) Symptoms Usually, it can last up to 20 years from the first rheumatic carditis to the onset of obvious symptoms of mitral regurgitation; once heart failure occurs , then progress is rapid. People with mild mitral regurgitation may have no obvious symptoms or only mild discomfort. Common symptoms of severe mitral regurgitation include: labor dyspnea, fatigue, orthopnea, etc., and significantly reduced activity tolerance. Hemoptysis and embolism are less common. In advanced right heart failure, liver congestion and swelling, tenderness, ankle edema, pleural effusion or ascites may occur. Acute cases may quickly develop acute left heart failure or pulmonary edema.

(2) Signs 1. During heart auscultation, a systolic blowing murmur will appear in the apex area, with a loudness above level 3/6, mostly propagating to the left axilla, weakening during inhalation, high-pitched when the reflux volume is small, and rough when the valve is thickened. When the damage to the front lobe is predominant, the murmur is conducted to the left axilla or under the left scapula; when the damage to the posterior lobe is predominant, the murmur is conducted to the base of the heart. May be accompanied by systolic tremor. The first heart sound in the apical area is weakened or masked by a murmur. As the ejection period of the left ventricle is shortened, the aortic valve closes prematurely, causing the second heart sound to split. Patients with severe mitral regurgitation may have a low-pitched third heart sound. Hearing the mitral valve opening sound indicates mitral valve stenosis, but it cannot rule out mitral valve insufficiency. In patients with severe mitral regurgitation, a low-key, short mid-diastolic murmur can be heard in the apex area due to relative mitral stenosis caused by the large amount of blood passing through during diastole. In pulmonary hypertension, the second heart sound is elevated in the pulmonary valve area. 2. Other signs: arterial blood pressure is normal but pulse is thin. The heart boundary expanded to the lower left, and the apex area now touched a localized systolic lifting-like pulse, indicating left ventricular hypertrophy and enlargement. In pulmonary hypertension and right heart failure, jugular vein distention, liver enlargement, and lower limb edema may occur.

Differential diagnosis

The murmur of mitral regurgitation should be differentiated from the systolic murmur in the apical region in the following situations: (1) Relative mitral regurgitation can occur in hypertensive patients Heart disease, aortic regurgitation or myocarditis caused by various reasons, dilated cardiomyopathy, anemic heart disease, etc. Because the left ventricle or mitral valve annulus is significantly enlarged, resulting in relative insufficiency of the mitral valve and apical systolic murmur. (2) Functional apical systolic murmur About half of normal children and adolescents can hear a precordial systolic murmur, with a loudness of 1 to 2/6, short, soft in nature, not masking the first heart sound, and no atrium. and ventricular enlargement. It can also be seen in high-dynamic circulation states such as fever, anemia, and hyperthyroidism. The murmur will disappear after the cause is eliminated. (3) Ventricular septal defect: A rough holosystolic murmur can be heard in the 3rd to 4th intercostal space on the left sternal edge, often accompanied by systolic tremor. The murmur is conducted to the apex area, and the apical pulse appears to be lifting. Electrocardiogram and X-ray examination showed enlargement of the left and right ventricles. Echocardiography shows a continuous interruption of the ventricular septum, and contrast-enhanced sonography confirms the presence of a left-to-right shunt at the ventricular level. (4) Tricuspid regurgitation: A localized blowing-like holosystolic murmur can be heard at the lower left sternal border. The murmur can be enhanced during inhalation due to the increase in blood return to the heart, and weakened during expiration. In pulmonary hypertension, the second heart sound of the pulmonary valve is increased and the V wave of the jugular vein is enlarged. There may be liver pulsation and enlargement. Right ventricular hypertrophy can be seen on electrocardiogram and X-ray examination. Echocardiography can confirm the diagnosis. (5) Aortic valve stenosis A loud and rough systolic murmur can be heard in the aortic valve area at the base of the heart or in the apex area, which is conducted to the neck, accompanied by systolic tremor. There may be early systolic click sounds, and the apical pulse appears to be lifting. Electrocardiogram and X-ray examination show left ventricular hypertrophy and enlargement. Echocardiography can confirm the diagnosis.

