Aortic stenosis overview
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Resident Survival Guide |
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Aortic Stenosis Microchapters |
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Diagnosis |
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Treatment |
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Percutaneous Aortic Balloon Valvotomy (PABV) or Aortic Valvuloplasty |
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Transcatheter Aortic Valve Replacement (TAVR) |
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Case Studies |
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Aortic stenosis overview On the Web |
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American Roentgen Ray Society Images of Aortic stenosis overview |
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Risk calculators and risk factors for Aortic stenosis overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Mohammed A. Sbeih, M.D. [2]; Lakshmi Gopalakrishnan, M.B.B.S. [3]; Usama Talib, BSc, MD [4] Assistant Editor-In-Chief: Kristin Feeney, B.S. [5]
Overview
The aortic valve ensures that the blood moves forward from the left ventricle into the aorta and that it does not leak backwards during diastole. When functioning appropriately, the aortic valve does not impede the flow of blood between the left ventricle and the aorta and it does not leak. Under some circumstances, the aortic valve becomes narrower than normal impeding the flow of blood. This is known as aortic valve stenosis, or aortic stenosis, often abbreviated as AS.
Classification
Aortic stenosis can be classified broadly into four main categories:
ACC/AHA staging system (Stages A-D)
Stage A = at risk;
Stage B = progressive (mild-moderate);
Stage C = asymptomatic severe (C1 = normal LVEF, C2 = LVEF <50%);
Stage D = symptomatic severe (D1 = high-gradient, D2 = low-flow low-gradient with reduced LVEF, D3 = paradoxical low-flow low-gradient with normal LVEF). [1][2]
Pathophysiology
Aortic stenosis is the progressive narrowing of the aortic valve. aortic sclerosis (leaflet thickening without obstruction) is the earliest pathological stage, affecting approximately 25% of people over 65, with an approximately 2% annual rate of progression to AS[3]. While early disease shares features with atherosclerosis (lipid infiltration, inflammation), the current understanding is that disease initiation and disease progression are distinct processes. Progression is primarily driven by fibrosis, calcification, and biomineralization rather than a purely atherosclerotic process. This distinction is clinically important because it explains why statins failed to slow AS progression [4]. In contrast, rheumatic aortic stenosis is due to fusion of the commissures with valvular scarring and calcification.[5] Aortic stenosis causes an impedance to the antegrade blood flow not only at the level of the aortic valve itself, but also at the subvalvular (below the aortic valve) or supravalvular (above the aortic valve) levels. As a result, chronic pressure overload develops in the left ventricle. The left ventricle undergoes hypertrophy as an initial adaptive mechanism to overcome the increased afterload. This compensatory mechanism ends up being maladaptive by causing apoptosis of the hypertrophied myocytes and subsequent heart failure. [6] Hence, aortic stenosis is a progressive valvular disease which progression depends mainly on the degree of the narrowing of the aortic valve as well as on the maladaptive ventricular wall response.[7]
Causes
The frequency of causes of aortic stenosis varies with the age of the patient. calcific degeneration of a trileaflet valve is the most common cause of stenosis overall, and bicuspid aortic valve (present in 1-2% of the population) is the most common congenital predisposition. [3]
Differentiating Aortic Stenosis from other Disorders
Aortic stenosis must be differentiated from other cardiac or pulmonary causes of dyspnea, weakness, and dizziness. Furthermore, if there is left ventricular outflow tract obstruction, it is critical to identify whether the obstruction is subvalvular, valvular or supravalvular or due to hypertrophic cardiomyopathy (HOCM).
Epidemiology and Demographics
Aortic stenosis primarily affects older adults and the majority of cases are due to calcific degeneration. AS affects 1% to 2% of persons aged 65 years or older and approximately 12% of those older than 75 years. Calcific AS affects approximately 12.6 million people globally and accounts for more than 100,000 deaths annually.[2] AS is the most common valvular heart disease in high-income countries, and its global prevalence increased 124% between 1990 and 2017. [8]
Risk Factors
The most common risk factor for the subsequent development of aortic stenosis is congenital bicuspid aortic valve. Rheumatic fever is another risk factor for the subsequent development of aortic stenosis (rheumatic heart disease). Risk factors that may speed up the progression of degenerative calcific aortic stenosis include: hypertension, diabetes mellitus, hyperlipoproteinemia, uremia and smoking.
