Valvular heart disease is heart lesions mainly involving the valve lesions.
Valvular heart disease - OverviewHeart valve where the valve or some animal organs which can open and close the membranous structure.Valve between the heart's four chambers (room), passive open or closed to ensure that the circular flow of blood in one direction. Film in the role of the heart will never stop the blood circulation activities are very common and very critical: the valve is a guard to prevent blood reflux into the ventricular just leave.
Between the atrium and the ventricle in between the ventricle and blood vessels leave the ventricle, has a valve. Blood flow after the valve will be closed, issue the heartbeat sound we hear on TV.
The heart of the left and right atrioventricular orifice and aortic mouth, pulmonary artery valve lesions can be. The clinical features of endocardial murmur and the corresponding changes in the pulse and blood circulation disorders. A
Parts of the lesion can make a judgment based on heart sounds, pulse and ECG results. Two or more parts of the lesions that combined valvular heart disease difficult to diagnose.
Valvular heart disease - Brief Introduction
Valvular heart disease (valvular heart diseases), cardiac lesions mainly involving the valve lesions.
About 1/3 of cases have occurred in various types of heart disease valvular heart disease, the vast majority of rheumatic carditis caused by a small number of degenerative changes or congenital deformity caused.
Of rheumatic disease process, about 3/4 cases of lesions invading the heart, caused by the myocardium, endocardium, pericardium, and valvular lesions. Recurrent rheumatic endocarditis, the resulting chronic valvular heart disease, including mitral valve disease is the most common (about 95%), followed by aortic valve disease (25%) and tricuspid valve disease (10% ) and pulmonary valve disease is rare (<1%).
Aortic valve disease occur in isolation are also less often jointly with mitral valve disease. Heart valve disease can be manifested as simple narrow, simple regurgitation or both the joint presence.
Heart valve disease - mitral valve diseaseMitral stenosis
The vast majority of rheumatic endocarditis caused by a small number of congenital malformations and left atrial tumor, vegetation or thrombosis non-valve tissue obstruction of the mitral valve hole caused.
Rheumatic mitral stenosis, rheumatic heart disease, about half of patients aged 20 to 40 years for the most common, women have a higher prevalence of about 2-fold in men.
① pathological anatomy and pathophysiology. Mitral stenosis is about 2 years until the formation of self-rheumatic endocarditis. Divided into three pathological types: diaphragm type, before and after the leaf edge is generally based on the severity of the lesions of different fibrous thickening, adhesions, sometimes calcification, valve hole stenosis, valvular lesions lighter activities are generally unrestricted ; funnel-type diaphragm valve disease itself is more serious, tendons, adhesions occurred, shortened, so that the margins of the valve to about 1cm organizations are stretched to form a funnel-shaped, front flap can still be activities, but subject to certain restrictions; funnel type valve with severe fibrosis, abnormal chordal papillary muscle shortened, so that the valve stiff, narrow funnel-shaped.
Hemodynamic changes caused by mitral stenosis is significantly correlated with stenosis severity. Clinical generally based on the size of the division of the narrow valve hole diameter degree of stenosis as mild (> 1.2cm), moderate (0.8 ~ 1.2cm) and severe (<0.8cm) three. When the narrow valve hole reduced to below 1.2 ~ 1.5cm, you can change as follows: diastolic left atrial flow out to the left ventricular blood flow limited, the increased left atrial pressure, left atrial - left ventricular diastolic pressure gradient increases, and thus left atrial hypertrophy, expansion, pulmonary vein and pulmonary microvascular corresponding increased pressure and expansion, and the formation of pulmonary congestion; cardiac output can not, as normal as increased or not increased after exercise, or even anti-can decline. Generally mild to moderate stenosis, compensatory mechanisms that rely on left atrial still capable of maintaining near-normal cardiac output, cardiac output after exercise, not only does not increase, often, however, reduced; pulmonary microvascular pressure increased more than the plasma colloidal osmotic pressure (30mmHg) can produce pulmonary edema; but the following compensatory mechanisms to prevent its occurrence: alveolar and microvessel organization, particularly the alveolar basement membrane thickening, lymphatic reflux strengthen; pulmonary artery spasm blood flow by reducing to prevent pulmonary microvascular pressure increased too much; but the small pulmonary arteries spasm, allows pulmonary hypertension is more obvious, right heart load more weight and lead to right heart failure; right heart failure, pulmonary artery pressure is reduced, but also indirectly to pulmonary microvascular pressure without being unduly increased.
