Chronic aortic regurgitation

Article written and reviewed by Dr Luca Moretti

Chronic aortic regurgitation is persistent regurgitation from the aorta into the left ventricle that develops slowly enough to permit structural adaptation. The ventricle dilates, increases its mass and generates a large total stroke volume to preserve forward output. This compensation explains an asymptomatic phase that may last for decades, but it does not prevent the overload from leading to fibrosis, increased end-systolic volume and loss of contractile function.

Modern management does not consist simply of waiting for symptoms to appear, but of identifying the point at which still-reversible adaptation begins to turn into myocardial damage. To do so, clinical history is integrated with quantitative echocardiography, serial volume measurements, magnetic resonance imaging, exercise testing and markers of subclinical dysfunction: surgical thresholds should therefore be interpreted as prognostic signals along this trajectory, not as isolated numbers to be rounded.

Causes include bicuspid aortic valve, cusp prolapse or degeneration, sequelae of endocarditis, rheumatic heart disease and dilation of the aortic root or ascending aorta. The general page on aortic regurgitation describes the entire spectrum; here the focus is on chronic remodeling, surveillance and selection of the timing of intervention.

Ventricular adaptation and transition to heart failure

During each diastole the ventricle simultaneously receives pulmonary venous return and blood flowing back from the aorta; end-diastolic volume therefore increases and the Frank-Starling mechanism allows a greater total stroke volume to be generated. Thanks to this adaptation, forward stroke volume can remain normal even when a substantial proportion of blood returns backward during the next cycle.

Remodeling combines dilation and eccentric hypertrophy. Addition of sarcomeres in series enlarges the cavity, while increased myocardial mass limits systolic wall stress. Unlike pure experimental volume overload, aortic regurgitation also imposes a pressure component because the ventricle must eject a large volume against aortic pressure.

Increased compliance initially keeps diastolic pressure low despite the larger volume, allowing the patient to exercise without substantial congestion. At this stage, however, heart rate and arterial pressure continue to modulate regurgitation: a long diastole provides more time for backward flow, while hypertension increases the driving force.

Forward stroke volume is the difference between total stroke volume and regurgitant volume. LVEF calculated from ventricular volumes includes total ejection and may appear normal even when effective output and contractility are already reduced. Therefore, in severe regurgitation an LVEF only slightly above the limits of the healthy population is not necessarily reassuring.

Chronic mechanical stress activates metalloproteinases, collagen remodeling, neurohormonal signaling and cell death. Interstitial fibrosis progressively increases stiffness; replacement fibrosis creates a substrate that is more difficult to reverse. Longitudinal strain may decline before LVEF because subendocardial fibers are particularly vulnerable.

End-systolic volume reflects both loading conditions and the ability of the ventricle to empty. A serial increase in LVESVi is associated with worse outcomes and may be more reproducible than diameter in cavities that have remodeled nonuniformly. End-systolic diameter remains, however, the measure on which historical indications are based and must be obtained using rigorous technique.

The transition phase begins when filling pressures rise, contractile reserve declines and effective output falls. The change becomes especially evident during exercise, when the ventricle can no longer reduce end-systolic volume and the rise in capillary pressure causes dyspnea, while resting measurements may still remain near the limits of normality.

Progression is not uniform. Etiology, severity, blood pressure, sex, body size, aortic compliance and myocardial disease all influence chamber dimensions. Women may develop significant damage at smaller absolute diameters; indexing to body surface area reduces, without eliminating, the risk of underestimation.

Sudden deterioration in a chronic lesion suggests superimposed endocarditis, rupture of a fenestration, dissection, ischemia or arrhythmia. The condition becomes acute-on-chronic: the ventricle is dilated, but the new amount of regurgitation exceeds its reserve and produces pulmonary edema or shock.

Remodeling also involves the left atrium. In early stages the atrium may be less dilated than in mitral regurgitation because it receives the load only through the rise in ventricular filling pressures; with diastolic dysfunction and functional mitral regurgitation, atrial volume and pressure increase. Atrial size is therefore an indicator of chronicity and loading, not a direct measure of the severity of aortic regurgitation.

The right ventricle is initially spared until increasing pulmonary pressure imposes an additional load. In late stages, pulmonary vasoconstriction and remodeling cause right-sided overload, and annular dilation may add tricuspid regurgitation: a multichamber progression indicating that the optimal window for isolated correction has already been passed.

