Assessment of left ventricular diastolic function. Diastolic function. Chronic diastolic heart failure
New recommendations for assessing left ventricular diastolic function from the European Association of Imaging Techniques have been published. of cardio-vascular system(European Association of Cardiovascular Imaging) and the American Society of Echocardiography: "Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging."
Previous Recommendations on this topic, issued in 2009 by the same organizations, were replete with a large number of indicators required to make a judgment about the presence and severity of left ventricular diastolic dysfunction. This required a fairly long time to conduct an echocardiographic study, complicated the analysis of the data obtained, and limited the use of the Recommendations in wide clinical practice.
The main goal of the new Guidelines is to simplify the approach and thus increase the usefulness of the recommendations in daily clinical practice. The authors of the new guidelines believe that in most clinical situations, filling pressure and left ventricular diastolic function can be reliably assessed using a few simple echocardiographic parameters. The values of four indicators are recommended to be used to identify impaired diastolic function:
- ratio of mitral flow velocity E to average speed movement of the mitral annulus E/e’ avg (> 14)
- left atrial volume index (> 34 ml/sq. m)
- maximum tricuspid regurgitation velocity (> 2.8 m/sec)
speed of movement of the mitral valve ring e’ (septal e’< 7 см/сек и латеральная e’ < 10 см/сек)
The Recommendations discuss the peculiarities of assessing diastolic function of the left ventricle in various diseases, cardiac arrhythmias and various clinical situations. The new Recommendations really simplify the assessment of left ventricular diastolic function in many ways and, in my opinion, are more successful than the previous ones. Studying this document will be useful for all doctors involved in echocardiography.
The medical and social significance of diseases of the cardiovascular system is extremely high in all countries, including the Republic of Belarus, since they make a major contribution to the formation of the structure of morbidity, disability and mortality.
Changes in the cardiovascular system in such patients are consistent and are characterized by progressive disturbances in its structure and function. The term “cardiovascular continuum” is increasingly used in the literature to describe these changes.
Violation of the diastolic function of the myocardium, loss of the ability of the walls of the left ventricle to relax during diastole in this case is considered as one of the earliest pathological manifestations. It is necessary to emphasize the high prevalence of diastolic dysfunction. Thus, in patients with arterial hypertension (AH), diastolic dysfunction of the left ventricular (LV) myocardium occurs in 50-90% of cases and closely correlates with the degree of increase in blood pressure (BP), duration of the disease, etc. .
In modern medical literature there is information that signs of diastolic myocardial dysfunction are detected in almost any heart disease. Often, diastolic myocardial dysfunction is observed in patients with chronic heart failure (CHF). For a long time, CHF was associated primarily with a decrease in myocardial contractility, observed with systolic dysfunction. However, clinical symptoms often occur in patients with preserved systolic myocardial function. The development of CHF in them is largely associated with impaired diastolic function of the heart. The incidence of diastolic myocardial dysfunction as a cause of CHF increases sharply with age. The prevalence of preserved LV systolic function among patients with CHF in various age groups is presented in Table. 1.
Table 1. Prevalence of preserved left ventricular systolic function among patients with CHF in different age groups
Information on the prevalence of preserved LV systolic function among patients of older age groups with CHF is widely presented in the medical literature. So, as a result of the work carried out by I.A. Sharoshina's (2003) study found that LV systolic function is preserved in more than 60% of patients with CHF aged 60 years and older, and it occurs in 47% of patients with CHF aged 66–75 years and in 64% over 75 years. According to the National Heart Failure Project (2003), in the USA, CHF with preserved LV systolic function occurs in more than 50% of women over 65 years of age and in a third of men of the same age. In geriatric practice, CHF with preserved LV systolic function is more common among women and in patients with hypertension (but without reliable indications of a history of myocardial infarction). Elevated blood pressure (160/100 mmHg) during the current examination is also much more often observed in patients with CHF with preserved LV systolic function.
It is important to note the pathogenetic relationship between high blood pressure, left ventricular hypertrophy (LVH), the development of LV diastolic dysfunction and CHF. An increase in blood pressure leads to an increase in afterload on the LV, and then compensatory development of LVH occurs. The hypertrophied myocardium loses its ability to relax. For complete filling of blood, the LV acts as a compensatory mechanism left atrium, which has to contract with a greater load. The progression of the processes leads to an increase in LV filling pressure, and then to an increase in pressure in the pulmonary circulation. Initially, changes in the heart are adaptive in nature and do not manifest themselves clinically. Clinical symptoms (for example, shortness of breath) are observed first during physical exertion, then tolerance to them decreases, shortness of breath occurs with light exertion and even at rest.
Along with the pathogenetic connection, a relationship has been established between the degree of impairment of the diastolic function of the heart and the severity of CHF, as well as tolerance to physical activity and quality of life. Diastolic dysfunction in patients with CHF is a prognostically significant factor.
It is necessary to distinguish between the concepts of “diastolic dysfunction” and “diastolic heart failure”. Diastolic heart failure always includes diastolic dysfunction, but the presence of diastolic myocardial dysfunction does not always indicate clinical heart failure. In turn, diastolic myocardial dysfunction most often precedes disturbances in systolic cardiac function. According to European recommendations, three conditions are required to establish a diagnosis of diastolic heart failure: the presence of symptoms of CHF; normal or slightly reduced ejection fraction (>45-50%); decreased rate of diastolic relaxation, diastolic compliance, or left ventricular diastolic compliance.
The impetus for the study of myocardial diastolic dysfunction was the introduction of echocardiography into research and then into clinical practice. Assessing mitral blood flow using echocardiography is a common method for diagnosing diastolic dysfunction. V n Normally, typical indicators of mitral blood flow in diastole have two peaks: wave E and wave A. The first reflects the early (E) phase of LV filling, the second - the atrial (A) component of LV diastolic filling. The E/A ratio and the time of deceleration of early transmitral flow are also used as main criteria. If necessary, determined additional indicators, such as the duration of the isovolumetric relaxation phase, atrial filling fraction, VTIE/VTIA ratio, S/D ratio, etc. If LV diastolic function is impaired, these indicators change.
Indicators | Norm | Variants of diastolic dysfunction | ||
slow relaxation | pseudo-normalization | restrictive type | ||
Basic | ||||
Peak E wave speed | < 0,53 см/с | Increase | ||
Peak speed of wave A | > 0.70 cm/s | Decrease | ||
E/A ratio | E/A<1 для лиц моложе 60 лет | Increase | ||
Early transmitral flow deceleration time | Reduction less than 150ms | Reduction less than 150ms | ||
Additional | ||||
Duration of the isovolumetric relaxation phase | Increase more than 100 ms | Decrease | ||
VTIE/VTIA ratio | Decrease | |||
Atrial filling fraction | Increase | Decrease | ||
S/D ratio | Increase due to D-wave | Decrease less than 0.75 | ||
Peak volumetric filling rate | Decrease less than 160 ml/s x m2 | |||
Table 2. Indicators for determining diastolic dysfunction and the main variants of its violation
The first, earliest version of diastolic dysfunction is characterized by delayed relaxation (abnormal relaxation). When relaxation is impaired, there is a decrease in the volume of blood entering the ventricle during the early filling phase and an increase in the contribution of the atria. The second, more severe pattern of impaired diastolic function is called pseudonormalization. At this stage of development of diastolic dysfunction, ventricular relaxation occurs even more slowly and not completely. Without a compensatory increase in intraatrial pressure, the ventricle is unable to accommodate the required volume of blood. An increase in intraatrial pressure restores the early transmitral pressure gradient. Further progression of diastolic dysfunction leads to the development of an even more severe model called restrictive.
Taking into account the widespread prevalence of diastolic cardiac dysfunction and its significance in the cardiovascular continuum, there is an understanding of the need for its correction in patients with cardiovascular diseases. It has been proven that the state of diastolic function can be used as a criterion for the effectiveness of therapy. Theoretically, drugs that reduce LVH, improve active relaxation, and increase LV compliance should help improve diastolic function. The most powerful positive effect on the state of diastolic function of the heart was noted with the use of angiotensin-converting enzyme inhibitors (ACE inhibitors) and calcium antagonists (CA).
Data on the beneficial effect of ACE inhibitors on the diastolic function of the heart in patients with hypertension have been obtained in most studies. Improvement in LV diastolic function is observed in a fairly short time - as a rule, after 8-16 weeks of therapy, i.e. even before a statistically significant regression of LV hypertrophy. According to A.D. Kuimova et al., in patients with hypertension, LV diastolic function improved when prescribed lisinopril, regardless of the presence of CHF. A study conducted at the Department of Therapy of BelMAPO revealed a positive effect enalapril on the state of diastolic function of the heart.
Improving the diastolic function of the heart is of practical importance when choosing therapy in patients with hypertension and CHF. ACE inhibitors are effective in the initial stages, including asymptomatic LV dysfunction, and in the most advanced stages of decompensation. These drugs improve cardiomyocyte relaxation and LV compliance, reduce blood pressure and cause regression of LVH. In 2005, new data on effectiveness were obtained perindopril in elderly patients with CHF with impaired diastolic function.
For the treatment of CHF, any ACE inhibitor can be prescribed, but preference should be given to drugs whose effectiveness has been proven in studies. C.G. Brilla et al. showed that during therapy with lisinopril, there is a significant increase in the ratio of peak velocities of transmitral blood flow E/A and a decrease in the time of isovolumetric relaxation, i.e. diastolic function improves. According to O.S. Sychev, application diroton in patients with coronary artery disease, it improves the diastolic function of the heart and causes an antiarrhythmic effect in patients with supraventricular and ventricular cardiac arrhythmias. Improvement in the main indicators characterizing myocardial diastolic function was noted when used in elderly patients ednita .
Calcium antagonists also have a beneficial effect on LV diastolic dysfunction by controlling blood pressure, reducing myocardial oxygen demand, causing dilatation of the coronary arteries and reversal of LV hypertrophy. The pathophysiological rationale for the use of AKs is their ability to improve myocardial relaxation and thereby increase ventricular diastolic filling. However, if their positive effect in patients with hypertension is undeniable, the effect on the survival of patients with CHF and the progression of this disease has not been sufficiently studied. For example, AKs are the drugs of choice in the treatment of diseases accompanied by severe LV hypertrophy, but the addition of severe systolic disorders and congestive heart failure to LV hypertrophy makes their use impractical and even dangerous due to a decrease in the pumping function of the heart and an increased risk of death.
In patients with preserved systolic heart function and existing diastolic dysfunction, only third-generation dihydropyridine AKs can be used, of which only amlodipine is currently available on the Belarusian pharmaceutical market. This drug, along with ACE inhibitors, has the most pronounced ability to cause regression of left ventricular hypertrophy and improve the diastolic function of the heart. Research conducted by M.R. Bohua et al. showed that normodipine has a beneficial effect on remodeling processes: causes reverse development of LV myocardial hypertrophy, improves diastolic function of the heart. The decrease in the mass, thickness and rigidity of the LV walls, and the increase in diastolic compliance under the influence of normodipine are due to subtle biochemical processes occurring in the myofibrils, the relaxation of which depends on the removal of excess Ca 2+ from the intracellular space and blocking the formation of pathological collagen. It is preferable to prescribe amlodipine to patients with angina pectoris, a rare heart rhythm, as well as contraindications for the use of other drugs (diabetes mellitus, broncho-obstructive diseases, metabolic disorders).
Among other groups of drugs that improve diastolic heart function, it is necessary to note angiotensin receptor blockers, since their action is in many ways similar to the effects of ACE inhibitors. The positive effect of beta-blockers may be due to a decrease in heart rate and, as a result, prolongation of diastole.
In general, it should be noted that the evidence base for the use of drugs in the treatment of CHF with diastolic dysfunction is small, so additional research is required to justify the feasibility of prescribing groups of drugs in the treatment of CHF, accompanied by LV diastolic dysfunction with preserved systolic function.
Diastolic heart failure. This type of heart failure reflects a situation in which the heart is unable to accept the necessary venous return of blood. This may be due to filling obstructions (stenoses of the pulmonary vein collectors or atrioventricular valves, triatrial heart) or poor ventricular relaxation (pulmonary stenosis, aortic stenosis, cardiomyopathy). The latter option typically requires increased venous pressure to maintain adequate cardiac output. Newborns often experience temporary physiological “stiffness” of the right ventricle. The combination of the latter factor with increased afterload (due to semilunar valve stenosis or high TVR) leads to the rapid development of low cardiac output syndrome soon after birth (“critical” heart disease).
Diastolic heart function assessed by transmitral and transtricuspid diastolic blood flow, in which the early filling flow (peak E on EchoCG) and the atrial systole flow (peak A) are distinguished.
In the fetus the E/A ratio is less than one, ventricular filling depends mainly on atrial systole. After birth, as the myocardium matures and its resistance decreases, the role of passive filling increases; in the period from one to 3-6 months, the E/A ratio becomes more than one.
In most cases, disturbances in systolic and diastolic heart functions combine.
Hypoxia and ischemia.
