Aortic insufficiency: causes, symptoms, diagnosis, treatment

Aortic insufficiency can be caused either by the primary lesion of the aortic valve flaps, or by aortic root damage, which now accounts for more than 50% of all cases of isolated aortic valve insufficiency.

[1],

What causes aortic insufficiency?

Rheumatic fever is one of the main valvular causes of aortic insufficiency. Wrinkling of the leaflets due to infiltration with connective tissue prevents them from closing but the time of diastole, thereby forming a defect in the center of the valve - the "window" for regurgitation of blood into the cavity of the left ventricle. The concomitant fusion of the commissure limits the opening of the aortic valve, which leads to the appearance of concomitant aortic stenosis.

Infective endocarditis

Insufficiency of the aortic valve can be caused by the destruction of the valve, perforation of its valves or the presence of growing vegetation, preventing the valves from closing in the diastole.

Calcified aortic stenosis in the elderly leads to the development of aortic insufficiency in 75% of cases, both due to the age-related expansion of the fibrous ring of the aortic valve, and as a result of dilatation of the aorta.

Other primary valve causes of aortic insufficiency:

• trauma, leading to rupture of the ascending part of the aorta. There is a violation of fastening commissure, which leads to a prolapse of the aortic valve into the cavity of the left ventricle;
• Congenital two-leaf valve due to incomplete closure or prolapse of the valves;
• a large septal defect of the interventricular septum;
• membranous subaortic stenosis;
• complication of radiofrequency catheter ablation;
• Myxomatous degeneration of the aortic valve;
• destruction of the biological valve prosthesis.

Aortic root injury

The defeat of the root of the aorta can cause the following diseases:

• age (degenerative) dilatation of the aorta;
• cystic necrosis of aortic media (isolated or as part of the Marfan syndrome);
• aortic dissection;
• imperfect osteogenesis (osteopsatyrosis);
• syphilitic aortitis;
• ankylosing spondylitis;
• Behcet's syndrome;
• psoriatic arthritis;
• arthritis with ulcerative colitis;
• recurrent polychondritis;
• Reiter's syndrome;
• giant cell arteritis;
• systemic hypertension;
• the use of some drugs that depress the appetite.

Aortic insufficiency in these cases is formed due to the pronounced widening of the ring of the aortic valve and the root of the aorta, followed by separation of the valves. Subsequent dilatation of the root is inevitably accompanied by excessive tension and bending of the valves, which then thicken, shrivel and become incapable of completely covering the aortic opening. This aggravates the aortic valve insufficiency, leads to a further expansion of the aorta and closes the vicious circle of pathogenesis ("regurgitation increases regurgitation").

Regardless of the cause, aortic insufficiency always causes dilatation and hypertrophy of the left ventricle with subsequent expansion of the mitral ring and possible dilatation of the left atrium. Often at the place of contact of the regurgitation flow and the wall of the left ventricle on the endocardium, "pockets" are formed.

[2], [3], [4], [5], [6]

Variants and causes of aortic insufficiency

Valve:

• Rheumatic fever.
• Calcifying aortic stenosis (CAS) (degenerative, senile).
• Infective endocarditis.
• Injuries of the heart.
• Congenital bivalve valve (a combination of aortic stenosis and aortic valve insufficiency).
• Meeksomatous degeneration of the valves of the aortic valve.

The defeat of the root of the aorta:

• Age (degenerative) enlargement of the aorta.
• Systemic arterial hypertension.
• Stratification of the aorta.
• Collagenoses (ankylosing spondyloarthritis, rheumatoid arthritis, giant cell arteritis, Reiter's syndrome, Ehlers-Danlos syndrome, Behcet's syndrome).
• Congenital heart defects (defect of interventricular septum with prolapse of aortic valve flaps, isolated subaortic stenosis). -
• Reception of anorectics.

Pathophysiology of aortic insufficiency

The main pathological factor in aortic insufficiency is an overload of the volume of the left ventricle, which entails a series of compensatory adaptive changes in the myocardium and the entire circulatory system.

The main determinants of the regurgitation volume; the area of the regurgitation opening, the diastolic pressure gradient on the aortic valve, and the duration of the diastole, which in turn is a derivative of the heart rate. Thus, bradycardia contributes to an increase, and tachycardia - a decrease in the volume of aortic valve insufficiency.

