aortic valve stenosis
Introduction
Introduction to aortic stenosis Aortic stenosis refers to an increase in the opening of the aortic valve, resulting in increased resistance to blood flow from the left ventricle to the aorta as the left ventricle contracts. The normal aortic valve area exceeds 3.0 cm2. Mild stenosis when the valve area was reduced to 1.5 cm2; moderate stenosis at 1.0 cm2; severe stenosis at <1.0 cm2. In North America and Europe, aortic stenosis is mainly seen in the elderly, caused by valvular scarring and calcification. Aortic stenosis caused by this cause often occurs after the age of 60, and often has no symptoms before 70 to 80 years old. The disease can also be caused by rheumatic fever (which occurs mostly in children). Aortic stenosis caused by rheumatic fever is often associated with mitral valve disease, including stenosis, reflux, or both. In young people, the most common cause of aortic stenosis is birth defects (see birth defects). In infancy, a narrow aortic valve may not be a problem, but it will gradually become a prominent problem as it ages. When their heart grows with age, the aortic valve is still the original size, the valve may have only two leaves instead of the normal three-leaf, or the shape of the valve is abnormal. Over time, the valve becomes stiff and narrow due to calcium salt deposition. basic knowledge Proportion of disease: in the elderly, the incidence of aortic stenosis is 1% to 2% Susceptible people: infants, elderly people around 60 years old Mode of infection: non-infectious Complications: congestive heart failure, cerebral embolism, infective endocarditis
Cause
Cause of aortic stenosis
Rheumatic fever (20%):
Aortic stenosis can be caused by sequelae of rheumatic fever, congenital stenosis or senile aortic valve calcification. 80% of patients with aortic stenosis are male. Simple rheumatic aortic stenosis is rare, often associated with aortic regurgitation and mitral valve disease. Pathological changes are adhesions and fibrosis at the valve junction, and the deformation of the valve exacerbates the damage of the valve, leading to calcium deposition and further stenosis.
Congenital aortic stenosis (20%):
It can be single leaf, two leaf or three leaf. The single-leaf type is already stenotic at birth, and the fissure and calcification of the valve are progressively aggravated, causing severe left ventricular outflow tract obstruction, and the child dies within a year. 50% of congenital aortic stenosis is bilobal and 30% is trifoliate. The two kinds of leaflet malformations may have no obvious stenosis in the childhood valve mouth, but the abnormal leaflet structure degenerates due to eddy current impact, causing thickening of the valve leaflets, calcification, stiffness, and finally leading to stenosis of the valve orifice, and may also be combined with insufficiency. Aortic root eddy current impact can occur after stenosis and expansion (see "Congenital Cardiovascular Disease" chapter "Aortic stenosis" section).
Senile aortic valve calcification (10%):
It is a degenerative change that accounts for 18% of elderly patients. The valve undergoes degenerative changes, fibrosis and calcification, and leaflet fusion. The stenosis of the valve is relatively light, and some patients may be accompanied by a regurgitation.
Pathogenesis
The main pathophysiological changes after aortic stenosis are increased left ventricular resistance during systole, which increases left ventricular contractility to increase transvalvular pressure gradient and maintain normal cardiac output at rest. This gradually causes left ventricular hypertrophy, leading to decreased left ventricular diastolic compliance, increased end-diastolic pressure; although resting cardiac output is still normal, but increased cardiac output during exercise. After severe stenosis of the valve, the pressure gradient across the valve is reduced, left atrial pressure, pulmonary artery pressure, pulmonary capillary compression and right ventricular pressure can be increased, and cardiac output is reduced. Decreased cardiac output can cause hypoxia, hypotension and arrhythmia, and insufficient blood supply to the brain can cause dizziness, syncope and other manifestations of cerebral hypoxia. Left ventricular hypertrophy, increased contractility, significantly increased myocardial oxygen consumption, further aggravating myocardial ischemia.
Prevention
Aortic stenosis prevention
Rheumatic heart disease can be prevented. If it can effectively control the infection of a chain pharyngitis, it will not get rheumatic fever, and rheumatic heart disease will not occur. The main preventive measures are:
1, primary prevention
Refers to the prevention of the first episode of rheumatic fever, the key is early diagnosis and treatment of methyl chain tonsillitis, where fever, sore throat or discomfort, headache, abdominal pain, pharyngeal congestion and sputum tonsils have secretions should be swallowed swab culture before treatment To determine the presence or absence of a chain growth, if positive, should start antibiotic treatment immediately.