The end result insufficient oxygen delivery to cells is their hypoxia and death. However, this process may be based on different mechanisms - hypoxia itself or ischemia. Both of these terms reflect a malnutrition of organs and tissues, but have different physiological meanings. With hypoxia, the oxygen content in the blood flowing to the tissues is reduced, and with ischemia, the volume of blood flowing is reduced. Congenital defects can be accompanied by both of these mechanisms of circulatory disorders, and they affect both the heart itself and other organs. Typical examples are aortic stenosis and transposition of the great arteries.
For aortic stenosis with significant hypertrophy of the left ventricular myocardium, the growth of small coronary vessels lags behind the needs, blood flow is disrupted mainly in the subendocardial layers of the myocardium, and ischemia of this zone occurs. When the great arteries are transposed, the volume of blood flow into the coronary vessels is not reduced, but blood with a sharply reduced oxygen content comes from the aorta, which leads to myocardial hypoxia.
Type of circulatory disorder determines therapeutic and surgical measures: in case of ischemia, it is necessary to strive to restore the volume of blood flow, in case of hypoxia - to increase the oxygen content in the blood.
Oxygenation index.
This index is used to evaluate efficiency artificial ventilation. It reflects the intensity of the effort required to achieve a given oxygenation of arterial blood and is calculated by the formula: IR = (Average Fp2 100)/pO2, where IR is the oxygenation index, Average pressure in the respiratory tract (cm water column), F02 - fractional oxygen content in the inhaled mixture (decimal fraction), pa02 - partial pressure of oxygen in arterial blood (mm Hg). The higher the index, the more severe the patient's condition.
Chronic diastolic heart failure
Diastolic CHF is heart failure with normal or slightly reduced contractile function of the left ventricle, but with a pronounced impairment of its diastolic relaxation and filling, which is accompanied by an increase in end-diastolic pressure in the ventricle, stagnation of blood in the pulmonary circulation and other signs of heart failure. Thus, there are 3 main criteria for identifying diastolic CHF as one of the special forms of cardiac decompensation (recommendations of the working group of the European Society of Cardiology, 1998).
1. The presence of clinical signs of CHF (shortness of breath, fatigue, moist rales in the lungs, edema, etc.).
2. Normal or slightly reduced myocardial contractility (LVEF greater than 45–50%).
3. The presence of objective signs indicating impaired relaxation and filling of the LV and/or signs of increased LV stiffness.
The identification of diastolic CHF is of great practical importance, since this form of CH occurs in 20–30% of patients with clinical signs of cardiac decompensation, and there are fundamental differences in the treatment tactics of such patients. However, two important practical circumstances should be kept in mind:
1. The progression of diastolic CHF over time leads to such a sharp decrease in LV filling that the value of CI and EF begins to decrease, i.e. signs of LV systolic dysfunction appear.
2. In almost all patients with CHF, in whom the process of decompensation from the very beginning has the character of systolic CHF and is accompanied by a clear decrease in EF and CI, more or less pronounced signs of LV diastolic dysfunction can be identified, which significantly aggravates hemodynamic disorders.
Thus, a clear division of CHF into two pathophysiological variants - systolic and diastolic - is valid mainly in the early stages of CHF formation (S.N. Tereshchenko et al. 2000). An advanced process of cardiac decompensation is, as a rule, a combination of disorders of the diastolic and systolic functions of the LV
Chronic diastolic heart failure
DEFINITION
Diastolic CHF is HF with normal or slightly reduced contractile function of the LV, but with a pronounced impairment of its diastolic relaxation and filling, which is accompanied by an increase in end-diastolic pressure in the ventricle, stagnation of blood in the pulmonary circulation and other signs of HF. This form of heart failure occurs in 20-30% of patients with clinical signs of cardiac decompensation.
There are 3 main criteria for identifying diastolic CHF (European Association of Cardiology, 2004): the presence of clinical signs of CHF (shortness of breath, fatigue, moist rales in the lungs, edema); normal or slightly reduced myocardial contractility (LVEF greater than 45-50%); objective signs indicating impaired relaxation and filling of the LV and/or signs of increased LV stiffness. The division of CHF into two pathophysiological mechanisms is possible in the early stages. The advanced process of cardiac decompensation is a combination of disorders of the diastolic and systolic functions of the left ventricle.
ETIOLOGY
The occurrence of LV diastolic dysfunction is based on 2 reasons: disruption of active relaxation of the ventricular myocardium, which is associated with damage to the energy-intensive process of diastolic Ca2+ transport; deterioration of the compliance of the LV walls, which is caused by changes in the mechanical properties of cardiomyocytes, the state of the connective tissue stroma (fibrosis), pericardium, as well as changes in the geometry of the ventricle. The diastolic form of CHF most often develops with severe hypertrophy of the ventricular myocardium, severe cardiac fibrosis, prolonged chronic myocardial ischemia, a significant increase in afterload, and pericarditis.
PATHOGENESIS
As a result of slowing down the active relaxation of the LV and reducing its compliance in diastole, normal ventricular filling pressure (less than 12 mm Hg) can no longer ensure its sufficient filling with blood. The first consequence of LV diastolic dysfunction is an increase in EDP in the ventricle, which helps maintain normal EDV and cardiac output. The second consequence of LV diastolic dysfunction is various options for the redistribution of diastolic blood flow from the atrium to the ventricle during diastole.
The flow of blood from the atrium into the ventricles occurs in two phases: in the rapid filling phase, when, under the influence of the pressure gradient between the atrium and the ventricle, about 60-75% of the total diastolic blood volume enters the latter; during atrial systole as a result of its active contraction (25% of the total blood volume). The early stages of impairment of LV diastolic function are characterized by a moderate decrease in the rate of isovolumic relaxation and early filling volume. As a result of this structural restructuring of diastole, a pronounced overload of the left atrium occurs, an increase in its volume and pressure in it. In later stages, a “restrictive” type of diastolic dysfunction develops. LA overload contributes to the early onset of supraventricular cardiac arrhythmias, atrial fibrillation and flutter. The third consequence of diastolic dysfunction is an increase in pressure in the venous bed of the pulmonary circulation and stagnation of blood in the lungs.
For diastolic CHF, LV dilatation is not typical until diastolic dysfunction is accompanied by a violation of the pumping function of the heart. LV diastolic dysfunction, increased ventricular pressure and pressure in the pulmonary circulation contribute to the activation of the body's neurohormonal systems. This contributes to the retention of Na+ and water in the body, the development of edema syndrome and a tendency to vasoconstrictor effects. Late stages of diastolic CHF are characterized by a significant increase in LV EDP, ineffective LA systole and a critical decrease in LV filling. Due to high pressure in the pulmonary artery, hypertrophy and dilation of the right ventricle develops, followed by signs of right ventricular heart failure. Diastolic CHF is characterized by a predominance of left ventricular failure.
CLINICAL PICTURE
It is characterized by symptoms of congestive left ventricular HF against the background of normal systolic function of the left ventricle, signs of impaired relaxation, detected by Doppler echocardiography. Diastolic CHF is more common in elderly and senile patients. Patients with hypertension, coronary artery disease, aortic stenosis, HA.
MP. diabetes mellitus, have a high risk of developing diastolic CHF. Patients complain of shortness of breath during exercise, orthopnea and dry cough, which appear in a horizontal position of the patient with a low headboard; fatigue and decreased performance. Physical examination may reveal orthopnea; congestive moist rales in the lower parts of the lungs; increased apical impulse; “double” apical impulse; presystolic gallop rhythm (pathological IV tone); atrial fibrillation is often detected.
INSTRUMENTAL DIAGNOSTICS
The use of modern instrumental studies allows us to determine the signs of LV diastolic dysfunction, ensure the absence of significant disturbances in LV systolic function, and establish the cause of diastolic CHF (coronary heart disease, myocardial infarction, angina).
Echocardiography
Echocardiographic criteria for the absence of LV systolic dysfunction are: 1. LV ejection fraction (EF) more than 45-50%. 2. LV EDV index is less than 102 ml/m.” 3. SI greater than 2.2 l/min/m.” Often, with diastolic dysfunction, EF remains normal, but may be increased (more than 60%). This indicates the presence of a hyperkinetic type of blood circulation in patients with diastolic CHF. In 70% of patients with diastolic CHF, echocardiographic signs of severe LV hypertrophy are detected.
To assess diastole and LV function, the following are determined: the maximum speed of the early peak of diastolic filling (Vmax Peak E), the maximum speed of transmitral blood flow during left atrium systole (Vmax Peak A), the ratio of the maximum speeds of early and late filling (E/A) , LV isovolumic relaxation time (IVRT), early diastolic filling deceleration time (DT).
LV isovolumic relaxation time (IVRT), which is the interval between the end of flow in the LV outflow tract and the beginning of flow through the mitral valve, is a good indicator of the rate of initial ventricular relaxation. Normally, LV IVRT is no more than 70-75 ms, and early diastolic filling deceleration time (DT) is 200 ms. At the end of diastole, during LA contraction, the blood flow rate increases again, forming a second peak (Peak A), and when the mitral valve closes it returns to the zero line.
With normal diastolic function, the Dopplerogram is dominated by the peak of early diastolic filling, which is 1.5-1.7 times higher than the peak of late ventricular filling (Table 63).
Table 63.
Normal values of LV diastolic function
Dopplerograms of transmitral blood flow reveal a decrease in the amplitude of peak E and an increase in the height of peak A. The E/A ratio decreases to 1 and below. At the same time, an increase in the LV isovolumic relaxation time (1VRT) is determined to be more than 90-100 ms and the early diastolic filling deceleration time (DT) is more than 220 ms. This type of LV diastolic dysfunction is called the “delayed relaxation” type. The most common factors leading to the formation of this type of LV diastolic dysfunction are chronic or transient myocardial ischemia in patients with coronary artery disease, cardiosclerosis of any origin, myocardial hypertrophy, pericardial lesions, and bundle branch block.
Further progression of intracardiac hemodynamic disturbances leads to an increase in left atrium pressure and an increase in the atrioventricular pressure gradient during the rapid filling phase. There is a significant acceleration of early diastolic filling of the ventricle (Peak E) with a simultaneous decrease in blood flow velocity during atrial systole (Peak A). An increase in LV end-diastolic pressure contributes to limiting blood flow during atrial systole. A pathological “pseudo-normalization” of LV diastolic filling occurs with an increase in the values of the maximum speed of early diastolic filling (Peak E) and a decrease in the speed of atrial filling (Peak A). As a result, the E/A ratio increases to 1.6-1.8 or more. These changes are accompanied by a shortening of the isovolumic relaxation phase (IVRT) of less than 80 ms and a deceleration time of early diastolic filling (DT) of less than 150 ms.
A restrictive type of diastolic dysfunction is observed in congestive heart failure, indicating a significant increase in LV filling pressure.
Often the described signs of LV diastolic dysfunction precede disturbances in its systolic function. An adequate assessment of LV diastolic function using the described method is possible in patients with a heart rate less than 90 per minute, in the absence of mitral stenosis, aortic, or mitral insufficiency.
Radiography
X-ray of the chest organs makes it possible to detect the absence of pronounced cardiomegaly and assess the condition of the pulmonary circulation. In most cases, signs of venous congestion of the lungs are detected, sometimes in combination with signs of pulmonary arterial hypertension. Instrumental studies allow us to identify the following signs of diastolic CHF: absence of LV systolic dysfunction (according to echocardiography); the presence of ECG and EchoCG signs of severe LV hypertrophy (symmetric or asymmetric); presence of echoCG signs of LV diastolic dysfunction (type of “slow relaxation” - decrease in the amplitude of peak E; increase in the height of peak A; decrease in the E/A ratio to 1 or lower; “restrictive” type of diastolic dysfunction - increase in the height of peak E; decrease in the amplitude of peak A , increasing the E/A ratio to 1.8 and higher); absence of pronounced cardiomegaly on radiographic examination; an increase in PA wedge pressure detected during catheterization of the right heart and PA.
There are no generally accepted algorithms for the treatment of diastolic CHF. According to the recommendations of the European Association of Cardiology (2004), several principles of drug therapy can be distinguished:
1. Restoring sinus rhythm in patients with supraventricular tachyarrhythmia (atrial fibrillation or flutter) leads to a significant improvement in diastolic filling of the ventricles by restoring the normal physiological sequence of contraction of the atria and ventricles.
A decrease in heart rate helps reduce afterload, intramyocardial tension and myocardial oxygen demand. To correct heart rate, beta-blockers (atenolol, metoprolol, carvedilol) and calcium antagonists - verapamil and diltiazem - are used.
3. To reduce stagnation in the pulmonary circulation, it is advisable to use diuretics that reduce blood volume and pressure in the pulmonary artery.
To influence the factors that determine diastolic filling of the ventricles and the degree of diastolic dysfunction, ACE inhibitors can be used, which are more effective in the treatment of patients with diastolic CHF. Calcium antagonists (verapamil and diltiazem) can improve active relaxation of the myocardium and diastolic filling of the ventricles, reduce myocardial mass, and improve the passive elastic properties of the heart muscle. β-blockers may be the drug of choice. The positive effect of long-term use of beta-blockers is associated with a decrease in the degree of LV myocardial hypertrophy and a decrease in the stiffness of the heart muscle. The presence of a negative inotropic effect limits the use of these drugs in patients with severe cardiac decompensation (NYHA FC III-1V). It is advisable to use β-blockers in patients with hypertension or coronary artery disease when there is tachycardia or tachyarrhythmia.
