Category: Heart anatomy

The reasons:

Rheumatic valvular stenosis (soldering and calcification usually occurs along the edges of the valves). Fibro-calcific aortic stenosis (valve degenerative changes are associated with collagen destruction and accumulation of calcium deposits in the valves : this process begins in the sinus region of Valsalva and extends to the cusps. Congenital valve stenosis.

The end result of all the above forms of aortic valve stenosis is the fusion of commissures and narrowing of the aortic orifice. When degeneration and calcification of the valve develop, it is practically impossible to differentiate these conditions.

EchoCG changes in this defect are due to the syndrome of systolic LV overload In the M- and B-modes, the following signs are usually revealed: 1. a change in the morphology of the AK leaflets (fibrosis or calcification); 2. decrease in the degree of divergence of the AK leaflets in systole less than 15 mm (normal 18-20 mm); 3. an increase in the expulsion period from the LV more than 350 ms (normally up to 330 ms); 4. marked hypertrophy of the LV walls (usually more than 15 mm).
 
 When Doppler study from the top, you can estimate the degree of stenosis according to systolic pressure gradient (Rao): minimum stenosis – pressure gradient up to 20 mm Hg (at least 8 mm), moderate –40 mm Hg, expressed to 80 mm Hg and extremely pronounced above 80 mm Hg. However, this method of measurement is not possible in all patients. There are other ways to estimate the pressure gradient on the aortic valve:

Rao = adsis. – (Tzs / KSRlzh) x 245, where, Rao – pressure gradient on the aorta, BPM – systolic blood pressure, Tzs – thickness of the posterior wall of the left ventricle, KSRlzh – final systolic size of the LV. It is necessary to emphasize that when reducing the area of ​​the joint-stock company hole by 20 – 40% (the norm is more than 2.5 cm 2 ), it practically does not affect the work of the heart and hemodynamic parameters suffer only if its area becomes less than 1.5 cm 2 .

Calcification and reduction of divergence Doppler flow in AK stenosis of AK valves up to 11 mm

The reasons:

Rheumatism (often associated with mitral valve insufficiency. Infective endocarditis. Congenital valve insufficiency (can be combined with valve stenosis). Relative aortic insufficiency (syphilitic aortitis, dissecting aortic aneurysm, ankylosing spondylitis, Marfan disease, aorto-arteritis, etc.)

As with mitral insufficiency, structural changes in the heart with this defect are due to volume overload syndrome (primarily of the left ventricle). In M-mode, one can detect: 1. fibrosis (calcification) of AK valves (more often with rheumatic or atherosclerotic lesions) with their separation into diastole, 2. small-amplitude diastolic flutter of the anterior cusp of MK (under the action of reverse blood flow from the aorta), 3. dilatation LV cavity.

B-mode: 1. LV from ellipsoid becomes more spherical in shape with dilatation of its cavity in severe cases (DAC exceeds 7 cm), 2. hypertrophy and hyperkinesis of the LV walls. DehoKG has the greatest information content in diagnosing this defect and determining its severity, especially color scanning. The regurgitation flow in the apical or parasternal position looks like a signal of different color (due to turbulence), starting from the aortic valve and penetrating into the LV cavity. Several methods of indirectly assessing the severity of regurgitation AO have been proposed: 1. the length of the regurgitation jet (1st order – up to 2 cm, 2nd stage – 2-4cm, 3rd stage – 4-6cm, 4th stage – more than 6cm), 2. the area of ​​the regurgitation jet according to short axis (1st. – up to 0.2cm 2 , 2nd . – 0.2 – 0.6cm 2 , 3rd. – 0.6 – 1.2cm 2 4st. –More than 1.2 cm 2 ), 3. the area of ​​the jet of regurgitation from the apical position (1st .- up to 1.5 cm 2 , 2nd . – 1.5-4 cm 2 , 3rd. – 4 – 8 cm 2 , and 4 tbsp. – more than 8 cm 2 ), 4. maximum speed aortic regurgitation in the mode of continuous-wave doppler (a speed of more than 3 m / s indicates how severe aortic insufficiency was ruled. 5. both of the regurgitation fraction (FF volume more than 50% of the stroke volume also characterizes severe aortic insufficiency).

It must be emphasized that none of these signs is absolute in assessing the severity of the defect. It can be judged as a whole only by the totality of all indicators as a whole.

signs of LV volume overload small-amplitude “shake” of the anterior cusp of the MK in early diastole

The regurgitation flow on the AK The regurgitation flow on the AK from the parasternal position

The regurgitation flow on the AK in the color doppler mode from the apical access Figure 2.4 EchoCG with aortic insufficiency.