Symptoms, clinical examination and natural history

During the long compensated phase, patients may perceive a forceful heartbeat in the chest or neck without functional limitation. A gradual reduction in activity may mask symptoms; asking about reproducible activities and comparing them over time is more reliable than a generic question. Family members and activity devices may document an unrecognized decline.

Exertional dyspnea results from increased filling pressures and inability to augment forward output. Fatigue and reduced endurance are equally important. Orthopnea, paroxysmal nocturnal dyspnea and edema indicate an advanced stage, often accompanied by dysfunction and functional regurgitation of the atrioventricular valves.

Palpitations may reflect the large stroke volume or ectopic beats. Angina may occur because of reduced diastolic coronary perfusion pressure and increased demand from the hypertrophied ventricle, with or without coronary artery disease. Syncope is atypical and should prompt evaluation for arrhythmias, concomitant stenosis or nonvalvular disorders.

Examination may show a broad displaced apical impulse, a brisk collapsing pulse and a wide pulse pressure. The murmur is early diastolic, decrescendo and high-pitched; in chronic disease, duration tends to correlate with severity more than intensity does. Blood pressure, vascular stiffness and jet direction can alter its audibility.

The Austin Flint murmur is a mid-diastolic apical murmur caused by interaction of the regurgitant jet with the anterior mitral leaflet and transmitral filling flow. A systolic murmur at the base may reflect high flow and does not automatically imply stenosis. A third heart sound and crackles indicate increased volume and pressure.

The natural history of asymptomatic patients with normal LVEF and dimensions is relatively favorable under surveillance, but is not benign. The likelihood of symptoms or an indication for intervention increases with severity, age, chamber dimensions and rate of change. Observational studies show that waiting until volumes become very large reduces postoperative recovery and survival.

Exercise testing is useful when asymptomatic status is uncertain. Reproducible symptoms, lower-than-expected exercise capacity or an abnormal hemodynamic response alter assessment. Exercise echocardiography may show absent reserve and increased pressures, but these data complement rather than replace validated indications.

BNP and NT-proBNP reflect wall stress and filling pressures. Persistently elevated or rising values are associated with higher risk, but depend on age, rhythm, renal function and obesity. They should be compared serially in the same patient and not used as an isolated trigger for surgery.

Quality of life should be assessed with specific questions. A young patient may continue sedentary work but give up sport; an older patient may report stability because he or she no longer leaves home. A change in NYHA class is late and coarse. Walking distance, oxygen consumption and achieved workload provide more sensitive information in uncertain cases.

A very wide pulse pressure also depends on arterial compliance. In an older person with stiff arteries, high systolic pressure may coexist with a diastolic pressure that is not particularly low; in a young person with compliant arteries, peripheral signs may be striking. Physical examination suggests the hemodynamic state but does not reliably grade regurgitation.

Echocardiography, magnetic resonance and severity criteria

Echocardiography should answer four questions: which structure is diseased, which mechanism creates the regurgitant orifice, how much blood regurgitates, and how the ventricle and aorta are responding. The mere presence of color Doppler flow does not define clinically significant disease; small physiologic or trivial jets are common.

Morphology distinguishes tricuspid, bicuspid or unicuspid valves, prolapse, retraction, perforation, calcification and root dilation. An eccentric jet directed toward the septum often suggests right coronary cusp prolapse; the relationship is not absolute and should be confirmed by visualizing the free edge.

The vena contracta is relatively independent of the driving pressure, and a width greater than 6 mm supports severe regurgitation, whereas less than 3 mm supports mild regurgitation. In oblique or multiple jets, or with a noncircular orifice, one-dimensional measurement loses accuracy. Three-dimensional vena contracta may help, but image quality and cutoffs are not uniform across platforms.

PISA derives EROA and regurgitant volume from flow convergence. In the aortic position the convergence zone is often constrained, eccentric and difficult to align; errors in radius are amplified because the radius is squared. EROA of at least 30 mm² and regurgitant volume of at least 60 mL are criteria for severe regurgitation when measurement is technically reliable.

Comparison between stroke volume in the left ventricular outflow tract and at another valve can be used to calculate regurgitant volume and fraction. Errors in diameter measurements propagate, and multiple valve lesions invalidate the assumption. A regurgitant fraction of at least 50% is severe and has direct physiological meaning: at least half of total stroke volume does not contribute to net forward output.

