Aortic regurgitation

Article written and reviewed by Dr Luca Moretti

Aortic regurgitation, or aortic insufficiency, is the valvular heart disease in which the valve does not close completely during diastole and allows some of the ejected blood to return from the aorta to the left ventricle. Competence, however, does not depend on the cusps alone: it results from the functional unit formed by the cusps, virtual annulus, sinuses of Valsalva, sinotubular junction and aortic root, so a lesion of any of these components may generate regurgitation.

The distinction between acute aortic regurgitation and chronic aortic regurgitation is both pathophysiological and therapeutic. A sudden loss of competence in a normal-sized ventricle may produce pulmonary edema and shock within hours; regurgitation of equal severity that develops slowly may be tolerated for years through dilation and eccentric hypertrophy. Jet severity, speed of onset and the myocardium's capacity to adapt must be considered together.

Epidemiology varies with age, sex and geographic setting. In Western registries, degenerative cusp disease, bicuspid aortic valve and root dilation predominate; in many regions rheumatic heart disease still has substantial importance. At least moderate regurgitation is more common in men and increases with age, but forms caused by bicuspid valve, endocarditis and heritable aortic disease also affect young adults.

Etiology, mechanisms and pathophysiology

A useful classification starts from cusp motion and distinguishes regurgitation with normal motion associated with annular or root dilation, excessive motion due to prolapse, and restricted motion due to retraction, calcification or restriction. This functional interpretation, analogous to the principles used in mitral repair, directly links the observed lesion to its mechanism and therefore to the possibility of repair.

Root dilation separates the commissures, widens the sinotubular junction and reduces central coaptation. It may result from hypertension and sporadic degeneration, bicuspid valve, Marfan syndrome, Loeys-Dietz syndrome, pathogenic ACTA2 variants or other thoracic aortopathy genes. Geometry should be described at the annulus, sinuses, junction and tubular segment because a single diameter does not identify the responsible segment or aortic risk.

Chronic cusp causes include bicuspid valve, myxomatous degeneration, fenestrations, prolapse, rheumatic retraction and calcification. In bicuspid disease the fused cusp and raphe may become stiff or prolapse; regurgitation is often eccentric and may be associated with root dilation. Rheumatic heart disease causes thickening and retraction of the margins, frequently with stenosis and mitral involvement.

The most important acute causes are infective endocarditis and type A aortic dissection. Infection may perforate or destroy a cusp, tear a fenestration, create an abscess or cause avulsion; dissection may dilate the root, displace a commissure or produce a flap that interferes with closure. Chest trauma, iatrogenic complications and sudden prosthetic dysfunction are less common but must be recognized.

During diastole, regurgitant volume depends on the effective orifice area, the duration of diastole and the pressure difference between the aorta and ventricle. Bradycardia and hypertension therefore prolong or intensify conditions favoring regurgitation, whereas tachycardia and controlled reduction of arterial pressure may reduce it; excessive tachycardia, however, impairs filling and increases myocardial oxygen demand.

In chronic disease, with every cardiac cycle the ventricle receives pulmonary venous return plus regurgitant blood. Total stroke volume increases to preserve forward output and the ventricle develops eccentric hypertrophy: sarcomeres are added in series, end-diastolic volume rises and increased mass limits wall stress. Compliance initially maintains relatively low filling pressure despite very large volumes.

The compensated phase is not biologically inert: volume overload, sometimes elevated systolic pressure and wall tension activate neurohormonal signaling, matrix changes and fibrosis. In this setting, ejection fraction may remain apparently normal because it measures total ejection, including the portion that will return from the aorta; therefore an LVEF of 55% does not have the same reassuring meaning as it would in a ventricle without volume overload.

As remodeling progresses, contractile reserve is exhausted, end-systolic volume increases and filling pressure rises. Reduced forward output causes fatigue, while transmission of pressure to the left atrium and pulmonary capillaries causes dyspnea. Replacement fibrosis and dysfunction may not fully regress after intervention if correction is performed late.

In acute disease the ventricle has no time to dilate. A large amount of blood enters a poorly compliant cavity and abruptly raises diastolic pressure, potentially causing premature mitral valve closure or diastolic mitral regurgitation. Aortic diastolic pressure falls, coronary perfusion decreases and forward output collapses: pulmonary edema, ischemia and cardiogenic shock may coexist.

Wide pulse pressure is characteristic of hemodynamically significant chronic regurgitation, in which systolic pressure rises because of the high stroke volume and diastolic pressure falls because of runoff. In acute disease, output may be so low that wide pulses and peripheral signs do not develop. The absence of classic findings therefore does not exclude a lethal lesion.

