Mitral valve stenosis
Clinical Presentation
Heart valve disease refers to damage to the heart caused by anatomical or/and functional abnormalities of the heart’s valves. The etiology of heart valve disease is divided into congenital and acquired. The incidence of congenital heart valve disease has not changed significantly in the last three to four decades; however, the common causes of acquired heart valve disease have changed significantly due to population aging, economic development, and improvement in disease prevention and control. In developed countries, mitral valve prolapse and senile degenerative changes have become the major causes of valve disease, and valve disease associated with intravenous drug use is on the rise, whereas the incidence of rheumatic heart disease is decreasing year by year, but rheumatic heart valve disease remains the most common cause of acquired heart disease in children and adolescents in developing countries. Echocardiography is an important noninvasive tool in the diagnosis and management of valvular disease. The lesion pattern of valve disease can be divided into stenosis and insufficiency, compared with the more frequent etiologies that lead to insufficiency lesions. Both regurgitant, and stenotic heart valve disease increase the hemodynamic burden on the left or right ventricle, or both ventricles, ultimately leading to heart failure. More than 15% of heart failure visits in China are due to heart valve disease, and pharmacological treatment has limited efficacy in valve disease, with surgery being the only way to correct hemodynamic abnormalities in patients with heart valve disease. The clinical prognosis of patients with heart valve disease has improved significantly in the last 20 years, mainly due to the development of noninvasive monitoring techniques for left ventricular function, the application of prosthetic valves, and advances in valve reconstruction techniques.
(I) Clinical manifestations
1, symptoms The normal mitral valve orifice area is 4-6 cm, the orifice area > 2 cm2 of mild mitral stenosis patients are generally asymptomatic, when the mitral valve is severely stenosed, the orifice area 1, 5 cm2 for mild stenosis; 1, 0 ~ 1, 5 cm2 for moderate stenosis; 55 mm, embolism history or a significant reduction in cardiac output as a risk factor for the occurrence of body circulation embolism. 80% of the body circulation embolism patients have Atrial fibrillation. 2/3 of the embolisms were cerebral artery embolisms, and the rest were peripheral and visceral (splenic, renal, and mesenteric) artery embolisms in that order. 1/4 of the embolisms were recurrent and multiple embolisms. Occasionally, a tipped globular thrombus or free floating globular thrombus in the left atrium may suddenly obstruct the mitral valve orifice, leading to sudden death. In atrial fibrillation and right heart failure, thrombus can form in the right atrium causing pulmonary embolism.
3. Right heart failure is a common complication in the late stage. In this stage, the left atrial pressure decreases due to the obvious reduction of right heart blood output, and the thickening of alveolar and pulmonary buy capillary walls, so the dyspnea is reduced, and the risk of acute pulmonary edema and hemoptysis is reduced. The clinical manifestations are the signs and symptoms of right heart failure.
4, infective endocarditis Simple mitral stenosis is rarely complicated by infective endocarditis.
5, Pulmonary infection Common.
Treatment
1.Medical treatment Internal treatment is mainly aimed at patients with mild to moderate mitral stenosis with mild symptoms and class I-II cardiac function. It mainly includes: ① Avoid overexertion and stress, and prevent infection. Penicillin can be used to prevent β-hemolytic streptococcal infection and infective endocarditis; ② control of heart rate: especially important for those with atrial fibrillation. Multiple drugs (e.g., digitalis, β-blockers, calcium antagonists) are often needed in combination; ③ diuretics: can reduce pulmonary stasis and significantly improve the patient’s symptoms; ④ digitalis drugs: can slow down the ventricular rate of patients with atrial fibrillation and improve the symptoms of right heart failure; ⑤ anticoagulation: for patients with high-risk factors for embolism in the body circulation, such as atrial fibrillation, post-operative mechanical valve replacement or a history of previous embolism, anticoagulation therapy can effectively The efficacy of anticoagulation in patients with mitral stenosis without a history of embolism and in sinus rhythm has yet to be studied.
2, Percutaneous balloon valvuloplasty is primarily used for simple mitral stenosis without significant valve calcification, fair elasticity, and no left atrial thrombus.
3.Surgical treatment Surgical treatment is mainly mitral valve replacement.
