Aortic insufficiency: causes, symptoms, diagnosis, treatment

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

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What causes aortic insufficiency?

Rheumatic fever is one of the main valvular causes of aortic insufficiency. Wrinkling of the valves due to connective tissue infiltration prevents them from closing during diastole, thereby creating a defect in the center of the valve - a "window" for regurgitation of blood into the left ventricular cavity. The accompanying fusion of the commissures limits the opening of the aortic valve, which leads to the appearance of concomitant aortic stenosis.

Infective endocarditis

Aortic valve insufficiency may be caused by valve destruction, perforation of its cusps, or the presence of growing vegetations that prevent the cusps from closing during diastole.

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

Other primary valvular causes of aortic regurgitation:

• trauma that leads to rupture of the ascending aorta. There is a disruption of the commissure attachment, which leads to prolapse of the aortic valve into the left ventricular cavity;
• congenital bicuspid valve due to incomplete closure or prolapse of the valves;
• large septal ventricular septal defect;
• membranous subaortic stenosis;
• complication of radiofrequency catheter ablation;
• myxomatous degeneration of the aortic valve;
• destruction of the biological valve prosthesis.

Aortic root lesion

The following diseases can cause damage to the aortic root:

• age-related (degenerative) dilation of the aorta;
• cystic necrosis of the aortic media (isolated or as a component of Marfan syndrome);
• aortic dissection;
• osteogenesis imperfecta (osteopstasis);
• syphilitic aortitis;
• ankylosing spondylitis;
• Behcet's syndrome;
• psoriatic arthritis;
• arthritis in ulcerative colitis;
• relapsing polychondritis;
• Reiter's syndrome;
• giant cell arteritis;
• systemic hypertension;
• use of certain appetite suppressants.

Aortic insufficiency in these cases is formed due to a pronounced expansion of the aortic valve ring and the aortic root with subsequent separation of the cusps. Subsequent dilation of the root is inevitably accompanied by excessive tension and bending of the cusps, which then thicken, wrinkle and become unable to completely cover the aortic opening. This aggravates aortic valve insufficiency, leads to further expansion of the aorta and closes the vicious circle of pathogenesis ("regurgitation increases regurgitation").

Regardless of the cause, aortic insufficiency always causes dilation and hypertrophy of the left ventricle with subsequent expansion of the mitral annulus and possible development of dilation of the left atrium. Often, "pockets" form on the endocardium at the site of contact of the regurgitant flow and the wall of the left ventricle.

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Types and causes of aortic insufficiency

Valve:

• Rheumatic fever.
• Calcific aortic stenosis (CAS) (degenerative, senile).
• Infective endocarditis.
• Heart injuries.
• Congenital bicuspid valve (combination of aortic stenosis and aortic valve insufficiency).
• Myxomatous degeneration of the aortic valve leaflets.

Aortic root lesion:

• Age-related (degenerative) dilation of the aorta.
• Systemic arterial hypertension.
• Aortic dissection.
• Collagenoses (ankylosing spondylitis, rheumatoid arthritis, giant cell arteritis, Reiter's syndrome, Ehlers-Danlos syndrome, Behcet's syndrome).
• Congenital heart defects (ventricular septal defect with prolapse of the aortic valve leaflets, isolated subaortic stenosis). -
• Taking anorectics.

Pathophysiology of aortic insufficiency

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

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

A gradual increase in end-diastolic volume leads to an increase in systolic tension of the left ventricular wall with subsequent hypertrophy, accompanied by a simultaneous expansion of the left ventricular cavity (eccentric hypertrophy of the left ventricle), which promotes uniform distribution of the increased pressure in the left ventricular cavity to each motor unit of the myocardium (sarcomere) and thereby helps maintain stroke volume and ejection fraction within normal or suboptimal limits (compensation stage).

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

Acute aortic insufficiency

The most common causes of acute aortic insufficiency are infective endocarditis, aortic dissection, or trauma. Acute aortic insufficiency is characterized by a sudden increase in the diastolic volume of blood entering the unchanged left ventricle. Insufficient time for the development of adaptive mechanisms leads to a sharp increase in the EDV in both the left ventricle and 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 quickly compensatory expand soon leads to a decrease in the volume of ejection into the aorta.

The resulting compensatory tachycardia is insufficient to maintain sufficient cardiac output, which contributes to the development of pulmonary edema and/or cardiogenic shock.