② clinical manifestations and laboratory tests. Symptoms of mitral stenosis severity, vary. Mild stenosis can be asymptomatic or mild; moderate stenosis is more caused by pulmonary congestion and cardiac output to reduce the symptoms, such as difficulty breathing, cough, palpitations, hemoptysis, cyanosis, fatigue, pulmonary edema, heart former area pain, huskily, difficulty in swallowing. Right heart failure, the symptoms can reduce, but the weakness is more obvious. Atrial fibrillation atrial thrombus loss can cause embolism symptoms.
Apex beat palpation signs: Typical short, precordial diastolic tremor; percussion sector increased heart; auscultation the first heart sound of mitral valve area hyperthyroidism and brittle, the second heart sound after mitral valve slap tone drum and the diastolic murmur, was the first ring light systolic enhanced features; split second heart sound (S2), the pulmonary second sound (P2), hyperthyroidism. In addition, severe stenosis with pulmonary hypertension and right ventricular dilatation, they can still have the relativity of tricuspid insufficiency early systolic regurgitation murmur and (or) relative pulmonary regurgitation early diastolic splashing murmur, acute pulmonary congestive bronchial wheeze; pulmonary edema, pulmonary moist rales. In late lesions, right heart failure, jugular vein distention, hepatomegaly, lower extremity edema.
X-ray chest X-ray: mild stenosis change is not obvious or lighter; have typical X-ray manifestations of moderate to severe stenosis, left atrial enlargement, after the right side of the bit-slice heart shadow a double shadow of the right anterior oblique barium meal examination showed lower esophageal left atrial enlargement compression backward position; left column oblique see right ventricle; aortic smaller. Pulmonary artery segment protrudes, and left and right pulmonary artery widened lung fields due to blood stasis and texture increased, the expansion of the pulmonary veins. The above performance with the stenosis severity increased.
ECG: right axis deviation, clockwise transposition Ⅰ and II, aVL, aVR lead in the P-wave widening (> 0.11 seconds) and a notch or amplitude increased. Moderate to severe stenosis and more right ventricular hypertrophy with strain. Lesions heavier or older with atrial fibrillation can also be associated with other arrhythmias.
Echocardiography: M-type echocardiographic left atrial enlargement icon mitral curve diastolic peak E decreased slowly, the F point disappeared and showed a flat line, namely battlements like change; flap diastolic anterior lobe showed activities in the same direction; and right ventricle performance. Two-dimensional ultrasound shows before and after the valve tip adhesion was bulging with the activities, opening rates were significantly smaller (normally 2 ~ 3cm), the first valve body diastolic left room, was a balloon-like change. Diastolic Doppler ultrasound, not only by mitral left ventricular side of the measured turbulence, but also by the frequency shift size projections blood flow between the flow rate and atrioventricular pressure gradient and poor parameter.
③ the differential diagnosis. The disease difficult to diagnose, but to be other causes of mitral valve obstruction, such as congenital mitral stenosis, left atrial myxoma, as well as a variety of reasons (such as medium-sized ventricular septal defect, patent ductus arteriosus , mitral regurgitation, aortic insufficiency) due to "relative" mitral stenosis differentiated the latter noise of short duration, mitral valve slap tone, noise loudness in the application of antihypertensive drugs reduced, is enhanced after the boost drug can be identified.
The ④ complications. Mainly atrial fibrillation, congestive heart failure, pulmonary infection, embolism, infective endocarditis, recurrent laryngeal nerve by the expansion of pulmonary artery compression caused by paralysis, hoarseness, dysphagia of the esophagus because of the oppression of left atrial enlargement .
The ⑤ prognosis. The possibility of whether surgery depends on the narrow valve hole and the degree of cardiac enlargement, complications and other factors. Mild stenosis, asymptomatic, no complications, the prognosis is good, and can be maintained with mild to moderate labor for more than 20 years; moderate to severe stenosis, symptoms and cardiac enlargement, and about 40% survive for 20 years; able to surgical treatment the prognosis is better.