Angiotensin II receptor blockers (losartan, valsartan, candesartai) have a more pronounced effect on local tissue RAS, myocardial hypertrophy and its elastic properties than traditional ACE inhibitors. Nitrates do not have a direct effect on diastolic relaxation, the formation of hypertrophy and cardiac fibrosis, but they reduce the myocardial oxygen demand, reduce ischemia of the heart muscle and thus can indirectly affect the elasticity of the ventricular myocardium. Cardiac glycosides are contraindicated in the treatment of patients with diastolic CHF.
The main principles of long-term treatment of patients with diastolic CHF are: restoration of sinus rhythm and full atrial systole in patients with supraventricular tachyarrhythmias. reduction of tachycardia (verapamil and beta-blockers), reduction of signs of blood stagnation in the pulmonary circulation, long-term use of drugs that have the properties of reversing the development of ventricular myocardial hypertrophy: ACE inhibitors; b-blockers; calcium antagonists; angiotensin II receptor antagonists, use of nitrates.
Until recently, the calculation of SV, EF and other hemodynamic parameters was carried out on the basis of measurements of the M - modal echocardiogram recorded from the left parasternal approach. For the calculation, the degree of anteroposterior shortening of the LV is taken into account, that is, the ratio of EDR and KSR. The calculation is carried out according to the L. Teicholz formula:
Where V is the volume of the LV (ESV or EDV) and D is the anteroposterior size of the LV in systole or diastole. SV is defined as the difference between EVA and ESR, and PV is defined as the ratio of SV to EDC.
Currently, most researchers have abandoned this method of determining hemodynamic parameters, since the calculation of EDV and ESV of the LV, according to this method, is based on measuring EDV and ESV of only a small part of the LV at its base and does not take into account the entire complex geometry of the ventricular cavity. The Teicholz method is also not suitable for determining stroke volume in the majority of patients with coronary artery disease who have local focal disturbances in LV contractility. This requires the practitioner to be very careful about these measurements and calculations.
^ Disk method (modified Simpson method). Significantly more accurate calculations of global LV contractility can be obtained by quantitative assessment of two-dimensional echocardiograms. The most suitable method for this purpose is the Simpson method (disk method), based on the planimetric determination and summation of the areas of 20 disks, which are unique cross-sections of the LV at different levels. To calculate the systolic and diastolic volumes of the LV, two mutually perpendicular two-dimensional images of the heart are obtained from the apical approach in the positions of the two-chamber and four-chamber heart. After highlighting the internal contour of the LV with the cursor in both projections, the latter is automatically divided into 20 disks (a and b) of the same height and their area (S) is calculated:
To calculate the LV volume (V), the areas of the 20 discs are summed, and the sum is multiplied by the height of each LV disc (L/20):
where L is the length of the LV.
This is how the KDO and KSO values are obtained.
Area-length method. In the absence of regional contractility disorders, another simple method for determining stroke volume can be used using two-dimensional echocardiography. On an echocardiogram of a four-chamber or two-chamber heart recorded from the apical approach, the area of the LV cavity (A) and its length (L) are determined planimetrically. LV volume (V) is determined by the formula:
where A is the area of the LV in the image and L is the length of the LV cavity.
Further calculation of hemodynamic parameters is carried out using classical formulas:
where MO is minute volume, UI is stroke index, SI is cardiac index, S is body surface area, determined by special nomograms.
^ Doppler echocardiography method . Determination of SV, EF and other hemodynamic parameters using Doppler echocardiography is based on measuring the volumetric blood flow through the aortic valve. For this purpose, from the apical access in the positions of a two-chamber or five-chamber heart, Doppler location of the LV outflow tract is performed in pulse mode, setting the control volume in the center of the outflow tract 10 mm proximal to the closed cusps of the aortic valve, and a systolic spectrum of linear blood flow velocity in the LV outflow tract is obtained. . In this case, the average linear blood flow velocity (V) and the linear blood flow velocity integral (LVOT VTI) are automatically calculated, i.e. the sum of all momentary values of linear velocity during the expulsion of blood into the aorta. The latter can also be represented as the product of Vcp (m/s) by the duration of the expulsion period (ET) in seconds: LVOT VTI = Vcp ET (cm).
It is clear that the same SV value can be obtained by multiplying the average linear blood flow velocity by the duration of systole (ET, in s) and the cross-sectional area of the aorta:
^ ASSESSMENT OF DIASTOLIC FUNCTION OF THE LEFT VENTRICLE
I LV diastolic function is assessed by the results of a study of transmitral diastolic blood flow in pulsed Doppler mode.
Define:
1) the maximum speed of the early peak of diastolic filling (Vmax Peak E);
2) the maximum speed of transmitral blood flow during systole of the left atrium 1 (Vmax Peak A);
3) area under the curve (velocity integral) of early diastolic filling (MVVTI Peak E)
4) atrial systole (MV VTI Peak A);
5) the ratio of the maximum speeds (or speed integrals) of early and late filling (E/A);
6) LV isovolumic relaxation time - IVRT (measured by simultaneous recording of aortic and transmitral blood flow in a constant-wave mode from the apical access);
7) early diastolic filling deceleration time (DT).
Normally, the diastolic blood flow through the mitral valve when recorded in Doppler compression has a two-wave form. After the mitral valve opens, the speed of blood flow through the left atrioventricular orifice quickly increases to a maximum and then just as quickly decreases almost to the zero line. This early diastolic peak (Peak E) corresponds to the rapid filling phase of the LV and is normally about 0.62 m/s. LV isovolumic relaxation time (IVRT), which is the interval between the end of flow in the LV outflow tract and the beginning of flow through the mitral valve, is a good indicator of the rate of initial ventricular relaxation. Normally, LV IVRT is no more than 70-75 ms, and early diastolic filling deceleration time (DT) is 200 ms.
At the end of diastole, during LA contraction, the blood flow rate increases again, forming a second peak (Peak A), and then returns to the zero line when the mitral valve closes. With normal diastolic function, the Dopplerogram is dominated by early diastolic filling (Peak E), which is 1.5-1.6 times higher than the peak of late ventricular filling (Peak A).
| Vmax Peak E | Vmax Peak A | E/A | IVRT | D.T. |
| 0.62 m/s | 0.35 m/s | 1,5-1,6 | 70-75 ms | 200 ms |
^ DIASTOLIC DYSFUNCTION OF THE LEFT VENTRICLE
The initial stages of impairment of LV diastolic function, not accompanied by an increase in ventricular EDP and LA pressure, are characterized by a decrease in the rate of isovolumic relaxation and the volume of early diastolic filling. In this case, the LA volume immediately before the start of its contraction, i.e. at the end of diastole, increases markedly. The result of this, according to the Frank-Starling law, is a stronger contraction of the LA and an increase in the atrial filling fraction (peak A). In other words, at the initial stage of development of diastolic dysfunction, a slowdown in LV relaxation leads to a redistribution of diastolic filling in favor of the atrial component and a significant part of the diastolic blood flow occurs during active LA systole.
Dopplerograms of transmitral blood flow reveal a decrease in the amplitude of peak E and an increase in the height of peak A. The E/A ratio decreases to 1.0 and below. At the same time, an increase in the LV isovolumic relaxation time (IVRT) is determined to be more than 90-100 ms and the early diastolic filling deceleration time (DT) is more than 220 ms.
This type of LV diastolic dysfunction is called type "slow relaxation". The most common factors leading to the formation of this type of LV diastolic dysfunction are chronic or transient myocardial ischemia in patients with coronary artery disease, cardiosclerosis of any origin (including post-infarction), myocardial hypertrophy, pericardial lesions, blockades! bundle branches, etc.
Further progression of intracardiac hemodynamic disturbances leads to an increase in left atrium pressure and an increase in the atrioventricular pressure gradient during the rapid filling phase. This is accompanied by a significant acceleration of early diastolic filling of the ventricle (Peak E) with a simultaneous decrease in blood flow velocity during atrial systole (Peak A). An increase in LV end-diastolic pressure further restricts blood flow during atrial systole. A kind of pathological “pseudo-normalization” of LV diastolic filling occurs with an increase in the values of the maximum speed of early diastolic filling (Peak E) and a decrease in the speed of atrial filling (Peak A). As a result, the E/A ratio increases to more than 1.6-1.8. These changes are accompanied by a shortening of the isovolumic relaxation phase (IVRT) of less than 70 ms and a deceleration time of early diastolic filling (DT) of less than 150 ms.
Such, " restrictive» type of diastolic dysfunction typically observed in congestive heart failure, indicating increased LV filling pressure. Often the described signs of LV diastolic dysfunction precede disturbances in its systolic function, and the “restrictive” type is prognostically less favorable.
^ ASSESSMENT OF REGIONAL CONTRACTILITY DISORDERS OF THE LEFT VENTRICLE
Detection of local disturbances in LV contractility using two-dimensional echocardiography is important for the diagnosis of CAD. The examination is usually performed from the apical access along the long axis in the projection of the two and four chamber hearts, as well as from the left parasternal access in the true and short axes.
In accordance with the recommendations of the American Association of Echocardiography, the LV is conventionally divided into 16 segments located in the plane of three cross sections of the heart, recorded from the left parasternal approach along the short axis.
An image of 6 basal segments - anterior (A), anteroseptal (AS), posteroseptal (IS), posterior (I), posterolateral (IL) and anterolateral (AL) - is obtained by locating at the level of the mitral valve leaflets (SAX MV), and the middle parts of the same 6 segments - at the level of the tapillary muscles (SAX PL). Images of the 4 apical segments - anterior (A), septal (S), posterior (I) and lateral (L) - are obtained by locating from the parasternal approach at the level of the apex of the heart (SAX AP).
The general idea of the local contractility of these segments is well complemented by three longitudinal “slices” of the LV, recorded from the parasternal approach along the long axis of the heart, as well as in the apical position of the four-chamber and two-chamber heart.
In each of these segments, the nature and amplitude of myocardial movement, as well as the degree of its systolic thickening, are assessed. There are 3 types of local disorders of the contractile function of the LV, united by the concept of “asynergy”:
1. Akinesia - absence of contraction of a limited area of the heart muscle.
2. Hypokinesia - a pronounced local decrease in the degree of contraction.
3. Dyskinesia - paradoxical expansion (bulging) of a limited area of the heart muscle during systole.
The main causes of local disturbances in LV myocardial contractility are:
1. Acute myocardial infarction (MI).
2. Post-infarction cardiosclerosis.
3. Transient painful and silent myocardial ischemia, including ischemia induced by functional stress tests.
4. Constant ischemia of the myocardium, which still retains its viability (the so-called “hibernating myocardium”).
5. Dilated and hypertrophic cardiomyopathies, which are often also accompanied by uneven damage to the LV myocardium.
6. Local disturbances of intraventricular conduction (blockade, WPW syndrome, etc.).
7. Paradoxical movements of the IVS, for example, with volume overload of the RV or bundle branch blocks.
Two-dimensional echocardiogram recorded from the apical approach in the position of the four-chamber heart in a patient with transmural myocardial infarction and apical segment dyskinesia (“dynamic aneurysm” of the LV). Dyskinesia is determined only during LV systole
Violations of local contractility of individual segments of the LV in patients with coronary artery disease are usually described on a five-point scale:
1 point - normal contractility;
2 points - moderate hypokinesia (slight decrease in the amplitude of systolic movement and thickening in the studied area);
3 points - severe hypokinesia;
4 points - akinesia (lack of movement and thickening of the myocardium);
5 points - dyskinesia (systolic movement of the myocardium of the segment under study occurs in the direction opposite to normal).
Of important prognostic significance is the calculation of the so-called local contractility index (LCI), which is the sum of the contractility scores of each segment (2S) divided by the total number of LV segments examined (n):
High values of this indicator in patients with MI or post-infarction cardiosclerosis are often associated with an increased risk of death.
^ ACQUIRED HEART DEFECTS
STENOSIS OF THE LEFT ATRIOVENTRICULAR ORIFICE (MITRAL STENOSIS)
Stenosis of the left atrioventricular orifice is characterized by partial fusion of the anterior and posterior leaflets of the mitral valve, a decrease in the area of the mitral orifice, and obstruction of diastolic blood flow from the left atrium to the left ventricle.
There are two characteristic echocardiographic signs of mitral stenosis detected by M-modal examination:
1) a significant decrease in the speed of diastolic closure of the anterior leaflet of the mitral valve;
2) unidirectional movement of the front and rear valve leaflets. These signs are better identified by M-modal examination from a parasternal approach along the long axis of the heart.
Determination of the speed of diastolic closure of the anterior leaflet of the mitral valve in a healthy person (a) and in a patient with stenosis of the left atrioventricular orifice (6).
