What causes mitral valve stenosis?
(I) Causes of morbidity
Due to recurrent rheumatic fever, early mitral valve stenosis is characterized by edema at the valve
In the later stages of the healing process, due to fibrin deposition and fibrous degeneration, adhesions and fusion at the anterior and posterior leaflet junctions, valve thickening, roughness, sclerosis, calcification, and tendon shortening and mutual adhesions are gradually formed, limiting valve mobility and opening, resulting in valve stenosis.
(B) Pathogenesis
In the early stage of rheumatic mitral stenosis, edema, inflammation and exudate formation mainly occur at the junction of the valve and its base, and later in the healing process, due to fibrin deposition and fibrous degeneration, adhesions and fusion at the junction of the anterior and posterior leaflets, thickening, roughness, sclerosis and calcification of the valve, as well as shortening of the tendon cords and mutual adhesions, restrict the valve mobility and opening, resulting in stenosis. According to the degree of lesion, mitral stenosis can be divided into 4 types.
(1) septal type: mainly adhesions at the mitral junction; the valve itself may not be thickened or may be mildly thickened; valve elasticity and mobility are good; occasionally there are mild adhesions of the tendon cords, and the disease is mostly mild.
(2) septal thickening type (valve thickening type): further development of the septal type, in addition to junctional adhesions, the anterior and posterior valves thicken, but the anterior valve elasticity and mobility is still good, the posterior valve mobility is often impaired or even loss of mobility, the tendon cords may have mild adhesions and calcification.
(3) septal funnel type: In addition to stenosis, the anterior and posterior leaflets are obviously thickened and adherent, and the anterior valve is still mostly movable but has been restricted, while the posterior valve has mostly lost its mobility, as it is often accompanied by adhesions, contractures and fusion of the tendon cords, making the valve appear as a funnel-shaped change with a large upper and small lower orifice.
(4) Funnel type: The anterior and posterior mitral leaflets are obviously fibrotic and calcified, with marked restriction of valve mobility, poor elasticity, adhesions, contractures, and fusion of the tendons and papillary muscles, resulting in a rigid and funnel-shaped valve, mostly accompanied by mitral valve closure insufficiency.
As mitral stenosis obstructs the diastolic drainage of the left atrium and gradually expands, blood stagnates in the left atrium, predisposing to atrial fibrillation and thrombosis, the latter often starting at the apex of the auricle and spreading along the lateral wall of the atrium to the annulus. Older thrombi can be mechanized, fibrotic and calcified, often attached to the atrial wall, while fresher thrombi can be attached to its surface, and once dislodged, can cause embolism of the body artery and produce corresponding symptoms. When the left atrium fails to compensate, the increased intra-atrial pressure can lead to pulmonary stasis. Long-term pulmonary stasis and fibrosis cause the lungs to lose elasticity and become stiff, affecting respiratory function and gas exchange. Microscopically, the alveolar wall layer is significantly thickened, often with interstitial edema and increased collagen, and sometimes “heart failure cells” containing iron-containing hemoglobin are seen in the alveoli. The pulmonary capillaries are enlarged and varicose due to stasis, the walls of small pulmonary arteries are thickened and narrowed, and increased pulmonary vascular resistance can lead to pulmonary hypertension, while the common pulmonary artery and its large branches are often significantly dilated. Pulmonary hypertension increases the afterload of the right ventricle, and the right ventricle becomes hypertrophied and enlarged, followed by the enlargement of the right atrium. When the right heart fails to compensate, right heart failure and signs of stasis in the body circulation occur. On the other hand, because of the reduced diastolic filling of the left ventricle, the left ventricle may shrink, and in severe cases, it may atrophy, especially in the outflow tract. Because of the underfilling of the left ventricle, the systolic ejection volume is reduced, so it can be accompanied by the relative reduction of the inner diameter of the aortic root and the weakening of the pulsation.