The ⑥ prevention. Mild stenosis in asymptomatic persons, generally do not need special treatment, but should avoid heavy physical activity and prevention of rheumatic activity relapse; moderate to severe stenosis and symptoms, and given the appropriate treatment should be based on the degree of cardiac decompensation. But the fundamental treatment of this disease is to lift the valve hole is narrow, in order to reduce the pressure gradient between the left atrial-left ventricular, to return to normal or near normal cardiac function. It should be timely to consider surgery expansion. Indications for surgery are as follows: lesions of the diaphragm type, may also consider the diaphragm funnel-shaped; the age of 20 to 45 years; appropriate cardiac function Ⅱ ~ Ⅲ grade IV level features also consider; merge pregnancy to the first five 6 months of surgery is appropriate; if combined with active rheumatism, endocarditis complications, you control three months after surgery due. To lift the valve hole stenosis can be surgical or interventional catheter dilatation.
Funnel or associated with mitral regurgitation should be considered for valve ring plasty or artificial valve replacement. For details see mitral stenosis.
Congenital mitral stenosisThe pathological changes mainly for valvular thickening, at the junction of fusion, chordal papillary muscle thickening, shortening, etc., resulting in the valve hole is narrow, or the left atrium valve ring formation, mitral parachute-like deformity, single papillary muscle symptoms, abnormal mitral valve arch caused by valve hole obstruction. Congenital mitral stenosis simple existence are rare, and more with atrial septal defect with the presence of form Lutengbahe's syndrome. It will also patent ductus arteriosus closure of ventricular septal defect, aortic stenosis coexist. Congenital mitral stenosis or obstruction for the children of the former cases, children with poor growth, pale, fatigue, shortness of breath, recurrent lung infections, syncope, pulmonary edema. Signs and laboratory tests and acquired mitral stenosis. Surgery to replace the artificial valve.
Due to mitral valve clogged left atrial myxoma in the left atrial myxoma is the most common form of cardiac tumors, more common in women, mostly originated in the left side of the myxoma atrial septal nearly oval fossa, a few may originate in the right atrium and left ventricle or right ventricle, often pedunculated tumor connected. Patients with valvular heart without other lesions; but blocked by the tumor in the droop of the diastolic mitral valve hole, so that the left atrial flow injection of the left ventricular blood blocked, the cause of mitral stenosis similar symptoms and signs, in addition to the easy be misdiagnosed as mitral stenosis, can also be misdiagnosed as infective endocarditis, rheumatic activity or myocarditis. With mitral stenosis and identify key points are:
① no rheumatic fever history;
② sudden onset, the symptoms are often compared with the signs and X-ray examination findings significantly;
The ③ signs and symptoms of intermittent, supine become obscure or disappear;
④ more atrial fibrillation;
⑤ ultrasound echocardiography to show the rear in the mitral valve, systolic and diastolic are the aperture of a cotton wool back to the acoustic diagnosis can be funded. For details see
Mitral regurgitation
The mutual synergy of the mitral valve leaflets, annulus, chordae, papillary muscles, atrial and ventricular free wall of six anatomical device is to ensure the normal mitral valve function important factor in any one occurrence of dysfunction can be caused by mitral regurgitation. Mitral insufficiency cause of a lot, but the most common rheumatic and other degenerative, infective endocarditis, papillary muscle dysfunction, cardiac trauma, primary cardiomyopathy and congenital valve malformations caused by
Rheumatic mitral incomplete statistics of the Shanghai area a group of 13 032 cases of rheumatic heart disease, simple mitral regurgitation accounted for 3.8%, close to insufficiency associated with stenosis of 27%.
① pathological anatomy and pathophysiology. Due to recurrent endocarditis, valve hardening, shortening or deformity, tendons adhesion, fusion, chordal and papillary muscle thickening and shortening or fusion, and the endocardium caused by valve does not shut down caused by regurgitation.
