Mitral stenosis (mitralstenosis) is a sequela of rheumatic heart disease and is commonly seen in adults. Patients present with symptoms such as shortness of breath, hemoptysis and cough, as well as weakness, palpitations and dizziness, depending on the degree of stenosis and compensatory function. Cardiac function can be classified into five classes based on the severity of the disease, which provides the basis for selection of patients for surgery.
Mitral stenosis Mitral stenosis (mitralstenosis) is a sequela of rheumatic fever. Very rarely, it is a congenital stenosis or an age-related mitral annulus or subannular calcification. Two-thirds of patients with mitral stenosis are women. Approximately 40% of patients with rheumatic heart disease (rheumatic heart disease) have simple mitral stenosis.
Where the face is dull, with purple cheeks and mild cyanosis of the lips. It is mostly seen in patients with mitral stenosis in rheumatic heart valve disease. It refers to a type of rheumatic heart disease called mitral stenosis, which is an autoimmune disease. The patient’s face is characterized by purplish redness of both cheekbones and lips, like after exercise, and is an important part of the physician’s visualization.
Mitral Stenosis – Disease Symptoms
Mitral stenosis usually occurs for up to 10 years from the initial rheumatic heart disease to the appearance of obvious mitral stenosis symptoms; thereafter, 10 to 20 years of gradual loss of motion.
1. Early symptoms.
Dyspnea laboratorial dyspnea, mainly due to reduced compliance of the lungs. With the development of the disease, dyspnea can occur with daily activities, as well as telescopic breathing. When there are triggers such as exertion, emotional excitement, respiratory infection, sexual intercourse, pregnancy or rapid atrial fibrillation, acute pulmonary edema can be induced.
2. Cough.
Mostly at night during sleep and after labor. Mostly dry cough; coughing mucus-like or pus-like sputum when complicated by bronchitis or lung infection. Significant enlargement of the left atrium compressing the bronchus may also cause coughing.
3.Hemoptysis
(1) Blood in sputum or hemoptysis, associated with bronchitis, pulmonary infection, and pulmonary congestion or capillary rupture; often accompanied by nocturnal paroxysmal dyspnea; hemoptysis may also occur in advanced bleeding pulmonary infarction of mitral stenosis.
(2) Massive hemoptysis, caused by a sudden increase in left atrial pressure, resulting in bronchial vein rupture and bleeding. It is mostly seen in patients with early mitral stenosis and only mild or moderate pulmonary artery augmentation. ③ Pink foamy sputum, which is caused by capillary rupture, is a characteristic of acute pulmonary edema.
4. Chest pain.
Approximately 15% of patients with mitral stenosis present with chest pain, which may be caused by increased tension in the hypertrophied right ventricular wall, along with decreased cardiac output resulting in right ventricular ischemia. It can be relieved by mitral valve dissection or dilatation.
5, Thromboembolism.
Thromboembolism occurs in 20% of patients with mitral stenosis during the course of the disease, 80% of whom have atrial fibrillation. Embolism can occur in the cerebral vessels, coronary arteries, and renal arteries, and can recur in some patients. Or it may be a multi-occurrence embolism.
6. Other symptoms.
Left atrial enlargement and left pulmonary artery dilatation may compress the left recurrent laryngeal nerve, causing hoarseness; significant enlargement of the left atrium may compress the esophagus, causing dysphagia; in right ventricular failure, symptoms such as loss of appetite, bloating, and nausea may occur.
Mitral valve stenosis – disease characteristics
1, heart auscultation apical region diastolic late low-pitched rumble-like murmur, incremental, limited, obvious in left lateral recumbency, may be accompanied by diastolic tremor. The first heart sound in the apical region is hyperactive and beat-like. The mitral opening sound (OS) can be heard in 80% to 85% of patients at the left sternal margin between 3 and 4 ribs or laterally within the apical region, which is followed by the second heart sound, short and loud in high pitch and obvious during exhalation, and is caused by tremor of the main valve (anterior mitral leaflet) of the septal orifice during opening. The presence of septal mitral stenosis is highly suggestive of mitral stenosis and the presence of a certain degree of valve flexibility and mobility, which is helpful in the diagnosis of septal mitral stenosis and has some significance in deciding on surgical treatment. As a result of pulmonary hypertension, there may be hyperacusis and splitting of the second heart sound of the pulmonary valve. In severe pulmonary hypertension, a high-pitched, decreasing early to mid-diastolic murmur can be heard between the 2nd and 4th ribs at the left sternal border, blowing in a wind-like fashion, along the left sternal border toward the tricuspid region, and increasing during inspiration. This is due to the dilatation of the pulmonary artery and its annulus, resulting in a murmur of relative pulmonary valve insufficiency (Graham-Settll murmur). An early systolic pulmonary valve murmur can sometimes be heard, which is distinct during expiration and decreases during inspiration. In patients with severe mitral stenosis, right ventricular enlargement due to pulmonary hypertension causes enlargement of the tricuspid annulus, resulting in relative tricuspid valve insufficiency. During right ventricular systole, part of the blood flow returns to the right atrium through the tricuspid valve orifice, resulting in a full systolic blowing murmur in the tricuspid region, which is conducted to the apical region and is apparent during inspiration.