Particularly pronounced hemodynamic disturbances are observed in patients with concentric left ventricular hypertrophy caused by pressure overload and discrepancy between the sizes of the left ventricular cavity and the EDV. This situation occurs in the case of aortic dissection against the background of systemic hypertension, as well as in acute aortic valve insufficiency after balloon commissurotomy in congenital aortic stenosis.

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Chronic aortic insufficiency

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

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

Further enlargement of the left heart chambers, combined with increased systolic wall stress, leads to concomitant concentric hypertrophy of the left ventricle. Thus, aortic valve insufficiency is a combination of volume and pressure overload (compensation stage).

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

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Pathophysiological mechanisms of left ventricular adaptation in aortic insufficiency

Spicy:

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

Chronic (compensated):

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

Chronic (decompensated):

• inadequate hypertrophy and increased afterload;
• increased myocardial fiber sliding and loss of 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 have no (or almost no) symptoms. Signs characteristic of a decrease in cardiac reserve or myocardial ischemia usually develop in the 4th or 5th decade of life after the formation of severe cardiomegaly and myocardial dysfunction. The main complaints (dyspnea during physical exertion, orthopnea, paroxysmal nocturnal dyspnea) accumulate gradually. Angina pectoris appears in the late stages of the disease; attacks of "nocturnal" angina become excruciating and are accompanied by profuse cold sticky sweat, which is caused by a slowdown in the heart rate and a critical drop in arterial diastolic pressure. Patients with aortic valve insufficiency often complain of intolerance to heartbeats, especially in a horizontal position, as well as of unbearable chest pain caused by the heart beating against the chest. Tachycardia, which occurs during emotional stress or during exertion, causes palpitations and head shaking. Patients are particularly bothered by ventricular extrasystoles due to a particularly strong post-extrasystolic contraction against 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 a diastolic murmur beginning immediately after the second sound. It differs from the murmur of pulmonary regurgitation by its early onset (i.e. immediately after the second sound) and increased pulse pressure. The murmur is best heard with the patient sitting or leaning forward, holding his breath at the height of expiration. With severe aortic insufficiency, the murmur quickly reaches a peak and then slowly decreases throughout diastole (decrescendo). If regurgitation is caused by primary valve damage, the murmur is best heard at the left edge of the sternal border in the third or fourth intercostal space. However, if the murmur is mainly due to dilation of the ascending aorta, the auscultatory maximum will be the right edge of the sternal border.

The severity of aortic insufficiency correlates most closely with the duration of the murmur rather than its intensity. With moderate aortic insufficiency, the murmur is usually limited to early diastole, high-pitched, and reminiscent of a push. With severe aortic insufficiency, the murmur lasts throughout diastole and may acquire a "scraping" tone. If the murmur becomes musical ("dove cooing"), this usually indicates "eversion" or perforation of the aortic valve leaflet. In patients with severe aortic insufficiency and left ventricular decompensation, equalization of pressure in the left ventricle and aorta at the end of diastole leads to the disappearance of this musical component of the murmur,

Mid- and late diastolic apical murmur (Austin-Flint murmur) is quite often detected in severe aortic insufficiency, and it can appear with an unchanged mitral valve. The murmur is caused by the presence of resistance to mitral blood flow due to high EDP, as well as oscillation of the anterior mitral valve leaflet under the influence of regurgitant aortic flow. In practice, it is difficult to distinguish Austin-Flint murmur from mitral stenosis murmur. Additional differential diagnostic criteria in favor of the latter: increased 1st tone (flapping 1st tone) and mitral valve opening tone (click).

Symptoms of acute aortic insufficiency

Because of the limited ability of the left ventricle to tolerate severe aortic regurgitation, such patients often develop signs of acute cardiovascular collapse, with weakness, severe dyspnea, and hypotension caused by decreased stroke volume and increased left atrial pressure.

The condition of patients with severe aortic valve insufficiency is always severe, accompanied by tachycardia, severe peripheral vasoconstriction and cyanosis, sometimes congestion and pulmonary edema. Peripheral signs of aortic insufficiency, as a rule, are not expressed or do not reach the same degree as in chronic aortic valve insufficiency. Double Traube tone, Duroziez noise and bispherical pulse are absent, and normal or slightly increased pulse pressure can lead to a serious underestimation of the severity of valve damage. The apical impulse of the left ventricle is normal, and jerky movements of the chest are absent. The first tone is sharply weakened due to premature closure of the mitral valve, the closing tone of which is occasionally heard in the middle or end of diastole. Signs of pulmonary hypertension with an accentuation of the pulmonary component of the second tone, the appearance of the third and fourth heart sounds 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 EDP and a drop in the diastolic pressure gradient across the aortic valve.