The normal adult mitral orifice area is about 4-6 cm2 and the orifice length is 3-3.5 cm. when the orifice area is <2.5 cm2 or the orifice length is <1.2 cm, clinical symptoms of different degrees will appear. Clinically, mitral stenosis is classified as mild (2.5 to 1.5 cm2; >1.2 cm), moderate (1.5 to 1.0 cm2; 1.2 to 0.8 cm), and severe (1.0 to 0.6 cm2; <0.8 cm) stenosis according to the degree of orifice area reduction and length diameter shortening. The natural course of mitral stenosis can be divided into 3 stages according to the corresponding hemodynamic changes that occur with the degree of stenosis.
(1) Left atrial compensatory phase: Mild to moderate mitral stenosis is due to obstruction of left atrial return to the left ventricle during diastole, and compensatory enlargement and hypertrophy of the left atrium occurs to enhance contractility, resulting in increased active atrial blood displacement during late diastole and delaying the rise in mean left atrial pressure.
(2) Left atrial failure phase: With the aggravation of mitral stenosis, the compensatory enlargement, hypertrophy and enhanced contractility of the left atrium can hardly overcome the hemodynamic obstruction caused by valve stenosis, and then the left atrial pressure gradually increases, which then affects pulmonary venous return, leading to a successive increase in pulmonary venous and pulmonary capillary pressure, enlargement of the canal diameter and luminal stasis. On the one hand, it can cause a decrease in pulmonary compliance, respiratory dysfunction and hypoxemia; on the other hand, when the pulmonary capillary pressure is significantly elevated, plasma and even blood cells leak out of the capillaries, and when lymphatic drainage is not timely, plasma and blood cells leak into the alveoli, which can cause acute pulmonary edema and signs of acute left atrial failure.
(3) Right heart involvement period: long-term pulmonary stasis decreases pulmonary compliance, which can reflexively cause small pulmonary artery spasm and contraction, leading to pulmonary hypertension. Long-term pulmonary hypertension can further cause thickening of the intima and middle layer of small pulmonary arteries and further narrowing of the vascular lumen, which aggravates pulmonary hypertension and forms a vicious circle. Pulmonary hypertension inevitably increases the right ventricular afterload, thickening the right ventricular wall and enlarging the right heart cavity, eventually causing right heart failure. At this point, pulmonary stasis and left atrial failure symptoms are reduced instead.
What are the early symptoms of mitral stenosis?
Clinical manifestations
1, symptoms mitral stenosis patients due to the severity of stenosis, the speed of progression, living conditions, occupation, labor intensity and compensatory mechanism, its clinical manifestations can be very different, the main clinical symptoms are.
(1) dyspnea: When mitral stenosis enters the stage of left atrial failure, it can produce different degrees of dyspnea. In the early stage, it only appears during heavy physical labor or strenuous exercise, and can be relieved with a little rest, often without drawing the patient’s attention. As the degree of mitral stenosis increases, later shortness of breath is felt even at rest, and there are often episodes of nocturnal paroxysmal dyspnea. With further development of the disease, it is often impossible to lie down and requires semi-recumbent or seated breathing. These symptoms are often aggravated by infection (especially respiratory tract infection), tachycardia, emotional excitement and atrial fibrillation.
(2) Hemoptysis: the incidence is about 15%-30%, mostly in patients with moderate or severe mitral stenosis, and can be as follows
(1) Massive hemoptysis: It is due to rupture of bronchial veins in the submucosa of the bronchus. Because of the presence of collateral circulation between the pulmonary veins and the bronchial veins, the sudden increase in pulmonary venous pressure can be transmitted to the small bronchial veins, causing the latter to rupture and bleed. The hemorrhage can reach hundreds of milliliters, and because the decrease in pulmonary venous pressure often terminates on its own after hemorrhage, hemorrhagic shock rarely occurs, but one must be alert to asphyxia due to hemoptysis. Hemoptysis due to mitral stenosis occurs more often in the early stages of pulmonary stasis, which is not a manifestation of pulmonary hypertension, and later, due to thickening of the varicose vein wall, hemoptysis is rare.