Gradual increase of end-diastolic volume leads to increased systolic wall stress of the left ventricle with subsequent hypertrophy, accompanied by simultaneous expansion of the cavity of the left ventricle (eccentric hypertrophy of the left ventricle) that facilitates uniform distribution of the increased pressure in the cavity of the left ventricle at each motor unit infarction (sarcomere) and thus contributes to the retention of the impact volume and the ejection fraction in normal or suboptimal limits (stage to compensation).

An increase in the volume of regurgitation leads to a progressive expansion of the left ventricular cavity, a change in its shape to a spherical one, an increase in diastolic pressure in the left ventricle, an increase in the systolic tension of the left ventricular wall (afterload), and a reduction in the ejection fraction. The fall of the ejection fraction is due to, inhibition of contractility and / or increase in afterload (decompensation stage).

Acute aortic insufficiency

The most common causes of acute aortic insufficiency are infective endocarditis, aortic dissection or trauma. With acute aortic valve insufficiency, a sudden increase in the diastolic volume of blood enters the unchanged left ventricle. The lack of time for the development of adaptive mechanisms leads to a sharp increase in BWW both in the left ventricle and in the left atrium. For some time the heart works according to the Frank-Starling law, according to which the degree of contraction of the myocardial fibers is a derivative of the length of its fibers. However, the inability of the heart chambers to rapidly compensate expansion soon leads to a decrease in the volume of ejection into the aorta.

The resulting compensatory tachycardia is not sufficient to maintain a sufficient cardiac output, which contributes to the development of pulmonary edema and / or cardiogenic shock.

Particularly pronounced hemodynamic disorders are observed in patients with concentric hypertrophy of the left ventricle, due to pressure overload and a discrepancy between the size of the cavity of the left ventricle and BWW. This situation occurs in the case of aortic dissection against a background of systemic hypertension, as well as with acute aortic valve failure after balloon commissurotomy with congenital aortic stenosis.

[7], [8], [9], [10]

Chronic aortic insufficiency

In response to an increase in blood volume in chronic aortic insufficiency, a number of compensatory mechanisms are included in the left ventricle, contributing to its adaptation to an increased volume without increasing the filling pressure.

A gradual increase in the diastolic volume allows the ventricle to expel a larger stroke volume, which determines the normal cardiac output. This is ensured by longitudinal replication of sarcomeres and the development of eccentric left ventricular myocardial hypertrophy, so the load on the sarcomere remains normal for a long time, preserving the pre-load reserve. The ejection fraction and fractional shortening of the left ventricular fibers remain within normal limits.

Further increase in the cavities of the left heart, combined with increased systolic wall tension, leads to concomitant concentric hypertrophy of the left ventricle. Thus, aortic valve failure is a combination of volume and pressure overload (compensation stage).

Subsequently, both the depletion of the preload reserve and the development of an inappropriate volume of left ventricular hypertrophy occur, followed by a decrease in the ejection fraction (decompensation stage).

[11], [12], [13], [14],

Pathophysiological mechanisms of adaptation of the left ventricle with aortic insufficiency

Sharp:

• tachycardia (shortening of diastolic regurgitation time);
• the Frank-Starling mechanism.

Chronic (compensated):

• eccentric type of hypertrophy (volume overload);
• geometric changes (spherical view);
• mixing the diastolic volume-pressure curve to the right.

Chronic (decompensated):

• inadequate hypertrophy and increased afterload;
• increased slip of the myocardial fibers and loss of the Z-register;
• suppression of myocardial contractility;
• fibrosis and cell loss.

Symptoms of aortic insufficiency

Symptoms of chronic aortic insufficiency

In patients with severe chronic aortic insufficiency, the left ventricle gradually expands, while the patients themselves do not (or almost do not have) symptoms. The signs characteristic for the reduction of cardiac reserve or myocardial ischemia develop, as a rule, in the 4th or 5th decade of life after the formation of severe cardiomegaly and myocardial dysfunction. The main complaints (dyspnea with exercise, orthopnea, paroxysmal nocturnal dyspnea) accumulate gradually. Angina appears in the late stages of the disease; attacks of "night" angina pectoris become painful and accompanied by copious cold sticky sweat, which is caused by a slowing of the heart rate and a critical drop in arterial diastolic pressure. Patients with aortic valve failure often complain of intolerance to heart attacks, especially in the horizontal position, as well as difficult to bear pain in the chest caused by heart beats to the chest. Tachycardia, which occurs with emotional stress or during exercise, causes palpitations and shaking of the head. Patients are especially worried about ventricular extrasystoles due to a particularly severe post-extrasystolic contraction on the background of an increase in the volume of the left ventricle. All these complaints appear and exist long before the onset of symptoms of left ventricular dysfunction.

