Aortic Valve Replacement (AVR)

Overview

Aortic valve regurgitation (AVR) is defined as diastolic aortic blood reflux into the left ventricle (LV). Acute AR is characterized by significant pulmonary edema and hypotension and is considered a surgical emergency. Chronic severe AVR results in a combination of LV volume and pressure overload. It is accompanied by systolic hypertension and wide pulse pressure, which explain peripheral physical symptoms such bounding pulses.

Systolic hypertension causes an increase in afterload, which leads to progressive LV dilatation and systolic dysfunction. Echocardiography is the most significant diagnostic test for AVR. It enables the determination of the source of AVR as well as the severity of AR and its impact on LV size, function, and hemodynamics.

Many individuals with chronic severe AVR can live for years with normal LV function and no symptoms. These individuals do not require surgery, but they should be closely monitored for the onset of symptoms or LV dilation/dysfunction. Before the LV ejection fraction goes below 55% or the LV end-diastolic dimension reaches 55 mm, surgery should be considered.

Unless there are significant comorbidities or other contraindications, symptomatic individuals should have surgery. The major goal of vasodilator-based medicinal treatment is to postpone surgery in asymptomatic patients with normal LV function or to treat patients for whom surgery is not a possibility. 

The purpose of vasodilator treatment is to significantly lower systolic arterial pressure. Future therapeutics may concentrate on molecular pathways to avoid LV remodeling and fibrosis. 

 

Epidemiology of AVR

The frequency of chronic AVR and the occurrence of acute AVR remain unknown. Even in healthy individuals, tracing AVR by echocardiography is a common observation. It appears to impact men more than women (13 percent vs. 8.5 percent). AVR prevalence rises with age and is most common after the age of 50. The frequency of AVR in the United States is estimated to be between 4.9 and 10%. 

 

How AVR develops and causes clinical symptoms?

AVR induces an increase in the volume of the left ventricle. An increase in LV end-diastolic volume results in LV dilatation and eccentric hypertrophy. This enables for a higher stroke volume to be ejected. The total stroke volume expelled by the LV in AVR patients is the sum of the effective stroke volume and the regurgitant volume. As a result, AVR is linked to greater preload. According to Laplace's rule, LV dilatation raises LV systolic tension. This, together with the higher systolic blood pressure caused by the increase in total forward stroke volume, results in greater afterload.

The combination of LV dilation and hypertrophy compensates for LV function. However, as time passes, wall thickening fails to keep up with the hemodynamic load, resulting in a decrease in systolic function and ejection fraction.

The LV decompensates, resulting in reduced compliance and higher LV end-diastolic pressure and volume. Left atrial, pulmonary artery wedge, pulmonary arterial, right ventricular (RV), and right atrial pressures rise as the disease progresses, but effective (forward) cardiac output decreases. Due to pulmonary congestion, symptoms of heart failure such as dyspnea, orthopnea, and paroxysmal nocturnal dyspnea arise.

Greater LV mass necessitates increased myocardial oxygen use. In addition, the coronary perfusion pressure is lowered. Myocardial ischemia and exertional chest discomfort result as a result of this.

The compensatory mechanisms of the LV do not develop quickly enough in individuals with acute severe AR to accommodate the regurgitant volume burden. Rapid rises in LV diastolic pressures can result in abrupt pulmonary edema and cardiogenic shock. As a result of the abrupt acute rise in LV volume and pressure, even diastolic mitral regurgitation might develop. 

 

What are the possible causes of AVR?

AR is caused by aortic leaflet mal-coaptation caused by anomalies in the aortic leaflets, their supporting structures such as the aortic root and annulus, or both.

Primary Valve Disease:

Common causes include calcific aortic valve disease, which is usually associated with aortic stenosis (AS) but can be associated with some degree of AR; infective endocarditis, which changes the anatomy of the leaflets; and a tear or laceration in the ascending aorta, which leads to aortic cusp prolapse due to loss of commissural support.

AR can be caused by a congenitally bicuspid aortic valve (BAV) owing to insufficient closure or prolapse of the valve, while AS is a more common consequence of BAV. Less prevalent causes of congenital AR include unicommissural and quadricuspid valves, as well as fenestrated valve rupture.