(ii) Stasis hemoptysis: it is often a small amount of hemoptysis or blood in sputum due to rupture of endobronchial microvessels or interalveolar capillaries.
③Pink foamy sputum: a characteristic manifestation of acute pulmonary edema combined with alveolar capillary rupture.
④Pulmonary infarct hemoptysis: mitral stenosis, especially in those who are bedridden for a long time and atrial fibrillation, can cause pulmonary artery embolism and hemoptysis due to dislodged thrombus in the vein or right atrium, often in the form of gelatinous dark red sputum.
(5) Chronic bronchitis with blood in sputum: Bronchial mucosa is often edematous in patients with mitral stenosis, which can easily cause chronic bronchitis.
(3) Cough: Unless combined with respiratory tract infection or acute pulmonary edema, the cough is mostly dry, mostly at night or after labor, because of increased venous reflux, which aggravates pulmonary stasis and causes cough reflex; sometimes the left atrium, which is obviously enlarged, compresses the left bronchus and causes an irritating dry cough. Pulmonary stasis and bronchial mucous membrane edema and exudation, coupled with bronchial mucous membrane epithelial cells cilia function is reduced, easy to cause bronchial and lung infections, at this time there can be coughing sputum
(4) Palpitations: often due to arrhythmias such as atrial fibrillation. Rapid atrial fibrillation can induce acute pulmonary edema, causing dyspnea or aggravating it in asymptomatic patients, and forcing them to seek medical attention.
(5) Chest pain: Patients with mitral stenosis and severe pulmonary hypertension may experience posterior sternal or precordial pressure or chest pain, which often lasts longer than angina, and nitroglycerin is ineffective, and the mechanism of chest pain is not known. In addition, mitral stenosis combined with rheumatic coronary arteritis, coronary embolism or pulmonary infarction can also be chest pain, the elderly also need to pay attention to the combination of coronary heart disease.
(6) Hoarseness: Rarely, marked enlargement of the left atrium, enlarged bronchial lymph nodes and dilated pulmonary arteries can compress the left recurrent laryngeal nerve and cause hoarseness (Ortner syndrome).
(7) Other.
(i) Fatigue and weakness: reduced cardiac output due to mitral stenosis.
(ii) Dysphagia: caused by compression of the esophagus by the enlarged left atrium.
③If the left atrial appendage thrombus is dislodged: it can cause arterial (cerebral and visceral) embolism symptoms.
④When the right heart is involved in right heart failure: due to gastrointestinal stasis and dysfunction, it can cause loss of appetite, and due to hepatic stasis and hepatic decompensation, it can cause pain in the liver area, hepatomegaly, abdominal distension, lower limb edema, and wasting, etc.
2. Physical signs
(1) Apical diastolic murmur: The apical diastolic murmur is the most important sign for the diagnosis of mitral stenosis, and in the majority of cases, the diagnosis of mitral stenosis can be made on this basis. In typical cases, the murmur is often confined to the apical region, with a low-pitched, increasing, rumbling murmur in late diastole, and a late diastolic (presystolic) murmur that is often enhanced in sinus rhythm and persists until the first heart sound (S1), which disappears when atrial fibrillation occurs. The diastolic murmur of mitral stenosis is most easily heard when the chest wall in the apical region is lightly pressed with a bell-type stethoscope and when the patient is placed in the left lateral position. For the lighter murmur, the murmur can be enhanced by exercise, coughing, forceful expiration, or inhalation of isoamyl nitrite. In general, there is a relationship between the severity of mitral stenosis and the loudness of the diastolic murmur in the apical region, but the relationship is not necessarily proportional. The loudness of the murmur depends mainly on the blood volume and the flow rate of blood through the stenotic valve orifice. In a certain range, the murmur loudness is proportional to the degree of stenosis, but in severe stenosis, the murmur is reduced or even inaudible, which is called “mute mitral stenosis”, because the blood flow through the mitral valve orifice is significantly reduced. When mitral stenosis is combined with atrial fibrillation (mostly severe mitral stenosis), tachycardia or left atrial failure, the murmur will also be reduced; when cardiac function improves and the heart rate slows down, the murmur can be enhanced. In addition, the murmur is reduced in combined pulmonary hypertension and valve leaflet fixation, and is enhanced when cardiac output increases.