2, other signs mitral valve face is seen in patients with severe mitral stenosis, due to reduced cardiac output, the patient has purplish-red cheek and mild cyanosis of the lips and mouth. Cyanosis is also seen at the end of the extremities. In patients with mitral stenosis in childhood, an elevation of the precordial region is seen, with a shift of the left papilla toward the left upper atrium and a systolic lifting-like pulsation at the left sternal border. Significant jugular venous pulsation indicates the presence of severe pulmonary hypertension.
Mitral Stenosis-Hemodynamic and Cardiac Changes
In the early stage, when the left atrium is in compensation, due to mitral stenosis, the entry of blood from the left atrium into the left ventricle during diastole is blocked, resulting in some blood remaining in the left atrium at the end of diastole, which, together with blood coming from the pulmonary veins, increases the amount of blood in the left atrium more than normal. At this time, the myocardial fibers elongate to strengthen the contraction force and the heart chambers expand to accommodate more blood, resulting in compensatory expansion of the left atrium. Due to the increased load on the left atrium, myocardial metabolism is enhanced and myocardial fibers thicken, resulting in compensatory hypertrophy of the left atrium to maintain relatively normal blood circulation. In the later stage, with the prolongation of time or aggravation of the lesion, the compensatory limit is exceeded and the contractility of the left atrium is weakened and the left atrium becomes highly dilated (myogenic dilatation), resulting in the loss of compensatory left atrium. At this time, the left atrial blood cannot fully drain into the left ventricle during diastole, causing severe left atrial stasis, and the increased left atrial pressure prevents pulmonary venous blood from entering the left atrium, resulting in increased pulmonary venous pressure and subsequent pulmonary stasis.
As a result of the elevated pulmonary venous pressure and pulmonary stasis, the small arteries in the lungs may contract through neural reflexes, causing the pulmonary artery pressure to rise. Long-term elevated pulmonary artery pressure leads to compensatory dilation and hypertrophy of the right ventricle. Later, myogenic strain occurs in the right ventricle and myogenic dilatation develops. This is followed by right ventricular stasis. When the right ventricle is highly dilated, the right ventricular annulus is enlarged and the tricuspid valve becomes relatively incompetent. During systole, some of the right ventricular blood flows back into the right atrium, which increases the negative right atrium but can lead to right heart insufficiency and cause stasis in the circulation.
Mitral Stenosis – Etiology and Pathogenesis
The main pathophysiological change after mitral stenosis is the restriction of diastolic blood flow from the left atrium to the left ventricle, which results in abnormally high pressure in the left atrium, and a significant stenosis in the left ventricle. The main pathophysiological change after mitral stenosis is the restriction of diastolic blood flow from the left atrium into the left ventricle, resulting in an abnormal increase in left atrial pressure and an increase in the pressure step difference between the left atrium and left ventricle to maintain normal cardiac output. This increase in left atrial pressure can cause an increase in pulmonary venous and pulmonary capillary pressure, followed by dilation and stasis. In this case, the patient may have no obvious symptoms at rest, but during physical activity, the pulmonary venous and pulmonary capillary pressures increase further due to increased blood flow, resulting in immediate difficulty, cough, cyanosis, and even acute pulmonary edema. Long-term overload of pulmonary circulation blood volume can lead to a rise in pulmonary artery pressure. Long-term pulmonary hypertension causes spasm and sclerosis of the small pulmonary arteries, and causes hypertrophy and dilation of the right ventricle, which can then lead to right ventricular failure. At this time, pulmonary artery pressure decreases, blood flow in the pulmonary circulation decreases, and pulmonary stasis is relieved.
In simple mitral stenosis, left ventricular end-diastolic pressures and volumes are normal. Most patients with mitral stenosis exercise with an elevated left ventricular ejection fraction and reduced end-systolic volume. Approximately one quarter of those with severe mitral stenosis present with left ventricular dysfunction, as evidenced by reduced ejection fraction and other indices of systolic function, which may be the result of chronic preload reduction. Most patients with mitral stenosis have resting cardiac output in the normal range and a lower-than-normal increase in cardiac output during exercise; a few with severe stenosis have lower-than-normal resting cardiac output and a lower-than-normal increase in cardiac output during exercise, which is mainly due to impaired left and right ventricular function in addition to mitral stenosis. In addition, because of the enlarged left atrium, it is difficult to maintain normal cardiac electrical activity, so atrial fibrillation often occurs. Rapid atrial fibrillation with a fast ventricular rate can increase pulmonary capillary pressure, which can easily aggravate pulmonary stasis or induce pulmonary edema.