Mitral regurgitation, left ventricular part?? Room capacity increases, the pressure increased, while the left and cardiac output decrease. With mitral stenosis or left ventricular failure, too much blood in the left atrium diastolic flow can still be injected into the left ventricle and increase left ventricular load, left ventricular gradual expansion and hypertrophy, which may eventually cause the left heart failure. The left atrium, left ventricular expansion and pressure increased, which can cause lung congestion and increased pulmonary artery pressure, which may eventually cause right ventricular hypertrophy and failure.
② clinical manifestations and laboratory tests. More than mild regurgitation, no obvious symptoms; moderate due to the increased amount of blood back into the left atrium, reducing cardiac output, there may be heart palpitations, shortness of breath, fatigue, weakness, symptoms get worse after the event. The late lesions, may have symptoms of pulmonary edema, hemoptysis and right heart failure. The disease symptoms more than mitral stenosis late and light; but if it is associated with mitral stenosis, the earlier heavier.
Signs: mainly the apex can be heard due to a large number of left ventricular blood back into the left atrial systolic murmur, high tone and rough, mostly hair-like, exhale enhance loudness in grade Ⅲ or more . Lesions before valve-based, weakening of the first heart sound or can not smell, and noise can be left armpit and back conduction; after valve-based multi-conduction to the bottom of the heart. Moderate or severe regurgitation, left ventricular enlargement compared with the third heart sound and relative mitral stenosis short diastolic murmur. More S2 division and P2 hyperthyroidism. Such as mitral valve stenosis, the diastolic murmur long and loud, and no third heart sound.
③ X-ray chest radiograph. With mitral stenosis are similar to, and left ventricular, left atrial enlargement is more pronounced and obvious left atrial appendage.
The ④ ECG. Left axis deviation, left ventricular hypertrophy with strain, and atrial fibrillation were more common.
The ⑤ echocardiography map. M-mode echocardiography icon of left ventricular and left atrial enlargement is obvious, the left atrial posterior wall of the C concave depth> 4mm. Valve leaflets in systole before and after the show of the two-dimensional can not be closed. Pulse Doppler examination showed the left atrium near the mitral valve orifice in systolic turbulence shadow with the characteristic of the reflux of blood flow away from the probe.
⑥ differential diagnosis. Signs and laboratory findings, and more can be confirmed. Be closed with non-rheumatic mitral valve insufficiency and severe mitral stenosis due to relative tricuspid regurgitation identification.
⑦ complications and prognosis. Complicated by right heart failure, atrial fibrillation and arterial embolism compared with mitral valve stenosis is less, but more infective endocarditis. The patients, although the early and more asymptomatic, but symptoms if there illness can be rapid development and progression and poor prognosis. Timely surgical correction, the prognosis is excellent.
⑧ prevention. Basically similar to mitral stenosis. Moderate or severe regurgitation, and cardiac function in grade Ⅱ, cardiac enlargement, cardiothoracic ratio> 55 to 60 percent or more, you should consider mitral valve plasty or artificial valve replacement surgery. Older than 45 years of age should undergo coronary angiography if coronary heart disease and bypass surgery indications for surgical treatment. Cardiac function Ⅲ, accompanied by severe pulmonary hypertension greater surgical risk, the effect is also poor.
Congenital mitral valve regurgitation caused by congenital malformations tendons, shortening or absence of the valve leaflets is too short, too long or cleft, valve ring expansion of the abnormal. Patients with multiple cases for children, developmental delay, more heart palpitations, shortness of breath, weakness, fatigue, recurrent respiratory tract infections, and finally heart failure. Signs and laboratory tests and acquired mitral regurgitation. Treatment for mitral valve plasty or artificial valve replacement.
Mitral valve prolapse syndrome when the heart contracts, the abnormal mitral valve to the left room prolapse, most patients have a tone and the late Kara contraction (or) late systolic murmur, accompanied by ECG changes. The disease can occur at any age, is more common in women. The cause of many, mainly myxoid degeneration of mitral valve chordae is too long or broken, papillary muscle dysfunction or rupture. Prolapse degree of light due to hemodynamic changes, may be asymptomatic; severe accompanied by moderate to severe mitral regurgitation may be bleeding and cardiac output to reduce the symptoms. In severe cases, may have left ventricular failure. Infective endocarditis, pulmonary infection or embolism, Erzhi condition deteriorated rapidly. The main signs of contraction, late Kara audio, Department of prolapse into the left atrium valve jitter generated by the apical; late systolic murmur multi-step - Department of valvular insufficiency. ECG II, III, aVF ECG T-wave inversion and ST segment mild depress. M-mode echocardiography examination revealed contraction in late backward shift of the "hammock-like" waveform; two-dimensional visible prolapse into the left atrium valve image. Left ventricular angiography can help confirm the diagnosis. In the treatment of progressive mitral insufficiency with heart failure, the need to control heart failure, and timely to consider artificial mitral valve replacement.