Mitral valve closure insufficiency Start detailed exercise
Etiology
(A) Etiology Any factor that damages mitral valve structures (mitral annulus, leaflets, tendons, and papillary muscles) can lead to tricuspid valve closure insufficiency. Rheumatic heart disease and mucinous degeneration of the mitral valve are the most common causes of mitral valve insufficiency, with the former predominating in developing countries with more rheumatic fever and the latter more common in developed countries.
Clinical manifestations
(B) Clinical manifestations
1, symptoms Mild chronic mitral valve insufficiency patients can be asymptomatic for life, the average patient usually has to experience more than 20 years, to the late stage of the disease, before clinical symptoms, manifested as easy fatigue, weakness, palpitations, shortness of breath after exertion, and night paroxysmal dyspnea. Pregnancy and atrial fibrillation can induce pulmonary edema, but patients with chronic mitral valve closure insufficiency have a lower incidence of acute pulmonary edema because of significantly higher left atrial compliance. Palpitations are mainly due to atrial fibrillation, atrial flutter, and/or increased cardiac output per beat.
Acute mitral valve insufficiency, especially in severe tendon or papillary muscle rupture, is often manifested as acute pulmonary edema due to poor left atrial compliance and a dramatic increase in left atrial pressure and pulmonary vascular resistance. Right heart failure may occur with a significant increase in pulmonary artery pressure and manifests as hepatomegaly, abdominal distention, and edema. Patients develop left ventricular failure within hours or days, with reduced antegrade cardiac output, decreased blood pressure in the body circulation, and shock. Acute pulmonary edema and cardiogenic shock do not occur in all acute mitral valve insufficiency and may be asymptomatic or manifest only as pulmonary edema if only a small tendon rupture is present.
The clinical manifestations of acute and chronic mitral valve insufficiency differ and should be differentiated to allow for proper clinical decision making.
2, physical signs
(1) Auscultation: The main sign in patients with mitral valve closure insufficiency is a rough apical all-systolic blowing murmur that is conducted toward the axilla or left subscapular angle, with tremor in some patients. The murmur of mitral valve insufficiency is generally unaffected by respiration, but sudden standing and Valsalva maneuvers may enhance the murmur, while squatting attenuates it. In severe mitral valve insufficiency, the murmur may be reduced or even disappear due to a significant decrease in cardiac output. In acute mitral insufficiency, the murmur is usually softer and located in early systole.
(2) Other: enlarged cardiac border, apical pulsation shifted to the left and downward in a lifted pattern. Absolute arrhythmia in atrial fibrillation.
X-ray, echocardiography and electrocardiography
(C) Auxiliary examinations
1. Echocardiography Doppler echocardiography and color Doppler flow imaging are the most accurate noninvasive methods for diagnosing and evaluating mitral valve insufficiency. Echocardiography may reveal left atrial enlargement and/or enhanced systole; the left ventricle may be hyperdynamic. A serial echocardiogram can provide early detection of left ventricular hypokinesia in patients with asymptomatic mitral valve insufficiency. A ratio of 40% of the maximum area of the mitral regurgitant bundle/left atrial area as determined by color Doppler is considered severe regurgitation.
2, ECG Mainly left atrial enlargement and atrial fibrillation, and in severe cases, left ventricular hypertrophy. In some patients with advanced disease, right ventricular hypertrophy is also present on the ECG.
Complications
(d) Complications mainly include: ① atrial fibrillation is seen in 3/4 of patients with chronic severe mitral valve insufficiency; ② infective endocarditis is more common than mitral stenosis; ③ body circulation embolism is seen in large left atria and chronic atrial fibrillation, but is less common than mitral stenosis; ④ heart failure appears early in acute cases and only occurs late in chronic cases; ⑤ complications of mitral valve prolapse are: infective endocarditis, cerebrovascular embolism, arrhythmias, sudden death, tendon rupture, severe mitral valve insufficiency, and heart failure.
Treatment
(E) Treatment
1. Internal therapy is mainly used for compensated chronic mitral valve insufficiency and symptomatic treatment. In acute mitral valve closure insufficiency, intravenous vasodilators and intra-aortic balloon counterpulsation may be used prior to emergency mitral valve replacement. Patients receiving medical therapy should be reviewed periodically. Surgical intervention should be performed as soon as symptoms worsen and ancillary tests show progressive cardiac enlargement or deterioration of left ventricular function.
(1) Etiologic treatment: If mitral valve closure insufficiency is due to cardiomyopathy, the cause can be treated directly.