The cardinal symptom of chronic aortic insufficiency is diastolic noise, which begins immediately after the second tone. From the noise of pulmonary regurgitation, it is distinguished by an early onset (ie immediately after the 2nd tone) and increased pulse pressure. Noise is better listened to sitting or tilting the patient forward, with a delay in breathing at the height of the exhalation. With severe aortic valve insufficiency, the noise quickly reaches a peak and then slowly declines throughout the diastole (decrescendo). If regurgitation is caused by a primary lesion of the valve, the noise is best heard at the left edge of the sternum in the third to fourth intercostal space. However, if the noise is mainly due to the expansion of the ascending aorta, the auscultatory maximum will be the right edge of the sternum.

The severity of aortic insufficiency is most correlated with the duration of the noise, and not with its severity. With moderate aortic valve insufficiency, noise is usually limited to early diastole, high-frequency and resembles a push. With severe aortic insufficiency, the noise lasts the entire diastole and can acquire a "scraping" shade. If the noise becomes musical ("cooing a dove"), then this usually indicates an "eversion" or perforation of the aortic valve leaflet. In patients with severe aortic valve failure and left ventricular decompensation, the equalization at the end of the diastole of pressure in the left ventricle and aorta leads to the disappearance of this musical component of noise,

Mid- and late-diastolic noise at the apex (Austin-Flint noise) is often detected with severe aortic insufficiency, and it can appear with an unchanged mitral valve. Noise is due to the presence of resistance to mitral blood flow high KDD, as well as the oscillation of the anterior valve lobe mitral valve under the influence of aortic regurgitation flow. In practice, it is difficult to distinguish the noise of Austin-Flint from the noise of mitral stenosis. Additional differential diagnostic criteria in favor of the latter: amplification of I tone (clapping I tone) and the tone (click) of the opening of the mitral valve.

Symptoms of acute aortic insufficiency

Because of the limited ability of the left ventricle to carry out acute aortic regurgitation, these patients often develop signs of acute cardiovascular collapse, with the appearance of weakness, severe dyspnea and hypotension caused by a decrease in stroke volume and an increase in pressure in the left atrium.

The condition of patients with severe aortic valve insufficiency is always severe, accompanied by tachycardia, marked peripheral vasoconstriction and cyanosis, sometimes stagnation and pulmonary edema. Peripheral signs of aortic insufficiency, as a rule, are not expressed or reach the degree, as in chronic aortic valve insufficiency. There is no double Traube tone, Durozier noise and a bisperic pulse, and a normal or slightly increased pulse pressure can lead to a serious underestimation of the severity of the valve lesion. The apical impulse of the left ventricle is normal, and the jerky movements of the thoracic paw are absent. I tone is sharply weakened due to premature closure of the mitral valve, the tone of closure of which is occasionally heard in the middle or the end of the diastole. Often, signs of pulmonary hypertension with an emphasis on the pulmonary component of tone II, the appearance of III and IV heart tones are often expressed. The early diastolic murmur of acute aortic insufficiency is usually low-frequency and short, which is associated with a rapid increase in CRF and a drop in the diastolic pressure gradient on the aortic valve.

Physical examination

In patients with chronic severe aortic regurgitation, the following symptoms are often observed:

• The rocking of the head with every beat of the heart (symptom de Musset);
• the appearance of a collapsoid pulse or pulse of a "hydraulic pump" characterized by rapid expansion and rapid fall of the pulse wave (Corrigan's pulse).

The arterial pulse is usually well expressed, palpated and evaluated better on the radial artery of the patient's raised arm. The bisparic pulse is also unremarkable and palpable on the brachial and femoral arteries of the patient much better than on the carotid arteries. It should be noted a large number of auscultatory phenomena associated with increased pulse pressure. The double tone of Traube is manifested in the form of systolic and diastolic tremors heard over the femoral artery. In the phenomenon of Mueller, the pulsation of the tongue is noted. Double noise Durozier - systolic murmur over the femoral artery at its proximal compression and diastolic when distal compression. The pulse is capillary, i.e. A quincke symptom, can be determined by pressing the glass against the inner surface of the patient's lip or by examining the fingertips through the transmitted light.

