Aortic valve insufficiency (AVI) is a heart condition in which the aortic valve leaflets do not close completely, leading to a reverse blood flow (regurgitation) from the aorta into the left ventricle.

3D animation – aortic valve dilatation

3D-animation – aortic valve leaflet redundancy

Epidemiology

Aortic regurgitation (AR) is the third most common valvular heart disease. According to the Framingham study, its prevalence among the adult population is 4.9%, with moderate and severe forms occurring in 0.5% of people.
Men are affected more often than women.
In developed countries, the main causes of the disease are degenerative and atherosclerotic changes in the valve associated with age.
In countries with limited access to medical care, infectious diseases such as rheumatic fever and infective endocarditis remain the leading causes of aortic valve damage and can lead to earlier development of valvular pathology, often already in childhood.
The burden of AR is expected to grow in the coming decades due to an aging population and an increase in the prevalence of cardiovascular diseases. In addition, thanks to the development of echocardiographic studies, it has become possible to detect subclinical forms of AR.

Dilatation of the aortic annulus – 3D model

Leaflet redundancy of the aortic valve – 3D model

Etiology

Degenerative processes, including calcification, fibrosis, and leaflet prolapse, are often combined with aortic stenosis. Infective endocarditis leads to leaflet destruction, while rheumatic fever causes their deformation and progressive regurgitation.
Systemic connective tissue diseases (Marfan, Loeys-Dietz, vascular Ehlers-Danlos) cause aortic dilation and an increased risk of dissection (aortic dissection). Inflammatory processes (Takayasu’s disease, granulomatosis with polyangiitis) and autoimmune pathologies (SLE, antiphospholipid syndrome) lead to aortic remodeling and secondary AR.
Enlargement of the aortic valve annulus, associated with aneurysms, hypertension, and connective tissue diseases, causes leaflet separation. Prolapse, leaflet redundancy prevent their normal closure, enhancing regurgitation.
AR can also occur with paravalvular leaks after prosthetic valve implantation.

Rheumatic aortic valve stenosis – 3D model

Degenerative aortic valve stenosis – 3D model

Pathophysiology

Acute aortic regurgitation develops suddenly, most commonly due to infective endocarditis, aortic dissection, or valve trauma.

Acute volume overload and increased diastolic pressure – significant blood flow back into the LV during diastole causes a sharp increase in end-diastolic pressure (EDP). This reduces its compliance, increases the load on the left atrium, and causes blood congestion in the pulmonary circulation, leading to pulmonary edema.
Reduced effective cardiac output – despite the hyperdynamic work of the LV, most of the blood returns to it, leading to a drop in blood pressure, organ hypoperfusion, and cardiogenic shock.
Impaired coronary perfusion – high EDP in the LV reduces the pressure gradient between the aorta and coronary arteries, decreasing myocardial blood supply and causing ischemia.
Compensatory reaction – activation of the sympathoadrenal system causes tachycardia and vasoconstriction, trying to maintain cardiac output. However, this increases afterload and exacerbates regurgitation.

Acute AR quickly leads to pulmonary edema, hypotension, and shock, requiring emergency surgical intervention.

Chronic AR develops gradually, most often due to degenerative valve changes, bicuspid aortic valve, rheumatic fever, or aortic dilatation. The heart has time to adapt to the volume overload, but over time the compensatory mechanisms are depleted, leading to decompensation.

Eccentric LV hypertrophy – prolonged volume overload causes LV dilation with parallel growth of myocytes, which allows maintaining normal cardiac output.
Progressive LV dilation – in late stages, due to chronic LV volume increase, its walls lose elasticity, which reduces ejection fraction and leads to systolic dysfunction. The end-diastolic LV dimension exceeds 70 mm.
Impaired coronary blood flow – the enlarged LV requires more oxygen, but the decrease in aortic diastolic pressure worsens myocardial perfusion, contributing to ischemia.
Hemodynamic changes – low diastolic pressure (50 mm Hg) reduces coronary blood flow, and chronic pulmonary circulation overload causes increased pressure in the left atrium and pulmonary veins.
Development of heart failure – as the disease progresses, congestion develops in the pulmonary and systemic circulations, accompanied by dyspnea, orthopnea, paroxysmal nocturnal dyspnea, as well as peripheral edema and hepatomegaly.

Clinical manifestations

Acute AR manifests with a rapid deterioration of condition.

Sudden onset of dyspnea that progresses to pulmonary edema, accompanied by orthopnea and suffocation.
Pronounced hypotension and cardiogenic shock due to a sharp decrease in cardiac output, manifested by weakness, dizziness, and altered consciousness.
In some cases of infective endocarditis, fever, chills, and signs of sepsis may occur.