In addition to penicillin allergy, penicillin should be the drug of choice for all patients, for the following reasons:
1 All strains of Streptococcus hemolyticus are equally sensitive to penicillin.
2 After applying for more than 40 years, the average bacteriostatic and bactericidal concentration of penicillin against this bacteria did not change, still around 0.005g/ml.
3 There is no sign of resistance to penicillin.
4 There is no other antibiotic anti-streptococcal infection activity and clinical effect than penicillin G.
5 penicillin is relatively inexpensive, the antibacterial spectrum is narrow, so it will not inhibit the normal flora, can avoid double infection, and has fewer side effects than other effective antibiotics. Beta-penicillin is suitable for patients who can not complete oral penicillin treatment for 10 days; Personal history or family history; or geographical, socio-economic environment in patients with high RF area, intramuscular injection of benzathine alone is more painful, injection with benzathine penicillin plus procaine penicillin injection is not painful, mixed injection The dose of benzathine penicillin should be: 600,000 U for patients <27 kg and 1.2 million U for patients with >27 kg. For most small patients, a mixture of benzathine penicillin 900,000 U and procaine penicillin 300,000 U Good results can be obtained, but this preparation is not suitable for adolescent or adult patients. For areas with low RF incidence, penicillin V can be treated orally. Penicillin V has acid stability and absorption, and the concentration of penicillin produced is higher. High, for children and adults, the dose is 250mg, 3 times / d, a total of 10 days, must emphasize the importance of continuous medication for 10 days, even if the symptoms disappear after a few days of medication, should be served for 10 days, less than 10 Day effect Significantly reduced, but more than 10 days can not increase the efficacy, its treatment of streptococcal pharyngitis is the same or almost the same as oral penicillin, for adults, 2 times / d drug efficacy is not reliable, 3 to 4 times / d is better , but the maximum dose does not exceed 1g / d, followed by cephalosporin IV, VI 0.25g, 4 times / d, a total of 10 days, but can not be used for patients with penicillin anaphylactic shock, tetracycline has not been produced domestically, sulfadiazine can not eliminate the chain Cocci, therefore not used to treat streptococcal angina, but continuous use of sulfadiazine is effective in preventing RF recurrence.
2, secondary prevention (the prevention of rheumatic fever recurrence)
Continuous antibiotic treatment is needed for patients with a clear history of rheumatic fever or existing rheumatic diseases to prevent recurrence of rheumatic fever.
(1) Precautionary period: Depending on the risk of recurrence, in general, people with upper respiratory tract infections, crowded living, poor medical conditions, and multiple episodes of history have a high risk of recurrence and a long time to prevent medication. On the contrary, it can be shortened appropriately. Patients with rheumatoid carditis have a relatively high risk of recurrence of carditis. They should receive long-term antibiotic prophylaxis until adult or lifelong prevention. On the contrary, patients who have not had rheumatic carditis have recurrence. The risk of involvement is low and antibiotic prophylaxis can be stopped in a few years. In general, prevention should last until at least 5 years after the patient reaches the twenties or the last rheumatic fever.
(2) Prevention program:
1 intramuscular injection of benzathine penicillin G: a common solution is long-acting penicillin preparation benzathine penicillin G 1.2 million U, intramuscular injection, once every 4 weeks, in acute RF high-risk countries and regions, and high-risk patients, preferably every 3 weeks Intramuscular injection 1 time.
2 oral antibiotics: patients with low risk of RF recurrence, such as those who have reached the end of puberty or adolescence or at least 5 years without recurrent rheumatic fever, can be changed to oral antibiotic prophylaxis, according to the recommended doses:
A. Sulfadiazine: body weight > 27kg, dose 1.0g, 1 time / d, weight 27kg, 0.5g per day, side effects are light and rare, occasionally can cause leukopenia, should check blood cell count every 2 weeks, pregnancy Advanced patients are banned because sulfadiazine can cross the placental barrier and compete with the bilirubin in the fetus for albumin binding sites.
B. Penicillin V: The dose is 250mg, 2 times / d, the allergic reaction is the same as the intramuscular injection of penicillin, and the penicillin skin test should be used before use.