Aortic cusp prolapse develops in certain people with ventricular septal defect (VSD). Rheumatic disease causes fibrous infiltration of the AV cusps, which causes retraction, preventing normal opening during systole and closure during diastole. The fusion of the commissures may result in mixed AS and AVR. Rheumatic mitral valve disease is frequently accompanied with rheumatic aortic valve disease.

Progressive AVR can also be caused by myxomatous aortic valve degeneration. Secondary AVR may arise from thickening and scarring of the AV leaflets caused by membranous subaortic stenosis. AVR has also been documented as a complication of percutaneous aortic balloon valvotomy and transcatheter aortic valve replacement procedures.

Valvular AVR is becoming more prevalent as a result of structural degradation of a bioprosthetic valve. Aortic cusp avulsion or rupture is a rare cause of acute AVR. Other less prevalent causes of AVR include systemic lupus erythematosus, Takayasu disease, Whipple disease, rheumatoid arthritis, ankylosing spondylitis, Jaccoud arthropathy, syphilis, Crohn disease, and appetite suppressing medications.

 

Primary Aortic Root Disease:

Aortic annular dilatation causes the AV leaflets to separate, resulting in AVR. Age-related alterations, cystic medial necrosis, which is frequently linked with Marfan syndrome, or osteogenesis imperfecta can all produce degenerative changes in the aortic root. Ankylosing spondylitis, Behcet disease, psoriatic arthritis, arthritis associated with reactive arthritis, ulcerative colitis, relapsing polychondritis, and giant cell arteritis are all related with aortic root dilation.

Severe, chronic systemic hypertension can dilate the aortic annulus, causing AVR to progress. Retrograde aortic dissection can include and disturb the aortic annulus, resulting in AVR.

 

What are the symptoms and physical signs in those with AVR?

By Medical History:

Chronic AVR symptoms emerge gradually, sometimes over decades. Exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, angina pectoris, palpitations, and head pounding are all symptoms. Nocturnal angina occurs when the heart beat slows during sleep, leading the arterial diastolic pressure to drop to dangerously low levels.

 

By Physical Examination:

As a result of systolic hypertension and reduced diastolic pressure, AVR is related with widened pulse pressure. The apical LV impulse is hyperdynamic and laterally and inferiorly displaced. A strong systolic thrill may be felt near the base of the heart, the suprasternal notch, and above the carotid arteries. The huge forward stroke volumes and low aortic diastolic pressure induce it.

S1 is normal, whereas S2 is either raised (because to a dilated aortic root) or lowered (when the aortic leaflets are thickened). A high-frequency, blown, decrescendo diastolic murmur can be heard best in the third intercostal gap at the left sternum border. The murmur of AR is easier to detect near the end of expiration when the patient is leaning forward.

The murmur increases with squatting or isometric activity and reduces with blood pressure-lowering procedures. With moderate AVR, this murmur is early diastolic and progresses to holodiastolic with severe AVR.

Peripheral Signs of severe chronic AVR results from a widened pulse pressure are described below:

• Austin Flint murmur: Low pitched rumbling mid-diastolic murmur heard best at the apex. It is thought to be caused by premature closure of the mitral valve due to the jet of AR.
• Becker sign: Presence of visible pulsation of retinal arteries through an ophthalmoscope
• Bisferiens pulse: Biphasic pulse due to the backflow of blood in early diastole
• Corrigan sign: Water-hammer pulse with abrupt distention and quick collapse.
• de Musset sign: Head bobbing with each with arterial pulsation.
• Duroziez sign: Systolic murmur heard over the femoral artery when it is compressed proximally and a diastolic murmur when it is compressed distally with a stethoscope.
• Gerhardt sign: Pulsations of the spleen are detected in the presence of splenomegaly.
• Hill sign: Blood pressure in the lower extremity is greater than blood pressure in the upper extremity
• Mayne sign: Drop of diastolic blood pressure of greater than 15 mmHg on raising the arm
• Muller sign: Systolic pulsation of the uvula
• Quincke sign: Capillary pulsation (flushing and paling best seen at the root of the nail when pressure is applied to the tip of the nail).
• Rosenbach sign: Pulsation of the liver
• Traube sign: Booming "pistol-shot" systolic and diastolic sounds heard over the femoral artery
• It should be noted that these eponymous signs have varying sensitivities and specificities. Evidence regarding the impact of severity of aortic regurgitation on the manifestation of these signs is sparse.

