Residency · Residency · Cardiothoracic Surgery

Aortic Regurgitation: Repair and Replacement Strategies

Overview

Aortic regurgitation (AR) produces chronic volume overload that, if uncorrected, leads to irreversible left ventricular dilatation and systolic dysfunction. Unlike aortic stenosis, the timing of intervention in chronic AR is more nuanced, requiring careful surveillance of ventricular dimensions and function. This chapter covers the mechanisms of AR, indications for surgery, principles of aortic valve repair, and when replacement is preferred.

Etiology and Mechanisms

Leaflet (Cusp) Pathology

Several conditions cause AR through intrinsic leaflet disease. Bicuspid aortic valve can produce cusp prolapse from asymmetric leaflet stress or raphe calcification. Degenerative disease causes myxomatous changes leading to cusp prolapse, analogous to mitral valve prolapse. Rheumatic disease produces leaflet retraction and commissural fusion, causing central regurgitation. Endocarditis can create leaflet perforations or vegetations that prevent proper coaptation.

Root and Annular Pathology

AR frequently results from disease of the aortic root rather than the leaflets themselves. Aortic root aneurysm dilates the sinuses of Valsalva, pulling the commissures apart and causing central AR. Annuloaortic ectasia stretches the annulus beyond the leaflets' ability to coapt. Type A aortic dissection can produce AR when the dissection flap prolapses through the valve or distorts commissural geometry. Connective tissue disorders such as Marfan and Loeys-Dietz syndromes cause progressive root dilatation with secondary AR.

AR Etiology Summary

Carpentier-Inspired Functional Classification of AR

AR mechanisms are classified analogously to the Carpentier system used for the mitral valve. Type I involves normal cusp motion with a central jet, caused by annular or root dilatation or leaflet perforation. Type II involves cusp prolapse from excess tissue or an elongated free edge. Type III involves restrictive cusp motion from calcification, fibrosis, or retraction. This classification provides a systematic framework for planning repair.

Carpentier-Inspired Classification of AR

Pathophysiology

Chronic AR

In chronic AR, the regurgitant volume returns to the LV during diastole, creating volume overload. The ventricle compensates with eccentric hypertrophy, dilating to accommodate the increased end-diastolic volume. Total stroke volume increases to maintain forward cardiac output. Eventually, myocardial fibrosis develops, systolic function declines, and symptoms appear. Importantly, the LV can tolerate chronic AR for years before decompensation — a "long compensated phase" that makes timing of surgery challenging.

Acute AR

Acute AR is an entirely different clinical entity. Sudden volume overload falls on a non-adapted LV with normal compliance and normal size. The rapid increase in LV end-diastolic pressure causes pulmonary edema and cardiogenic shock. Causes include endocarditis, aortic dissection, and trauma. Acute severe AR is a medical emergency requiring urgent or emergent surgery.

Acute vs. Chronic AR Comparison

Hemodynamic Hallmarks

The hallmark of chronic AR is a wide pulse pressure (high systolic, low diastolic). Numerous eponymous physical signs reflect this: the water-hammer pulse of Corrigan, pistol-shot femorals (Traube sign), and head bobbing (de Musset sign). The Austin Flint murmur is a low-pitched diastolic rumble caused by the regurgitant jet impinging on the anterior mitral leaflet.

Indications for Surgery

ACC/AHA 2020 Guidelines

Class I indications include symptomatic severe AR (dyspnea, angina, heart failure), asymptomatic severe AR with LVEF at or below 55%, and severe AR in patients undergoing other cardiac surgery. Class IIa indications include asymptomatic severe AR with LVESD above 50 mm (or indexed LVESD above 25 mm/m2) and asymptomatic severe AR with progressive LV dilatation (LVEDD above 65 mm) when surgical risk is low. Moderate AR in patients undergoing other cardiac surgery is a Class IIb indication.

Timing: The Challenge of Chronic AR

The goal is to operate before irreversible LV dysfunction develops. Serial echocardiography every 6 to 12 months is needed for severe asymptomatic AR. Exercise testing can unmask symptoms in borderline cases. Cardiac MRI provides accurate LV volumes when echocardiographic findings are equivocal.

Aortic Valve Repair

Rationale for Repair

Repair avoids prosthesis-related complications (thromboembolism, anticoagulation, endocarditis, structural valve deterioration) and preserves native valve hemodynamics with no gradient and laminar flow. A growing body of evidence supports durable long-term results in selected patients, though best outcomes are achieved at experienced centers with dedicated valve repair programs.