C. Erythromycin: 250mg, 2 times / d, suitable for allergic to penicillin and sulfa drugs.
D. Chinese medicine such as honeysuckle, berberine, astragalus, cork, dandelion, radix isatidis, and andrographis paniculata; Chinese patent medicines such as silver yellow tablets, Yinqiao tablets, anti-inflammatory tablets, silver yellow needles, etc. have good effects on hemolytic streptococcal infection, choose application.
According to a recent WH0 report, 33,651 patients with RF or RHD were enrolled in secondary prevention for treatment in 1986-1990, but only about 63.2% of patients completed secondary prevention, 95.7% of whom used long-acting penicillin. Intramuscular injection once, 2.1% oral penicillin, 0.1% sulfadiazine, 2.1% erythromycin, 0.3% of patients had adverse reactions to penicillin, 53 cases of RF recurrence, accounting for 0.4% of patients/year, if not prevented The recurrence rate of rheumatic fever is as high as 60% of patients per year.
Complication
Aortic stenosis complications Complications Congestive heart failure, cerebral embolism, infective endocarditis
The disease can be complicated by the following diseases:
1, congestive heart failure: 50% to 70% of patients die of congestive heart failure.
2, embolism: more common in calcified aortic stenosis, the most common cerebral embolism, can also occur in the retina, limbs, intestines, kidneys and spleen and other organs.
3, subacute infective endocarditis: can be seen in the two-leaf aortic stenosis.
Symptom
Symptoms of aortic stenosis Common symptoms Snoring, respiratory and dyspnea, labor, syncope, systolic murmur, arrhythmia, paroxysmal nocturnal dyspnea, endocardial, elastic fiber, angina, angina, loss of consciousness
Light can be asymptomatic for many years. Severe stenosis may have syncope, angina or heart failure, and a small number of cases may be sudden death, ventricular fibrillation and cardiac arrest caused by myocardial ischemia.
1, symptoms
More common in men, simple rheumatic aortic stenosis is rare, mostly combined with dysfunction and/or mitral valve disease.
(1) left ventricular compensation period: mild to moderate aortic stenosis, can be asymptomatic for many years, the autopsy found that about 5% of patients with aortic stenosis can suddenly die without obvious symptoms.
(2) Left ventricular decompensation: The characteristic symptoms of severe aortic stenosis are angina, syncope and heart failure.
1 angina pectoris: angina pectoris occurs in aortic stenosis, often suggesting that the valve area is less than 0.8cm2, which is not easy to distinguish from coronary heart disease angina pectoris. Aortic valve stenosis may cause angina pectoris and myocardial hypertrophy due to increased oxygen demand and relative decrease in coronary flow. Insufficient oxygen supply, resulting in subendocardial myocardial ischemia, according to statistics, with or without angina, about 50% of patients with aortic stenosis over 40 years of age coexist with coronary heart disease.
2 syncope: often after labor or suddenly change from supine position to upright position, there is blackening or transient loss of consciousness, which may be the same as the mechanism of angina pectoris, that is, myocardial oxygen supply is reduced when myocardial oxygen demand increases, labor Sexual syncope is due to the expansion of peripheral blood vessels due to labor, but there is no corresponding increase in cardiac output. Erective syncope is caused by the inability to increase cardiac output during sudden standing. Sometimes sublingual nitroglycerin can also cause syncope when treating angina. Small doses of nitrate can cause significant relaxation of the peripheral veins, which leads to a decrease in the amount of blood return to the heart and a decrease in the preload of the heart. When the dose is increased, the peripheral resistance of the arterioles also relaxes, causing the left ventricular afterload to decrease, but the heart There is no corresponding increase in blood output, resulting in insufficient blood supply to the cerebral circulation. In addition, severe arrhythmias caused by myocardial ischemia, such as persistent ventricular tachycardia, high atrioventricular block, severe sinus bradycardia, etc. can also lead to Syncope or sudden death, patients with syncope or angina survive an average of 2 to 5 years.
3 left heart failure: from early labor dyspnea, and then to paroxysmal nocturnal dyspnea, sitting breathing and acute pulmonary edema, early heart failure may be related to left ventricular diastolic dysfunction; late is associated with systolic dysfunction, The life expectancy of patients with aortic stenosis and left heart failure is expected to be less than 2 years.