Infective endocarditis

Modes B and M: 1. the presence of moving on a narrow or wide base of echoes of different density (depending on the duration of the process) on the valves (chords), 2. the presence of characteristic signs for mitral or aortic regurgitation, 3. signs of pericarditis are often detected, 4. possible decrease in the LV pumping function.

Doppler mode – signs of regurgitation on the MC or AK. It should be emphasized that in 15 – 20% of cases, endocarditis on the valves is non-infectious in nature (Lupus endocarditis Libman-Sachs, tumors of various organs, conditions associated with antiphospholipid syndrome, etc.). In these cases, as a rule, no pronounced regurgitation is observed, since the valve collapses slightly. It is rather difficult to identify vegetations on modified valves (with existing defects, as well as in the case of prosthetic valves).

Echocardiographic evaluation of the function of valve prostheses has been and remains a difficult problem. These difficulties are connected with the following reasons: 1. the difference of many modifications of prostheses, which besides come in different sizes (in this connection, normal the values ​​of the pressure gradient on the aortic prosthesis vary from 12 to 30 mm Hg, and on the mitral – from 10 to 27 mm Hg. Art.); 2. The presence of a large number of acoustic artifacts that are difficult to distinguish from pathological echoes, especially in the area of ​​the ring. However, Doppler examination of the flow on prostheses and, especially, transesophageal echography, can provide valuable information in assessing their function. As a rule, the malfunction of the prosthesis is caused either by their stenosis (due to thrombosis, fibrosis, calcification, etc.), or failure (paraprosthetic fistulas, valvular insufficiency, etc.).

Since the standard values ​​of the pressure gradient on prostheses vary quite widely, it is possible to speak of stenosis only if there are results from previous studies (performed at best by the same doctor on the same machine). In the absence of concomitant regurgitation on the valves, a formula can be used to calculate the effective area of ​​the mitral opening of the prosthesis using the flow continuity equation, i.e. calculate the product of the LV outgoing path area and the flow rate in the outgoing path and divide by the flow rate through the MK prosthesis (Apv = Alvot X Vlvot / Vpv).

Attempting to quantify regurgitation through valve prostheses, especially in the mitral position, is extremely difficult with transthoracic access (due to the powerful acoustic shadow from the prosthetic material). In this case, the most informative may be color Doppler mapping or transesophageal examination. It should be remembered that a small stream of regurgitation (1 – 2 tbsp.) Can always be identified on a normally functioning prosthesis.

Thus, only using reference echocardiographic data, when the prosthesis is clearly functioning well (the results of postoperative echoCG studies), knowing the type and size of the prosthesis, one can evaluate its work in dynamics.

Prosthesis AK (paraprosthetic fistula with Prosthesis MK (ball prosthesis) regurgitation 2-3 tbsp.)

Depending on the anatomical features, primary defects (in the proximal part of the septum, at its base – partial atrioventricular canal, in the region of the coronary sinus) and secondary, located in the area of ​​the oval fossa, are isolated. EchoCG diagnosis of malformation includes the detection of the defect of the MPP and its indirect signs (volume overload of the right sections, pulmonary hypertension).

The defect of the septum in the form of a “discontinuous” signal is well visualized in B-mode from the parasternal access along the short axis at the level of the vessels or from the subcostal along the long axis. One should keep in mind the possibility of false positive diagnostics of the defect on the basis of this symptom only, since in the oval window area the partition is often very thin.

In addition, in the M – and B-modes reveal dilatation of the cavities of the PP and the pancreas with the expansion of the pulmonary trunk, as well as the paradoxical movement of the IUP. A Doppler study can detect low-speed left-right flow through the septum, which begins in the middle of ventricular systole and overlaps diastolic transmitral blood flow, and when assessing flow on the pulmonary trunk, an increase in pressure gradient and signs of pulmonary hypertension. When color Doppler mapping is clearly visible pathological flow through the WFP.

It should be noted that most authors do not consider the presence of an open oval window a congenital defect as such (cardiac hemodynamics does not suffer, since it is normally covered by a valve on the LP side). Contributes to the functioning of an open oval window only the formation of pulmonary hypertension of both heart (shunt) and pulmonary origin (in diseases of the lungs).

According to the localization, the defects of MZhP are divided into: 1. membranous; 2. infundibular (in the outgoing department of the IUP); 3.atrioventricular (defects of the bringing department); 4. muscle. The most frequently diagnosed and hemodynamically significant are defects in the membranous part of the IUP.