Patient Selection for Repair

Ideal candidates include patients with bicuspid or trileaflet valves with cusp prolapse and those with root dilatation but normal cusps. Less favorable candidates include those with severely calcified or retracted cusps (rheumatic disease) or extensive endocarditis destruction. Intraoperative assessment is critical, as the final repair decision is often made after direct valve inspection.

Repair Techniques

Cusp Repair

Several techniques address cusp pathology. Free-edge resuspension with PTFE neochordae shortens the prolapsing cusp (analogous to neochordae in mitral repair). Cusp plication folds excess tissue at the free edge. Cusp shaving thins thickened, fibrotic tissue to improve pliability. Patch repair with autologous or bovine pericardium addresses leaflet perforations from endocarditis. In bicuspid valves, raphe resection with midline plication creates a more symmetric opening.

Annuloplasty

Subcommissural annuloplasty uses pledgeted sutures at the commissural level to reduce annular diameter. External annuloplasty rings — circumferential or partial — stabilize the annulus and prevent re-dilatation, analogous to the mitral annuloplasty ring concept. Internal geometric annuloplasty achieves suture-based reshaping of the aortic annulus.

Root Remodeling and Reimplantation

When AR is secondary to root dilatation, root replacement with valve preservation is ideal. The Yacoub remodeling procedure replaces the sinuses while maintaining the native annulus. The David reimplantation procedure suspends the native valve inside a Dacron tube graft, fixing the annular diameter and preventing future dilatation.

Assessment of Repair

Intraoperative TEE assesses coaptation height (above 4 mm is ideal), effective height, and residual AR. An acceptable result is trace to mild AR immediately post-repair. A water test (filling the aortic root with saline) is performed before closing the aortotomy.

<image>Intraoperative illustration of aortic valve repair techniques for cusp prolapse. Panel A shows a surgeon's view of a trileaflet aortic valve with prolapse of the right coronary cusp, demonstrating the free-edge below the plane of the other cusps. Panel B shows free-edge resuspension using PTFE neochordae sutures to elevate the free edge to the correct coaptation plane. Panel C shows cusp plication with a horizontal mattress suture shortening the free edge. Panel D shows the post-repair result with symmetric coaptation of all three cusps. Coaptation height is measured and labeled (target > 4 mm).</image>

Aortic Valve Replacement for AR

When Replacement Is Preferred

Replacement is preferred when cusps are severely calcified or destroyed and not amenable to repair, in rheumatic disease with commissural fusion and leaflet retraction, with extensive endocarditis destruction (though some cases can be repaired with patches), at centers without expertise in aortic valve repair, and when an intraoperative repair attempt fails.

Technical Considerations Unique to AR

The annulus is often dilated, which must be accounted for during sizing. Aggressive debridement of calcium is critical to prevent paravalvular leak. In bicuspid valves with aortopathy, concomitant ascending aortic replacement should be considered if the diameter exceeds 4.5 cm.

Clinical Pearls

Chronic AR can be tolerated for years without symptoms, but the LV is silently dilating — serial imaging is mandatory to catch the transition from compensated to decompensated disease. The critical echocardiographic triggers for surgery in asymptomatic severe AR are LVEF at or below 55% and LVESD above 50 mm — do not wait for symptoms if these thresholds are met. Acute severe AR from dissection or endocarditis is a surgical emergency because the non-compliant LV cannot accommodate the sudden volume load, leading to rapid pulmonary edema and shock. Aortic valve repair is a viable and increasingly durable option for AR, particularly in bicuspid valve prolapse and root dilatation with normal cusps, but it requires dedicated expertise. When AR is caused by root dilatation, repairing only the cusps without addressing the root will lead to recurrence — valve-sparing root replacement (David) is the procedure of choice. The Carpentier-inspired classification of AR mechanisms (Type I, II, III) provides a systematic framework for repair planning. Coaptation height above 4 mm and effective height above 9 mm on post-repair TEE are strong predictors of durable repair.

References

• Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients with Valvular Heart Disease. Circulation. 2021;143(5):e72-e227.
• Boodhwani M, de Kerchove L, Glineur D, et al. Repair-oriented classification of aortic insufficiency: impact on surgical techniques and clinical outcomes. J Thorac Cardiovasc Surg. 2009;137(2):286-294.
• de Kerchove L, Boodhwani M, Glineur D, et al. Aortic valve repair: principles and results. Eur Heart J. 2019;40(26):2135-2142.
• David TE. Aortic valve sparing in different aortic valve and aortic root conditions. J Am Coll Cardiol. 2016;68(6):654-664.
• Aicher D, Fries R, Rodionycheva S, et al. Aortic valve repair leads to a low incidence of valve-related complications. Eur J Cardiothorac Surg. 2010;37(1):127-132.

Read this lecture as Markdown