4 sudden cardiac death: can be the first symptom of aortic stenosis, there may be repeated angina or syncope episodes, the cause of sudden death is mostly related to acute myocardial ischemia induced ventricular fibrillation or cardiac arrest.
2, signs
(1) Left ventricular compensation period:
1 The apex beats to the left and down.
2 The apical area can reach a slow lifting impulse; the aortic valve area can reach the systolic fine tremor.
3 The heart of the voiced voice expands to the lower left.
4 auscultation features:
A. Aortic valve area systolic murmur: heard in the aortic valve area a loud ( 3 ~ 4 / VI level), rough, high pitch, long time-limited hair-like jet systolic murmur, this noise is due to Systolic blood flow through the stenotic valve, caused by eddy currents in the ascending aorta, the murmur is rhomboid, appears after S1, in the contraction, peaks in the late stage, and disappears after S2, to the bilateral carotid and clavicle Lower arterial conduction, with the severity of aortic stenosis, the louder the noise, the longer the duration, and the peak of the diamond is shifted back, but when the severe aortic stenosis is accompanied by cardiac insufficiency or tachycardia, the murmur becomes shorter. And soft.
B. Aortic systolic early jetting sound: When the aortic valve is light and moderately stenotic, in the aortic valve area or the second auscultation area of the aortic valve, the early jetting sound can be heard, and there is a short and loud extra after S1. Sound, a sudden opening of the aortic valve causes high-speed blood flow to impact the narrow aortic valve and cause vibration, more common in children, adolescent congenital aortic stenosis; if rheumatic aortic stenosis, due to valve adhesion, thickening It affects the valve activity, so it is rarely heard.
C. A2 attenuated and reversed aortic valve area: In severe aortic stenosis, due to mechanical or electrical delay of left ventricular contraction, left ventricular ejection time is significantly prolonged and S2 reverse splitting occurs (paradoxical splitting). The result is that the first component of the second heart sound (aortic valve component) is delayed after the second component (pulmonary valve component). After deep inhalation, the pulmonary artery flap is delayed, the reverse split disappears, and the deep exhalation occurs. Increase the left heart return blood, so that the aortic valve closure is more delayed, so the inverse split aggravation, when the severe valve thickening, calcification, A2 can be weakened or even disappeared.
D. Others: In the middle and severe aortic stenosis, left ventricular hypertrophy, due to decreased left ventricular compliance, resulting in left ventricular diastolic left atrial contraction, so the apical area can smell S4; severe aortic stenosis can be accompanied Mild reflux, so you can often hear mild diastolic watery murmurs in the third and fourth intercostals of the left sternal border.
E. Vascular signs: The pulse is weak and slow, the systolic blood pressure is reduced, the diastolic blood pressure is normal, and the pulse pressure difference is small.
(2) Left ventricular decompensation period:
1 When the left aortic stenosis causes left ventricular enlargement: Relative mitral regurgitation can occur, and systolic murmurs can be heard in the apical region 2~3/VI, while the latter improves left ventricular function and left ventricular systolic The noise can be alleviated, and vice versa.
2 When the left heart is insufficiency: S4 galloping can be heard in the apex area.
Examine
Aortic stenosis
1, X-ray inspection
Mild aortic stenosis and normal heart shadow; middle and severe stenosis can be seen as follows:
1 left ventricular centripetal hypertrophy does not increase the proportion of cardiothoracic, because the ventricular cavity does not increase significantly, only the fourth bow of the anterior slice is round bulging;
2 liters of aortic protrusion and stenosis and expansion;
3 fluoroscopy can be seen in the aortic valve calcification;
4 left ventricular enlargement and pulmonary congestion in heart failure;
5 two-leaf aortic valve can sometimes be associated with aortic coarctation, chest radiograph can be seen by the collateral vessels caused by the lower edge of the rib.
2, ECG
Left axis and left ventricular hypertrophy and strain of the electric axis; may have atrioventricular block, left bundle branch block; V1 lead P wave inversion or V1ptf<0.03mms when left atrial enlargement, due to myocardial fibrosis, chest Pathological Q waves can appear in the lead.