Elevated lipoprotein(a) [Lp(a)] a recognized risk factor for both the development and progression of AS. Mendelian randomization studies and meta-analyses have established Lp(a) as a causal, genetically determined risk factor for calcific aortic valve disease. Patients in the highest Lp(a) tertile demonstrate 41% faster hemodynamic progression of AS. The 2022 European Atherosclerosis Society consensus statement identifies Lp(a) as causally associated with both aortic valve microcalcification and macrocalcification.[4][5][6][7]
Chronic kidney disease/end-stage renal disease is also a significant risk factor, as recognized by the AHA scientific statement on AS in CKD.[9]
Male sex and older age (≥65 years) are independent risk factors. [2]
Natural History, Complications and Prognosis
Left untreated, aortic valve stenosis can lead to angina, syncope, congestive heart failure, atrial fibrillation, endocarditis, and sudden cardiac death. Surgical treatment of aortic stenosis also carries risks and potential complications that include vascular complications and mitral valve injury.
Diagnosis
History and Symptoms
The main symptoms of aortic stenosis include angina, syncope and congestive heart failure. The current literature emphasizes that symptomatic severe AS is associated with an annual mortality rate as high as 50% if not treated with valve replacement, and the 1-year mortality was 50.7% with standard medical care in the PARTNER trial[2]. Other symptoms include dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea.
Physical Examination
Aortic stenosis is most often diagnosed when it is asymptomatic and can sometimes be detected during routine examination of the heart and circulatory system. The major signs include pulsus parvus et tardus (a slow-rising, small volume carotid pulse), a lag time between apical and carotid impulses, and a distinct systolic ejection murmur.
Electrocardiogram
The electrocardiogram in the patient with moderate to severe aortic stenosis may reveal left ventricular hypertrophy and heart block.
Cardiac Stress Test
Exercise testing should not be performed in symptomatic patients with severe AS (Stage D1, aortic velocity ≥4.0 m/s or mean gradient ≥40 mm Hg) because of the risk of severe hemodynamic compromise (Class III: Harm). However, in asymptomatic patients with severe AS (Stage C1), exercise testing is reasonable (Class IIa) to assess physiological changes and confirm the absence of symptoms.[1]
Chest X-ray
Chest X-ray may be used as a diagnostic tool in the evaluation of aortic stenosis. Findings associated with aortic stenosis include left ventricular hypertrophy and calcification of the aortic valve.
CT Scan
CT Aortic Valve Calcium Scoring
Noncontrast CT aortic valve calcium scoring is now recommended by both ACC/AHA and ESC/EACTS guidelines as a key adjunctive tool to adjudicate AS severity, particularly in patients with discordant echocardiographic findings (e.g., low-flow, low-gradient AS). Sex-specific calcium score thresholds have been established: ≥2,065 Agatston units (AU) in men and ≥1,274 AU in women indicate severe AS. CT calcium scoring is also recommended in paradoxical low-flow low-gradient AS with preserved LVEF.[10]
MRI
Cardiac MRI (CMR) has an expanding role in AS evaluation, particularly for: Myocardial fibrosis assessment via late gadolinium enhancement (LGE) and T1 mapping/extracellular volume (ECV) quantification. LGE-detected midwall fibrosis is independently associated with a 2.14-fold increased risk of all-cause mortality in AS patients.[11]
The EVOLVED trial (2025) randomized asymptomatic patients with severe AS and midwall LGE to early intervention vs. conservative management, establishing CMR-detected fibrosis as a biomarker for risk stratification.[12]
CMR is the reference standard for LV mass and volume assessment and can detect subclinical myocardial damage before LVEF declines.[13]
Echocardiography
Echocardiography is the best non-invasive test to evaluate the aortic valve anatomy and function. TTE is indicated in patients with signs or symptoms of AS or a bicuspid aortic valve for accurate diagnosis (Class I) [1]. Doppler echocardiography allows the measurement of the maximum jet velocity and can be used to estimate the effective orifice area of the aortic valve as well as the gradient across the aortic valve using the modified Bernoulli equation (gradient = 4 x velocity2). The flow must be constant, so as the velocity increases, the valve area decreases proportionally. severe AS is defined by aortic Vmax ≥4 m/s or mean gradient ≥40 mm Hg, with AVA typically ≤1.0 cm² (or indexed AVA ≤0.6 cm²/m²), but a high velocity or high gradient alone meets the definition of severe AS — AVA is not required [1]. Moreover , the role of global longitudinal strain (GLS) by speckle tracking echocardiography as a more sensitive indicator of subclinical myocardial dysfunction than LVEF, with prognostic value in asymptomatic severe AS[14]
Attention to technical details is important as they may lead to underestimation of the severity of the aortic stenosis.[5] Echocardiography can also be used to assess the severity of left ventricular hypertrophy.