Treatment

(1) Medical treatment: appropriately avoid excessive physical labor and strenuous exercise, limit sodium intake, and protect heart function; for rheumatic heart disease, actively prevent streptococcal infection and rheumatism Activity and infective endocarditis; appropriate use of diuretics; vasodilators, especially those that reduce afterload, can reduce regurgitant flow and increase cardiac output by reducing left ventricular ejection resistance, thereby producing beneficial hemodynamic effects. Angiotensin-converting enzyme inhibitors can be used in chronic patients. In acute cases, intravenous infusion of sodium nitroprusside, nitroglycerin, or phentolamine can be used. Digitalis drugs should be used in patients with heart failure and are more effective in those with atrial fibrillation. Anticoagulant drugs can be used to prevent thromboembolism in patients with advanced heart failure.

(2) Long-term follow-up studies of surgical treatment show that the improvement of cardiac function in patients with mitral regurgitation after surgical treatment is significantly better than that of medical treatment; even in patients with heart failure or atrial fibrillation, surgical treatment The efficacy is also significantly better than drug treatment. Valve repair has a lower mortality rate, a higher long-term survival rate, and a smaller incidence of thromboembolism than artificial valve replacement. 1. Preoperative preparation Before surgical treatment, left and right heart catheterization and left ventriculography should be performed. These examinations are very helpful in diagnosing mitral regurgitation and clarifying primary cardiomyopathy or functional mitral regurgitation; hemodynamic examinations are helpful in estimating the severity of the disease of the affected valve leaflets; coronary artery Angiography can determine whether the patient needs coronary artery bypass grafting at the same time, because patients with coronary heart disease have high mortality and complications from surgery. 2. Indications for surgery ① Acute mitral regurgitation; ② Heart function grade 3 to 4, after active medical treatment; ③ No obvious clinical symptoms or heart function is grade 2 or below, and auxiliary examination shows progressive heart aggregation Large, left ventricular ejection fraction decreases. If the inner diameter of the left ventricle at the end of systole reaches 50 mm or the inner diameter at the end of diastole reaches 70 mm according to echocardiography, and the ejection fraction is ≤50%, surgical treatment should be performed as soon as possible. About half of the cases of rheumatic mitral regurgitation require valve replacement or valve plastic repair. It is difficult to accurately determine which treatment method can be used before surgery with existing diagnostic methods.

At present, neither artificial mechanical valve nor biological valve has been perfected, the incidence of postoperative complications is high, and the long-term efficacy is not satisfactory, so the clinical symptoms are mild, the heart function is Class I to II, physical examination, chest X-ray film For those who do not show significant left ventricular enlargement through echocardiography and echocardiography, surgical treatment should be postponed and regular follow-up examinations will be conducted to observe the development of the disease. On the other hand, the rate of development of left ventricular function attenuation is difficult to predict. In some cases with function level III or above, the left ventricular myocardium often exhibits permanent interstitial fibrous scar lesions, which not only increases the risk of surgery but also affects long-term treatment. Effect. Highly enlarged left atrium also adversely affects the effectiveness of surgical treatment. Therefore, when the left ventricle begins to show irreversible lesions, even if the clinical symptoms are not severe, it is the best time to perform surgical treatment. In recent years, the development of echocardiography has made it possible to detect the early development of left ventricular dysfunction through series of regular measurements of left ventricular cavity systolic volume and volume, ejection fraction, left ventricular regional systolic abnormalities and other changes, and provide a reference for the selection of surgical timing. . In cases where cardiac function has declined to grade III or IV, although the ejection fraction has dropped to 0.40, surgical treatment can still improve hemodynamics, increase the blood flow from the left ventricle to the aorta, alleviate clinical symptoms and prevent or delay left ventricular bleeding. Function continues to decline. For acute mitral regurgitation caused by iatrogenic or infective endocarditis and chordae tendineae rupture, if the symptoms of pulmonary venous hypertension and endocarditis are controlled by medical treatment, surgical treatment can be postponed and regular follow-up observation can be performed. If medical treatment fails to respond, immediate mitral valve repair surgery is required. Those with severe pulmonary vascular obstructive disease, chronic right heart failure, or those who have failed to respond to medical treatment are not suitable for surgical treatment. 3. Types of surgery ① Valve repair: It can preserve the natural valve to the maximum extent. Suitable for prolapse caused by mitral valve relaxation; excessive length or rupture of chordae tendineae; localized rheumatic mitral valve disease, soft anterior leaflet without shrinkage and no contracture of chordae tendineae although there is fibrosis or calcification; infectious intracardiac Inflammation of mitral valve vegetations or perforation lesions is limited, with no or only slight damage to the anterior leaflet. ② Artificial valve replacement: Replacement valves include mechanical valves and biological valves. Mechanical valves include ball valves, floating disc valves and tilted disc valves. Their advantages are strong wear resistance, but they have a high incidence of thromboembolism and require lifelong anticoagulation treatment. Insufficient anticoagulation may lead to thromboembolism or anticoagulation 10 years after surgery. The mortality and disability rate caused by excessive coagulation and bleeding can be as high as 50%; secondly, the eccentric blood flow of the mechanical valve has greater resistance to blood flow and a higher transvalvular pressure difference. Biological valves include porcine aortic valves, bovine pericardial valves and homologous dural valves. Their advantages are low thromboembolism rate, no need for lifelong anticoagulation and central blood flow similar to natural valves, but not as strong as mechanical valves. Degenerative calcification and damage may occur after 3 to 5 years, and about 50% of the valves will need to be replaced again after 10 years. Young patients and those with a high risk of atrial fibrillation or thromboembolism who require anticoagulation treatment should choose mechanical valves; if the valve annulus is small, artificial valves with better hemodynamic effects should be used; if there is a bleeding tendency or anticoagulant contraindications, a mechanical valve should be used. And young women who plan to become pregnant after valve replacement should use biological valves.