A small number of mitral stenoses have inaudible diastolic murmurs, the so-called mute mitral stenosis, which can be seen in very mild mitral stenoses, but clinically refers to those with severe mitral stenosis and pulmonary hypertension, mainly because of the following reasons: (1) severe stenosis (less than 1.0 cm2), valve thickening and adhesion, and reduced mobility, which slow down the blood flow through the mitral valve orifice and reduce the blood volume, resulting in The murmur is extremely light or even inaudible; ② pulmonary hypertension, significant enlargement of the right ventricle, and extreme cis-clockwise transposition force the left ventricle to shift back to the left, affecting the mitral murmur conduction. In addition, some patients with mitral stenosis when the cardiac function is significantly reduced and/or combined with atrial fibrillation and tachycardia, the original diastolic murmur can be significantly weakened or even disappeared, turning into mute mitral stenosis. The murmur may reappear as cardiac function improves, the arrhythmia corrects, or the ventricular rate slows. Occasionally, in mitral stenosis with aortic valve lesions, the apical diastolic murmur may diminish or disappear because of increased left ventricular end-diastolic pressure and reduced left interatrial transvalvular pressure difference. Other conditions such as pulmonary emphysema and large pericardial effusion may also affect murmur conduction, and pulmonary lesions may sometimes mask the diastolic murmur, at which point the patient should be asked to pause for breath before careful auscultation. Although no diastolic murmur can be heard in the apical region of mute mitral stenosis, other signs of mitral stenosis may still be present, such as hyperacusis of the first heart sound in the apical region, mitral valve opening beat, hyperacusis of the second heart sound in the pulmonary valve region, Graham-Stell murmur, and relative tricuspid incomplete murmur, etc. The corresponding changes in mitral stenosis are still present on X-ray, echocardiogram, and electrocardiogram; clinically There may be pulmonary stasis, left atrial failure and/or right heart failure manifestations.
(2) Hyperactive 1st heart sound (S1) and open valve sound: In mitral stenosis, the left atrial pressure is elevated, and at the end of diastole, there is still a large pressure difference between the left atrium and the ventricle, coupled with the reduced filling of the left ventricle in diastole, the anterior mitral valve leaflet is in a lower position in the ventricular cavity, and when the ventricle contracts, the leaflet suddenly and rapidly closes, producing a hyperactive flapping S1. It is a high-pitched, crisp, short, and loud heart sound that follows S2. The mechanism is that in mitral stenosis, the pressure step difference between the left atrium and the ventricle in early diastole is large, and the anterior leaflet of the stenotic mitral valve is pushed forcefully into the left ventricle by the high-pressure blood flow of the left atrium, but the opening is suddenly obstructed midway, causing a sudden increase in anterior leaflet tension and prompting the leaflet to close suddenly and briefly; in recent years, echocardiography has confirmed that the mitral valve opens, then suddenly and rapidly closes for a moment and then opens again. The presence of hyperactivity and opening sounds often indicates good mobility and elasticity of the anterior mitral leaflet, which is helpful in the diagnosis of septal mitral stenosis and in the choice of treatment with percutaneous balloon mitral valve dilatation. In funnel-type mitral stenosis, the orifice is stiff and funnel-shaped, and the valve loses elasticity, so S1 in the apical region is diminished and there is no opening sound, and it is often accompanied by a systolic murmur of incomplete closure.