In acute AVR, symptoms and physical findings are related to decreased stroke volume. Patients present with tachycardia, tachypnea, and pulmonary edema. Because the physical examination findings of acute AR are subtler than those of chronic AR, the diagnosis is difficult to make when a patient presents with dyspnea and shock. A high index of suspicion is essential for rapid diagnosis.

 

How AVR is evaluated and diagnosed?

The workup of aortic regurgitation includes the following tests.

• Echocardiography

The primary diagnostic technique is echocardiography, which gives an accurate evaluation of the aortic valve architecture, aortic root anatomy, and the LV.

Chronic AVR is characterized by left ventricular dilation. Until later phases, systolic function is normal, as shown by a drop in EF or an increase in end-systolic dimension.

With severe AVR, the central jet width is greater than 65 % of the LV outflow tract (LVOT), the regurgitant volume is 60 mL/beat, the effective regurgitant orifice area is greater than 0.30, the regurgitant fraction is 50%, the vena contracta is greater than 0.6 cm, and there is diastolic flow reversal in the proximal descending thoracic aorta.

In individuals with severe AVR, the continuous-wave Doppler profile of the AVR jet indicates a quick deceleration time. A high slope implies that pressures between the aorta and LV equalize more quickly during diastole.

In both acute and chronic AVR, a high-frequency diastolic flapping of the anterior mitral leaflet caused by the impact of the regurgitant jet may be seen.

A bedside transthoracic 2-dimensional and M-mode echocardiography (TTE) and/or transesophageal echocardiogram (TEE) can be used to diagnose acute AR (TE).

• Cardiac Magnetic Resonance

Cardiac MRI (CMR) is an alternate diagnostic method that is particularly useful in individuals who require further assessment despite echocardiography due to inadequate acoustical windows. It is the most precise noninvasive method for determining LV end-systolic volume, diastolic volume, and mass. The antegrade and retrograde flow volumes in the ascending aorta can be used to precisely estimate the severity of AVR.

• Cardiac Catheterization

If there is a disagreement between the clinical presentation and noninvasive imaging, angiography can offer information regarding the severity of AVR, hemodynamics, and coronary artery architecture. It entails injecting contrast material into the aortic root quickly and recording the right and left anterior oblique projections.

 

How AVR is treated?

Acute AVR:

Emergency surgery is recommended for severe acute AVR. Medical treatment is restricted and is only utilized to briefly stabilize the patient. To enhance forward flow, intravenous diuretics and vasodilators (such as sodium nitroprusside) are used to reduce afterload. To improve cardiac output, inotropes such as dopamine or dobutamine may be utilized. Beta-blockers are avoided because they lower CO and slow the heart rate, giving the LV more time to diastolic fill. Intra-aortic balloon counterpulsation is not recommended.

Surgery may be postponed in patients with acute AVR caused by active infective endocarditis who have been hemodynamically stable for 5 to 7 days after starting antibiotics. However, if hemodynamic instability or abscess development occurs, the procedure must be performed.

 

Chronic AVR:

Monitoring throughout the disease course: Asymptomatic individuals with mild or moderate AVR and normal cardiac size should be clinically and echocardiographically evaluated every 12 or 24 months. Asymptomatic patients with persistent severe AVR and normal LV function should be evaluated every 6 months.

Medical therapy: There are few indications for medical treatment in AVR. Vasodilator treatment should be used to treat systemic arterial hypertension associated with chronic AVR. It is preferable to use dihydropyridine calcium channel blockers or angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEIs/ARBs).