Papillary muscle dysfunction causes, the most common is caused by coronary heart disease or hypertensive heart disease, myocardial ischemia, resulting in a papillary muscle injury, necrosis, then fibrosis with dysfunction, and even lead to rupture, resulting in mitral regurgitation. Symptoms depends on the cause of the basic lesion of papillary muscle dysfunction and mitral regurgitation severity without a. Signs of the main apical systolic murmur, ischemia, papillary muscle dysfunction, mitral valve can not close a systolic murmur, ischemia improvement or recovery after the noise is diminished or disappeared, noise times can be a full-systolic change for the contraction of the mid-or late; the first heart sound to hyperthyroidism, can enhance deep inspiration. More ischemic ST-T changes in ECG. Echocardiography Figure examination diagnosed in capital. If necessary, can be used for left ventricular angiography. Often in dealing with medical treatment of basic disease and heart failure, medical treatment does not, you need to consider surgical treatment, including artificial valve replacement according to the disease, coronary artery bypass grafting and aneurysm resection surgery. For details see mitral regurgitation.
Valvular heart disease - tricuspid valve diseaseTricuspid atresiaTricuspid atresia tricuspid atresia is a cyanotic congenital heart disease, the incidence rate of about 1 to 5% of the congenital heart disease. Ranks third in cyanotic congenital heart disease Relay tetralogy of Fallot and aorta dislocation. The main pathological changes of tricuspid atresia or tricuspid lack of patent foramen ovale or atrial septal defect. For details see tricuspid atresia.
Tricuspid regurgitationTricuspid regurgitation tricuspid insufficiency (tricuspidinsufficiency) is rare in the valve leaflet involvement, mostly caused by pulmonary hypertension and tricuspid expansion. Due to congenital or acquired factors caused by the expansion of tricuspid valve disease or tricuspid annulus, resulting in tricuspid regurgitation tricuspid valve in systole can not be completely closed, said. There are two kinds of functional and organic disease, the former is mostly secondary to lesions lead to the expansion of the right ventricle, the incidence rate is very high, such as primary pulmonary hypertension, mitral valve disease, pulmonary valve or funnel stenosis, right ventricular myocardial infarction. Which congenital abnormalities such as Ebstein anomaly and a common atrioventricular canal, can also be acquired lesions, such as rheumatic inflammation, coronary artery lesions caused by tricuspid valve papillary muscle dysfunction, trauma, and endocarditis. Worse as the original prognosis of the disease incidence due to the nature and severity of heart failure may be due to primary pulmonary hypertension and chronic pulmonary heart disease prognosis is often compared with mitral valve disease or atrial septal defect caused by . Medical treatment can relieve symptoms, and curable surgery. For details see tricuspid regurgitation.
Ebstein malformationEbstein malformation Ebstein malformation is a rare congenital cardiac malformations. The first reported case in 1866 Ebstein, sometimes referred to as Ebstein's anomaly. The incidence of congenital heart disease accounted for 0.5 to 1%. Ebstein malformation refers to the tricuspid valve malformation, subsequent location of the valve and the septal leaflet below normal, not the level of the atrioventricular ring moved down near the apex of the right ventricular wall, the normal position of the anterior valve, resulting in the right atrium than normal, while smaller than the normal right ventricle can tricuspid regurgitation. Such deformity is often associated with the foramen ovale open or atrial septal defect and pulmonary stenosis. The right atrium and more blood pressure increased, which contains the blood portion of the atrial septal defect or foramen ovale into the left atrium, the parts are still in the tricuspid valve into the right ventricle, pulmonary stenosis, into the pulmonary circulation of the blood volume reduction, Therefore, arterial blood back into the left atrium, with mixed venous blood from the right atrium shunt to, through the mitral valve into the room left ventricle and systemic circulation. For details see Ebstein malformation.