Chronic AR remains asymptomatic for a long time due to the left ventricle’s adaptation to volume overload.

As the disease progresses, sensations of palpitations and increased pulsation appear, especially when lying down, which is associated with an increase in stroke volume and high pulse pressure.
Patients may complain of throbbing sensations in the head and neck area, caused by enhanced pulsation of large arteries.
Over time, shortness of breath develops during physical exertion. In severe cases, dyspnea becomes constant, accompanied by episodes of nocturnal dyspnea, indicating congestion in the pulmonary circulation.
Chest pain occurs in some patients and is caused by reduced coronary perfusion due to low diastolic pressure. Angina in AR more often develops at night when the heart rate slows down.
Late stages of the disease are accompanied by increasing symptoms of congestive heart failure, including peripheral edema, hepatomegaly, and ascites.

Diagnosis

Transthoracic echocardiography (TTE): is the key method for confirming the diagnosis of AR, assessing aortic valve morphology, degree of regurgitation, left ventricular (LV) size and function, as well as aortic dimensions.

Criteria for severe AR according to TTE data: vena contracta >6 mm; reverse diastolic flow in the descending aorta. Regurgitant volume >60 mL per cycle. Regurgitant fraction >50%. Effective regurgitant orifice area (EROA) ≥0.30 cm².

Grades of aortic regurgitation by transthoracic echocardiography

Parameter	Light AR (Grade I)	Moderate AR (Grade II)	Severe AR (III degree)
Vena contracta diameter	3 mm	3-6 mm	> 6 mm
Regurgitant volume	30 mL	30-60 mL	> 60 mL
Regurgitant fraction	30%	30-50%	> 50%
Effective regurgitant orifice area (EROA)	0.10 cm²	0.10-0.30 cm²	≥ 0.30 cm²
Reverse diastolic flow	Absent	Present, but not in descending aorta	Reverse flow in descending aorta

Transesophageal echocardiography (TEE): recommended when TTE provides insufficient information, especially in cases of suspected infective endocarditis or when planning surgical intervention.
Magnetic resonance imaging (MRI): rarely, but may be used to assess regurgitant volume and LV function, especially when echocardiography provides limited data.
Computed tomography (CT): used for detailed assessment of aortic size and condition, especially when dilation or aneurysm is suspected and for choosing the surgical approach.
Electrocardiography (ECG): helps identify signs of LV hypertrophy and other associated abnormalities.
Chest X-ray: may show enlarged heart size and signs of pulmonary congestion.

Treatment of aortic valve insufficiency

Risk factor modification

Blood pressure control, as systemic hypertension contributes to aortic root dilation and worsens leaflet coaptation.
Correction of hyperlipidemia, smoking cessation, and weight control.
Regular moderate-intensity physical activity improves heart function; however, intense strength training and sports with high static load (e.g., weightlifting) are contraindicated in severe AR.

Drug therapy

Hypotensive therapy is indicated for arterial hypertension and aortic dilation; both ACE and BPA are most effective in reducing LV afterload and dilatation.
In patients with Marfan syndrome, beta-blockers or calcium channel blockers are preferred to slow aortic dilation.
Diuretics are used in congestive heart failure to reduce cardiac load.
Beta-blockers are used for aortic dilation but are contraindicated in isolated severe AR without hypertension, as they may worsen hemodynamics.
Vasodilators are prescribed limitedly, in select cases of symptomatic AR with high vascular resistance.

Transcatheter aortic valve implantation (TAVI)

Widely used for aortic stenosis, but its use in isolated AR is limited. This is due to anatomical features: the absence of leaflet calcification reduces the stability of the implanted prosthesis, increasing the risk of paravalvular leaks and valve displacement.

Contraindications for TAVI in AR: isolated AR without leaflet calcification; significant aortic root dilation making prosthesis fixation unstable.

3D animation – transcatheter aortic valve implantation (TAVI)

Surgical treatment

Surgical correction remains the main treatment method for severe AR, especially in patients with symptoms or signs of LV dysfunction.

Surgical aortic valve replacement is indicated in the following cases:

Symptomatic severe AR;
Asymptomatic severe AR with LV EDD >70 mm, ESD >50 mm, or EF 50%;
Ascending aorta surgery is performed for significant aortic dilatation (>55 mm, and >50 mm in Marfan syndrome).

Mechanical or biological prostheses are used for surgical valve replacement. The choice depends on the patient’s age, contraindications to anticoagulants, and comorbidities.