Holodiastolic flow reversal in the descending aorta, especially with an end-diastolic velocity greater than 20 cm/s, is a strong sign. Its presence in the abdominal aorta further increases specificity. Age, arterial compliance, branch-vessel patency and heart rate should be taken into account.

The criteria that, when concordant and technically valid, define severe chronic regurgitation are:

• Morphology showing a large coaptation defect, flail cusp or perforation.
• Vena contracta greater than 6 mm.
• EROA at least 30 mm².
• Regurgitant volume at least 60 mL per beat.
• Regurgitant fraction at least 50%.
• Holodiastolic flow reversal prominent in the descending aorta.
• Ventricular dilation consistent with significant chronic volume overload.

A pressure half-time below 200 ms supports severe regurgitation and above 500 ms supports mild regurgitation, but it depends on compliance and pressure. The jet deceleration slope may steepen with diastolic dysfunction without an increase in orifice size. It should not be the decisive parameter in a hypertensive patient treated during the study or in a stiff ventricle.

Diameters and volumes should be indexed and compared serially. LVESD is measured perpendicular to the long axis while avoiding obliquity; biplane 2D Simpson and 3D methods calculate volumes. A small change within technical variability is not progression; use of the same laboratory and review of prior images improve reliability.

Cardiac magnetic resonance provides the best reproducibility for volumes and mass and directly quantifies aortic regurgitant flow with phase-contrast imaging. It is indicated when an eccentric jet limits echocardiographic assessment, parameters are discordant, or the decision depends on small differences. Regurgitant fraction and volume predict progression, although thresholds do not perfectly overlap with echocardiographic cutoffs.

CMR also characterizes focal fibrosis with late gadolinium enhancement and interstitial fibrosis with mapping. The presence of scar supports more advanced myocardial damage, but there is not yet a fibrosis threshold that by itself mandates intervention. CT or MR angiography completes assessment of the aortic root and aorta.

Global longitudinal strain may identify impaired subendocardial function despite preserved LVEF. The value depends on vendor, image quality, loading conditions and the normal reference range; serial changes on the same system are more credible than a single cutoff. Reduced GLS strengthens concern but does not replace symptoms or guideline thresholds.

Quantification should be performed with blood pressure under control. Marked hypertension increases regurgitation and jet size; recent vasodilation may reduce them. Reports and serial comparisons should document blood pressure and rhythm, because a hemodynamic change does not necessarily represent an anatomical change.

With multiple jets, total EROA is the sum of the individual orifices and a single vena contracta measurement underestimates the lesion. In bicuspid valves the jet is often eccentric; with a dilated root it may be central and broad. Consistency among method, mechanism and remodeling avoids false precision.

Surveillance and timing of intervention

Symptomatic severe regurgitation requires surgery when the patient is operable, regardless of LVEF. Symptoms should be attributed carefully, but once the relationship has been established, further dilation should not be awaited. Delay exposes the patient to heart failure and incomplete recovery.

In asymptomatic patients, the 2025 ESC/EACTS guidelines recommend surgery with LVEF ≤50%, LVESD >50 mm or LVESDi >25 mm/m², particularly in patients with a small body size. Surgery is also recommended when severe regurgitation accompanies an indication for CABG or aortic surgery.

The earlier recommendation is deliberately selective: surgery may be considered in low-risk patients with LVEF ≤55%, LVESDi >22 mm/m² or LVESVi >45 mL/m². The class IIb level reflects observational evidence and balances prevention of myocardial damage against operative mortality, prosthesis durability and lifetime reinterventions.

The trend can make a value below threshold clinically urgent. Progressive increase in end-systolic volume, reproducible decline in LVEF, worsening strain, rising BNP or symptoms during exercise should lead to Heart Team discussion. An unexpected measurement should first be verified to avoid surgery based on error.

Repair is preferable when an expert center expects a durable result. Prolapse of a noncalcified cusp and root dilation with preserved tissue are favorable scenarios; retraction, calcification and multiple fenestrations reduce the likelihood of durable repair. Repair should achieve a broad coaptation surface and stabilize the annulus and root.

Valve replacement is appropriate when repair is not reliable. Prosthesis selection is a lifetime decision. A mechanical prosthesis offers durability but requires a vitamin K antagonist; a bioprosthesis avoids permanent anticoagulation in the absence of another indication, but degenerates and may necessitate a later procedure.