As a result of high pressure in the LA, the valve leaflets are constantly in the open position during diastole and, unlike the norm, do not close after the completion of early rapid filling of the LV. The blood flow from the left atrium becomes constant (not interrupted) linear. Therefore, on the echocardiogram, there is a flattening of the curve of movement of the anterior leaflet and a decrease in the amplitude of wave A, corresponding to the systole of the left atrium. The shape of the diastolic movement of the anterior leaflet of the mitral valve instead of M-shaped becomes U-shaped.
In a two-dimensional echocardiographic study from a parasternal approach along the long axis of the heart, the most characteristic sign of mitral stenosis, detected already in the initial stages of the disease, is a dome-shaped diastolic protrusion of the anterior leaflet of the mitral valve into the LV cavity towards the IVS, which is called “parousia”.
In the later stages of the disease, when the mitral valve leaflets thicken and become rigid, their “sailing” stops, but the valve leaflets during diastole are located at an angle to each other (normally they are parallel), forming a peculiar cone-shaped shape of the mitral valve.
Scheme of diastolic opening of the mitral valve leaflets: a - normal (the leaflets are parallel to each other), b - funnel-shaped arrangement of the mitral valve leaflets in the initial stages of mitral stenosis, accompanied by a dome-shaped diastolic protrusion of the anterior leaflet into the LV cavity (“parousia”), c - cone-shaped MV on late stages of mitral stenosis (the leaflets are located at an angle to each other, rigid).
Parousia" of the anterior mitral valve leaflet in mitral stenosis (two-dimensional echocardiogram of the true axis access). There is also an increase in the size of the left atrium.
Decreased distolic divergence of the valve leaflets and the area of the mitral orifice during a two-dimensional study from a parasternal short-axis approach: a - normal, b - mitral stenosis.
Doppler echocardiographic study of transmitral diastolic blood flow allows us to identify several signs characteristic of mitral stenosis and associated primarily with a significant increase in the diastolic pressure gradient between the LA and LV and a slowdown in the decrease in this gradient during the period of LV filling. These signs include:
1) increase in the maximum linear velocity of early transmitral blood flow to 1.6-2.5 m.s1 (normally about 0.6 m.s1),
2) slowing down the decline in the rate of diastolic filling (flattening of the spectrogram),
3) significant turbulence of blood movement.
^ Dopplerograms of transmitral blood flow in normal conditions (a) and in mitral cases (b).
To measure the area of the left atrioventricular orifice, two methods are currently used. With two-dimensional echocardiography from a parasternal short-axis approach at the level of the tips of the valve leaflets, the area of the opening is determined planimetrically by tracing the contours of the opening with the cursor at the moment of maximum diastolic opening of the valve leaflets.
More accurate data are obtained by Doppler examination of transmitral blood flow and determination of the diastolic gradient of transmitral pressure. Normally it is 3-4 mm Hg. As the degree of stenosis increases, the pressure gradient also increases. To calculate the area of the hole, the time during which the maximum gradient is reduced by half is measured. This is the so-called half-life of the pressure gradient (Th2) - The pressure gradient reported by Doppler echocardiography is calculated using the simplified Bernoulli equation:
where DR is the pressure gradient on both sides of the obstruction (mm Hg), and V is the maximum
blood flow velocity of the distal obstruction (m s!).
This means that when AR is reduced by half, the maximum linear blood flow velocity decreases by 1.4 times (V2 = 1.4). Therefore, to measure the half-life of the pressure gradient (T1/2), it is enough to determine the time during which the maximum linear blood flow velocity decreases by 1.4 times. It has been shown that if the area of the left atrioventricular orifice is 1 cm2, the T1/2 time is 220 ms. From here the area of the hole S can be determined by the formula:
When T1/2 is less than 220 ms, the hole area exceeds 1 cm2, on the contrary, if T1/2 is more than 220 ms, the hole area is less than 1 cm2.
^ MITRAL VALVE INSUFFICIENCY
Insufficiency is the most common pathology of the mitral valve, the clinical manifestations of which (including auscultation) are often mild or absent altogether.
There are 2 main forms of mitral regurgitation:
1. Organic mitral valve insufficiency with wrinkling and shortening of the valve leaflets, calcium deposition in them and damage to subvalvular structures (rheumatism, infective endocarditis, atherosclerosis, systemic connective tissue diseases).
2. Relative mitral insufficiency caused by dysfunction of the valve apparatus, in the absence of gross morphological changes in the valve leaflets.
The causes of relative mitral insufficiency are:
1) prolapse of the mitral valve;
2) IHD, including acute MI (infarction of the papillary muscle and other mechanisms of valvular dysfunction);
3) diseases of the left ventricle, accompanied by its pronounced dilatation and expansion of the fibrous ring of the valve and/or dysfunction of the valve apparatus (arterial hypertension, aortic heart defects, cardiomyopathies, etc.);
4) rupture of tendon threads;
5) calcification of the papillary muscles and fibrous ring of the mitral valve.
^ Organic (a) and two variants of relative mitral valve insufficiency (b, c).
There are no direct echocardiographic signs of mitral regurgitation using one- and two-dimensional echocardiography. The only reliable sign of the organ - cervical mitral insufficiency - non-closure (separation) of the mitral valve leaflets during ventricular systole - is detected extremely rarely. Indirect echocardiographic signs of mitral regurgitation, reflecting hemodynamic changes characteristic of this defect, include:
1) increase in LA size;
2) hyperkinesia of the posterior wall of the left atrium;
3) increase in total stroke volume (according to the Simpson method);
4) myocardial hypertrophy and dilatation of the LV cavity.
The most reliable method for detecting mitral regurgitation is a Doppler study. The study is carried out from the apical access of a four-chamber or two-chamber heart in a pulse-wave mode, which allows you to sequentially move the control (gating) volume at various distances from the mitral valve leaflets, starting from the place of their closure and further towards the upper and lateral walls of the left atrium. In this way, a search is made for the regurgitation jet, which is clearly visible on Doppler echocardiograms in the form of a characteristic spectrum directed downward from the baseline zero line. The density of the spectrum of mitral regurgitation and the depth of its penetration into the left atrium are directly proportional to the degree of mitral regurgitation.
With the 1st degree of mitral regurgitation, the latter is detected immediately behind the mitral valves; with the 2nd degree, it extends 20 mm from the valves deep into the left atrium; with the 3rd degree, approximately to the middle of the left atrium; and with the 4th degree, it reaches the opposite wall of the atrium. .
It should be remembered that minor regurgitation, which is recorded immediately behind the mitral valve leaflets, can be detected in approximately 40-50% of healthy people.
Mapping of the Doppler signal in a patient with mitral insufficiency: a - mapping scheme (black dots indicate sequential movement of the control volume), b - Dopplerogram of the mitral blood flow recorded at the level of the left atrium outflow tract. Regurgitation of blood from the LV to the LA is indicated by arrows.
The color Doppler scanning method is the most informative and visual in identifying mitral regurgitation.
The blood stream returning to the left atrium during systole is colored light blue during color scanning from the apical access. The magnitude and volume of this regurgitation flow depends on the degree of mitral regurgitation.
At a minimal degree, the regurgitant flow has a small diameter at the level of the leaflets of the left atrioventricular valve and does not reach the opposite wall of the left atrium. Its volume does not exceed 20% of the total volume of the atrium.
With moderate mitral regurgitation, the reverse systolic blood flow at the level of the valve leaflets becomes wider and reaches the opposite wall of the left atrium, occupying about 50-60% of the atrium volume.
Severe mitral regurgitation is characterized by a significant diameter of the regurgitant blood flow already at the level of the mitral valve leaflets. The reverse flow of blood occupies almost the entire volume of the atrium and sometimes even enters the mouth of the pulmonary veins.
a - minimal degree (regurgitant blood flow has a small diameter at the level of the mitral leaflets and does not reach the opposite wall of the left atrium), 6 - moderate degree (regurgitant blood flow reaches the opposite wall of the left atrium), c - severe mitral valve insufficiency (regurgitant blood flow reaches the opposite wall LA and occupies almost the entire volume of the atrium).
^ AORTIC STENOSIS
Diagnostic criteria for aortic stenosis in an M-modal study are a decrease in the degree of divergence of the aortic valve leaflets during LV systole, as well as compaction and heterogeneity of the structure of the valve leaflets.
Normally, the movement of the aortic valve leaflets is recorded in the form of a kind of “box” during systole and in the form of a straight line during diastole, and the systolic opening of the aortic valve leaflets usually exceeds 12-18 mm. With severe stenosis, the opening of the valves becomes less than 8 mm. Leaf divergence within 8-12 mm may correspond to varying degrees of aortic stenosis.
a - systolic opening of the aortic valve (AV) leaflets in a healthy person,
b - systolic opening of the valves of the aortic valve in a patient with aortic stenosis.
At the same time, it should be borne in mind that this indicator, determined during the M-modal study, is not one of the reliable and reliable criteria for the severity of stenosis, since it largely depends on the magnitude of the stroke volume.
A two-dimensional B-mode study from parasternal access of the true axis of the heart allows us to identify more reliable signs of aortic stenosis:
1. Systolic deflection of the valve leaflets towards the aorta (an echocardiographic symptom similar to the “parousia” of the mitral valve leaflets with stenosis of the left atrioventricular orifice) or the arrangement of the leaflets at an angle to each other. These two signs indicate incomplete opening of the aortic valve during LV systole.
2. Severe hypertrophy of the LV myocardium in the absence of significant dilation of its cavity, as a result of which the EDV and ESV of the LV for a long time differ little from the norm, but there is a significant increase in the thickness of the IVS and the posterior wall of the LV. Only in advanced cases of aortic stenosis, when myogenic dilatation of the LV develops or mitralization of the defect occurs, an increase in the size of the LV is detected on the echocardiogram.
3. Poststenotic dilatation of the aorta, caused by a significant increase in the linear velocity of blood flow through the narrowed aortic opening.
4. Severe calcification of the aortic valve leaflets and aortic root, which is accompanied by an increase in the intensity of echo signals from the valve leaflets, as well as the appearance in the aortic lumen of many intense echo signals parallel to the walls of the vessel.
Two-dimensional echocardiogram recorded from a parasternal view of the true cardiac axis in a patient with aortic stenosis (6). There is noticeable thickening of the valves of the aortic valve, their incomplete opening in systole, significant post-stenotic expansion of the aorta and pronounced hypertrophy of the posterior wall of the LV and IVS.
^ Scheme of Doppler study of transaortic blood flow (a) and Dopplerogram (b) of a patient with aortic stenosis (apical position of the true LV axis)
.
Calculation of the area of the aortic valve with the help of Doppler and two-dimensional jocardiographic studies (scheme): a - planimetric determination of the area of the cross section of the LV outflow tract, b - Doppler determination of the linear velocity of systolic blood flow in the LV outflow tract and in the aorta (above the site of narrowing).
^ AORTIC INSUFFICIENCY
The main sign of aortic regurgitation with one-dimensional echocardiography (M-mode) is diastolic vibration of the anterior mitral valve leaflet, which occurs under the influence of reverse turbulent blood flow from the aorta to the LV.
Changes in a one-dimensional echocardiogram in aortic insufficiency: a - diagram explaining the possible mechanism of diastolic flutter of the anterior mitral valve leaflet, b - one-dimensional echocardiogram in aortic insufficiency (diastolic flutter in the anterior leaflet of the mitral valve and IVS is noticeable)
Another sign - non-closure of the aortic valve leaflets in diastole - is not detected so often. An indirect sign of severe aortic insufficiency is also the early closure of the mitral valve leaflets as a result of a significant increase in pressure in the LV.
Two-dimensional echocardiography for aortic insufficiency is somewhat inferior in information content to the M-modal study due to lower temporal resolution and the inability in many cases to register diastolic vibration of the anterior leaflet of the mitral valve. EchoCG usually reveals significant LV dilatation.
The most informative in diagnosing aortic insufficiency and determining its severity is Doppler echocardiography, especially color Doppler scanning.
Aortic diastolic regurgitation, when using the apical or left parasternal color Doppler position, appears as a mottled flow originating from the aortic valve and extending into the LV. This pathological regurgitant diastolic blood flow must be distinguished from the normal physiological blood flow in diastole from the LA to the LV through the left atrioventricular orifice. In contrast to the transmitral diastolic blood flow, the blood stream regurgitating from the aorta comes from the aortic valve and appears at the very beginning of diastole, immediately after the closure of the aortic valve leaflets (II tone). Normal diastolic blood flow through the mitral valve occurs a little later, only after the end of the isovolumic relaxation phase of the LV.
^ Doppler echocardiographic signs of aortic insufficiency.
Quantification of the degree of aortic regurgitation is based on measuring the half-life time (T1/2) of the diastolic pressure gradient between the aorta and LV. The rate of regurgitant blood flow is determined by the pressure gradient between the aorta and LV. The faster this speed decreases, the faster the pressure between the aorta and the ventricle equalizes and the more pronounced is the aortic insufficiency (with mitral stenosis, the opposite relationship exists). If the half-life of the pressure gradient (T1/2) is less than 200 ms, severe aortic regurgitation occurs. With T1/2 values greater than 400 ms, we are talking about a low degree of aortic insufficiency.
