Julius I. Ejiofor and Ashraf A. Sabe
This chapter is a revision and update of that included in the previous editions of the TSRA Review written by Amjad Syed (2nd edition), Ravi K. Ghanta (1st edition), and Bryan M. Burt (1st edition).
Background
Aortic insufficiency (AI) is the regurgitation of blood across the aortic valve which results in diastolic reflux of blood from the aorta into the left ventricle. It can be acute or chronic.
Mechanisms of AI
Mechanisms of aortic insufficiency can be divided into two main categories: functional aortic annular (ventricular/aortic junction) and primary leaflet pathology. Functional aortic annular regurgitation results from an imbalance of cusp to annular dimensions. Potential causes include aortic dissection, aortic root aneurysm, connective tissue disorders. Primary aortic leaflet pathology may be caused by calcific or myxomatous degeneration, congenitally bicuspid, infective endocarditis, rheumatic disease, and anorectic medications [fenfluramine and phenteramine]).
Pathophysiology
In acute AI, the regurgitant blood into the LV in diastole causes a sudden increase in LVEDV and reduces effective or forward stroke volume. This leads to rapid rise in LVEDP leading to increased mean LA and pulmonary venous pressures, producing varying degrees of pulmonary edema. In the acute setting, two compensatory mechanisms attempt to maintain and effective cardiac output: increased contractility due to the Frank-Starling mechanism (increase LVEDV), and an increased HR.
In contrast, chronic AI is a slow, insidious process, leading to numerous compensatory mechanisms to maintain cardiac output for a long time, hence keeping the patient asymptomatic for a long time. Eventually, as the LV enlarges, heart failure ensues and the patient manifests symptoms.
Causes of acute AI include infective endocarditis, aortic dissection, and trauma while causes of chronic AI include cusp calcific or myxomatous degeneration, aortic and aortic root aneurysms.
Diagnosis
Physical exam
A widened pulse pressure occurs due to augmentation of the total cardiac output resulting in distention of peripheral arterial system followed by quick collapse secondary to regurgitant flow through AV. Clinically, this manifest through many eponymous signs such as a water-hammer pulse, De Musset sign (head bobbing), Quincke’s pulses (alternating flushing and blanching of the nails), and pistol shot sounds (shot-like sounds heard over the femoral arteries). On auscultation the typical murmur heard with AI is a diastolic decrescendo murmur.
Echocardiography
TTE is the diagnostic modality of choice. Severity of AI is determined by jet width (as % of LVOT diameter), vena contracta width (narrowest diameter of the jet), regurgitant volume, regurgitant fraction, and effective regurgitant orifice area. Diastolic blood flow reversal may be noted in the descending aorta. AI is classified as severe when the jet width is >65% of the LVOT, the vena contracta is >0.6 cm, the regurgitant volume is ≥60 ml per beat, the regurgitant fraction is ≥50%, and regurgitant orifice area is ≥0.30 cm2. AI is also severe if the pressure half-time is <300ms.
Classification of AI
Analogous to Carpentier’s classification for mitral valve disease, El Khoury devised a classification system to categorize the etiology of AI. The classification provides a systematic approach to guide repair techniques.
Class I: Normal cusp motion with FAA dilation or cusp perforation
- Class Ia: Proximal ascending aorta dilation (STJ)
- Class Ib: Proximal dilation (sinuses of Valsalva) and Distal dilation (STJ)
- Class Ic: Isolated FAA dilation (dilation of the ventriculo-aortic junction)
- Class Id: Cusp perforation and FAA dilation
Class II: Cusp prolapse: due to excessive cusp tissue or due to commissural disruption e.g., aortic dissection
Class III: Cusp restriction: leaflet/cusp retraction/thickening e.g., bicuspid or degenerative or fibrosing disease (Reiter’s syndrome, Ankylosing spondylitis)
It is worth noting that two or more simultaneous pathologic mechanisms may occur in a given patient leading to a component of both central and eccentric regurgitation.
Stages of AR according to the 2020 AHA/ACC guidelines:
- At risk (bicuspid or sclerotic valve with normal hemodynamics)
- Progressive (mild-moderate AR with normal LVEF, possible LV Dilation)
C1) Asymptomatic normal LVEF (≥55%) and mild to moderate LV dilation (LVESD <50 mm).