Clinical presentation and natural history

Patients with mild or moderate chronic regurgitation are often asymptomatic, and even severe disease may remain silent for a long time because forward output is maintained. The history should therefore reconstruct actual performance over time: slower walking pace, avoidance of hills, new pauses or abandonment of usual activities are more informative than simply answering no when asked about dyspnea.

Exertional dyspnea develops when filling pressures rise or output fails to adapt to exercise. Orthopnea and paroxysmal nocturnal dyspnea follow; pulmonary edema belongs to the decompensated phase or acute disease. Fatigue and reduced endurance reflect lower forward output, concomitant anemia, deconditioning or combinations of these factors.

Palpitations may represent awareness of a hyperdynamic heartbeat or extrasystoles; atrial fibrillation develops later than in mitral disease but may occur with atrial dilation and heart failure. Nocturnal or exertional angina may result from low aortic diastolic pressure, increased ventricular mass and concomitant coronary artery disease. Syncope is not a typical symptom and should prompt investigation for arrhythmias or another disorder.

In severe acute disease, sudden dyspnea, orthopnea, agitation, diaphoresis, chest or back pain when dissection is present, and fever or embolic phenomena in endocarditis predominate. Hypotension, cold extremities, oliguria and altered mental status indicate hypoperfusion. Presentation may rapidly become fatal and diagnosis must proceed alongside stabilization.

On examination in chronic disease, the apical impulse is broad and displaced laterally. The pulse is brisk and collapsing, pulse pressure widens and peripheral capillary or arterial pulsations may appear; these historical eponyms have educational value but limited sensitivity and specificity. They do not replace proper blood pressure measurement and imaging.

The diastolic murmur is high-pitched and decrescendo, best heard along the left sternal border with the patient seated, leaning forward and in expiration. A jet from a dilated root may radiate to the right. Duration tends to increase with severity in chronic disease; in acute disease, rapid pressure equalization may make it short and soft.

An apical mid-diastolic Austin Flint murmur may result from interference of the jet with the anterior mitral leaflet and suggests significant regurgitation, without implying organic mitral stenosis. A systolic ejection murmur is common because of high transaortic flow and does not necessarily indicate associated stenosis. A third heart sound indicates volume overload and increased filling pressures.

Natural history is heterogeneous. In asymptomatic patients with preserved function and dimensions, immediate annual risk may be low but rises with dilation, reduced LVEF, increasing end-systolic volumes, BNP, reduced strain and aortic progression. An isolated value close to a threshold should be confirmed and interpreted within its serial trajectory.

The onset of symptoms or dysfunction marks a prognostic change. Intervention before advanced dysfunction offers a greater probability of normalization of volumes and good survival; persistently reduced LVEF, very high end-systolic volume and myocardial fibrosis are associated with incomplete recovery. Surveillance is therefore not passive waiting but scheduled measurement of remodeling.

Diagnosis and multimodality quantification

Transthoracic echocardiography is the first test. It should identify etiology, cusp number and tissue, jet direction, root and aortic dimensions, regurgitation severity, ventricular volumes and function, associated valve disease and pulmonary pressure. Blood pressure and heart rate at the time of the study are part of the interpretation.

Assessment is integrated: no single parameter is sufficiently robust in every anatomy and hemodynamic condition. Jet area within the left ventricle should not be used alone because it depends on gain, Nyquist limit, pressure, eccentricity and wall impingement. Eccentric jets may appear small because of the Coandă effect despite a significant orifice.

The vena contracta is the narrowest portion of the jet immediately downstream from the orifice. A width greater than 6 mm supports severe regurgitation and less than 3 mm supports mild regurgitation, but the assumption of a regular orifice may fail with multiple or eccentric jets. Three-dimensional vena contracta area may better describe noncircular orifices, although it depends on image quality and standardization.

The PISA method uses the flow-convergence radius and aliasing velocity to calculate flow rate and effective regurgitant orifice area. An area of at least 30 mm² and a regurgitant volume of at least 60 mL per beat are criteria of severe disease. In the aortic position, convergence may be difficult to visualize, nonhemispheric or constrained by the wall; poor measurements should not be converted into apparently precise numbers.

Pulsed-wave Doppler in the descending aorta documents holodiastolic flow reversal. Prominent reversal throughout diastole, with end-diastolic velocity above 20 cm/s, is a strong sign of severe regurgitation; measurement in the abdominal aorta increases specificity. Aortic compliance, heart rate, blood pressure and collateral flow modify the finding, particularly in older patients.