Mitral Stenosis-Pathologic Changes
The pathologic changes begin with inflammatory edema and redundancy formation at the valve junction and base, extensive leaflet thickening due to fibrosis and/or calcium deposits, adhesions, fusion of tendons, shortening, and leaflet stiffness, resulting in orifice deformation and stenosis, which becomes a cleft-like orifice when stenosis is significant. According to the degree of lesion, there are septal and funnel types. The septal type has no or mild lesions in the main valve body and is still mobile; the funnel type has significant leaflet thickening and fibrosis, significant adhesions and shortening of the tendon cords and papillary muscles, stiffening of the entire valve in a funnel shape, and significant restriction of movement. It is often associated with varying degrees of incomplete closure. Stenosis is further aggravated by leaflet calcification and can lead to thrombosis and embolism. In congenital mitral stenosis, there is leaflet thickening, junctional fusion, tendon thickening or shortening, papillary muscle hypertrophy or fibrosis, and there may be a stenotic annulus above the valve and a fibrous band below the valve. The most characteristic feature is a parachute deformity of the mitral valve with only one papillary muscle, in which the tendons of both leaflets are attached to this papillary muscle and the entire valve is opened with a parachute.
Mitral stenosis – diagnosis
1. History/symptoms.
The earliest symptom is paroxysmal dyspnea at night, and in severe cases, seated breathing; in extremely severe cases, pulmonary edema, cough, coughing pink foamy sputum, mostly aggravated after sleep or activity, may be accompanied by coughing sputum, blood in sputum, hemoptysis, and as the disease progresses, dyspnea may be reduced when swelling of the lower limbs and little urination occur.
2. Physical examination reveals.
Apical face with mild cyanosis of the lips and mouth. The precordial region is elevated, a fine diastolic tremor can be palpated in the apical region, and the cardiac border is enlarged to the left at the third intercostal space. The apical S1 is hyperactive and tapping, and the open tapping sound can be heard from the left sternal margin between the Ⅲ and Ⅳ intercostal spaces to the superior apical area. The early diastolic splash-like murmur, (Graham-Steell murmur) intensifies during deep inspiration.
3.Auxiliary examination.
X-ray examination showed prominent pulmonary artery trunk, large left atrium, large right ventricle, elevated left main bronchus, and left atrial pressure traces visible in the esophagus. ECG showed: P-wave widening >0.11s with tangential traces, right ventricular hypertrophy; atrial fibrillation may be present in later stages. UCG showed mitral valve thickening, adhesions, calcification, orifice stenosis, left atrial and right ventricular cavity enlargement, and atrial thrombus; Doppler ultrasound showed subdiastolic turbulence spectrum in mitral valve.
4, Differential diagnosis.
It should be differentiated from mitral stenosis of other etiologies.
Mitral stenosis – treatment
1, compensatory treatment.
Avoid excessive physical labor and strenuous exercise to protect cardiac function; patients with rheumatic heart disease should be actively prevented from streptococcal infection and rheumatic activity as well as infective endocarditis.
2. Those with clinical symptoms in the decompensated phase of treatment.
It is appropriate to take oral diuretics and limit sodium intake. When right heart failure is obvious or rapid atrial fibrillation occurs, digitalis preparations can relieve symptoms and control the ventricular rate. If persistent atrial fibrillation is present for less than one year, pharmacological or electrical resuscitation therapy should be considered. For long-term heart failure with AF, anticoagulation therapy can be used to prevent thrombosis and arterial embolism.
3, the treatment of closure is to lift the mitral stenosis and reduce the transvalvular pressure step difference. The following surgical methods are often used.
(1) percutaneous puncture mitral valve balloon detachment. This is an interventional cardiac catheterization technique that is indicated for simple mitral stenosis. This method can expand the mitral orifice area to more than 2.0 cm2, significantly reduce the mitral transvalvular pressure step difference and left atrial pressure, improve the cardiac index, and effectively improve clinical symptoms. Percutaneous mitral balloon dissection does not damage the subvalvular structures and can avoid complications in skilled operators; moreover, it is not necessary to open the chest, which is safer, and patients have less injury and faster recovery.
(2) There are two types of mitral valve separation: closed and direct vision. The closed type mostly uses the dilator method through the left ventricle, which has the best effect on the septal type. The indications for surgery are that the patient is not older than 55 years old, has cardiac function at grade 2 to 3, no rheumatic activity or infective endocarditis within the last six months, no thrombus in the atrium on preoperative examination, no or only mild mitral valve incompetence or aortic valve lesions and the left ventricle is not large. The procedure should be performed within the sixth month of pregnancy in cases of combined pregnancy. In patients with moderate or severe mitral insufficiency, suspected intra-atrial thrombosis, severe calcification of the valve, or significant fusion and shortening of the tendon cords, direct visual separation should be performed.
(3) The indications for prosthetic valve replacement are: cardiac function at grade 3 to 4 with significant mitral valve insufficiency and/or aortic valve lesion and left ventricular enlargement; severe valve calcification that prevents separation and repair; and stenosis due to calcified atheroma. Mechanical or biological valves are commonly used. Mechanical valves are durable and do not cause calcification or infection, but require lifelong anticoagulation; they are contraindicated in patients with ulcerative or bleeding disorders. Biologic valves do not require anticoagulation, but can fail due to infective endocarditis or valve calcification or mechanical injury over several years. With the development of technology, trans-femoral and transapical interventional valve techniques are becoming increasingly mature, and it is hoped that in the near future, patients will be able to avoid open-heart valve surgery altogether.