Valvular heart disease - aortic valve diseaseValvular aortic stenosis simple narrow rheumatic rare. Usually appear in childhood or adolescence, a few are congenital valve malformations were mostly calcified aortic valve stenosis, can also be caused by congenital malformations or rheumatic; adulthood.
① pathological anatomy and pathophysiology. Congenital aortic valve single lobe or two leaf deformities, caused by different degrees of stenosis, adult and more may be associated with calcification; calcified valve to lose the original shape was dome-shaped, scattered irregular calcification clumps, rigid valve, valve small; by rheumatic valve at the junction adhesion, fusion, and the valve hole to release limited caused by stenosis.
The normal aortic valve hole is about 3cm2, stenosis <1cm2, left ventricular ejection resistance increases, the systolic blood pressure, left ventricular and aortic systolic pressure gradient increases, ventricular hypertrophy increases myocardial oxygen consumption; stroke volume decreases; induced coronary blood supply caused by angina, arrhythmias and left ventricular failure.
② clinical manifestations and laboratory tests. Symptoms due to the severity of the stenosis without. Mild cases may be asymptomatic or mild symptoms. Severe stenosis, cardiac output decreased significantly, organized organ blood supply shortage of symptoms such as malaise, fatigue, exertional dyspnea, dizziness, cardiac arrhythmia, left heart failure or sudden death.
Signs: early systolic jet sound for the aortic valve area, and followed by subsequent rough and loud ejection systolic murmur, grade Ⅲ loudness to the conduction of the suprasternal notch and neck, many accompanied by tremor can reverse split of second heart sound, systolic pressure lower blood pressure show a smaller pulse pressure. Pulse smaller.
X-ray chest X-ray: left ventricle increases, the ascending aorta by stenosis caused by rapid blood flow suddenly slow down expansion in the lateral pressure increase due to the narrow, even visible aortic calcification. ECG: left ventricular hypertrophy and strain, may be associated with the performance of the left bundle branch block and arrhythmia.
Echocardiography: thickening of the aortic valve, back to the acoustic enhancement, open to slow down, open amplitude decreases (normal is 1.5cm). Aortic diastolic diameter and systolic internal diameter decreases. Doppler ultrasound shows the systolic pressure gradient and the degree of stenosis of the left ventricular systolic turbulence of blood through the aortic valve hole, which can be calculated.
Left heart catheterization and angiography: left ventricular systolic pressure significantly higher than the aorta increased. Left ventricular angiography showed small valve hole; ascending aortic dilatation and emptying time of the contrast agent.
③ diagnosis and differential diagnosis. According to the signs is not difficult to diagnose. If the younger age at onset, multi-line congenital malformation of the aortic valve Echocardiography; age of onset of valve calcification calcified aortic valve stenosis; a history of rheumatic fever and severe regurgitation and atrial fibrillation, rheumatic. The disease still need to aortic stenosis, subaortic stenosis, pulmonary valve stenosis and aortic atherosclerosis and other identification.
The ④ prognosis. This disease is mild, moderate stenosis better prognosis can be asymptomatic for more than 10 years, severe stenosis often occurs in syncope, angina pectoris, or sudden death. Are usually left heart failure after an average survival of only a few years. Cause of death of adult cases, 10 to 20 percent of sudden death.
The ⑤ prevention. Appropriate restrictions on physical activity according to the patient, pay attention to the prevention of infection, angina, heart failure onset. Symptoms, ECG left ventricular hypertrophy, myocardial disorders, cardiac enlargement, left ventricular and aortic systolic pressure gradient> 6.67kPa (50mmHg), should be considered artificial aortic valve replacement; if accompanied by coronary heart disease you need at the same time for the aorta - coronary artery bypass grafting.
Stenosis of the aortic valve in the valve-like membrane in the aortic sinus at the top of localized or diffuse stenosis. Its clinical manifestations are valvular stenosis similar to cardiac auscultation aortic contraction of the early jet sound; the right upper limb pulse strong and powerful, blood pressure is higher than the left upper extremity, which is narrow after the blood spray directed at the innominate artery due. Aortic stenosis, X-ray chest examination no l expansion, but expansion of the aortic sinus performance. The diagnosis requires the use of echocardiography, left heart catheterization and retrograde ascending aortic angiography. The principles of treatment for severe lesions required surgical correction of the stenosis.