C2) Asymptomatic abnormal LV systolic function (LVEF <55) or severe LV dilation (LVESD 50 mm or indexed LVESD >25 mm/m2)
D) Symptomatic severe AR (LVEF >55%), mild to moderate LV dysfunction (LVEF 40% to 55%), or severe LV dysfunction (LVEF <40%)
Valve guidelines for AI
Current recommendations for management of chronic AI depend on the presence of symptoms, LV function, and LV dimensions. Patients with severe AI with symptoms or an EF ≤55% should undergo aortic valve repair or replacement (Class I). Isolated AV surgery is currently not recommended for patients who are asymptomatic, even with severe chronic AI, as long as they have normal LV function and LV dimensions. In asymptomatic patients with normal function (EF>50%), it is reasonable to perform surgery when the LV end-systolic diameter (LVESD) >50 mm (Class IIa) or LV end-diastolic diameter (LVESD) >65mm(Class IIb).
Patients with acute AI will have symptoms and management of acute AI is by early aortic valve repair or replacement. Vasodilators and inotropic agents, which augment forward flow and reduce LVEDP, may be helpful to manage the patient temporarily prior to surgery.
Surgical treatment
Acute severe AI typically requires early or immediate surgical intervention (repair or replacement) as these patients are typically quite symptomatic. Current recommendations for management of chronic AI depend on the presence of symptoms, LV function, and LV dimensions as stated above. Patients with AI with and without aortic root aneurysms have traditionally been treated with isolated aortic valve replacement or composite valve and root replacement (Bentall procedure) or with valve sparing root replacement. See chapter on aortic stenosis and aortic root aneurysm for technical details of these procedures. Here we focus on techniques for aortic valve preservation and repair, which promises to substantially reduce the shortcomings of both bioprosthetic and mechanical replacement prostheses, while improving long term survival and patient quality of life. It is important to note that transcatheter aortic valve replacement is not approved for pure isolated AI without aortic stenosis.
Aortic valve repair techniques
Cusp repair techniques
AI due to cusp perforation as in cases of resected fibroelastomas, fenestrations, or healed endocarditis can be repaired with a simple patch of autologous pericardium.
Repair of prolapsed cusp can be achieved by free margin plication or free margin resuspension, resulting in shortening. The degree of plication is determined using the other normal cusps as reference. Commissuroplasty can also be considered.
When AI is due to cusp restriction from focal calcification, this can be repaired by cusp shaving decalcification, and/or resection and patching (cusp extension). More significantly restricted or fused leaflets may require commissurotomy.
Aortic valve repair for AI in bicuspid AV is an emerging field and detailed repair techniques are beyond the scope of this review, as geometric orientation needs to be factored in.
Aortic valve annuloplasty
Early results of aortic valve repair showed that patients with circumferential annular stabilization have better results with lower incidence of late failures. Therefore, annular stabilization techniques should be used with the above cusp repair techniques to achieve long-term durability. For patients with root aneurysms, the valve-sparing root replacement using the reimplantation technique (by Tirone David) provides circumferential external annular stabilization (see aortic root chapter).
Subcommisural annuloplasty with pledgetted sutures with or without geometric ring has also been employed to reduce the circumferential length of the VAJ and stabilize the annulus. In the US, the HAART aortic annuloplasty device (Biostable Science & Engineering, Austin, TX) is a commercially available internal annuloplasty device designed to restore root geometry and provide annular stabilization. External annuloplasty devices are not commercially available in the United States. Several centers use Dacron grafts to serve as customized external annuloplasty rings. Four or five rings of the graft are cut and serve as the ring.
Outcomes
Early outcomes of aortic valve repair operations at high volume, experienced centers have been excellent. Several published series have demonstrated that these procedures can be done safely and with low mortality and morbidity, in carefully selected patients. Long-term durability for the varying techniques in isolated aortic valve repair remains an important area of study with opportunity for significant improvement.
Suggested Readings
- 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):286–94.
- Boodhwani M, El Khoury G. Aortic valve repair: indications and outcomes. Curr Cardiol Rep. 2014;16(6):490.
- Nishimura RA, Otto CM, Bonow RO et al. 2020 AHA/ACC Guideline for the Management of Patients with Valvular Heart Disease. J Am Coll Cardiol. 2021;77(4):e25-e197.
- David, Tirone E. “Aortic Valve Repair and Aortic Valve-Sparing Operations.” Cardiac Surgery in the Adult, 5e Eds. Lawrence H. Cohn, and David H. Adams. McGraw-Hill, 2017
- Arnaoutakis, George, Bavaria, Joseph “Aortic Valve Repair.” Rob & Smith’s Operative Cardiac Surgery, 6th Eds. Thomas L. Spray, and Michael A. Acker. CRC Press, 2019.