(3) Pulmonary valve closure sound (P2) hyperactivity and S2 splitting: When mitral stenosis leads to pulmonary hypertension, it can produce P2 hyperactivity and S2 splitting, sometimes with claudication. As pulmonary hypertension progresses, the pulmonary arteries may become dilated, and jet-like systolic murmurs and pulmonary artery ejection sounds (early systolic karate) may be heard in the pulmonary valve area. When the pulmonary artery is severely dilated, it can produce relative pulmonary valve closure insufficiency, and an early diastolic blowing murmur, or Graham-Stell murmur, can be heard in the pulmonary valve auscultation area. When mitral stenosis progresses to the stage of right heart involvement, it may produce relative tricuspid valve insufficiency, and a systolic murmur may be heard in the tricuspid valve auscultation area.
(4) Other signs.
(1) The patient has a “mitral valve face” with red cheeks and mild cyanosis of the lips.
(2) In children or adolescents, there may be an anterior elevation with elevated pulsations.
③Tap-like S1 and diastolic tremor may be palpable in the apical region.
④The heart border may be pear-shaped on auscultation and expand to the left when the right ventricle is enlarged.
⑤Dry and moist woven grass can be heard in the lungs when pulmonary stasis and pulmonary edema occur.
⑥In the case of right heart failure, there are signs of large circulation stasis.
Diagnosis
The diagnosis of typical mitral stenosis can be made qualitatively on the basis of clinical manifestations, especially cardiac auscultation, and experienced physicians can also assess the severity of mitral stenosis, but accurate quantitative diagnosis depends on laboratory tests. The most effective ancillary tests to confirm the diagnosis of mitral stenosis are echocardiography, followed by x-ray, and electrocardiography, which is only used as an adjunctive diagnostic tool.
Diagnosis of the degree of mitral stenosis and the type of pathology: The degree of mitral stenosis and the quantitative diagnosis should be determined by a comprehensive analysis, which can generally be estimated from the following aspects.
If a patient with mitral stenosis has compensated cardiac function, the stenosis is mild; if there is recurrent left atrial failure, pulmonary edema episodes, and/or signs of right heart failure, the stenosis is more severe.
2. Changes in the turbinate boundary on physical examination In patients with mitral stenosis, if there is right ventricular hypertrophy and pulmonary hypertension, the turbinate boundary is enlarged to the left and right (mainly to the left), and the heart waist is full, showing typical mitral heart changes, and the degree of enlargement is often proportional to the degree of mitral stenosis.
The degree of enlargement is often proportional to the degree of mitral stenosis. 3, cardiac auscultation findings In patients with atrial fibrillation, mitral stenosis is more severe, and vice versa is lighter; in patients with paroxysmal atrial fibrillation, mitral stenosis is lighter than in those with persistence. Note the time distance between the mitral valve opening sound and the second heart sound; the closer they are, the more severe the mitral stenosis. As for the diastolic murmur in the apical region, in mild to moderate stenosis, its loudness is mostly proportional to the diastolic pressure difference between the left atrium and ventricle and the degree of stenosis, whereas in severe stenosis, the murmur is reduced. A hyperactive, split second heart sound (S2) in the pulmonary valve region with a Graham-Stell murmur indicates the presence of significant pulmonary hypertension, which is corroborative of a more severe mitral stenosis. In addition, the presence of a systolic murmur in the tricuspid region due to tricuspid valve insufficiency also indicates a more severe mitral stenosis.
In addition to corroborating the above auscultation findings, the electrocardiogram can also refer to the R-Sl time, which is the time distance between the beginning of the R wave (or Q wave) on the electrocardiogram and the closing component of the S1 mitral valve. Normal R-S1 is 40-60ms, mild mitral stenosis is 50-70ms, moderate is 80-90ms, and severe is >100ms. S2- and open valve sound (S2-OS) time distance measurement also has some reference value, if S2-OS >90ms, it is mostly mild mitral stenosis; if <50ms, it is more severe mitral stenosis.