^ Determination of the degree of aortic insufficiency based on Doppler studies of regurgitant diastole and blood flow through the aortic valve. T1/2
- half-life of the diastolic pressure gradient in the aorta and left ventricle.
^ TRILEAFTER VALVE INSUFFICIENCY
Tricuspid valve insufficiency often develops secondarily, against the background of pancreatic decompensation caused by pulmonary hypertension (cor pulmonale, mitral stenosis, primary pulmonary hypertension, etc.). Therefore, organic changes in the leaflets of the valve itself, as a rule, are absent. M-modal and two-dimensional echocardiographic studies can reveal indirect signs of the defect - dilatation and hypertrophy of the RV and RA, corresponding to the volume overload of these parts of the heart. In addition, a two-dimensional study reveals paradoxical movements of the IVS and systolic pulsation of the inferior vena cava. Direct and reliable signs of tricuspid regurgitation can only be detected with Doppler examination. Depending on the degree of insufficiency, a stream of tricuspid regurgitation is detected in the right atrium at different depths. Sometimes it reaches the inferior vena cava and hepatic veins. It should be remembered that in 60-80% of healthy individuals, slight regurgitation of blood from the pancreas to the RA is also detected, however, the maximum speed of reverse blood flow does not exceed 1 m-s1.
Dopplerogram of tricuspid insufficiency: a - diagram of Doppler scanning from the apical position of the four-chamber heart, b - Dopplerogram of tricuspid regurgitation (marked by arrows).
^ DIAGNOSIS OF PERICARDIAL LESIONS
Echocardiographic examination allows diagnosing various types of pericardial lesions:
1) dry pericarditis,
2) the presence of fluid in the pericardial cavity (exudative pericarditis, hydropericardium,
3) constrictive pericarditis.
Dry pericarditis is known to be accompanied by thickening of the pericardial layers and an increase in the echogenicity of the posterior pericardial layer, which is clearly revealed by M-modal examination. The sensitivity of one-dimensional echocardiography in this case is higher than that of two-dimensional scanning.
Effusion in the pericardial cavity. In the presence of a pathological effusion in the pericardial cavity, exceeding the normal volume of serous fluid (about 30-50 ml), an echocardiogram reveals separation of the pericardial layers with the formation of an echo-negative space behind the posterior wall of the LV, and diastolic separation of the pericardial layers is of diagnostic importance. The movement of the parietal layer of the pericardium decreases or disappears completely, while the excursion of the epicardial surface of the heart increases (epicardial hyperkinesia), which serves as an indirect sign of the presence of fluid in the pericardial cavity.
Quantitative determination of the volume of effusion in the pericardial cavity using echocardiography is difficult, although it is believed that 1 cm of echo-negative space between the pericardial layers corresponds to 150-400 ml, and 3-4 cm corresponds to 500-1500 ml of fluid.
^ One-dimensional (a) and two-dimensional (6) echo cardiogram for effusion pleurisy. There is compaction and moderate separation of the pericardial layers.
Two-dimensional echocardiogram in a patient with a significant amount of pericardial effusion (PE). Fluid is detected behind the posterior wall of the left ventricle, in the region of the apex of the heart and in front of the right ventricle.
Constrictive pericarditis is characterized by fusion of the pericardial layers into a single conglomerate, followed by calcification and the formation of a dense, immobile capsule surrounding the heart (“armored” heart) and complicating the process of diastolic relaxation and filling of the ventricles. Severe disturbances in diastolic function underlie the formation and progression of heart failure.
One-dimensional or two-dimensional echocardiographic examination can detect thickening and significant compaction of the pericardial layers. The echo-negative space between the layers is filled with an inhomogeneous layered mass, less echo-dense than the pericardium itself. Signs of impaired blood supply to the heart in diastole and myocardial contractility are also revealed.
1. Early diastolic paradoxical movement of the IVS into the LV cavity with subsequent development of hypokinesia and akinesia of the IVS.
2. Flattening of the diastolic movement of the posterior wall of the LV (M-mode).
3. Reduction in the size of the ventricular cavities.
4. Reducing the collapse of the inferior vena cava after a deep breath (normally, the collapse of the inferior vena cava is about 50% of its diameter).
5. Decrease in stroke volume, ejection fraction and other indicators of systolic function.
A Doppler study of transmitral blood flow reveals a significant dependence of the rate of LV diastolic filling on the phases of respiration: it increases during exhalation and decreases during inhalation.
Changes during breathing in the amplitude of the Doppler signal of the transmitral diastolic blood flow in a patient with constrictive pericarditis: a - diagram of ultrasound Doppler scanning, b - Dopplerogram of diastolic blood flow (during inspiration, a significant decrease in blood flow velocity is determined)
CARDIOMYOPATHIES
Cardiomyopathies (CM) are a group of myocardial diseases of unknown etiology, the most characteristic features of which are cardiomegaly and progressive heart failure.
There are 3 forms of ILC:
1) hypertrophic cardiomyopathy,
2) dilated cardiomyopathy,
3) restrictive CMP.
^ Hypertrophic cardiomyopathy (HCM) is characterized by
1) pronounced hypertrophy of the LV myocardium,
2) a decrease in the volume of its cavity
3) impaired LV diastolic function.
The most common form is asymmetrical HCM with predominant hypertrophy of the upper, middle or lower third of the IVS, the thickness of which can be 1.5-3.0 times the thickness of the posterior wall of the LV.
Of interest is ultrasound diagnostics of the so-called obstructive form of HCM with asymmetrical lesions of the IVS and obstruction of the LV outflow tract (“subaortic subvalvular stenosis”). Echocardiographic signs of this form of HCM are:
1. Asymmetrical thickening of the IVS and limitation of its mobility.
2. Anterior systolic movement of the mitral valve leaflets.
3. Covering the aortic valve in mid-systole.
4. The appearance of a dynamic pressure gradient in the LV outflow tract.
5. High linear velocity of blood flow in the LV outflow tract.
6. Hyperkinesia of the posterior wall of the left ventricle.
7. Mitral regurgitation and dilatation of the left atrium.
Echocardiographic signs of hypertrophic cardiomyopathy
:a - diagram of asymmetric IVS hypertrophy, b - two-dimensional echocardiogram from the parasternal access of the true axis of the heart. A pronounced thickening of the IVS is determined.
Anterior systolic movement of the mitral valve leaflet in a patient with hypertrophic cardiomyopathy: a - diagram explaining the possible mechanism of anterior systolic movement, b - one-dimensional echocardiogram, on which the systolic movement of the anterior mitral valve leaflet (marked by red arrows) and significant thickening of the IVS and the posterior wall of the LV are clearly visible.
The shape of a Dopplerogram of the systolic blood flow in the outflow tract of the left ventricle in a patient with hypertrophic cardiomyopathy, reflecting the appearance of a dynamic pressure gradient in the outflow tract and aorta, caused by the covering of the aortic valve in mid-systole. An increase in the maximum linear blood flow velocity (Vmax) is also noticeable.
^ Dilated cardiomyopathy (DCM) characterized by diffuse damage to the heart muscle and is accompanied by
1) a significant increase in the cavities of the heart,
2) mild myocardial hypertrophy,
3) a sharp decrease in systolic and diastolic function,
4) a tendency to rapid progression of signs of heart failure, the development of mural thrombi and thromboembolic complications.
The most characteristic echocardiographic signs of DCM are significant dilatation of the LV with normal or reduced thickness of its walls and a decrease in EF (below 30-20%). Enlargement of other chambers of the heart (RV, LA) is often noted. As a rule, total hypokinesia of the LV walls develops, as well as a significant decrease in blood flow velocity in the ascending aorta and the LV outflow tract and in the PA (Doppler mode). Intracardiac mural thrombi are often visualized.
Two-dimensional (a) and one-dimensional echocardiography (b) in a patient with dilated cardiomyopathy. Significant dilatation of the left ventricle, as well as the right ventricle and atria with normal thickness of their walls is determined.
^ Restrictive cardiomyopathy. The concept of restrictive cardiomyonatia (RCMP) combines two diseases: endocardial fibrosis and eosinophilic fibroplastic Loeffler's endocarditis. Both diseases are characterized by:
1) significant thickening of the endocardium,
2) hypertrophy of the myocardium of both ventricles,
3) obliteration of the cavities of the LV and RV,
4) pronounced diastolic dysfunction of the ventricles with relatively preserved systolic function.
One-dimensional, two-dimensional and Doppler echocardiographic studies in RCM can detect:
1. Thickening of the endocardium with a decrease in the size of the ventricular cavities.
2. Various options for paradoxical movement of the IVS.
3. Prolapse of the mitral and tricuspid valves.
4. Severe diastolic dysfunction of the ventricular myocardium of a restrictive type with an increase in the maximum speed of early diastolic filling (Peak E) and a decrease in the duration of isovolumic relaxation of the myocardium (IVRT) and the slowdown time of early diastolic filling (DT).
5. Relative insufficiency of the mitral and tricuspid valves.
6. Presence of intracardiac wall thrombi.
Changes revealed on a two-dimensional echocardiogram (a) and Dopplerogram of transmitral blood flow (b) in a patient with restrictive cardiomyopathy. There is a noticeable significant thickening of the IVS and the posterior wall of the LV, a decrease in the ventricular cavities, and an increase in the size of the left atrium. A Dopplerogram reveals signs of LV diastolic dysfunction of a restrictive type (a significant increase in the E/A ratio, a decrease in the duration of IVRT and DT).
Two-dimensional echocardiograms (a, b) recorded from the apical position of the four-chamber heart in a patient with a mural thrombus in the cavity of the left ventricle (in the apex region).
Main literature
1. N. Schiller, M.A. Osipov Clinical echocardiography. 2nd edition, Practice 2005. 344 p.
2. Mitkov V.V., Sandrikov V.A. Clinical guide to ultrasound diagnostics in 5 volumes. M.: Vidar. 1998; 5: 360 s.
3. Feigenbaum X. Ultrasound diagnostics. M.: Medicine. 1999;416p.
additional literature
1.M.K.Rybakova, M.E. Alekhin, V.V. Mitkov. Practical guide to ultrasound diagnostics. Echocardiography. Vidar, Moscow 2008. 512 p.
2. A. Kalinin, M.N. Alekhine. Assessment of the state of the atrial myocardium in the mode of two-dimensional gray scale deformation in patients with arterial hypertension with slight hypertrophy of the left ventricle. Journal "Cardiology" No. 8, 2010.
3. Yu.N. Belenkov. Left ventricular remodeling; A complex approach. Heart failure. 2002, T.3, No. 4, 163 p.
4. A.V.Grachev. The mass of the left ventricular myocardium in patients with arterial hypertension with various echocardiographic types of geometry of the left ventricle of the heart. Journal "Cardiology" No. 3, 2000.
5. Yu.A. Vasyuk, A.A. Kazina Features of systolic function and remodeling in patients with arterial hypertension. Heart failure No. 2, 2003.
6. A.V.Preobrazhensky, B.A. Sidorenko, M.N. Alekhin et al. Left ventricular hypertrophy in hypertension. Part 1. Criteria for diagnosing left ventricular hypertrophy and its prevalence. “Cardiology” No. 10, 2003, 104 p.
Congenital heart defects are found in 1% of children born alive. Most of these patients die in infancy and childhood, and only 5-15% survive to puberty. With timely surgical correction of congenital heart disease in childhood, the life expectancy of patients is significantly longer. Without surgical correction, patients with small VSDs, small ASDs, moderate pulmonary stenosis, small patent ductus arteriosus, bicuspid aortic valve, minor stenosis of the aortic mouth, Ebstein's anomaly, corrected by transposition of the great vessels usually survive to adulthood. Patients with tetralogy of Fallot and a patent AV canal are less likely to survive into adulthood.
9.1. VENTRICULAR SEPTAL DEFECT
VSD is the presence of communication between the left and right ventricles, leading to pathological discharge of blood from one chamber of the heart to another. Defects can be located in the membranous (upper) part of the interventricular septum (75-80% of all defects), in the muscular part (10%), in the outflow tract of the right ventricle (supracrestal - 5%), in the inflow tract (atrioventricular septal defects - 15%). For defects located in the muscular part of the interventricular septum, the term “Tolochinov-Roger disease” is used.
Prevalence
VSD is the most common congenital heart defect in children and adolescents; it occurs less frequently in adults. This is due to the fact that in childhood, patients undergo surgical intervention; in some children, VSDs close on their own (the possibility of independent closure remains even in adulthood with small defects), and a significant proportion of children with large defects die. In adults, defects of small and medium size are usually detected. VSD can be combined with other congenital heart defects (in descending order of frequency): coarctation of the aorta, ASD, patent ductus arteriosus, subvalvular pulmonary artery stenosis, subvalvular aortic stenosis, mitral stenosis.
HEMODYNAMICS
In adults, VSDs persist due to the fact that they were either not identified in childhood or were not operated on in a timely manner (Fig. 9-1). Pathological changes in VSD depend on the size of the opening and the resistance of the pulmonary vessels.