A pressure half-time below 200 ms supports rapid pressure equalization and therefore severity, whereas a value above 500 ms favors mild disease. It is influenced, however, by ventricular and aortic compliance, diastolic pressure and vasodilator therapy. In acute disease it may be very short; in diastolic dysfunction it may overestimate severity.

The main quantitative and semiquantitative echocardiographic criteria for severe aortic regurgitation include:

• Vena contracta width greater than 6 mm.
• Effective regurgitant orifice area at least 30 mm².
• Regurgitant volume at least 60 mL per beat.
• Regurgitant fraction at least 50%.
• Holodiastolic flow reversal in the descending aorta, with end-diastolic velocity above 20 cm/s.
• Pressure half-time below 200 ms as a supportive, not isolated, finding.

The ventricular response provides a consistency check. Severe chronic regurgitation should cause dilation, except in early presentation, a small cavity or erroneous measurements; a normal cavity is instead compatible with acute disease. Linear dimensions are simple and historically validated, but indexed 2D or 3D volumes better describe nongeometric ventricles and differences in body size.

Transesophageal echocardiography is indicated when transthoracic imaging does not define mechanism or severity, when endocarditis or dissection is suspected and when repair is being planned. Two-dimensional and three-dimensional views localize prolapse, perforation, fenestration, raphe and commissural geometry. In an unstable patient it should not delay surgery when the diagnosis and indication are already clear.

Cardiac magnetic resonance is particularly useful when echocardiography and the clinical picture are discordant. Phase-contrast quantification measures forward and reverse aortic flow and derives regurgitant volume and fraction; standard cine imaging provides reproducible ventricular volumes and characterization of fibrosis. Plane-selection errors, aliasing, turbulence and distance from the valve require expert protocols.

CT does not routinely quantify regurgitation but defines the aorta, annulus, cusps, calcium and coronary arteries. It is essential in dissection when the patient is stable enough for transport and in surgical or transcatheter planning. In aortopathy, measurements should be obtained perpendicular to the vessel axis and compared using the same technique.

Exercise testing unmasks symptoms in a patient who reports being asymptomatic and documents functional capacity and blood pressure response; exercise echocardiography may assess contractile reserve, but no universally accepted thresholds are sufficient to replace established indications. BNP and longitudinal strain add prognostic information and help in borderline cases.

Catheterization is reserved for persistent discordance or unresolved concomitant assessments. Aortography is semiquantitative and depends on technique and hemodynamics; invasive pressure measurement may document equalization in acute disease. Coronary angiography is performed according to age, probability of coronary artery disease and the planned procedure.

Treatment, indications for intervention and follow-up

Treatment depends on timing of onset, severity, symptoms, ventricular response, valvular and aortic anatomy, risk and the feasibility of durable repair. Decisions in severe cases should be made in a Heart Valve Centre capable of integrating imaging, interventional cardiology, valve surgery and aortic surgery.

Severe acute aortic regurgitation generally requires urgent surgery. Intravenous vasodilators and inotropes may reduce load and support output as a bridge; bradycardia should be avoided and intra-aortic balloon counterpulsation is contraindicated because it increases regurgitation during diastole. Endocarditis and dissection require parallel etiologic treatment without waiting for a pharmacological response that cannot correct the lesion.

In chronic disease, hypertension should be treated, preferably with agents that reduce afterload such as ACE inhibitors, angiotensin receptor blockers or dihydropyridine calcium-channel blockers according to the clinical profile. Therapy is indicated for blood pressure and heart failure, not as a substitute for surgery. In normotensive asymptomatic patients with preserved function, routine vasodilation has not been shown to reliably defer intervention.

Surgery is recommended in patients with symptomatic severe regurgitation regardless of LVEF, provided benefit is not futile. It is also recommended in asymptomatic patients with LVEF no higher than 50%, LVESD greater than 50 mm or indexed LVESD greater than 25 mm/m², especially in smaller individuals. These thresholds indicate remodeling that is already prognostically relevant.

The 2025 ESC/EACTS guidelines allow earlier intervention to be considered, with a lower recommendation level, in low-risk asymptomatic patients with LVEF no higher than 55%, LVESDi greater than 22 mm/m² or LVESVi greater than 45 mL/m². These are not automatic indications: measurement quality, trends, sex, body size, repairability, risk and patient preferences should be discussed.