EchoCG examination includes visualization of the defect itself in the B-mode, identification of signs of hypertrophy and volume overload of the pancreas in the M-mode, as well as an assessment of the degree of pulmonary hypertension using Doppler research. As a rule, when Doppler studies at the level of the defect in systole (and sometimes in diastole) high-speed flows with a high pressure gradient of 40–90 mm are detected. Hg Art. (the larger the size of the defect – the smaller the pressure gradient) with the directionality of the flow above the zero line. Therefore, hemodynamically insignificant defects of the muscular part are usually high-speed, and with Eisenmenger syndrome, which often complicates large membranous defects, the nature of the discharge becomes low-speed and bidirectional (left-right at the beginning of systole, and right-left at the end)

Color mapping allows you to visualize the defect and the direction of blood flow much faster, and also recognize multiple defects. It should be borne in mind that the size of the diagnosed MZhP detected during the EchoCG examination is usually 20–30% less than the true size.

Distinguish: valve; subvalvular and supravalvular variants of isolated pulmonary artery stenosis (ISLA).

In 10% of cases, ISLA is accompanied by a DMPP or an open oval window (Fallot triad). In valvular stenosis, the narrowing is located in the valve area, represented by the diaphragm with a central or eccentric orifice. Valve ring hypoplazirovanno.

In a one-dimensional echocardiography study (M-mode) reveal: hypertrophy of the anterior wall of the right ventricle, hypertrophy of the interventricular septum (less often), thickening of the valve cusps of the pulmonary artery, increased excursion of the tricuspid valve, prolapse of the valve of the tricuspid valve. In the study in B-mode, it is characteristic: arching the pulmonary valve valves into the output path of the right ventricle, post-stenotic dilatation of the pulmonary artery, hypertrophy of the pancreatic wall and increased echo signal from the endocardium of the pancreas. The most valuable information is provided by the Doppler EchoCG, which allows to judge the degree of pulmonary hypertension and calculate the pressure gradient at the site of stenosis. The following degrees of stenosis are distinguished: insignificant (systolic pressure gradient up to 25 mm Hg), moderate (25–50 mm Hg), marked stenosis (50–75 mm Hg.and extremely pronounced stenosis (systolic pressure gradient exceeds 75 mmHg.). As a rule, when the pressure gradient is less than 25 mmHg, this defect rarely requires any active intervention.

The defect includes 4 components: stenosis of the pulmonary artery, ventricular septal defect, destructive aorta, right ventricular hypertrophy.

The most important 2 components of this defect are: stenosis of the pulmonary artery and ventricular septal defect. Pulmonary stenosis can be infundibular, at the level of the valve, pulmonary trunk, or in the subinfibular zone. The combination of valvular and infundibular stenosis is most characteristic. Dextraposition of the aorta can be in varying degrees of severity. Hypertrophy of the right ventricle is secondary and occurs as a result of obstruction of the output tract. The right-sided aortic arch is observed in 20-30%.

One-dimensional echocardiography reveals: aortic dilatation, aortic destraction (location of the anterior aorta wall and interventricular septum at different depths), hypertrophy of the anterior wall of the right ventricle, hypertrophy of the interventricular septum, reduction of the diameter of the pulmonary artery, reduction of the left atrium. A two-dimensional study is characterized by direct visualization of the ventricular septal defect, aortic dislocation and its dilatation in the parasternal projection of the long axis, as well as direct visualization of the stenosis of the pulmonary artery and its localization. Doppler echocardiography reveals turbulent flow in the pulmonary artery stem and the presence of a systolic pressure gradient.

Parasternal position along the long and parasternal position along the short axes Diagram and EchoCG with Fallot’s tetrad.

Open arterial duct

The duct departs from the aorta at the level of the left subclavian artery and flows into the pulmonary artery at the site of its division into two branches. One-dimensional study reveals signs of volume overload of the left heart (an increase in the cavity of the left ventricle and atrium). In a two-dimensional study, direct visualization of the duct from the supraternal access is possible in the form of an echo-free space between the descending aorta and the pulmonary artery. The Doppler-EchoG has the highest sensitivity and specificity in detecting a defect, which allows to detect systolic and diastolic turbulent flows in the pulmonary artery above the valve.

Normally, the septal cusps of the mitral and tricuspid valves are fixed at the same level; with Ebstein’s anomaly, this distance is increased to 1.4-3.2 cm, the tricuspid opening (fibrous ring) remains in the normal position. The shifted valves of the tricuspid valve (septal and posterior) in the right ventricle divide it into two parts: atrialized (the portion of the right ventricle between the fibrous ring and the displaced valves) and the cavity of the right ventricle itself. Defect combined with secondary DMPP or open oval window.

The two-dimensional EchoCG is the most informative in identifying this defect : 1. The septal valve is displaced into the cavity of the right ventricle in the projection of 4-chambers from the apex (more than 20 mm in adults and 15 mm in children); 2. atrialized right ventricle; 3. dilatation of the right atrioventricular orifice; 4. open oval window or DMPP (observed in 85% of cases).