Rice. 9-1. Anatomy and hemodynamics of VSD. A - aorta; PA - pulmonary artery; LA - left atrium; LV - left ventricle; RA - right atrium; RV - right ventricle; IVC - inferior vena cava; SVC - superior vena cava. A short solid arrow indicates a ventricular septal defect.With a small VSD (less than 4-5 mm), the so-called restrictive defect, the resistance to blood flow through the shunt is high. Pulmonary blood flow increases slightly, pressure in the right ventricle and pulmonary vascular resistance also increase slightly.
With a medium-sized VSD (5-20 mm), a moderate increase in pressure in the right ventricle occurs, usually not exceeding half the pressure in the left ventricle.
With a large VSD (greater than 20 mm, non-restrictive defect), there is no resistance to blood flow, and the pressure levels in the right and left ventricles are equal. An increase in blood volume in the right ventricle leads to increased pulmonary blood flow and increased pulmonary vascular resistance. With a significant increase in pulmonary vascular resistance, the discharge of blood from left to right through the defect decreases, and when pulmonary vascular resistance predominates over the resistance in the systemic circulation, a discharge of blood from right to left may occur with the appearance of cyanosis. With a large discharge of blood from left to right, pulmonary hypertension and irreversible sclerosis of the pulmonary arterioles (Eisenmenger syndrome) develop.
In some patients, perimembranous VSDs or defects in the area of the right ventricular outflow tract can be combined with aortic regurgitation as a result of sagging of the aortic valve leaflet into the defect.
Complaints
Small-sized (restrictive) defects are asymptomatic. Medium-sized VSDs lead to delayed physical development and frequent respiratory tract infections. With large defects, as a rule, patients have signs of right and left ventricular failure: shortness of breath on exertion, enlarged liver, swelling of the legs, orthopnea. When Eisenmenger syndrome occurs, patients begin to experience severe shortness of breath even with minor physical activity, chest pain without a clear connection with physical activity, hemoptysis, and episodes of loss of consciousness.
Inspection
Children with a medium-sized VSD are usually retarded in physical development, and they may have a cardiac hump. The discharge of blood from right to left leads to the appearance of changes in the fingers in the form of “drumsticks”, cyanosis, which increases with physical activity, and external signs of erythrocytosis (see Chapter 55 “Tumors of the Blood System”, Section 55.2 “Chronic Leukemia”).
Palpation
Systolic flutter is detected in the middle part of the sternum, associated with turbulent blood flow through the VSD.
Auscultation hearts
The most characteristic sign is a rough systolic murmur along the left edge of the sternum with a maximum in the III-IV intercostal spaces on the left with irradiation to the right half of the chest. There is no clear correlation between the volume of the systolic murmur and the size of the VSD - a thin stream of blood through a small VSD may be accompanied by a loud noise (the saying “much ado about nothing” is true). A large VSD may not be accompanied by noise at all due to equalization of blood pressure in the left and right ventricles. In addition to noise, auscultation often reveals splitting of the second sound as a result of prolongation of the systole of the right ventricle. In the presence of a supracrestal VSD, a diastolic murmur of concomitant aortic valve insufficiency is detected. The disappearance of noise with VSD is a sign not of improvement, but of deterioration of the condition, which appears as a result of equalization of pressure in the left and right ventricles.
Electrocardiography
The ECG with small defects is not changed. With a medium-sized VSD, there are signs of hypertrophy of the left atrium and left ventricle, deviation of the electrical axis of the heart to the left. With a large VSD, the ECG may show signs of hypertrophy of the left atrium and both ventricles.
X-ray study
For small defects, no changes are detected. With a significant discharge of blood from left to right, signs of enlargement of the right ventricle, increased vascular pattern due to an increase in pulmonary blood flow and pulmonary hypertension are revealed. With pulmonary hypertension, its characteristic radiological signs are observed.
Echocardiography
In 2D mode, the VSD can be directly visualized. Using the Doppler mode, turbulent blood flow from one ventricle to another is detected, the direction of discharge is assessed (from left to right or right to left), and the pressure in the right ventricle is determined by the pressure gradient between the ventricles.
Catheterization cavities hearts
Catheterization of the cavities of the heart makes it possible to detect high pressure in the pulmonary artery, the value of which is crucial for determining the tactics of patient management (operative or conservative). With catheterization, it is possible to determine the ratio of pulmonary blood flow and blood flow in the systemic circulation (normally the ratio is less than 1.5:1).
TREATMENT
Small VSDs usually do not require surgical treatment due to their favorable course. Surgical treatment of VSD is also not performed when the pressure in the pulmonary artery is normal (the ratio of pulmonary blood flow to blood flow in the systemic circulation is less than 1.5-2:1). Surgical treatment (closure of VSD) is indicated for medium or large VSD with a pulmonary to systemic blood flow ratio of more than 1.5:1 or 2:1 in the absence of high pulmonary hypertension. If the resistance of the pulmonary vessels is 1/3 or less of the resistance in the systemic circulation, then progression of pulmonary hypertension after surgery is usually not observed. If there is a moderate or pronounced increase in pulmonary vascular resistance before surgery after radical correction of the defect, pulmonary hypertension persists (it may even progress). With large defects and increased pressure in the pulmonary artery, the result of surgical treatment is unpredictable, since, despite the closure of the defect, changes in the pulmonary vessels persist.
It is necessary to carry out prevention of infective endocarditis (see Chapter 6 "Infective endocarditis").
FORECAST
The prognosis is usually favorable with timely surgical treatment. The risk of infective endocarditis with VSD is 4%, which requires timely prevention of this complication.
9.2. Tetralogy of Fallot
Tetralogy of Fallot is a congenital heart defect characterized by the presence of four components: 1) a large, high-lying VSD; 2) pulmonary artery stenosis; 3) dextroposition of the aorta; 4) compensatory hypertrophy of the right ventricle.
Prevalence
Tetralogy of Fallot accounts for 12-14% of all congenital heart defects.
HEMODYNAMICS
In tetralogy of Fallot, the aorta is located over the large VSD and over both ventricles, resulting in equal systolic pressures in the right and left ventricles (Figure 9-2). The main hemodynamic factor is the relationship between the resistance to blood flow in the aorta and in the stenotic pulmonary artery.
With little resistance in the pulmonary vessels, pulmonary blood flow may be twice that of the systemic circulation, and arterial oxygen saturation may be normal (acyanotic tetralogy of Fallot).
With significant resistance to pulmonary blood flow, blood shunts from right to left, resulting in cyanosis and polycythemia.
Pulmonary artery stenosis can be infundibular or combined, less commonly valvular (for more details, see Chapter 8 “Acquired heart defects”).
During exercise, blood flow to the heart increases, but blood flow through the pulmonary circulation does not increase due to the stenotic pulmonary artery, and excess blood is dumped into the aorta through the VSD, so cyanosis increases. Hypertrophy occurs, which leads to increased cyanosis. Right ventricular hypertrophy develops as a result of constantly overcoming an obstacle in the form of pulmonary artery stenosis. As a result of hypoxia, compensatory polycythemia develops - the number of red blood cells and hemoglobin increases. Anastomoses develop between the bronchial arteries and the branches of the pulmonary artery. In 25% of patients, a right-sided location of the aortic arch and descending aorta is found.
CLINICAL PICTURE AND DIAGNOSTICS
Complaints
The main complaint of adults with tetralogy of Fallot is shortness of breath. In addition, heart pain unrelated to physical activity and palpitations may be bothersome. Patients are prone to pulmonary infections (bronchitis and pneumonia).
Inspection
Cyanosis is noted, the severity of which may vary. Sometimes cyanosis is so pronounced that not only the skin and lips turn blue, but also the mucous membrane of the oral cavity and conjunctiva. Characterized by a lag in physical development, changes in the fingers (“drumsticks”), nails (“watch glasses”).
Palpation
Systolic tremors are detected in the second intercostal space to the left of the sternum above the area of pulmonary artery stenosis.
Auscultation hearts
Listen to the rough systolic murmur of pulmonary artery stenosis in the II-III intercostal spaces to the left of the sternum. The second tone above the pulmonary artery is weakened.
Laboratory research
Complete blood count: high erythrocytosis, increased hemoglobin content, ESR sharply reduced (to 0-2 mm/h).
Electrocardiography
The electrical axis of the heart is usually shifted to the right (angle α from +90° to +210°), signs of right ventricular hypertrophy are noted.
Echocardiography
Echocardiography can detect the anatomical components of the tetralogy of Fallot.
X-ray study
Increased transparency of the pulmonary fields is noted due to a decrease in blood supply to the lungs. The contours of the heart have a specific shape of a “wooden clog shoe”: a reduced arch of the pulmonary artery, an emphasized “waist of the heart”, a rounded and raised apex of the heart above the diaphragm. The aortic arch may be on the right.
COMPLICATIONS
The most common occurrences are strokes, pulmonary embolism, severe heart failure, infective endocarditis, brain abscesses, and various arrhythmias.
TREATMENT
The only method of treatment is surgical (radical surgery - plastic surgery of the defect, elimination of pulmonary artery stenosis and displacement of the aorta). Sometimes surgical treatment consists of two stages (the first stage is to eliminate pulmonary artery stenosis, and the second is to perform VSD repair).
FORECAST
In the absence of surgical treatment, 3% of patients with tetralogy of Fallot survive to 40 years of age. Deaths occur due to strokes, brain abscesses, severe heart failure, infective endocarditis, and arrhythmias.
9.4. PENTAD OF FALLOT
Pentade of Fallot is a congenital heart defect consisting of five components: four signs of tetralogy of Fallot and ASD. Hemodynamics, clinical presentation, diagnosis and treatment are similar to those of tetralogy of Fallot and ASD.
9.5. ATRIAL SEPTAL DEFECT
ASD is the presence of communication between the left and right atria, leading to pathological discharge of blood (shunting) from one chamber of the heart to another.
Classification
Based on anatomical location, primary and secondary ASD, as well as a venous sinus defect, are distinguished.
Primary ASD is located below the fossa ovale and is part of a congenital heart defect called patent atrioventricular canal.
The secondary ASD is located in the area of the fossa ovale.
A sinus venosus defect is a communication between the superior vena cava and both atria, located above the normal interatrial septum.
ASDs of other localizations (for example, coronary sinus) are also identified, but they are extremely rare.
Prevalence
ASD accounts for about 30% of all congenital heart defects. It is more often found in women. 75% of ASDs are secondary, 20% are primary, 5% are venous sinus defects. This defect is often combined with others - pulmonary stenosis, abnormal drainage of the pulmonary veins, mitral valve prolapse. ASDs can be multiple.
HEMODYNAMICS
Shunting blood from left to right leads to diastolic overload of the right ventricle and increased blood flow in the pulmonary artery (Fig. 9-3). The direction and volume of blood discharged through the defect depends on the size of the defect, the pressure gradient between the atria and the compliance (extensibility) of the ventricles.
With a restrictive ASD, when the area of the defect is smaller than the area of the atrioventricular orifice, there is a pressure gradient between the atria and blood discharge from left to right.
With a non-restrictive ASD (large in size), there is no pressure gradient between the atria and the volume of blood shunted through the defect is regulated by the compliance (extensibility) of the ventricles. The right ventricle is more compliant (so pressure in the right atrium drops faster than in the left), and blood shunts from left to right, causing dilation of the right chambers of the heart and increasing blood flow through the pulmonary artery.
In contrast to VSD, pulmonary artery pressure and pulmonary vascular resistance in ASD remain low for a long time due to the low pressure gradient between the atria. This explains the fact that ASD in childhood usually remains unrecognized. The clinical picture of ASD manifests itself with age (over 15-20 years) as a result of an increase in pressure in the pulmonary artery and the appearance of other complications - cardiac arrhythmias, right ventricular failure [in the latter case, the risk of pulmonary embolism and systemic arteries (paradoxical embolism) is high]. With age, with large ASDs, hypertension may appear due to an increase in peripheral vascular resistance as a result of anatomical changes in the pulmonary vessels, and blood discharge gradually becomes bidirectional. Less commonly, blood discharge may occur from right to left.
CLINICAL PICTURE AND DIAGNOSTICS
Complaints
Patients with ASD have no complaints for a long time. Anamnestic examination reveals frequent respiratory tract diseases - bronchitis, pneumonia. Shortness of breath, which occurs initially during exertion and then at rest, and rapid fatigue may be a concern. After 30 years, the disease progresses: palpitations (supraventricular arrhythmias and atrial fibrillation), signs of pulmonary hypertension (see Chapter 14 “Pulmonary Hypertension”) and heart failure of the right ventricular type develop.
Inspection
The examination allows us to determine some delay in physical development. The appearance of cyanosis and changes in the terminal phalanges of the fingers in the form of “drum sticks” and nails in the form of “watch glasses” indicate a change in the direction of blood discharge from right to left.
Palpation
The pulsation of the pulmonary artery (in the presence of pulmonary hypertension) is determined in the second intercostal space to the left of the sternum.
Auscultation hearts
When the defect is small, no auscultatory changes are detected, so ASD is usually diagnosed when signs of pulmonary hypertension appear.
The first heart sound is not changed. The second tone is split due to a significant lag in the pulmonary component of the second sound as a result of the flow of a large volume of blood through the right parts of the heart (extension of right ventricular systole). This splitting is fixed, i.e. does not depend on the phases of breathing.