(2) Vasodilators: can reduce preload and decrease regurgitant fraction. Angiotensin-converting enzyme inhibitors are commonly used. In acute mitral valve insufficiency, intravenous vasodilators and intra-aortic balloon counterpulsation may be used before emergency mitral valve replacement.
(3) Others: If atrial fibrillation is present, digitalis drugs and anticoagulants may be used. Diuretics are available in case of obvious heart failure.
2.Surgical treatment mainly includes valve replacement and mitral valve repair. The timing of surgery is an important and difficult clinical issue. Since abnormal left ventricular function is an adverse factor affecting the prognosis of surgery, and surgical treatment itself can disrupt the normal physiological state of the heart, which may further dilate the left ventricle and reduce the systolic function, patients should be followed up regularly to monitor the systolic function of the left ventricle, so that patients can receive surgical treatment as early as possible when the left ventricle is damaged. The timing of surgery cannot be determined solely by the presence or absence of clinical symptoms, because once a patient has symptoms, it means that left ventricular function is impaired and irreversible damage to the myocardium is occurring.
Aortic valve stenosis Start the detailed exercise
Etiology
(A) Etiology
While the incidence of rheumatic heart disease has been declining in recent years, degenerative valve changes have become an important cause of acquired aortic stenosis, and the main etiology of aortic stenosis varies among different age groups.
Clinical manifestations
(II) Clinical manifestations
1. Symptoms Patients with mild or moderate aortic stenosis may be asymptomatic for life, and a few patients with severe aortic stenosis may be asymptomatic for many years. The main symptoms of aortic stenosis are angina pectoris, syncope and dyspnea. In severe cases, pulmonary edema and sudden death may occur. Once these symptoms occur, the prognosis is poor if surgical treatment is not performed promptly. The average survival time of patients with congestive heart failure, syncope and angina is 2, 3 and 5 years, respectively.
(1) Angina: Angina can also occur in patients with aortic stenosis without coronary artery disease, and the clinical features of its angina are similar to those of coronary exertional angina. It is mainly due to the decrease in coronary reserve blood flow due to myocardial hypertrophy and the increase in myocardial oxygen consumption due to increased ventricular wall tension and contractility.
(2) Syncope: Syncope due to aortic stenosis is characterized by the fact that it often occurs during exercise or exertion. There are many causes of syncope in patients with aortic stenosis, such as decreased cerebral perfusion and cardiac arrhythmias. Supraventricular and ventricular arrhythmias can also induce hypotension and syncope, and even sudden death.
(3) Dyspnea: mainly exertional dyspnea. Decreased left ventricular compliance and/or left ventricular dilatation increases left ventricular end-diastolic pressure and left atrial pressure, and eventually pulmonary artery pressure, leading to exertional dyspnea. During the progression of the disease, nocturnal paroxysmal dyspnea, telangiectatic breathing and pulmonary edema may also occur as manifestations of left heart failure.
2. Physical signs
(1) Auscultation: The most important sign is the systolic jet murmur in the aortic valve area, which is enhanced and then diminished and transmitted to the neck, and the loudness of the murmur varies with the size of cardiac output. The murmur is reduced when the heart rate increases or the cardiac output decreases; it is enhanced after inhalation of isoamyl nitrite and extrasystole. Systolic murmurs in patients with aortic stenosis are usually best heard in the aortic valve region and may also be best heard in the apical region in older patients. Extreme elevation of left ventricular systolic pressure may occasionally cause mitral valve closure insufficiency, producing a corresponding murmur. In patients with aortic stenosis in sinus rhythm who have a large transvalvular pressure step difference, systolic S4 and S2 may be heard in the apical region or may be mildly split.
(2) Other: normal apical pulsation position, elevation-like, and in heart failure, enlarged heart borders with corresponding signs of left heart failure.
X-ray, echocardiography, electrocardiography
(C) Auxiliary elucidation
1.Electrocardiogram mainly shows left ventricular hypertrophy, ST segment changes and left bundle branch block can also be seen.
2, chest X-ray The posterior one anterior is often normal, late in heart failure, the left ventricle is enlarged and the aorta is dilated. On lateral x-ray, valve calcification is sometimes seen.
3.Echocardiography The main findings are left ventricular hypertrophy and valvular calcification. Left ventricular dilatation and decreased systolic shortening rate reflect impaired left ventricular function. Echocardiography allows estimation of the pressure step difference across the aortic valve. It is generally accepted that a valve orifice area >1, 0 cm2 is considered mild stenosis, 0, 75-1, 0 cm2 is moderate stenosis, and 6, 7 kPa (50 mmHg) is severe stenosis.