Aortic valve repair and valve-sparing operations

Reconstructive interventions are used in patients with aortic regurgitation caused by leaflet prolapse, local fibrous deformation, or aortic root dilation. The main repair techniques include:

Leaflet resection and plication – used for leaflet prolapse, which is eliminated by shortening and fixing the leaflet;
Leaflet reconstruction with autologous or animal pericardium – used for significant leaflet deformation when restoration is necessary without valve replacement;
Valve-sparing operations are preferred for young patients as they allow avoiding lifelong anticoagulant therapy. However, they require anatomically preserved leaflets and have stricter indications.

David procedure – the aortic valve is reimplanted into an artificial vascular graft, fixing the leaflets, which prevents their separation during aortic root dilation.

Yacoub procedure – remodeling of the aortic root by replacing its dilated part with a vascular graft without fixing the fibrous ring, preserving the native aortic valve.

FAQ

1. What is aortic valve insufficiency?

It is a condition where the valve leaflets do not close completely, and part of the blood returns from the aorta to the left ventricle during diastole.

2. Is there congenital aortic valve insufficiency?

Yes, congenital aortic insufficiency is common, although less common than acquired forms. It can be related to:
– Bicuspid aortic valve (the most common congenital anomaly predisposing to regurgitation);
– Developmental defects of the flaps (insufficient closure due to shortening or deformity);
– Connective tissue syndromes (Marfan, Ehlers-Danlos), in which dilatation of the aorta and valve zone is possible.
The congenital form often progresses slowly but requires regular monitoring as surgical correction may be required over time.

3. What are the symptoms of aortic insufficiency?

Symptoms depend on the form (acute or chronic) and severity:
– Acute AR: severe dyspnea, pulmonary edema, weakness, hypotension, shock (requires emergency care).
– Chronic AR:
– Early stages: asymptomatic course or palpitations, pulsation in the neck/head;
– Progression: dyspnea on exertion, angina pectoris (due to decreased coronary blood flow), nocturnal attacks of suffocation;
– Decompensation: edema, liver enlargement, decreased tolerance to physical activity.

4. What are the characteristic auscultation signs of aortic valve insufficiency?

A diastolic blowing murmur at the right upper sternal border (second intercostal space), intensifying when the patient is seated and leaning forward.

5. What are the recommendations for aortic insufficiency?

– Monitoring and correction of pressure to reduce LV stress.
– Regular examinations: EchoCG 1-2 times a year to assess the dynamics.
– Physical activity: moderate exercise (walking, swimming), but avoid heavy strength training.
– Prevention of endocarditis: antibiotic prophylaxis before dental/surgical interventions (as indicated).
– Surgical treatment: in case of symptoms or signs of LV dysfunction (PV <50%, КДР >70 mm).

Important:

For asymptomatic forms, monitoring is necessary, and when symptoms appear, timely consultation with a cardiologist is required to decide on surgery.

List of Sources

2021 ESC/EACTS Guidelines for the management of valvular heart disease. Vahanian A, Beyersdorf F, Praz F, Milojevic M, Baldus S, Bauersachs J, Capodanno D, Conradi L, De Bonis M, De Paulis R, Delgado V, Freemantle N, Gilard M, Haugaa KH, Jeppsson A, Jüni P, Pierard L, Prendergast BD, Sádaba JR, Tribouilloy C, Wojakowski W; ESC/EACTS Scientific Document Group. Eur Heart J. 2022 Feb 12;43(7):561-632. doi: 10.1093/eurheartj/ehab395.

Burden of valvular heart disease, 1990-2017: Results from the Global Burden of Disease Study 2017. Chen J, et al. J Glob Health. Sep 8;10(2):020404. doi: 10.7189/jogh.10.020404.

Aortic Valve Regurgitation: A Comprehensive Review. Oluwaseun A. Akinseye MD, MPH Aradhana Pathak MD Uzoma N. Ibebuogu MD. Current Problems in Cardiology. 2018 Aug; 43(8):315-334. doi: 10.1016/j.cpcardiol.2017.10.004.

TAVI and the future of aortic valve replacement. Howard C, Jullian L, Joshi M, Noshirwani A, Bashir M, Harky A. J Card Surg. 2019 Dec;34(12):1577-1590. doi: 10.1111/jocs.14226.

Aortic Valve Repair for Aortic Insufficiency Due to Cusp Prolapse. David TE. Ann Thorac Surg. 2023. Feb;115(2):436. doi: 10.1016/j.athoracsur.2022.06.047.

Aortic Regurgitation. Flint N, Wunderlich NC, Shmueli H, Ben-Zekry S, Siegel RJ, Beigel R. Curr Cardiol Rep. 2019 Jun 3;21(7):65. doi: 10.1007/s11886-019-1144-6.