Physical examination

Patients with chronic severe aortic regurgitation often experience the following symptoms:

• shaking of the head with each heartbeat (de Musset's symptom);
• the appearance of a collaptoid pulse or a “hydraulic pump” pulse, characterized by a rapid expansion and rapid decline of the pulse wave (Corrigan pulse).

The arterial pulse is usually well expressed, palpated and assessed better on the radial artery of the patient's raised arm. Bispherical pulse is also common and is palpated on the patient's brachial and femoral arteries much better than on the carotid arteries. It is worth noting a large number of auscultatory phenomena associated with increased pulse pressure. Traube's double tone manifests itself as systolic and diastolic impulses heard over the femoral artery. With Müller's phenomenon, pulsation of the uvula is noted. Durozieux's double noise is a systolic noise over the femoral artery with its proximal compression and diastolic with distal compression. The pericapillary pulse, i.e. Quincke's symptom, can be determined by pressing a glass to the inner surface of the patient's lip or examining the fingertips through transmitted light.

Systolic blood pressure is usually increased, and diastolic is sharply reduced. Hill's symptom is an excess of systolic pressure in the popliteal fossa over systolic pressure in the brachial cuff by more than 60 mm Hg. Korotkoff sounds continue to be heard even near zero, although intra-arterial pressure rarely falls below 30 mm Hg, therefore, the moment of "smearing" of Korotkoff sounds in phase IV usually correlates with true diastolic pressure. 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.

The apical impulse is diffuse and hyperdynamic, shifted downward and outward; systolic retraction of the parasternal region may be observed. At the apex, a wave of rapid filling of the left ventricle can be palpated, as well as a systolic thrill at the base of the heart, supraclavicular fossa, and over the carotid arteries due to increased cardiac output. In many patients, carotid thrill can be palpated or recorded.

Physical signs of aortic insufficiency

• Austin-Flint murmur is a mid-diastolic murmur at the apex of the heart that mimics mitral stenosis.
• Hill-Fleck sign - excess of arterial pressure in the arteries of the lower extremities over the pressure in the upper extremities (measured with a tonometer, a reliable difference of more than 15 mm Hg).
• Corrigan's pulse is a rapid increase and rapid fall in the amplitude of the arterial pulse. The sign is determined by palpation of the radial artery, and it intensifies when raising the arm - "water pump pulse", collapsing pulse.
• Duroziez's sign is an intermittent systolic-diastolic murmur over the femoral artery when it is compressed.
• Quincke's sign is increased pulsation of the capillaries of the nail bed.
• Traube's sign is a double tone heard over the femoral artery when it is slightly compressed.
• De Musset's sign is a shaking of the head in the sagittal plane.
• Meine's sign is a decrease in diastolic blood pressure when raising the arm by more than 15 mm Hg.
• Rosenbach's sign - liver pulsation.
• Becker's sign is increased pulsation of the retinal arteries.
• Müller's sign - pulsation of the uvula.
• Gerhard's sign - pulsation of the spleen.

Diagnosis of aortic insufficiency

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Electrocardiography

Chronic severe aortic insufficiency results in left axis deviation and signs of diastolic volume overload, which is expressed in changes in the shape of the initial components of the ventricular complex (pronounced Q waves in lead I, 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. Inverted T waves and ST segment depression are often detected, reflecting the severity of left ventricular hypertrophy and dilation. Acute aortic valve insufficiency is characterized by nonspecific changes in the ST segment and T wave in the absence of signs of left ventricular myocardial hypertrophy.

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Chest X-ray

Typical cases show downward and leftward expansion of the cardiac shadow, resulting in a noticeable enlargement along the longitudinal axis and an insignificant enlargement in the transverse direction. Calcification of the aortic valve is not typical for "pure" aortic insufficiency, but is often diagnosed with a combination of aortic valve insufficiency and aortic stenosis. Marked enlargement of the left atrium in the absence of signs of heart failure indicates the presence of concomitant mitral valve disease. Marked aneurysmal dilation of the aorta suggests aortic root disease (eg, in Marfan syndrome, cystic medial necrosis, or annuloaortic ectasia) as the cause of aortic insufficiency. Linear calcification of the wall of the ascending aorta is observed in syphilitic aortitis, but it is highly nonspecific and may occur in degenerative lesions.