• Staging of Chronic AR: Chronic AR is classified into 4 stages based on the 2020 ACC/AHA Guideline for the Management of Patients with Valvular Heart Disease:
• Stage A: Patients at risk for AR. These patients have no hemodynamic consequences or symptoms.
• Stage B: Progressive AR. Patients have mild to moderate AR but normal LV systolic function and no clinical symptoms.
• Stage C: Asymptomatic severe AR. Patients will have AR jet width greater or equal to 65% of the left ventricular outflow tract (LVOT). Stage C is subclassified further depending on LV systolic function as :

1. C1: Normal LVEF (>50%) and mild to moderate LV dilation (LVESD <50 mm).
2. C2: Reduced LVEF (<50%) with severe LV dilation (LVESD >50 mm).

• Stage D: Symptomatic severe AR. Findings of severe AR jet on echocardiography. It can have either normal or abnormal LVEF. Symptoms include exertional dyspnea, angina, or heart failure.

 

Surgical treatment: Treatment guidelines for AR are based on the 2020 American Heart Association/American College of Cardiology recommendations. Aortic valve replacement (AVR) is the preferred therapy for individuals with severe symptomatic chronic AR and severe asymptomatic chronic AVR with LV systolic failure (LVEF 50 percent).

 

AVR is also a viable choice for individuals with severe AVR who are asymptomatic and have normal LV function (LVEF 50 percent) but have substantial LV dilatation (LVESD index >25 mm/m2 or LVESD >50 mm).

AVR can also be explored for patients with severe AVR who are asymptomatic and have normal LV systolic function at rest (LVEF 50 percent, stage C1) but have increasing significant LV dilatation (LV end-diastolic dimension >65 mm) given the procedure's minimal surgical risk.

Despite the fact that the guidelines recommend valvular surgery when symptoms, left ventricular systolic dysfunction, or left ventricular dilatation develop, newer studies that show evidence of subclinical myocardial dysfunction and irreversible myocardial fibrosis in patients with chronic AR call the current recommendations on the timing of intervention into question. 

 

Prognosis of AVR

Acute AVR:

The operational risk in acute severe aortic regurgitation is significantly higher than in chronic severe aortic regurgitation. Patients with acute AVR often have aggravating conditions such as infective endocarditis or a dissecting aneurysm, which reduces their prognosis.

Chronic AVR:

Even if the AVR is severe, asymptomatic chronic AVR is commonly linked with a generally positive prognosis for many years. Quantitative measurements of AVR severity, as well as LV size and systolic function, are good predictors of clinical prognosis. If LV dysfunction is discovered early, before EF drops significantly, before LV dilation, and before symptoms arise, it is more likely to be reversible. Surgery is required before permanent alterations occur because surgery improves cardiac death rates in high-risk individuals.

When an AVR patient becomes symptomatic, his or her condition rapidly deteriorates. Congestive cardiac failure, acute pulmonary edema, and abrupt death are all possibilities. Only 30% of individuals with NYHA Class III or IV symptoms survive four years without surgery.

 

Complications of AVR

The early stages of chronic AR are subclinical, and there may be no indications or symptoms. However, as the disease advances, it has an impact on cardiac hemodynamics and functioning. It can cause progressive left ventricular systolic dysfunction, congestive heart failure, ischemic cardiomyopathy, arrhythmia, and possibly abrupt death. In individuals with congestive symptoms or exercise intolerance, the advantages of surgery exceed the dangers; consequently, valve surgery is well warranted to prevent problems.

 

Conclusion

Aortic valve regurgitation (AVR) is a valvular heart disease characterized by inadequate aortic valve closure, resulting in blood reflux from the aorta into the left ventricle (LV) during diastole.

Aortic regurgitation can be acute (due to bacterial endocarditis or aortic dissection) or chronic (due to a congenital bicuspid valve or rheumatic fever), and it can be caused by a valvular defect or an aortic abnormality.

Most instances of acute AVR result in fast decrease of LV function, followed by pulmonary edema and cardiac decompensation. Chronic AR can be compensated for a long time and only become symptomatic when left heart failure occurs.

An S3 and a high-pitched, decrescendo early diastolic murmur are heard on auscultation. A widened pulse pressure is another distinguishing diagnostic feature. The most significant diagnostic tool, both for establishing the diagnosis and assessing the degree of illness, is echocardiography.

Conservative therapy for asymptomatic individuals comprises of symptom control and physical activity as tolerated. Patients who are symptomatic or have substantially diminished LV function require surgical intervention, most typically aortic valve replacement.