Subvalvular aortic valve stenosis in the left ventricle at the outlet of the abnormal aortic root diaphragm caused by the narrow, many involving the mitral valve. Often accompanied by PDAs, clinical performance and valve type were similar, but the low murmur position, the lower part of the precordial the loudest, and no aortic contraction of the early jet sound. X-ray chest examination no l expansion of aortic stenosis, valvular calcification, and left ventricular angiography showed a subaortic constant filling defect can be identified with valvular stenosis. Treatment is surgical excision subaortic diaphragm.
Aortic insufficiency with chronic aortic regurgitation, rheumatic for the most common, and often accompanied by a narrow. In addition, or congenital valvular abnormalities caused or go far due to various causes, such as aortic atherosclerosis, Mull party's syndrome or syphilitic aorta caused by aortic root expansion caused by the relative regurgitation. Acute aortic insufficiency seen in infective endocarditis, aortic dissection, chest contusion involving the aortic valve, and myxoid degeneration of valve leaflets rupture caused by.
The pathophysiology of aortic blood flow back into the diastolic left ventricle, artery diastolic left ventricular volume increases and expansion; systolic left ventricular compensatory contraction to enhance stroke volume increases to maintain normal heart cardiac output. Left ventricular secondary hypertrophy, oxygen consumption increased. Artery diastolic, systolic blood pressure, pulse pressure, reduced coronary perfusion and myocardial blood supply. A long time, the occurrence of left heart failure. Acute aortic regurgitation, left ventricular sudden load increase and expansion, increased wall tension, and can rapidly lead to left heart failure.
The clinical manifestations and laboratory tests are mainly the following aspects:
① symptoms. Acute soon symptoms, even death within a short time. Chronic, lesions less long-term asymptomatic; moderate or severe regurgitation, in addition to palpitations, fatigue, dizziness, and angina diastolic blood pressure is too low to the brain and the heart blood supply is not caused by pressure, pulse pressure is too large caused by head turn movement. Severe left ventricular failure.
② signs. The main signs of the third intercostal space of the left sternal border generated by aortic blood reflux to the left ventricular early diastolic descending splashing kind of murmur, can be spread to the apex?? Take the most clear. Pulse pressure, peripheral vascular signs, such as lips and nails, capillary pulsation, the radial artery the palpable flush pulse, femoral artery can be heard gunshot sounds (stethoscope bell-shaped chest pressed in the femoral artery, could be heard and sharp sound with the pulse) and Di Luo Ji Ai Shi Zheng (stethoscope bell-shaped chest a little pressure on the artery can be heard two noises). Performance and aortic regurgitation were positively correlated.
③ X-ray chest radiograph. Widened ascending aorta, twisted, extended elongation under the left ventricle to the left, the entire heart shadow was boot-shaped; left anterior oblique view shows left ventricular shadow extends backwards, often covering or overlapping in the spine.
The ④ ECG. Left axis deviation, left ventricular hypertrophy, may be associated with left ventricular strain levy.
The ⑤ echocardiography map. M-mode ultrasound examination showed left ventricular outflow tract and aortic root diameter increases, the diastolic mitral curve arising from the aorta back to the bloody impact of small high-frequency vibration. Two-dimensional visible aortic valve can not close. Doppler ultrasound examination showed aortic diastolic turbulence.
The ⑥ Selective ascending aortic angiography. There are a lot of contrast agent through the aortic mouth back into the left ventricle.
Diagnosis based on noise and blood pressure changes, it is not difficult to diagnose.
Complications and prognosis of the disease are more prone to infective endocarditis, left ventricular failure or sudden death. Mild long-term no obvious symptoms, the prognosis is comparatively good; severe, low diastolic blood pressure reduction in coronary blood supply, can be faster heart failure and poor prognosis.
Treatment if the symptoms, especially those with angina or heart decompensation, increased pulse pressure, diastolic blood pressure, heart to the cardiothoracic ratio> 55 to 60% should be considered for the artificial aortic valve replacement.