Valve surgery is also recommended in severe regurgitation when the patient is undergoing coronary artery bypass grafting or ascending aortic surgery. Aortic diameter may constitute an indication independent of valvular severity and follows specific thresholds according to genotype, root phenotype, bicuspid valve, growth, family history and pregnancy.

Valve repair avoids a prosthesis and its complications but requires good-quality cusps and dedicated expertise. Isolated prolapse, selected fenestrations and root-related regurgitation may be corrected with plication or resuspension, annuloplasty and valve-sparing root replacement. Adequate effective height and stable coaptation are determinants of durability.

Surgical replacement remains the standard when repair is not expected to be durable. Mechanical and biological prostheses are selected according to age, life expectancy, anticoagulation, bleeding risk, pregnancy and future strategy. If an aneurysm coexists, the procedure may include root replacement with coronary reimplantation or supracoronary replacement of the ascending aorta.

TAVI for pure regurgitation is more difficult than for stenosis: calcium and stable anchoring are often absent, while the annulus and root are dilated. Risks include embolization, residual leak, need for a second device and coronary obstruction. Dedicated devices have improved outcomes in high-risk patients; the 2025 guidelines allow TAVI to be considered in selected symptomatic patients with severe disease who are inoperable at expert centers, but do not make it equivalent to surgery in operable patients.

Follow-up of asymptomatic severe regurgitation with preserved function is at least annual and becomes every three to six months when measurements or LVEF approach thresholds or change rapidly. Mild or moderate disease requires longer intervals tailored to etiology and the aorta. Each visit should reassess symptoms, blood pressure, examination findings, diameters and volumes using comparable techniques.

A confirmed serial increase is more meaningful than small fluctuations between laboratories. Aortic measurements should be repeated with the same modality; a diameter greater than 40 mm generally requires baseline CT or magnetic resonance imaging and surveillance of the entire segment. Patients should receive precise instructions to report dyspnea, declining performance, edema, sudden chest pain or persistent fever.

Physical activity and pregnancy depend on severity, function and aortic diameters. Mild-to-moderate regurgitation with normal function is often compatible with exercise; severe lesions or aortopathy require individualized assessment and restriction of intense static effort. Preconception counseling is essential if the root is dilated or a heritable aortopathy is present.

Complications and prognosis

Chronic volume overload leads to ventricular dilation, systolic dysfunction and heart failure. The transition may be gradual and initially subclinical; once extensive fibrosis has developed, the ventricle may not recover completely. Preventing this damage is the primary purpose of surgical thresholds and surveillance.

Heart failure presents with pulmonary congestion, reduced output or both. Atrial fibrillation, ischemia, infection, anemia, hypertension and renal failure may precipitate it. In acute disease, pulmonary edema and shock are direct manifestations of the lesion rather than end stages of prolonged remodeling.

Myocardial ischemia results from reduced aortic diastolic pressure, increased ventricular mass and wall tension, and associated coronary artery disease. It may occur even without epicardial stenoses. In acute disease, the combination of hypotension and elevated end-diastolic pressure markedly reduces the coronary perfusion gradient.

Atrial and ventricular arrhythmias become more likely with dilation and fibrosis. Palpitations and syncope require monitoring and investigation for independent causes; valve correction does not necessarily eliminate an established substrate. Atrial fibrillation is anticoagulated according to thromboembolic risk and prosthesis type.

Initially post-capillary pulmonary hypertension may progress to vascular remodeling and right ventricular dysfunction. Tricuspid regurgitation, systemic congestion, hepatic and renal dysfunction identify advanced disease and increase operative risk. Late correction may not fully normalize these changes.

Endocarditis, septic emboli, abscess and atrioventricular block are complications of the infectious form. In dissection, tamponade, coronary or organ malperfusion, rupture and aortic regurgitation occur in combination. These conditions follow emergency pathways in which regurgitation is part of a broader disease process.

After repair, residual or recurrent regurgitation may develop because of loss of coaptation, annular dilation or cusp deterioration. After replacement, patient-prosthesis mismatch, thrombosis, endocarditis, paravalvular leak and structural valve degeneration may occur. The baseline postoperative echocardiogram is the reference for subsequent follow-up.

Prognosis is favorable when the lesion is corrected before dysfunction develops and when the aorta and valve are treated comprehensively. Advanced symptoms, reduced LVEF, high end-systolic volume, fibrosis, renal failure, pulmonary hypertension and frailty worsen outcomes. Success therefore does not simply mean absence of postoperative regurgitation, but functional recovery and prevention of irreversible damage.