Complications

Complications in chronic patients are similar to those of mitral stenosis but appear later. Infective endocarditis is more common and embolism is less common. When acute and chronic patients undergo chordae tendineae rupture, acute left heart failure or even acute pulmonary edema will occur within a short period of time, and the prognosis is poor. In acute mitral regurgitation, a sudden increase in a large amount of regurgitated blood from the left atrium can cause a sharp increase in pressure in the left atrium and pulmonary veins, causing acute pulmonary edema.

Auxiliary examination

(1) X-ray examination In patients with mild mitral regurgitation, no obvious abnormalities may be found. In severe cases, the left atrium and left ventricle are significantly enlarged, and the significantly enlarged left atrium can push and compress the esophagus. In pulmonary hypertension or right heart failure, the right ventricle becomes enlarged. Pulmonary venous congestion, interstitial pulmonary edema and Kerley B lines can be seen. There is often calcification of the mitral valve leaflets and annulus. Left ventriculography can quantify mitral regurgitation.

(2) Electrocardiogram examination: The electrocardiogram of patients with mild mitral regurgitation may be normal. In severe cases, left ventricular hypertrophy and strain may occur; in pulmonary hypertension, left and right ventricular hypertrophy may occur. People with chronic mitral regurgitation and left atrial enlargement often have atrial fibrillation. In sinus rhythm, the P wave is widened and bimodal, indicating an enlarged left atrium.

(3) Echocardiography is the most accurate non-invasive diagnostic method for detecting and quantifying mitral regurgitation. On two-dimensional echocardiography, it can be seen that the reflection of the anterior and posterior leaflets of the mitral valve is enhanced and thickened. The valve opening does not close properly during systole; when the chordae tendineae are ruptured, the mitral valve may show a flail-like change. On the long axis of the left ventricle, the valve leaflets can be seen hooking toward the left atrium like a gooseneck during systole, and in diastole. Whiplash drifting toward the left ventricle. M-mode ultrasound shows an increase in the EF slope of the anterior leaflet of the mitral valve during diastole and an increase in leaflet activity; enlargement of the left atrium and overexpansion during systole; enlargement of the left atrium and hyperactivity of the ventricular septum. Doppler ultrasound showed left atrial systolic regurgitation. Contrast echocardiography of the left heart shows that the contrast agent returns from the left ventricle to the left atrium during systole.

(4) Radionuclide examination Radionuclide blood pool imaging showed enlargement of the left atrium and left ventricle, and an increase in the end-diastolic volume of the left ventricle. In pulmonary hypertension, enlargement of the main pulmonary artery and right ventricle can be seen.

(5) Right heart catheterization showed increased pressure in the right ventricle, pulmonary artery and pulmonary capillaries, and increased pulmonary circulation resistance. Left heart catheterization showed increased pressure in the left atrium, with significant V waves in the pressure curve, while cardiac output reduce.

Prevention

Mitral regurgitation is mainly caused by repeated attacks of rheumatic fever. Therefore, preventing repeated attacks of rheumatic fever is the key to preventing the occurrence and development of this disease. Rheumatic Mitral Regurgitation Valvular regurgitation often has no obvious symptoms in the early stages. By the time obvious symptoms appear, the disease has become more serious. Therefore, early detection and early prevention and treatment are very important. For example, patients with mitral regurgitation who have clear rheumatic heart valve disease should visit the hospital regularly. Hospital diagnosis and treatment, severe lesions may be treated by valve surgery. Valvuloplasty or valve replacement is performed depending on the condition.