3. Echocardiography (UCG)
(1) M-type and two-dimensional UCG: aortic valve leaf thickening, its M-shaped motion curve can be thickened multiple echoes, valve leaf opening amplitude is reduced, M-shaped UCG aortic valve activity curve diamond-shaped hexagonal box anteroposterior diameter Reduced, the distance between the anterior and posterior leaves of normal people is 15 ~ 25mm, in the absence of left ventricular discharge, the distance between the anterior and posterior leaves is less than 15mm, suggesting aortic stenosis, two-dimensional UCG shows aortic valve thickening, deformation The echo is enhanced, the activity is stiff, and the opening is limited. On the short axis diagram of the aorta, the valve mouth is triangular, eccentric or irregular. The area of the valve is measured on a two-dimensional map, which is normally 2 to 4 cm 2 .
Indirect signs: the amplitude of the M-shaped motion curve in the aortic root is reduced, and the tremor wave disappears; the ventricular septum and the posterior wall of the left ventricle are symmetrically thickened, the left ventricular cavity can be enlarged or normal, and the left atrium can be enlarged later.
Transesophageal UCG can more clearly show the three leaflets of the aorta and its opening and closing activities, especially the examination of the superior structure of the valve is superior to the transthoracic UCG.
Three-dimensional, four-dimensional UCG can observe the aortic valve and its lobes from different angles, the subvalvular structure, more two-dimensional, M-type intuitive, has entered clinical use, and its practicality is being further improved.
(2) Doppler UCG: increased aortic valve flow velocity, spectral Doppler measurable and high-speed jet spectrum of aortic valve, often greater than 2m / s; color Doppler display colorful mosaic on the aortic valve The blood flow, cross-valve pressure step can reflect the degree of stenosis and hemodynamic changes of the valve to some extent. The peak pressure difference p and the average pressure difference Pm are commonly used. p may overestimate the severity of the stenosis. Degree, Pm refers to the average value of all instantaneous pressure differences at both ends of the systolic aortic valve. It is also a commonly used index in cardiac catheterization, which can accurately reflect the degree of aortic valve stenosis. See Table 1, a simpler method is to directly measure the peak blood flow velocity of the aortic valve, 2 ~ 3m / s is mild stenosis; 3 ~ 4m / s is moderate stenosis; greater than 4m / s is severe stenosis.
Ultrasound diagnosis of aortic stenosis should be based on two-dimensional and M-type, Doppler can be used as a reference and detection of hemodynamics.
4, cardiac catheterization
Left heart catheterization can not only accurately determine the transvalvular pressure difference and the valve area, but also judge the severity and evaluate the left heart function.
(1) Record and measure the peak-to-peak pressure difference, maximum differential pressure and mean pressure difference of the left ventricle-aorta.
(2) Right heart catheter thermodilution method to measure cardiac output.
(3) Calculate the aortic valve area using the Golin formula.
(4) Coronary angiography for suspected coronary heart disease.
(5) For suspected aortic valve, subvalvular stenosis can be identified according to different parts of the pressure curve and left ventricular angiography.
Diagnosis
Diagnosis and diagnosis of aortic stenosis
diagnosis
Rheumatic aortic stenosis, more common in adolescents, with a history of rheumatic fever, most with aortic regurgitation and mitral valve disease, rare rheumatic aortic stenosis, elderly degenerative aortic stenosis, with age A gradual increase in aortic valve degeneration and calcification, which can occur in patients with a normal valve or mild valvular dysplasia, with no adhesion and fusion at the leaflet junction, and the latter with the rheumatoid aorta Pathological identification of stenosis, congenital aortic valve two-leaf deformity accounted for more than 50% of congenital aortic valve abnormalities, after a few decades, aortic stenosis gradually formed, of which about 40% with aortic valve Incomplete closure, the diagnosis of aortic stenosis can be based on medical history and physical signs, combined with X-ray, electrocardiogram, echocardiography and left cardiac catheterization, generally can be diagnosed.
Differential diagnosis
1. Identification of rheumatic, congenital and degenerative aortic stenosis.
2, the differential diagnosis of congenital aortic stenosis is divided into aortic stenosis, aortic stenosis and aortic stenosis three types, with the most valvular stenosis, less subvalvular stenosis, and the stenosis of the stenosis is the least .
3, pulmonary stenosis, aortic stenosis and pulmonary stenosis identification.
4, hypertrophic cardiomyopathy, especially obstructive hypertrophic cardiomyopathy when systolic jet murmur occurs in the left sternal border, it needs to be differentiated from aortic stenosis.