5.Electrocardiographic examination If there is right ventricular hypertrophy and strain with atrial fibrillation, it mostly indicates more severe mitral stenosis.
6.X-ray examination If the mitral stenosis is moderate or above, it shows that the aortic node is narrowed, the pulmonary artery segment is prominent, the left atrium and right ventricle are enlarged, the hilar shadow is deepened, and the cardiothoracic ratio is increased to 60% to 80%, and the Kerley B line or A line is visible.
7.UCG examination can directly measure the valve area and the size of the left atrium and right ventricle, which has quantitative diagnostic value for mitral stenosis.
The pathological type of mitral stenosis is judged according to the clinical manifestations, aiming to provide reference for patients to choose the best treatment plan. In general, the septal and septal thickening types are characterized clinically by rare atrial fibrillation, apical S1 hyperactivity in a tapping pattern, frequent mitral valve opening sounds, and pre-systolic enhancement of the diastolic murmur; these two types are mostly mild to moderate mitral stenosis. The septal funnel type is a further development of the above-mentioned pathological types. Its clinical features include hyperactive S1 in the apical region during auscultation, but it is not crisp, and the opening sounds are unclear or even inaudible, and atrial fibrillation is present in about half of the cases. The clinical features of the funnel type are that most of them have atrial fibrillation, low S1 in the apical region, no opening sound, reduced diastolic murmur, often without presystolic augmentation, and often systolic murmur due to mitral valve incompetence.
In general, septal and septal thickening types can be treated with percutaneous balloon mitral valve dilatation (PBMV) or surgical closed dilatation; septal funnel type should be tried with closed dilatation under extracorporeal circulation, which can also be changed to direct visual separation depending on the condition; and funnel type mostly requires valve replacement.
What should be considered before treatment of mitral stenosis?
(A) Treatment
1.Medication
(1) Left atrial compensatory phase.
(1) Prevention of rheumatic activity and treatment of streptococcal infection in the throat.
(2) Avoid strenuous activities and heavy physical work. Some data show that when the heart rate increases from 70 beats/min to 80 beats/min during activity, the atrioventricular transvalvular pressure difference can be increased by 1 times.
(3) Pay attention to the combination of work and rest, and a light and vitamin-rich diet to keep cardiac function in the compensatory phase for a longer period of time to slow down the progress of the disease.
(2) Period of left atrial failure.
(1) Chronic pulmonary stasis phase: appropriate rest should be taken and water and sodium intake should be restricted. Drug therapy to reduce preload, diuretics can be given, such as hydrochlorothiazide (dihydroketorol) 25-50mg, 1 to 2 times / d; choose intravenous dilators to reduce the amount of return blood, can use nitroglycerin 10-20mg into 500ml of liquid slowly intravenous drip, after the condition improves, change to long-acting nitrate oral, such as isosorbide mononitrate 50mg, 1 time / d; can Oral beta blockers to slow down the heart rate and prolong the ventricular diastole.