Echocardiography

Recommended for patients with aortic valve insufficiency for the following purposes (Class I):

• Verification and assessment of the severity of acute or chronic aortic insufficiency (level of evidence B).
• Diagnosis of the cause of chronic aortic valve insufficiency (including assessment of the morphological features of the aortic valve, the size and morphology of the aortic root), as well as the degree of left ventricular hypertrophy, the size (or volume) and systolic function of the left ventricle (level of evidence B).
• Evaluation of the severity of aortic insufficiency and the degree of aortic enlargement in patients with dilated aortic valves (level of evidence B).
• Determination of left ventricular volumes and function over time in asymptomatic patients with severe aortic valve insufficiency (level of evidence B).
• Dynamic observation of patients with mild, moderate and severe aortic insufficiency when new symptoms appear (level of evidence B).

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Additional echocardiographic techniques to assess the severity of aortic insufficiency

When examining in color Doppler scanning mode, either the area of the initial jet at the aortic cusps is measured during parasternal examination of the aortic valve along the short axis (in case of severe aortic valve insufficiency, this area exceeds 60% of the area of the fibrous ring), or the thickness of the initial part of the jet during parasternal placement of the sensor and examination of the aorta along the true axis. In case of severe aortic insufficiency, the transverse size of the initial jet is >60% of the size of the fibrous ring of the aortic valve.

The half-life time on the Doppler spectrum of aortic insufficiency is determined during examination using continuous-wave Doppler (if it is <400 ms, then the regurgitation is considered severe).

Using continuous-wave Doppler, the magnitude of the slowing of the decline in the Doppler spectrum of the aortic valve insufficiency jet is determined (if this indicator is >3.0 m/s2, ^aortic regurgitation is considered severe). Unfortunately, the magnitude of the last two indicators largely depends on the number of heart contractions.

The presence of left ventricular dilation also indicates severe aortic insufficiency.

Finally, in severe aortic valve insufficiency, a reverse blood flow occurs in the ascending aorta.

All of the above signs can describe severe aortic regurgitation, but there are no signs that reliably differentiate mild aortic insufficiency from moderate aortic insufficiency using Doppler echocardiography.

In addition, in everyday practice, a four-stage division of the aortic valve insufficiency jet is also used:

• Stage I - the regurgitant jet does not extend beyond half the length of the anterior mitral valve leaflet;
• II st. - the aortic insufficiency jet reaches or is longer than the end of the mitral valve leaflet;
• III st. - The jet reaches half the length of the left ventricle,
• IV stage - the jet reaches the apex of the left ventricle.

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Radionuclide methods and magnetic resonance imaging

Radionuclide angiography or MRI are indicated for primary or dynamic examination of left ventricular volumes and function at rest in patients with aortic insufficiency when echocardiography results are uninformative (class I, level of evidence B). MRI is also justified for assessing the severity of aortic valve insufficiency when echocardiography results are uninformative (class IIa, level of evidence B)/

Load tests

Can be carried out in the following cases.

• In patients with chronic aortic insufficiency to assess the functional status and identify new symptoms during exercise with an ambiguous clinical picture (class IIa, level of evidence B).
• In patients with chronic aortic valve insufficiency, to assess functional status and detect new symptoms during exercise if a high level of physical activity is expected (class IIa, level of evidence C).
• When performing radionuclide angiography simultaneously to assess left ventricular function in symptomatic and asymptomatic patients with chronic aortic insufficiency (class IIb, level of evidence B).

Cardiac catheterization

Cardiac catheterization is performed for the following indications:

• Cardiac catheterization in combination with aortic root angiography and left ventricular pressure measurement is indicated to assess the severity of aortic valve insufficiency, left ventricular function, and aortic root size when noninvasive test results are inconsistent with or contradict clinical manifestations in patients with aortic insufficiency (Class I, Level of Evidence B).
• Coronary angiography is indicated before aortic valve replacement surgery in patients at risk of coronary artery disease (Class I, Level of Evidence C).

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

• before cardiac surgery if the results of noninvasive tests are adequate, consistent with clinical manifestations and there is no need for coronary angiography (class III, level of evidence C);
• in asymptomatic patients when noninvasive tests are informative (class III, level of evidence C).