Systolic blood pressure is usually increased, and the diastolic blood pressure is sharply reduced. Hill's symptom is that the systolic pressure in the popliteal fossa exceeds systolic pressure in the shoulder cuff by more than 60 mm. Gt; Art. Korotkov's tones continue to be heard even near the zero mark, although intra-arterial pressure rarely falls below 30 mm Hg. Therefore, with the true diastolic pressure, the moment of "lubrication" of Korotkov's tones in the IV phase, as a rule, correlates. With the development of signs of heart failure, peripheral vasoconstriction may appear, thereby increasing diastolic pressure, which should not be regarded as a sign of moderate aortic valve insufficiency.

Apical impulse diffuse and hyperdynamic, shifted downward and outward; systolic retraction of the parasternal region can be observed. At the top, you can palpate the wave of rapid filling of the left ventricle, however, as well as systolic trembling on the basis of the heart, the supraclavicular fossa, over the carotid arteries due to increased cardiac output. In many patients, carotid tremor can be palpated or recorded.

Physical signs of aortic insufficiency

• The noise of Austin-Flint is a mesodiastolic murmur at the apex of the heart, imitating mitral stenosis.
• The hallmark of Hill-Fleck is the excess of arterial pressure on the arteries of the lower extremities over the pressure on the upper extremities (measurement by a tonometer, a reliable difference of more than 15 mm Hg).
• Corrigan's pulse is a rapid increase and a rapid fall in the amplitude of the arterial pulse. The symptom is determined with the help of palpation of the radial artery, and it increases with the raising of the hand - the "pulse of the water pump", collapsing the pulse.
• The Durozier symptom is an intermittent systolo diastolic murmur over the femoral artery when it is compressed.
• Sign of Quincke - increased pulsation of the capillaries of the nail bed.
• Traube attribute is a double tone, heard over the femoral artery with its easy compression.
• The symptom de Musset is the swaying of the head in the sagittal plane.
• A symptom of Maine is a decrease in diastolic blood pressure when the arm is raised by more than 15 mm. Gt; Art.
• The sign of Rosenbach is a pulsation of the liver.
• Sign Becker - increased pulsation of the arteries of the retina.
• The sign of Mueller is the pulsation of the tongue.
• The sign of Gerhard is the pulsation of the spleen.

Diagnosis of aortic insufficiency

[15], [16], [17], [18]

Electrocardiography

Chronic severe aortic insufficiency leads to a deviation of the axis of the heart to the left and the appearance of signs of diastolic overload volume, which is manifested in a change in the shape of the initial components of the ventricular complex (pronounced Q-wave in I lead, AVL, V3-V6) and a decrease in the K-wave in lead VI. Over time, these signs decrease and the overall amplitude of the QRS complex increases. Often there are inverted teeth T and depression of the ST segment that reflects the severity of left ventricular hypertrophy and its dilatation. For acute aortic valve insufficiency, nonspecific changes in the ST segment and T wave are characteristic in the absence of signs of myocardial hypertrophy of the left ventricle.

[19], [20], [21], [22], [23], [24], [25]

Radiography of chest organs

In typical cases, the expansion of the shadow of the heart is observed downward and to the left, which leads to a noticeable increase along the longitudinal axis and an insignificant increase in the diameter. Calcification of the aortic valve is not typical for "pure" aortic insufficiency, but it is often diagnosed when aortic valve and aortic stenosis fail. A distinct increase in the left atrium in the absence of signs of heart failure indicates the presence of concomitant mitral valve damage. Severe aneurysmal aortic dilatation suggests aortic root injury (eg, in Marfan syndrome, cystic necrosis of the mediastinum, or annuloaortal ectasia) as a cause of aortic insufficiency. Linear calcification of the wall of the ascending aorta is observed with syphilitic aortitis, but it is very nonspecific and can occur with degenerative lesions.

Echocardiography

It is recommended for patients with aortic valve insufficiency for the following purposes (class I):

• Verification and assessment of severity of acute or chronic aortic insufficiency (level of evidence B).
• Diagnosis of the cause of chronic aortic valve failure (including evaluation of the morphological features of the aortic valve, the size and morphology of the aortic root), and the degree of left ventricular hypertrophy, size (or volumes) and systolic function of the left ventricle (level of evidence B).
• Assessment of the severity of aortic insufficiency and the extent of aortic augmentation in patients with aortic aortic dilatation (level of evidence B).
• Determination of volumes and functions of the left ventricle in dynamics in asymptomatic patients with severe aortic valve insufficiency (level of evidence B).
• Dynamic observation of patients with mild, moderate and severe aortic insufficiency with the appearance of new symptoms (level of evidence B).