Cardiac Catheterization
Left and right heart catheterization as well as angiography may be useful in the assessment of the patient prior to aortic valve replacement surgery. invasive hemodynamic assessment is one option but is no longer the primary recommended approach for discordant findings. CT calcium scoring and dobutamine stress echocardiography are now the preferred noninvasive methods for adjudicating severity in discordant cases. Cardiac catheterization is primarily performed for coronary angiography prior to planned valve intervention, not routinely for hemodynamic assessment of AS severity[1]
Aortic Valve Area
The aortic valve area is the size of the orifice for blood to flow from the left ventricle to the aorta. The aortic valve area is reduced in aortic stenosis, and the aortic valve area is the metric that is used to gauge the need for aortic valve replacement surgery. The pressure gradient across a narrowed aortic valve cannot be used to gauge the need for valve replacement as the gradient may be low in patients with impaired left ventricular function.
Aortic Valve Area Calculation
The calculation of the aortic valve area is an indirect method used to determine the area of the aortic valve. The calculated aortic valve orifice area is currently one of the measures for evaluating the severity of aortic stenosis. An aortic valve having an area ≤1.0 cm² (or indexed AVA ≤0.6 cm²/m²) considered to be severe aortic stenosis.[1]
There are many ways to calculate the aortic valve area. The most commonly used methods involve measurements taken during echocardiography. For interpretation of these values, the aortic valve area is generally divided by the body surface area.
Treatment
General Approach
Choice of SAVR vs. TAVR
AVR (either SAVR or TAVR) is recommended for symptomatic severe AS. The choice between SAVR and TAVR should be made by a multidisciplinary heart valve team based on age, surgical risk, anatomy, comorbidities, and patient preference — not simply based on whether the patient "can tolerate surgery[2][15]. If severe left ventricular dysfunction is present in the setting of aortic stenosis, it is of utmost importance to differentiate between true severe aortic stenosis and pseudo-severe aortic stenosis as these two entities have different pathophysiologies and different outcomes after aortic valve replacement. Medical therapy reduces symptoms but does not prolong life. TAVR is a Class I recommendation for patients ≥80 years or with life expectancy <10 years, and either SAVR or TAVR is Class I for patients aged 65-80 years. SAVR is preferred for patients <65 years with life expectancy >20 years[2][10]. Aortic valvuloplasty can be considered in those patients who are too sick for surgery or transcatheter aortic valve implantation.The section should mention the concept of shared decision-making (Class I, ACC/AHA) in choosing between SAVR and TAVR, considering expected patient longevity vs. valve durability.[10]
Discussion of early intervention in asymptomatic severe AS:
For asymptomatic severe AS, current guidelines now recognize several Class I and IIa indications for AVR even without symptoms: LVEF <50%, symptoms on exercise testing, very severe AS (Vmax ≥5 m/s), BNP >3× normal, and rapid progression (≥0.3 m/s/year). The RECOVERY trial (10-year follow-up, 2026) and AVATAR trial demonstrated survival benefit with early surgery in asymptomatic very severe AS.[1][2][10][16]
Medical Therapy
While medical therapy may improve the symptoms of patients with aortic stenosis, medical therapy does not prolong life expectancy. Aortic valve replacement remains the definitive treatment for symptomatic aortic stenosis and it improves both the symptoms and life expectancy of the patients. When pharmacological therapies are used, extreme caution must be taken in the administration of vasodilators as an excess in vasodilation may lead to hypotension, a reduction in perfusion pressure to the heart, a further decline in cardiac output and further hypotension. This vicious circle can be fatal and must be avoided at all costs.
The 2020 ACC/AHA guidelines give a Class IIb recommendation for renin-angiotensin-aldosterone system (RAAS) blockade in patients undergoing TAVR, based on observational data showing lower 1-year mortality.[1]
Surgery
Surgical intervention may be a necessary component of treatment for symptomatic severe aortic stenosis. Aortic valve replacement is the mainstay of treatment of symptomatic aortic stenosis, as it improves both the symptoms and life expectancy in aortic stenosis patients, in contrast to medical therapy alone which may improve the symptoms without prolonging life expectancy.[12]
Percutaneous Aortic Balloon Valvotomy (PABV) or Aortic Valvuloplasty
Surgical aortic valve replacement is the mainstay of the treatment of aortic stenosis as it improves both symptoms and life expectancy. However, some patients may not be surgical candidates due to coexisting comorbidities. Hence, minimally invasive treatment such as percutaneous aortic balloon valvotomy (PABV) maybe an alternative to surgery as a palliative strategy. PABV is a procedure during which one or more balloons are placed across a stenotic valve and then inflated in order to cause a decrease the severity of aortic stenosis. This is to be distinguished from transcatheter aortic valve implantation (TAVI) which is a different method that involves replacement of the valve percutaneously.