Complications
1, arrhythmia 10% can occur atrial fibrillation, atrial fibrillation makes the clinical condition deteriorate rapidly, and severe hypotension, syncope or pulmonary edema can occur in acute cases. Left ventricular hypertrophy, subendocardial ischemia or coronary embolism can lead to ventricular arrhythmias, and aortic valve calcification and conduction system can lead to atrioventricular block, both of which can cause syncope or even death.
2, sudden cardiac death usually occurs in those who have had symptoms before. Sudden death rarely occurs in asymptomatic people, and the incidence is only 1% to 3%.
3. Infective endocarditis is uncommon. The risk of infective endocarditis is greater in younger people with less severe valve malformations than in older people with calcific valve stenosis.
4, Embolism of the body circulation Rare. Emboli can come from calcium in calcific stenotic valves or from microthrombi in thickened mitral valves.
5, heart failure Once left ventricular failure occurs, the natural history is significantly shorter, so end-stage right ventricular failure is rare.
6, gastrointestinal bleeding Bleeding is insidious and chronic, and bleeding stops after prosthetic valve replacement.
Treatment
1.Medical treatment Since asymptomatic patients have a good prognosis and rarely die suddenly, medical treatment can be taken. Physical activity can be appropriately limited according to the patient’s degree of stenosis. Educate patients to prevent infective endocarditis. Regular follow-up echocardiography is done to determine the progression of stenosis, left ventricular hypertrophy, etc. When symptoms of angina pectoris, low cardiac output, or heart failure appear, surgical treatment should be performed as soon as possible. For those who cannot be operated, digoxin and diuretics can be used to temporarily improve the symptoms of heart failure, and nitrates should be used cautiously to treat angina pectoris. Because vasodilators can reduce peripheral resistance and left ventricular filling pressure, resulting in a decrease in cardiac output and fatal hypotension, patients with aortic stenosis are prohibited from vasodilators, especially angiotensin-converting enzyme inhibitor therapy. Anticoagulation is required in patients with atrial fibrillation.
2.Surgical treatment Once the symptoms of aortic stenosis appear or the transvalvular pressure difference >50mmHg at rest, the patient should have aortic valve replacement as soon as possible. Patients with significant left heart failure or low ejection fraction are at greater risk for surgery. Age sometimes increases the risk of surgery, but old age itself is not a contraindication to surgery. In patients with comorbid coronary artery disease, it is best to also
3. Balloon valvuloplasty Because valvular calcification is more common in aortic stenosis and because aortic balloon valvuloplasty has been shown not to reduce mortality and has a high rate of postoperative restenosis, aortic balloon valvuloplasty is currently used only in patients with aortic stenosis who have progressive heart failure but cannot tolerate surgery or to temporarily improve the patient’s condition to complete elective aortic valve replacement.
Aortic regurgitation Start the breakdown exercise
Etiology
(I) Etiology Aortic valve insufficiency can be caused by abnormalities of the aortic valve and/or aortic root.
1. Chronic aortic valve insufficiency
(1) Diseases leading to chronic aortic valve abnormalities: aortic valve diastasis, rheumatic heart disease, infective endocarditis, and degenerative leaflet calcification. Degenerative disease leading to leaflet calcification is the most common cause of chronic aortic valve insufficiency, and it often leads to both aortic valve insufficiency and stenosis.
(2) Diseases causing aortic root lesions: Maffan syndrome, aortic coarctation, hypertension combined with aortic annular dilatation, syphilitic aortitis, ankylosing spondylitis, osteogenesis imperfecta, and systemic lupus erythematosus.
2.Acute aortic closure insufficiency
(1) Infective endocarditis: it is the most common cause of acute aortic valve closure insufficiency.
(2) Aortic coarctation: Acute proximal aortic coarctation is also a major cause of acute aortic valve closure insufficiency. However, certain clinical manifestations of proximal coarctation, such as pericardial effusion with filling, acute myocardial infarction, or aortic dissection, are often more critical than acute aortic valve insufficiency.
Clinical manifestations
(II) Clinical manifestations
1. Symptoms Patients with mild or moderate chronic aortic valve closure insufficiency are usually asymptomatic, and even patients with severe chronic aortic valve closure insufficiency can be asymptomatic for many years, but once symptoms appear, the disease progresses rapidly. The main symptoms are as follows.