[26], [27], [28], [29]

Additional echocardiographic techniques for assessing the severity of aortic insufficiency

In a color Doppler scan, either the initial jet area of the aortic valves is measured in a parasternal aortic valve short axis study (in severe aortic valve failure, this area exceeds 60% of the area of the fibrous ring), or the thickness of the initial part of the jet for parasternal sensor location and study aorta of the original axis. In severe aortic insufficiency, the transverse size of the initial jet is> 60% of the size of the fibrous aortic valve ring.

Determine the half-life time on the Doppler spectrum of aortic insufficiency in studies with continuous wave Doppler (if it is <400 ms, then regurgitation is considered severe).

With the help of the continuous-wave Doppler, the magnitude of deceleration of the decline in the Doppler spectrum of the aortic valve failure jet is determined (at a value of> 3.0 m / s ^2, aortic regurgitation is considered severe). Unfortunately, the value of the last two parameters depends to a large extent on the number of cardiac contractions.

The presence of dilatation of the left ventricle also supports a severe aortic insufficiency.

Finally, with severe aortic valve insufficiency in the ascending aorta, a reverse flow of blood appears.

All of the above signs can describe severe aortic regurgitation, but there are no signs that reliably separate mild aortic insufficiency with Doppler-echocardiography from a moderate-sized one.

In addition, in everyday practice, a four-stage subdivision of aortic valve failure is also used:

• I Art. - the jet of regurgitation does not exceed half the length of the anterior valve lobe;
• II century. - a jet of aortic insufficiency reaches or is longer than the end of the valve leaf;
• III century. - The jet reaches half the length of the left ventricle,
• IV century. - The jet reaches the top of the left ventricle.

[30], [31]

Radionuclide methods and magnetic resonance imaging

Radionuclide angiography or MRT is indicated for primary or dynamic examination of left ventricular volume and function at rest in patients with aortic insufficiency with non-informative results of the EchoCG study (class I, level of evidence B). Conducting MRI is also justified for assessing the severity of aortic valve failure with non-informativity of Echocardiographic results (class IIa, level of evidence B) /

Load tests

Can be conducted in the following cases.

• In patients with chronic aortic insufficiency for evaluation of functional status and detection of new symptoms in case of an ambiguous clinical picture (class IIa, level of evidence B).
• In patients with chronic aortic valve failure to assess functional status and identify new symptoms in case of exercise, if a high level of physical activity is assumed (class IIa, level of evidence C).
• With simultaneous radionuclide angiography for evaluation of left ventricular function in symptomatic and asymptomatic patients with chronic aortic insufficiency (class IIb, level of evidence B).

Cardiac catheterization

Cardiac catheterization is carried out according to the following indications:

• Cardiac catheterization in combination with angiography of the aortic root and measurement of pressure in the left ventricular cavity is indicated for assessing the severity of aortic valve failure, left ventricular function and aortic root size if the results of non-invasive tests do not correspond or contradict clinical manifestations in patients with aortic insufficiency I, level of evidence B).
• Coronary angiography is indicated before the operation of aortic valve replacement in patients at risk for coronary artery disease (class I, level of evidence C).

At the same time, cardiac catheterization (in combination with angiography of the aortic root and measurement of pressure in the left ventricular cavity) is not indicated for assessing the severity of aortic valve insufficiency, left ventricular function and aortic aortic sternum:

• before surgical intervention at the heart, if the results of non-invasive tests are adequate, consistent with clinical manifestations and there is no need for coronary angiography (class III, level of evidence C);
• in asymptomatic patients with informative non-invasive tests (class III, level of evidence C).

Thus, the severity of aortic insufficiency is assessed according to the following criteria.

[32], [33], [34], [35], [36]

Criteria for the severity of aortic insufficiency according to the ACC / ANA algorithms (2006)

Criteria	Aortic insufficiency
	Lightweight	Moderate Gravity	Heavy

Quality

Angiography	1 +	2+	3-4 +
Width of color Doppler flow	Central flow, width less than 25% of LVEF	Significantly than with mild, but without signs of severe aortic insufficiency	Central flow, width more than 65% of LVEF
Doppler-width vena contracta, cm	<0.3	0.3-0.6	> 0.6

Quantitative (catheterization or ZHKKG)

Volume reorgitatsii, ml / number of reductions	<30	30-59	> 60
Fraction of regurgitation,%	<30	30-49	> 50
Area of the opening of the regurgitation, cm 2	<0.10	0.10-0.29	> 0.30

Additional Essential Criteria

Volume of the left ventricle

-

-

Increased

[37], [38], [39], [40]

Indications for consultations of other specialists

In the presence of indications for surgical treatment, a consultation of a cardiosurgeon is recommended.