②Acute pulmonary edema: mitral stenosis combined with acute pulmonary edema is based on left atrial failure, although its clinical manifestations are similar to those of left ventricular failure pulmonary edema, there are both similarities and differences in the management of the two. The similarities include the application of semi-recumbent position, oxygen, alternating ligature tourniquet on the extremities, morphine or pethidine injection, sedation, rapid diuresis, use of vasodilators and aminophylline, and removal of causative factors. The difference is that digitalis should be used with caution when pulmonary edema due to mitral stenosis is present, and it should not be used as the first choice for the treatment of acute pulmonary edema. In mitral stenosis, the diastolic filling of the left ventricle is less than normal, and the anterior and posterior loads of the left ventricle are not large or even smaller than normal, so there is no need to use digitalis to strengthen its contraction; however, the application of digitalis also strengthens the contraction of the right ventricle, which may increase the amount of blood injected into the pulmonary artery from the right ventricle, leading to an increase in pulmonary edema. Mitral stenosis combined with acute pulmonary edema may still be treated with digitalis in appropriate amounts, but only in combination with tachyarrhythmic atrial fibrillation, pronounced sinus tachycardia and supraventricular tachycardia, which is mainly used to slow down the ventricular rate rather than to increase myocardial contractility. If the ventricular rate is still not significantly reduced after the application of digitalis, it can be slowly injected intravenously under cardiac monitoring with 0,5-2mg propranolol or 2,5-5mg verapamil diluted with 20ml of 5% glucose solution, which can often receive better results. In terms of vasodilators preferred to dilate the vein-based drugs, such as nitroglycerin 10-20mg added to 5% glucose solution 500ml intravenous drip, in order to reduce the amount of cardiac blood return, improve pulmonary stasis. If medical treatment is ineffective, emergency percutaneous balloon mitral valve dilatation or surgical closed detachment can be performed in units where available to relieve valve stenosis as soon as possible.
Mitral stenosis combined with hemoptysis: general principles of management include close observation of the condition, prevention of asphyxia, lying in a flat position, oxygenation in cases of respiratory distress and hypoxia, and appropriate use of hemostatic agents such as carbachol, phenolsulfonamide, vitamin K, and aminocaproic acid. However, it must be pointed out that posterior pituitary hormone, which is often used clinically for pulmonary hemoptysis, should not be used because it has a strong vasoconstrictive effect, which can increase blood pressure, increase pulmonary artery resistance, and increase cardiac load. On the contrary, vasodilators can be applied to reduce pulmonary venous pressure, either nitroglycerin 0,3-0,6mg sublingually every 0,5-1 hour or intravenous drip. In addition, powerful diuretics can be used to reduce pulmonary venous pressure. Emergency percutaneous balloon mitral valve dilatation can be performed for hemoptysis that fails to respond to medical treatment.
Mitral stenosis combined with thromboembolism: The formation of left atrial appendage thrombus is positively correlated with the degree of left atrial enlargement and the duration of atrial fibrillation. In order to prevent the formation of left atrial appendage thrombus in patients with combined chronic atrial fibrillation, it is advisable to give long-term anti-platelet aggregation drugs, such as aspirin 0,15-0,3g, 1 time/d, or ticlopidine 0,25g, 2 times/d for 3 days, and then change to 0,25g, 1 time/d for 3 months, and then change to aspirin for maintenance. When chronic atrial fibrillation is combined with fresh thrombosis of the left atrium, the valve lesion is consistent with septal type or septal thickening type features, percutaneous balloon mitral valve dilatation can be considered after 3 to 4 weeks of warfarin anticoagulation therapy. If the valve lesion is septal funnel type or funnel type, surgical mitral valve dilatation or prosthetic valve replacement is indicated, and postoperative anticoagulation therapy is still required. Because atrial stuttering may occur after resetting AF, it sometimes takes 3 to 4 weeks to restore effective atrial contraction, therefore, to prevent thrombus dislodgement, anticoagulation therapy should be continued 3 to 4 weeks after resetting. In rheumatic heart disease combined with heart failure, anticoagulation therapy can help prevent venous thrombosis and pulmonary embolism in patients with a history of one or more previous thromboembolisms and in patients at high risk for thromboembolism (i.e., patients with atrial fibrillation, prosthetic mechanical heart valves). However, to date, there is no strong evidence that anticoagulation reduces pulmonary and circulatory embolism in patients with sinus rhythm who have no prior history of thromboembolism. In case of thromboembolism, if the embolized artery is large, the onset is within 12 hours, the patient has good cardiac function, and the surgical field is accessible, arteriotomy can be performed to remove the embolus; the main medical treatment is anticoagulation.