A systolic murmur is heard over the pulmonary artery as a result of the ejection of an increased volume of blood from the right ventricle. In case of primary ASD, a systolic murmur of relative insufficiency of the mitral and tricuspid valves is also heard at the apex of the heart. A low-frequency diastolic murmur may be heard over the tricuspid valve due to increased blood flow through the tricuspid valve.
With an increase in pulmonary vascular resistance and a decrease in blood discharge from left to right, the auscultatory pattern changes. The systolic murmur over the pulmonary artery and the pulmonary component of the second sound intensify; both components of the second sound can merge. In addition, a diastolic murmur of pulmonary valve insufficiency appears.
Electrocardiography
In case of secondary ASD, complexes are noted rSR’ in the right precordial leads (as a manifestation of delayed activation of the posterobasal sections of the interventricular septum and expansion of the outflow tract of the right ventricle), deviation of the electrical axis of the heart to the right (with hypertrophy and dilatation of the right ventricle). In case of a venous sinus defect, first degree AV block and lower atrial rhythm are observed. Heart rhythm disturbances in the form of supraventricular arrhythmias and atrial fibrillation are characteristic.
X-ray study
X-ray examination reveals dilatation of the right atrium and right ventricle, dilatation of the trunk of the pulmonary artery and its two branches, the symptom of “dancing the roots of the lungs” (increased pulsation as a result of increased pulmonary blood flow due to blood discharge).
Echocardiography
Echocardiography (Fig. 9-4) helps detect dilatation of the right ventricle, right atrium, and paradoxical motion of the interventricular septum. If the defect size is sufficient, it can be detected in two-dimensional mode, especially clearly in the subxiphoid position (when the position of the interatrial septum is perpendicular to the ultrasound beam). The presence of a defect is confirmed by Doppler ultrasound, which makes it possible to identify the turbulent flow of shunted blood from the left atrium to the right or, conversely, through the interatrial septum. Signs of pulmonary hypertension are also detected.
Catheterization cavities hearts
Catheterization of the cardiac cavities is performed to determine the severity of pulmonary hypertension.
TREATMENT
In the absence of severe pulmonary hypertension, surgical treatment is performed - ASD repair. If there are symptoms of heart failure, therapy with cardiac glycosides, diuretics, and ACE inhibitors is necessary (for more information, see Chapter 11 “Heart Failure”). In patients with primary ASD and venous sinus defect, prophylaxis of infective endocarditis is recommended (see Chapter 6 “Infective endocarditis”).
FORECAST
With timely surgical treatment, the prognosis is favorable. In non-operated patients, deaths before the age of 20 are rare, but after 40 years the mortality rate reaches 6% per year. The main complications of ASD are atrial fibrillation, heart failure, and rarely paradoxical embolism. Infective endocarditis with secondary ASD occurs very rarely. In cases of small ASD, patients live to a ripe old age.
9.6. OPEN DUCT ARTERIUS
Patent ductus arteriosus is a defect characterized by non-closure of the vessel between the pulmonary artery and the aorta (ductus arteriosus) within 8 weeks after birth; The duct functions in the prenatal period, but its non-closure leads to hemodynamic disturbances.
Prevalence
Patent ductus arteriosus is observed in the general population with an incidence of 0.3%. It accounts for 10-18% of all congenital heart defects.
HEMODYNAMICS
Most often, the ductus arteriosus connects the pulmonary artery and the descending aorta below the origin of the left subclavian artery; less often, it connects the pulmonary artery and the descending aorta above the origin of the left subclavian artery (Fig. 9-5). 2-3 days (less often 8 weeks) after birth, the duct closes. In premature babies, with fetal hypoxia, fetal rubella (in the first trimester of pregnancy), the duct remains open. There is a discharge (shunting) of blood from the descending aorta into the trunk of the pulmonary artery. Further manifestations of the defect depend on the diameter and length of the patent ductus arteriosus and the resistance to blood flow in the duct itself.
With a small duct size and high shunt resistance, the volume of discharged blood is insignificant. The flow of excess blood into the pulmonary artery, left atrium and left ventricle is also small. The direction of blood discharge during systole and diastole remains constant (continuous) - from the left (from the aorta) to the right (to the pulmonary artery).
With a large diameter of the duct, a significant excess amount of blood will flow into the pulmonary artery, leading to an increase in pressure in it (pulmonary hypertension) and overloading the left atrium and left ventricle with volume (the consequence of this is dilatation and hypertrophy of the left ventricle). Over time, irreversible changes in the pulmonary vessels (Eisenmenger syndrome) and heart failure develop. Subsequently, the pressure in the aorta and pulmonary artery is equalized, and then in the pulmonary artery it becomes higher than in the aorta. This leads to a change in the direction of blood discharge - from the right (from the pulmonary artery) to the left (to the aorta). Subsequently, right ventricular failure occurs.
CLINICAL PICTURE AND DIAGNOSTICS
The manifestations of the defect depend on the size of the patent ductus arteriosus. A patent ductus arteriosus with a small discharge of blood may not manifest itself in childhood and may manifest itself with age as fatigue and shortness of breath during physical exertion. With a large volume of discharged blood from childhood, there are complaints of shortness of breath during physical exertion, signs of orthopnea, cardiac asthma, pain in the right hypochondrium due to liver enlargement, swelling of the legs, cyanosis of the legs (as a result of discharge of blood from right to left into the descending aorta), cyanosis of the left arm ( with a patent ductus arteriosus above the origin of the left subclavian artery).
With a small volume of blood discharge from left to right, there are no external signs of a defect. When blood is discharged from right to left, cyanosis of the legs appears, changes in the toes in the form of “drumsticks”, changes in the fingers of the left hand in the form of “drumsticks”.
Palpation
With intense blood discharge from left to right, systolic trembling of the chest is determined above the pulmonary artery and suprasternally (in the jugular fossa).
Auscultation hearts
The typical auscultatory manifestation of a patent ductus arteriosus is a continuous systole-diastolic (“machine”) murmur due to constant unidirectional blood flow from the aorta to the pulmonary artery. This noise is high-frequency, intensifies towards the second tone, is better heard under the left collarbone and radiates to the back. In addition, a mid-diastolic murmur may be heard at the apex of the heart due to increased blood flow through the left atrioventricular orifice. The sonority of the second tone can be difficult to determine due to the loud noise. When the pressure in the aorta and pulmonary artery is equalized, the noise from continuous systole-diastolic turns into systolic, and then disappears completely. In this situation, the accent of the second tone over the pulmonary artery begins to clearly emerge (a sign of the development of pulmonary hypertension).
Electrocardiography
If the blood discharge is small, no pathological changes are detected. When the left parts of the heart are overloaded with a large volume of excess blood, signs of hypertrophy of the left atrium and left ventricle are noted. Against the background of severe pulmonary hypertension, the ECG reveals signs of hypertrophy of the right ventricle.
Echocardiography
With significant sizes of the patent ductus arteriosus, dilatation of the left atrium and left ventricle is observed. A large patent ductus arteriosus can be detected in two dimensions. In Doppler mode, a turbulent systole-diastolic flow is determined in the pulmonary artery, regardless of the size of the duct.
X-ray study
If the shunt is small, the radiographic picture is usually unchanged. With pronounced blood discharge, an enlargement of the left chambers of the heart and signs of pulmonary hypertension (bulging of the pulmonary artery trunk) are detected.
TREATMENT
If signs of heart failure appear, cardiac glycosides and diuretics are prescribed (see Chapter 11 “Heart failure”). It is recommended to prevent infectious endarteritis before and for six months after surgical correction of the defect (see Chapter 6 “Infective endocarditis”).
Surgical treatment in the form of ligation of the patent ductus arteriosus or occlusion of its lumen must be carried out before the development of irreversible changes in the pulmonary vessels. After surgical treatment, signs of pulmonary hypertension may persist or even progress.
COMPLICATIONS
With an open ductus arteriosus, complications may occur: infectious endarteritis, pulmonary embolism, ductal aneurysm, its dissection and rupture, calcification of the duct, heart failure. Infectious endarteritis usually develops in the pulmonary artery opposite the open ductus arteriosus as a result of constant trauma to the wall of the pulmonary artery with a stream of blood. The incidence of infectious endarteritis reaches 30%.
FORECAST
Timely surgery eliminates the pathological discharge of blood from the aorta into the pulmonary artery, although signs of pulmonary hypertension may persist throughout life. The average life expectancy without surgical treatment is 39 years.
To diagnose coarctation of the aorta, correct measurement of blood pressure in the legs is important. To do this, the patient is placed on his stomach, a cuff is placed on the lower third of the thigh, and auscultation is performed in the popliteal fossa using a technique similar to that when measuring pressure in the arms (with determination of systolic and diastolic levels). Normally, the pressure in the legs is 20-30 mm Hg. higher than on the hands. With coarctation of the aorta, the pressure in the legs is significantly reduced or not detected. A diagnostic sign of aortic coarctation is considered to be a difference in systolic (or mean) blood pressure in the arms and legs of more than 10-20 mmHg. Approximately equal pressure is often noted on the arms and legs, but after physical activity (treadmill) a significant difference is determined. The difference in systolic blood pressure in the left and right arms indicates that the origin of one of the subclavian arteries is located above or below the obstruction.
Palpation
Determine the absence or significant weakening of the pulse in the legs. You can detect increased pulsating collaterals in the intercostal spaces, in the interscapular space.
Auscultation hearts
The accent of the second tone is detected over the aorta due to high blood pressure. Systolic murmur is characteristic at the Botkin-Erb point, as well as under the left clavicle, in the interscapular space and on the vessels of the neck. With developed collaterals, a systolic murmur is heard over the intercostal arteries. With further progression of hemodynamic disorders, a continuous (systolic-diastolic) murmur is heard.
Electrocardiography
Signs of left ventricular hypertrophy are detected.
Echocardiography
A suprasternal examination of the aorta in two-dimensional mode shows signs of narrowing. With a Doppler study, turbulent systolic flow is determined below the site of narrowing and the pressure gradient between the dilated and narrowed parts of the aorta is calculated, which is often important when deciding on surgical treatment.
X-ray study
With the long-term existence of collaterals, usuration of the lower parts of the ribs is detected as a result of compression by their dilated and tortuous intercostal arteries. To clarify the diagnosis, aortography is performed, which accurately identifies the location and degree of coarctation.
TREATMENT
A radical treatment method for coarctation of the aorta is surgical excision of the narrowed area. Drug therapy is carried out depending on the clinical manifestations of the defect. For symptoms of heart failure, cardiac glycosides, diuretics, and ACE inhibitors are prescribed (for more details, see Chapter 11 “Heart Failure”). Treatment for hypertension may be necessary.
PROGNOSIS AND COMPLICATIONS
Without surgical treatment, 75% of patients die by age 50. As a result of high blood pressure, typical complications may develop: strokes, kidney failure. An atypical complication of hypertension is the development of neurological disorders (for example, lower paraparesis, impaired urination) due to compression of the spinal cord roots by the dilated intercostal arteries. Rare complications include infectious endoaortitis and rupture of the dilated aorta.
9.8. CONGENITAL AORTIC STENOSIS
Congenital stenosis of the aortic mouth is a narrowing of the outflow tract of the left ventricle in the area of the aortic valve. Depending on the level of obstruction, stenosis can be valvular, subvalvular, or supravalvular.
Prevalence
Congenital aortic stenosis accounts for 6% of all congenital heart defects. Valve stenosis is most often noted (80%), less often subvalvular and supravalvular. In men, aortic stenosis is observed 4 times more often than in women.
HEMODYNAMICS
Valvular stenosis (see Fig. 9-7). Most often, the aortic valve is bicuspid, with the opening located eccentrically. Sometimes the valve consists of one leaf. Less commonly, the valve consists of three leaflets, fused together by one or two adhesions.
With subvalvular stenosis, three types of changes are noted: a discrete membrane under the aortic valves, a tunnel, muscle narrowing (subaortic hypertrophic cardiomyopathy, see Chapter 12 “Cardiomyopathies and Myocarditis”).
Supravalvular stenosis of the aortic ostium can be in the form of a membrane or hypoplasia of the ascending aorta. A sign of hypoplasia of the ascending aorta is considered to be a ratio of the diameter of the aortic arch to the diameter of the ascending aorta of less than 0.7. Often supravalvular stenosis of the aortic mouth is combined with stenosis of the branches of the pulmonary artery.
Supravalvular aortic stenosis in combination with mental retardation is called Williams syndrome.
Aortic stenosis is often combined with other congenital heart defects - VSD, ASD, patent ductus arteriosus, coarctation of the aorta.
In any case, an obstacle to blood flow is created and the changes described in Chapter 8 “Acquired heart defects” develop. Over time, valve calcification develops. The development of poststenotic expansion of the aorta is characteristic.
CLINICAL PICTURE AND DIAGNOSTICS
Complaints
Most patients with minor stenosis do not complain. The appearance of complaints indicates severe stenosis of the aortic mouth. There are complaints of shortness of breath during exercise, fatigue (due to reduced cardiac output), fainting (as a result of cerebral hypoperfusion), and chest pain during exercise (due to myocardial hypoperfusion). Sudden cardiac death may occur, but in most cases this is preceded by complaints or changes in the ECG.