(1) Palpitations: associated with increased volume per beat. Palpitations may be the only symptom before the onset of dyspnea. It is especially pronounced in the left lateral recumbent position.
(2) Angina pectoris: It can occur in patients with normal coronary regurgitation and is more likely to occur with combined aortic stenosis, which is mainly due to reduced coronary perfusion due to diastolic hypotension caused by diastolic aortic valve closure insufficiency.
(3) Congestive heart failure: Nocturnal paroxysmal dyspnea may be the first symptom, but exertional dyspnea and telangiectatic breathing, as well as peripheral edema, may also occur. Patients may feel fatigued and weak.
(4) Other: Rare symptoms include profuse sweating and periodic carotid artery pain and induration. Patients with acute aortic valve closure insufficiency have primarily clinical manifestations of acute pulmonary stasis, ranging from dyspnea to acute pulmonary edema depending on the degree of regurgitation. There are often significant palpitations.
2, physical signs
(1) Auscultation: The typical murmur of aortic valve closure insufficiency is a decreasing diastolic blowing murmur that is most pronounced at the left sternal margin when sitting in an anterior tilt. The length of the murmur depends on the regurgitant flow, mild regurgitation only causes a short early diastolic murmur, with the increase in regurgitant flow, gradually become a full diastolic murmur. Aortic regurgitant blood can form functional mitral stenosis, and a soft mid-diastolic Austin Flint murmur can be heard in the apical region, which can be reduced by isoamyl nitrite inhalation. Increased cardiac output per beat results in a systolic murmur in the aortic valve region. S4 and S3 gallop rhythm may be heard in the late phase.
(2) Other: Patients with chronic aortic valve closure insufficiency have increased pulse pressure, resulting in a series of peripheral vascular signs, mainly including watery pulse, Musset’s sign, distinct carotid pulsation, capillary pulsation sign, arterial gunshot sound, and Du-roziez’s sign. Patients with acute aortic valve insufficiency have normal or only mildly increased pulse pressure, and peripheral vascular signs are rare.
X-rays, echocardiography
Auxiliary examinations
1.Echocardiography Echocardiography and Doppler are currently the most important noninvasive methods for diagnosing and evaluating aortic valve insufficiency. Echocardiography can show the function of the left ventricle, the size of the heart’s cavity diameter and the degree of left ventricular hypertrophy, which is an important tool to determine the timing of surgery. In addition it can detect strong ventricular contraction in the early stages of aortic regurgitation, mitral leaflet flutter due to regurgitant flow, and detect the flab of infected endocarditis. Doppler examination can determine the degree of regurgitation.
2. Chest X-ray Characteristically shows dilatation of the heart and aorta, and may show signs of left heart failure.
Complications
The main complications are: (1) infective endocarditis is more common; (2) ventricular arrhythmias are common and sudden cardiac death is rare; (3) heart failure appears early in acute cases and late in chronic cases.
Treatment
(E) Treatment
In general, surgery should be performed as soon as possible when a patient with chronic aortic valve insufficiency develops symptoms and/or evidence suggestive of impaired left ventricular systolic function. Patients with acute aortic valve insufficiency with significant heart failure should undergo emergency surgery. The surgical treatment of patients with aortic valve closure insufficiency mainly consists of the following modalities: ① valve replacement: is the main surgical tool for treating most patients with aortic valve closure insufficiency; ② valve repair: is indicated for a small number of simple aortic valve closure insufficiencies without valve calcification, such as aortic di- or tri-valvularization abnormalities. The treatment can also be used for aortic valve insufficiency caused by limited leaflet perforation due to infective endocarditis; ③Aortic root replacement: when the aortic valve leaflets are normal and the aortic regurgitation is only due to aortic root dilatation, aortic root replacement can be done.
2.Medical treatment: Patients with mild to moderate aortic regurgitation who have normal systolic function and no symptoms can be given medical treatment with close follow-up and observation of their condition. The main measures are: ① Remove the cause: treat the underlying disease, such as endocarditis and syphilis; ② Vasodilators: vasodilators can dilate small arteries, reduce systolic resistance, increase antegrade blood flow, reduce regurgitation, and reduce the severity of the lesion. For some patients with milder acute aortic regurgitation, vasodilators can also be used, and if necessary, sodium nitroprusside can be used for treatment.