⑤ Mitral stenosis combined with atrial fibrillation: if paroxysmal atrial fibrillation, drug of choice is amiodarone, which can often prevent paroxysmal atrial fibrillation episodes and maintain sinus rhythm at a dose of 0,2g, 3-4 times/d, gradually reduced to 0,2g, 1 time/d after 7-10 days, and continued until after percutaneous balloon mitral valve dilatation (PBMV) or mitral valve surgery, so that the mitral transvalvular pressure difference until it approaches normal. In persistent AF (defined as AF lasting longer than 3 months), mechanical obstruction of mitral stenosis that is not relieved should not be resuscitated with drugs or defibrillated with electric shock, as it is highly likely to recur. Because persistent AF can cause a 30% decrease in cardiac output, when complicated by rapid AF, it is advisable to control the ventricular rate rapidly, by giving 0.4 mg of trichothecene C (cydlam) in 20 ml of 10% glucose and injecting it slowly intravenously. After the ventricular rate is slowed down, digoxin 0,25mg can be applied orally once/d for long-term maintenance to maintain the ventricular rate at 60-80 beats/min at rest and <100 beats/min during daily activities. electric shock resuscitation or pharmacological resuscitation can be considered for persistent AF that has not recovered sinus rhythm after PBMV or mitral valve surgery is currently recommended.
(3) Percutaneous balloon mitral valve dilatation (PBMV) The fundamental problem in the treatment of mitral stenosis is to lift the mechanical stenosis of the valve and reduce the transvalvular pressure differential. Drug therapy can only temporarily reduce the symptoms, but cannot cure and control the progression of the disease.
2.Surgical treatment
(1) Closed mitral commissurotomy: The indications, contraindications, and efficacy of closed mitral commissurotomy are roughly the same as those of PBMV, but PBMV is less invasive, quicker to recover, and more easily accepted by patients. In recent years, due to the widespread implementation of PBMV, closed mitral valve dissection has been rarely performed.
(2) Open mitral commissurotomy: mitral stenosis combined with mitral valve insufficiency, or inability to accurately exclude intra-atrial thrombus, or severe calcification of the valve, or suspected severe fusion and shortening of the tendon cords, should be performed under direct visualization for mitral valve separation.
(3) Artificial heart valve replacement: Patients with mitral stenosis, heart function grade 3 to 4, and combined with obvious aortic valve lesions and/or mitral valve insufficiency, resulting in significant enlargement of the left ventricle, or extensive and severe calcification of the valve so that it cannot be separated and repaired and shaped, should perform artificial valve replacement. Mechanical valves or biologic valves are commonly used. Mechanical valves are made of titanium alloy or pyrolytic carbon and have the advantage of being durable, not causing rejection of the body, and not causing calcification or infection; the disadvantage is that they require lifelong anticoagulation and are contraindicated in patients with peptic ulcers or bleeding disorders. It is difficult to undergo other surgical procedures in the future and there is a risk of hemorrhagic complications. Biological valves are made from bovine pericardium or porcine heart valves treated to eliminate antigenicity, or from human dura mater selected by tissue mapping, with the advantage of not requiring long-term postoperative anticoagulation and minimal rejection; the disadvantage is that they can fail due to infectious endocarditis or after several years due to calcification and/or mechanical damage.
(B) Prognosis
The prognosis of patients with mitral stenosis depends on the severity of the stenosis, the degree of cardiac enlargement, the combination of other valve damage, and the possibility of surgical treatment. In the case of rheumatic heart disease, it also depends on the ability to control the recurrence of rheumatic activity with the prevention of complications. In terms of the natural course of rheumatic mitral stenosis, compensated patients generally remain in the light to moderate workforce for more than 20 years; if the heart is significantly enlarged, only 40% of patients survive for 20 years; from the onset of significant symptoms to incapacity averages about 7 years; from persistent atrial fibrillation to death is generally 5 years, although there are cases of up to 25 years.