TAVI is not standard therapy for operable adults with pure aortic regurgitation. Lack of calcium, a large annulus and associated aortopathy impair anchoring. It may be considered in a symptomatic patient with severe regurgitation who is judged inoperable and has suitable anatomy, preferably with dedicated systems and in a center able to manage embolization or conversion to surgery.

Treatment of hypertension reduces additional afterload. ACE inhibitors, angiotensin receptor blockers or dihydropyridines are rational choices according to comorbidities; standard heart-failure therapy is used when LVEF is reduced. In normotensive asymptomatic patients, vasodilators have not been shown to alter the natural history sufficiently to replace intervention.

In asymptomatic severe regurgitation far from intervention thresholds, clinical review and echocardiography are generally performed annually. When LVEF or chamber dimensions approach the limits, follow-up is performed every three to six months. Mild-to-moderate regurgitation is followed at longer intervals, adjusted according to aortic dimensions, etiology and progression.

Surveillance includes instructions about symptoms and blood-pressure measurement, not merely a scheduled echocardiogram. Any new dyspnea, decline in performance, edema or angina should prompt earlier reassessment. A dilated aorta requires imaging of its entire course and intervals based on diameter and growth rate.

The presence of coronary artery disease modifies both the procedure and prognosis. Coronary assessment precedes surgery according to age and pretest probability, using CT or invasive angiography. A need for revascularization may bring forward intervention for severe valve disease, while diffuse coronary disease increases risk and may account for part of the symptom burden.

Discussion of prosthesis choice should precede hospital admission. Anticoagulation, pregnancy plans, occupation, sport, bleeding risk, durability and the possibility of valve-in-valve procedures have different implications. In a young patient, an apparently simple choice determines a sequence of procedures rather than only the current operation.

Outcomes, complications and special situations

After timely correction, ventricular volumes and mass decrease. Reverse remodeling is greatest during the first months and may continue thereafter; a markedly dilated or fibrotic ventricle may remain abnormal. A baseline postoperative echocardiogram helps distinguish a pre-existing residual abnormality from new deterioration.

The complication of waiting too long is irreversible dysfunction. Once reserve has been lost, even technically perfect surgery may leave persistent heart failure. Chronic congestion promotes pulmonary hypertension, right ventricular dysfunction, tricuspid regurgitation, and renal and hepatic impairment.

Atrial fibrillation and ventricular arrhythmias are favored by dilation and scar. Anticoagulation follows thromboembolic risk and prosthesis type; valve replacement does not automatically eliminate the arrhythmic substrate. Syncope and tachyarrhythmias require independent evaluation.

Endocarditis may abruptly increase severity and produce an acute-on-chronic presentation. Persistent fever, a new embolic event or rapid deterioration require blood cultures and echocardiography. Antibiotic prophylaxis is reserved for high-risk categories, whereas oral hygiene and treatment of infectious foci are universal measures.

During pregnancy, reduced systemic vascular resistance may make regurgitation better tolerated than stenosis when ventricular function and the aorta are normal. Plasma-volume expansion and the postpartum period can nevertheless precipitate congestion; associated aortopathy adds a risk of dissection. Preconception assessment should define valve status, ventricular status, aortic root dimensions and genotype when indicated.

Moderate dynamic exercise is generally acceptable in nonsevere disease with normal function. Severe regurgitation, marked dilation or aortopathy require individualized exercise prescription and caution with high-intensity static exertion. Exercise testing can provide an objective baseline.

Prognosis depends less on the label of chronic disease than on the myocardial stage at the time of correction. Careful surveillance, reproducible measurements and early discussion of options help prevent advanced heart failure from becoming the first recognized manifestation.

After replacement, a bioprosthesis requires surveillance for structural valve deterioration and a mechanical prosthesis requires monitoring of anticoagulation. After repair, residual regurgitation, coaptation, and annular and root dimensions are assessed. Progression from mild to moderate regurgitation is not merely an incidental finding: the mechanism and rate of progression should be defined.

Optimal management is a continuous sequence: etiologic diagnosis, baseline measurement, serial comparison, recognition of transition and intervention before irreversible damage. Loss to follow-up is one of the most concrete risks of the long asymptomatic phase and should be prevented through recall systems and clearly assigned clinical responsibility.