Inspection, percussion
See "Aortic Stenosis" in Chapter 8, "Acquired Heart Defects."
Palpation
Systolic vibration is determined along the right edge of the upper part of the sternum and over the carotid arteries. When the peak systolic pressure gradient is less than 30 mm Hg. (according to echocardiography) tremors are not detected. Low pulse pressure (less than 20 mmHg) indicates significant severity of aortic stenosis. With valvular stenosis, a small slow pulse is detected.
Auscultation hearts
Characteristic is a weakening of the second tone or its complete disappearance due to the weakening (disappearance) of the aortic component. With supravalvular stenosis of the aortic mouth, the second sound is preserved. With valvular stenosis of the aortic mouth, an early systolic click is heard at the apex of the heart, which is absent in supra- and subvalvular stenoses. It disappears with severe valvular stenosis of the aortic mouth.
The main auscultatory sign of aortic stenosis is a rough systolic murmur with a maximum in the second intercostal space on the right and irradiation into the carotid arteries, sometimes along the left edge of the sternum to the apex of the heart. With subvalvular stenosis of the aortic mouth, differences in auscultatory manifestations are observed: an early systolic click is not heard, an early diastolic murmur of aortic valve insufficiency is noted (in 50% of patients).
Electrocardiography
With valvular stenosis, signs of left ventricular hypertrophy are detected. With supravalvular stenosis of the aortic mouth, the ECG may not be changed. With subvalvular stenosis (in the case of subaortic hypertrophic cardiomyopathy), pathological waves may be detected Q(narrow and deep).
Echocardiography
In two-dimensional mode, the level and nature of obstruction of the aortic opening (valvular, subvalvular, supravalvular) are determined. In Doppler mode, the peak systolic pressure gradient (the maximum pressure gradient when the aortic valve leaflets open) and the degree of stenosis of the aortic ostium are assessed.
When the peak systolic pressure gradient (with normal cardiac output) is more than 65 mm Hg. or the area of the aortic opening is less than 0.5 cm 2 / m 2 (normally the area of the aortic opening is 2 cm 2 / m 2), stenosis of the aortic orifice is considered severe.
Peak systolic pressure gradient 35-65 mm Hg. or an area of the aortic opening of 0.5-0.8 cm 2 /m 2 is considered as moderate aortic stenosis.
When the peak systolic pressure gradient is less than 35 mm Hg. or the area of the aortic opening is more than 0.9 cm 2 / m 2, stenosis of the aortic mouth is considered minor.
These indicators are informative only if left ventricular function is preserved and there is no aortic regurgitation.
X-ray study
Poststenotic dilatation of the aorta is detected. With subvalvular stenosis of the aortic mouth, there is no post-stenotic dilatation of the aorta. It is possible to detect calcifications in the projection of the aortic valve.
TREATMENT
In the absence of calcification, valvotomy or excision of a discrete membrane is performed. In cases of severe fibrotic changes, aortic valve replacement is indicated.
PROGNOSIS AND COMPLICATIONS
Aortic stenosis usually progresses regardless of the level of obstruction (valvular, supravalvular, subvalvular). The risk of developing infective endocarditis is 27 cases per 10,000 patients with aortic stenosis per year. With a pressure gradient of more than 50 mm Hg. the risk of infective endocarditis increases 3 times. With aortic stenosis, sudden cardiac death is possible, especially during physical exertion. The risk of sudden cardiac death increases with increasing pressure gradient - it is higher in patients with aortic stenosis with a pressure gradient of more than 50 mm Hg.
9.9. PULMONARY ARTERY STENOSIS
Pulmonary stenosis is a narrowing of the outflow tract of the right ventricle in the area of the pulmonary valve.
Prevalence
Isolated pulmonary artery stenosis accounts for 8-12% of all congenital heart defects. In most cases, this is valvular stenosis (the third most common congenital heart defect), but it can also be combined (in combination with subvalvular, supravalvular stenoses, and other congenital heart defects).
HEMODYNAMICS
The narrowing can be valvular (80-90% of cases), subvalvular, supravalvular.
With valvular stenosis, the pulmonary valve can be unicuspid, bicuspid or tricuspid. Poststenotic dilatation of the pulmonary artery trunk is characteristic.
Isolated subvalvular stenosis is characterized by infundibular (funnel-shaped) narrowing of the right ventricular outflow tract and an abnormal muscle bundle that prevents the ejection of blood from the right ventricle (both options are usually combined with VSD).
Isolated supravalvular stenosis can be in the form of localized stenosis, complete or incomplete membrane, diffuse hypoplasia, multiple peripheral pulmonary artery stenoses.
When the pulmonary trunk narrows, an increase in the pressure gradient between the right ventricle and the pulmonary artery occurs. Due to an obstruction in the path of blood flow, hypertrophy of the right ventricle occurs, and then its failure. This leads to increased pressure in the right atrium, opening of the foramen ovale and shunting of blood from right to left with the development of cyanosis and right ventricular failure. In 25% of patients, pulmonary artery stenosis is combined with a secondary ASD.
CLINICAL PICTURE AND DIAGNOSTICS
Complaints
Mild pulmonary stenosis is asymptomatic in most cases. With severe stenosis, rapid fatigue, shortness of breath and chest pain during physical activity, cyanosis, dizziness and fainting appear. Dyspnea with pulmonary stenosis occurs as a result of inadequate perfusion of working peripheral muscles, causing reflex ventilation of the lungs. Cyanosis in pulmonary artery stenosis can be of either peripheral (the result of low cardiac output) or central (the result of blood discharge through the patent foramen ovale) origin.
Inspection
You can detect pulsation of the enlarged right ventricle in the epigastric region. When tricuspid valve insufficiency occurs as a result of decompensation of the right ventricle, swelling and pulsation of the neck veins are detected. Also see the sections “Pulmonary Stenosis” and “Tricuspid Valve Insufficiency” in Chapter 8, “Acquired Heart Defects.”
Palpation
Systolic tremor is determined in the second intercostal space to the left of the sternum.
Auscultation hearts
The second tone with slight and moderate valvular stenosis of the pulmonary artery is not changed or is slightly weakened due to the lesser participation of the pulmonary component in its formation. With severe stenosis and a significant increase in pressure in the right ventricle, the second sound may disappear completely. With infundibular and supravalvular stenoses of the pulmonary artery, tone II does not change.
With valvular stenosis of the pulmonary artery in the second intercostal space to the left of the sternum, an early systolic click is heard at the moment of maximum opening of the pulmonary valve leaflets. The systolic click increases with exhalation. At other levels of stenosis (supravalvular, subvalvular), a systolic click is not heard.
The main auscultatory manifestation of pulmonary artery stenosis is a rough systolic murmur in the second intercostal space to the left of the sternum with irradiation under the left clavicle and into the back. With supravalvular stenosis, the noise radiates to the left axillary region and back. The duration of the systolic murmur and its peak correlate with the degree of stenosis: with moderate stenosis, the peak of the murmur is noted in the middle of systole, and its end is before the aortic component of the second sound; with severe stenosis, the systolic murmur is later and continues after the aortic component of the second sound; with supravalvular stenosis or peripheral stenosis of the branches of the pulmonary artery, there is a systolic or continuous murmur with irradiation into the pulmonary fields.
Electrocardiography
With minor stenosis of the pulmonary artery, no changes are detected on the ECG. With moderate and severe stenosis, signs of right ventricular hypertrophy are found. With severe pulmonary artery stenosis, signs of hypertrophy (dilatation) of the right atrium appear. Supraventricular arrhythmias may occur.
Echocardiography
Normally, the area of the valve opening of the pulmonary artery is 2 cm 2 / m 2. In case of valvular pulmonary artery stenosis, a dome-shaped protrusion of the thickened leaflets of the pulmonary artery valve into the trunk of the pulmonary artery during systole of the right ventricle is detected in two-dimensional mode. Thickening of the wall (hypertrophy) of the right ventricle is characteristic. Other levels of pulmonary artery obstruction and their nature are also determined. The Doppler mode allows you to determine the degree of obstruction by the pressure gradient between the right ventricle and the pulmonary trunk. Mild pulmonary stenosis is diagnosed when the peak systolic pressure gradient is less than 50 mmHg. Pressure gradient 50-80 mm Hg. corresponds to a moderate degree of stenosis. With a pressure gradient of more than 80 mm Hg. speak of severe pulmonary artery stenosis (the gradient can reach 150 mm Hg or more in cases of severe stenosis).
X-ray study
With valvular stenosis of the pulmonary artery, a post-stenotic expansion of its trunk is detected. It is absent in supra- and subvalvular stenoses. Characteristic depletion of the pulmonary pattern.
Catheterization cavities hearts
Catheterization of the cardiac cavities allows you to accurately determine the degree of stenosis by the pressure gradient between the right ventricle and the pulmonary artery.
TREATMENT AND PROGNOSIS
Minor and moderate valvular stenosis of the pulmonary artery usually proceeds favorably and does not require active intervention. Subvalvular muscular stenosis progresses more significantly. Supravalvular stenosis usually progresses slowly. When the pressure gradient between the right ventricle and the pulmonary artery increases by more than 50 mm Hg. in case of valvular stenosis, valvuloplasty is performed (after valvotomy, 50-60% of patients develop pulmonary valve insufficiency). If heart failure occurs, it is treated (see Chapter 11 “Heart failure”). Prevention of infective endocarditis is recommended (see Chapter 6 “Infective endocarditis”), since the risk of its development is quite high.
9.10. EBSTEIN ANOMALY
Ebstein's anomaly is the location of the posterior and septal leaflets of the tricuspid valve at the apex of the right ventricle, leading to an enlargement of the right atrium cavity and a decrease in the right ventricular cavity. Epstein anomaly accounts for about 1% of all congenital heart defects. The occurrence of this defect is associated with the intake of lithium into the fetus during pregnancy.
HEMODYNAMICS
The displacement of the attachment site of the two leaflets of the tricuspid valve into the cavity of the right ventricle leads to the fact that the latter is divided into the supravalvular part, which is combined with the cavity of the right atrium into a single chamber (atrialization of the right ventricular cavity) and a reduced subvalvular part (the cavity of the right ventricle itself) (Fig. 9-8). A decrease in the cavity of the right ventricle leads to a decrease in stroke volume and a decrease in pulmonary blood flow. Since the right atrium consists of two parts (the right atrium itself and part of the right ventricle), the electrical and mechanical processes in it are different (not synchronized). During right atrium systole, the atrialized portion of the right ventricle is in diastole. This results in decreased blood flow to the right ventricle. During right ventricular systole, right atrial diastole occurs with incomplete closure of the tricuspid valve, which results in the displacement of blood in the atrialized portion of the right ventricle back into the main portion of the right atrium. There is a significant expansion of the fibrous ring of the tricuspid valve, pronounced dilatation of the right atrium (it can hold more than 1 liter of blood), an increase in pressure in it and a retrograde increase in pressure in the inferior and superior vena cava. The expansion of the cavity of the right atrium and the increase in pressure in it help to keep the oval opening open and a compensatory decrease in pressure due to the discharge of blood from right to left.
CLINICAL PICTURE AND DIAGNOSTICS
Complaints
Patients may complain of shortness of breath during exercise, palpitations due to supraventricular arrhythmias (observed in 25-30% of patients and often cause sudden cardiac death).
Inspection
Cyanosis is detected when blood is shunted from right to left, signs of tricuspid valve insufficiency (see Chapter 8 “Acquired heart defects”). Characteristic signs of right ventricular failure (dilation and pulsation of the veins of the neck, enlarged liver and edema).
Percussion
The boundaries of relative cardiac dullness are shifted to the right due to the enlarged right atrium.
Auscultation hearts
The first heart sound is usually split. The appearance of III and IV heart sounds is possible. Systolic murmur is characteristic in the III-IV intercostal spaces to the left of the sternum and at the apex due to tricuspid valve insufficiency. Sometimes a diastolic murmur is heard associated with relative stenosis of the right atrioventricular orifice.
Electrocardiography
An ECG may show signs of Wolff-Parkinson-White syndrome in 20% of patients (more often there are right-sided accessory pathways). Characteristic signs are of right bundle branch block, the presence of signs of right atrium hypertrophy in combination with 1st degree AV block.
Echocardiography
All anatomical signs of Ebstein's anomaly are identified (Fig. 9-9): abnormal location of the tricuspid valve leaflets (their dystopia), enlarged right atrium, small right ventricle. In Doppler mode, tricuspid valve insufficiency is detected.
X-ray study
Cardiomegaly is noted (characteristic of the spherical shape of the heart shadow) with increased transparency of the pulmonary fields.
TREATMENT
When symptoms of heart failure appear, cardiac glycosides (contraindicated in the presence of Wolff-Parkinson-White syndrome) and diuretics are prescribed. Surgical treatment consists of tricuspid valve replacement or reconstruction.
FORECAST
The main causes of death: severe heart failure, thromboembolism, brain abscesses, infective endocarditis.