When Doppler echocardiography determine the failure of the tricuspid valve, assess the magnitude of pulmonary hypertension. One-dimensional echocardiography allows visualization of an increase in right heart, a paradoxical movement of an IVS, a delayed closure of the tricuspid valve (over 0.03 s), an increase in the excursion of the anterior flap of the tricuspid valve, simultaneous location of two atrioventricular valves.

Anatomical changes in the architectonics of the heart and great vessels that do not lead to gross impairment of the function of the cardiovascular system should be referred to small anomalies of heart development (MARS). The etiological cause of minor abnormalities of the heart, is hereditarily determined connective tissue dysplasia, which has various clinical manifestations depending on the degree of penetrance of the gene. Classification MARS is based on the principle of anatomical affiliation. There are the following MARS:

Aorta

1.A very narrow aortic root. 2. Limitarily wide aortic root. 3 Bicuspid AK. 4. Asymmetry of AK flaps. 5. Replacing the AK valves.

Double-leaf AK with prolapsed cusps without regurgitation.

Left ventricle

1. The transverse, longitudinal trabeculae (chord) in the LV cavity. 2. Systolic deformity of the outgrowth part of the IUP in the form of a roller (transient systolic roller) 3. Split, abnormally located, additional or hypertrophied papillary muscles.

1. Procuring MK (sagging 5-7 mm – Ι Art., 8-9 – ΙΙ Art., Above 9 mm – ΙΙΙeast; sagging up to 5 mm is considered a normal valve kinetics) .2. Ectopic fastening of chords to the wings of the MC.

To avoid subjectivity and subsequent overdiagnostics of MARS, their objectification is necessary, through quantitative evaluation. In cardiology practice, quantitative assessment is widely used in the study of the depth of mitral valve prolapse. Also, a quantitative approach is used in determining the length of the elongated Eustachian valve, dilatation of great vessels, atrioventricular orifices, and the number of additional trabeculae.

When it comes to referring any structural defect in the heart to MARS, it must be remembered that the principle of evaluation by functional significance is conditional. A bicuspid aortic valve usually does not lead to impaired aortic blood flow, but it is precisely with this developmental abnormality that the frequency of sudden death is higher than in the population. It is well known that whatever the tumor of the heart is: malignant, benign – it is malignant in its localization. For this reason, consideration of MARS only from the point of view of changing the structure of an organ without taking into account their effect on hemodynamic parameters and prognosis is dangerous and extremely harmful. On the other hand, the exaggeration of the functional significance of stigma in the heart is also not justified. In each case, the structural anomaly in the heart must be assessed in prognostic terms.It should also be emphasized that MARS can cause the appearance of the so-called functional heart murmurs (both systolic and diastolic).

 

HCM as a whole is characterized by:

1) severe LV myocardial hypertrophy,

2) a decrease in its cavity,

3) a violation of LV diastolic function.

Depending on the variant of hypertrophy, the following types of hcmp are distinguished: a) asymmetrical, b) symmetrical, c) apical. The asymmetrical type, in turn, may be accompanied by predominant hypertrophy of the upper, middle and lower third of the ICF, the thickness of which may be 1.5–3 times greater than the thickness of the LV LV wall. Clinically more severe, and the prognostic hazard is obstructive hypertrophic cardiovascular disease and obstruction of the output division of the LV (“subaortic subvalvular stenosis”). Echocardiography signs of this form of hcmp are: 1. Asymmetric thickening of MZhP and restriction of its mobility. 2. Perednesystolic movement of the valves MK. 3. AK cover during systole. 4. Hyperkinesis MZHP. 5. High pressure gradient in the outgoing LV. 6Mitral regurgitation and increase in LP.

Dilatsionny KMP (DCMP)

The most characteristic signs of DCM are: 1) significant dilatation of the LV (more than 40-50% of the standard values) with normal or reduced thickness of its walls, 2) a sharp violation of the systolic and diastolic functions of the LV (EF below 30-20%), 3) total LV hypokinesis, 4) a significant decrease in flow rates in the outgoing LV tract and pulmonary artery, 5) expansion of other heart chambers (LV, RV). When DCM in the cavities of the heart are often diagnosed near-wall thrombi.

Restrictive ILC (RCMP)

The concept of RCMP unites two diseases: endocardial fibrosis and eosinophilic fibroplastic endocarditis of Laeffer. Secondary RCMP can occur in diseases such as cardiac amyloidosis, hemochromatosis, and sarcoidosis. EchoCG in these diseases is characterized by: 1) symmetric hypertrophy of the LV wall, 2) reduced or normal LV cavity, 3) dilatation of the atria, 4) presence of granular induration in the myocardium, 5) increased echo signal from the LV endocardium, 6) signs of diastolic and systolic dysfunction LV, 7) the presence of a small pericardial effusion (not always).