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

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

Criteria	Aortic insufficiency
	Easy	Moderate severity	Heavy

Quality

Angiography	1 +	2+	3-4+
Color Doppler Flow Width	Central flow, width less than 25% of LVOT	Significantly higher than in mild but no signs of severe aortic insufficiency	Central flow, width more than 65% of the LVOT
Doppler width of vena contracta, cm	<0.3	0.3-0 6	>0.6

Quantitative (catheterization or echocardiography)

Repurgitation volume, ml/number of contractions	<30	30-59	>60
Regurgitation fraction, %	<30	30-49	>50
Area of regurgitation opening, cm2	<0.10	0.10-0.29	>0.30

Additional essential criteria

Left ventricular volume

-

-

Enlarged

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Indications for consultations with other specialists

If there are indications for surgical treatment, a consultation with a cardiac surgeon is recommended.

Treatment of aortic insufficiency

Goals of treatment for aortic insufficiency:

• Prevention of sudden death and heart failure.
• Relief of disease symptoms and improvement of quality of life.

Drug treatment of aortic insufficiency

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

Class I

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

Class IIa

• The use of vasodilators is justified as a short-term intervention to improve the hemodynamic profile of patients with severe symptoms of heart failure and severe aortic insufficiency and before aortic valve replacement (AVR). (Level of Evidence: C)

Class IIb

• Vasodilators may be useful as a long-term intervention in asymptomatic patients with severe aortic valve insufficiency who have left ventricular dilation with normal systolic function. (Evidence level B)

Class III

• The use of vasodilators is not indicated for long-term intervention in asymptomatic patients with mild to moderate aortic insufficiency and normal left ventricular systolic function. (Level of Evidence: B)
• The use of vasodilators is not indicated for long-term intervention in asymptomatic patients with systolic dysfunction who are candidates for aortic valve replacement. (Level of Evidence: C)
• The use of vasodilators is not indicated for long-term intervention in symptomatic patients with normal left ventricular function or mild to moderate systolic dysfunction who are candidates for aortic valve replacement. (Evidence level C)

Indications for surgical treatment of aortic insufficiency

Class I

• Aortic valve transplantation (AVT) is indicated in all symptomatic patients with severe aortic valve regurgitation, regardless of left ventricular systolic function. (Level of Evidence: B)
• AVR is indicated in asymptomatic patients with chronic severe aortic insufficiency and left ventricular systolic dysfunction (ejection fraction 50% or less) at rest. (Level of Evidence: B)
• AVR is indicated in patients with chronic severe aortic valve insufficiency undergoing coronary artery bypass grafting (CABG) or surgical interventions on the aorta or other heart valves. (Level of evidence C)

Class IIa

• AVR is justified in asymptomatic patients with severe aortic insufficiency and normal left ventricular systolic function (ejection fraction greater than 50%), but with the presence of severe left ventricular dilation (end-diastolic dimension greater than 75 mm or end-systolic dimension greater than 55 mm). (Level of evidence B.)

Class IIb.

• AVR is possible in patients with moderate aortic valve insufficiency during surgical interventions on the ascending aorta. (Level of evidence C.)
• AVR is possible in patients with moderate aortic insufficiency when performing LCS, (Level of evidence C.)
• AVR is considered in asymptomatic patients with severe aortic regurgitation and normal left ventricular systolic function at rest (ejection fraction greater than 50%) if the degree of left ventricular dilation exceeds 70 mm in end-diastolic dimension or 50 mm in end-systolic dimension, if there is evidence of progressive left ventricular dilation, decreased exercise tolerance, or an atypical hemodynamic response to exercise. (Evidence level C)

Class III

• AVR is not indicated in asymptomatic patients with mild, moderate, or severe aortic valve regurgitation and normal left ventricular systolic function at rest (ejection fraction greater than 50%) unless the degree of left ventricular dilation is moderate to severe (end-diastolic dimension less than 70 mm or end-systolic dimension greater than 50 mm). (Level of Evidence: B)

Prognosis for aortic insufficiency

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

In moderate to severe chronic aortic insufficiency, the prognosis is favorable for many years. About 75% of patients survive for more than 5 years after diagnosis, about 50% - for more than 10 years. Congestive heart failure, episodes of pulmonary edema, and sudden death are observed with severe left ventricular dilation. 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 in early death, which occurs due to acute left ventricular failure.