Treatment of aortic insufficiency

Objectives of aortic insufficiency:

• Preventing sudden death and heart failure.
• Relieving the symptoms of the disease and improving the quality of life.

Medication for aortic insufficiency

Assign to patients to increase cardiac output and reduce regurgitation volume.

Class I

• The use of vasodilators is indicated for long-term treatment of patients with severe aortic insufficiency who have symptoms of left ventricular disease or dysfunction in the event that surgical treatment is not recommended due to the presence of additional cardiac or extracardiac causes. (Level of Evidence: B.)

Class IIa

• The use of vasodilators is justified as a short-term effect for improving the hemodynamic profile of patients with severe symptoms of heart failure and severe aortic insufficiency and before aortic valve replacement (PAK). (Level of Evidence S.)

Class IIb

• The use of vasodilators is possible as a long-term effect in asymptomatic patients with severe aortic valve insufficiency, in whom expansion of the left ventricular cavity is noted while maintaining a normal systolic function. (Level of Evidence: B.)

Class III

• The use of vasodilators is not indicated as a long-term effect in asymptomatic patients with mild or moderate aortic insufficiency with normal systolic function of the left ventricle. (Level of Evidence: B.)
• The use of vasodilators is not indicated as a long-term effect in asymptomatic patients with systolic dysfunction who are candidates for aortic valve replacement. (Level of Evidence S.)
• The use of vasodilators is not indicated as a long-term effect in patients with symptoms of the disease with normal left ventricular function or with mild to moderate systolic dysfunction who are candidates for an aortic valve transplant. (Level of Evidence S.)

Indications for surgical treatment of aortic insufficiency

Class I

• Aortic valve transplantation (PAK) is indicated for all symptomatic patients with severe aortic valve failure, regardless of left ventricular systolic function. (Level of Evidence: B.)
• PAA is shown to asymptomatic patients with chronic severe aortic insufficiency and left ventricular systolic dysfunction (ejection fraction of 50% or less) at rest. (Level of Evidence: B.)
• PAA is indicated for patients with chronic severe aortic valve failure when performing aortocoronary shunting (ASCh) or surgical interventions on the aorta or other heart valves. (Level of Evidence S.)

Class IIa

• PAK is justified for asymptomatic patients with severe aortic insufficiency and normal systolic function of the left ventricle (ejection fraction more than 50%), but with the presence of severe diarrhea of the left ventricle (end-diastolic size greater than 75 mm or finitely systolic size> 55 mm). (Level of Evidence: B.)

Class IIb.

• PAK is possible in patients with moderate aortic valve insufficiency during surgical interventions in the ascending aorta. (Level of Evidence S.)
• PAA is possible in patients with moderate aortic insufficiency in the performance of LCS, (Level of evidence: C.)
• PAA is possible in asymptomatic patients with severe aortic regurgitation and normal systolic function of the left ventricle at rest (ejection fraction more than 50%) if the degree of expansion of the left ventricular cavity exceeds in the final diastolic size 70 mm or the systolic size - 50 mm, if there is evidence of progressive expansion of the left ventricular cavity, reduced tolerance to exercise, or there is an atypical hemodynamic response to exercise. (Level of Evidence S.)

Class III

• PAA is not indicated for asymptomatic patients with mild, moderate or severe aortic valve insufficiency and normal left ventricular systolic function at rest (ejection fraction greater than 50%) if the degree of dilatation of the left ventricle is not moderate or severe (end-diastolic size less than 70 mm or of course systolic more than 50 mm). (Level of Evidence: B.)

Prognosis for aortic insufficiency

The prognosis depends on the nature of the aortic valve failure.

With moderate or severe chronic aortic failure, the prognosis has been favorable for many years. About 75% of patients live more than 5 years after diagnosis, about 50% - more than 10 years. Congestive heart failure, episodes of pulmonary edema and sudden death are noted with pronounced dilatation of the left ventricle. Without surgical treatment, death usually occurs within 4 years after the onset of angina and within 2 years after the development of heart failure. Acute aortic insufficiency without timely surgical intervention ends with early death, which occurs as a result of acute left ventricular failure.