Both ACC/AHA and ESC/EACTS give PABV a Class IIb recommendation only as a bridge to SAVR or TAVR, or before urgent noncardiac surgery. It is not recommended as a definitive or standalone palliative therapy due to high restenosis rates.[10]
Transcatheter Aortic Valve Implantation
TAVR has been FDA-approved for all surgical risk categories (including low risk) since 2019, based on the PARTNER 3 and Evolut Low Risk trials [15]. In Transcatheter Aortic Valve Implantation (TAVI) also known as Percutaneous Aortic Valve Replacement (PAVR), a synthetic valve is advanced to the heart through a small hole made in the groin. This procedure is similar in its mechanism to the insertion of a stent, or performing balloon angioplasty albeit with much larger equipment. Traditional aortic valve replacement is an invasive surgical procedure, with considerable mortality and morbidity, especially in more fragile patients. In the newly developed TAVI procedure, the dysfunctional aortic valve is replaced percutaneously, which obviates the need for open heart surgery. TAVR has lower 30-day risk of atrial fibrillation (10% vs. 33%) and major bleeding compared to SAVR, but higher rates of permanent pacemaker implantation (15% vs. 6%) and paravalvular regurgitation. Long-term durability data for TAVR extend up to 10 years in older patients, compared to >20 years for surgical bioprosthetic valves.[2]
Follow Up
Follow up is recommended for all patients with operated and unoperated aortic stenosis. Asymptomatic patients with aortic stenosis should undergo follow up since aortic stenosis is an ongoing disease that progresses with time. The Follow Up time is following:
Severe AS (Stage C1): every 6-12 months
Moderate AS: every 1-2 years
Mild AS: every 3-5 years[2][1]
Prevention
Aortic stenosis associated with rheumatic heart disease can be minimized with antibiotic therapy in patients with documented streptococcal pharyngitis (strep throat).[15]Bicuspid aortic valve disease is a congenital variant and cannot be prevented. Three large RCTs (SALTIRE, SEAS, ASTRONOMER) and a Cochrane systematic review conclusively demonstrated that statins do not slow the progression of calcific AS or reduce the need for valve replacement. The 2020 ACC/AHA guidelines explicitly state there are no data to support statins for prevention of AS progression.[2][1]
Currently, no medical therapies have been proven to slow AS progression. Medications targeting calcification (bisphosphonates, denosumab) have also been ineffective. Lp(a)-lowering therapies are under investigation but no published data yet support their use for AS[2]
Precautions and Prophylaxis
The 2020 ACC/AHA guidelines do not recommend routine antibiotic prophylaxis for native valve AS (including bicuspid aortic valve). Prophylaxis is recommended only for the highest-risk groups: prosthetic cardiac valves (including TAVR), prosthetic material used for valve repair, previous IE, unrepaired cyanotic congenital heart disease, and cardiac transplant with valve regurgitation. The 2021 AHA scientific statement specifically considered and rejected expanding prophylaxis to patients with native valve AS, bicuspid aortic valve, or rheumatic heart disease. [1][2]
Clindamycin is no longer recommended for IE prophylaxis due to increased risk of Clostridium difficile infection. Preferred alternatives for penicillin-allergic patients include cephalexin, azithromycin, or doxycycline.[16]
Patients with severe aortic stenosis should avoid strenuous exercise and any exercise that greatly increases afterload such as weight lifting.
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 https://www.jacc.org/doi/10.1016/j.jacc.2020.11.018
- ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 doi:10.1001/jama.2024.16477
- ↑ 3.0 3.1 doi:10.1001/jama.2024.16477
- ↑ 4.0 4.1 doi:10.1001/jamacardio.2022.0987
- ↑ 5.0 5.1 5.2 DOI: 10.1093/eurheartj/ehac361
- ↑ 6.0 6.1 https://pubmed.ncbi.nlm.nih.gov/37078819/DOI: 10.1093/cvr/cvad062
- ↑ 7.0 7.1 https://jamanetwork.com/journals/jamacardiology/fullarticle/2820718?utm_source=openevidence&utm_medium=referral
- ↑ https://pubmed.ncbi.nlm.nih.gov/35241220/
- ↑ https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000000979?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org
- ↑ 10.0 10.1 10.2 10.3 10.4 https://pubmed.ncbi.nlm.nih.gov/37587584/
- ↑ https://pubmed.ncbi.nlm.nih.gov/35113967/
- ↑ 12.0 12.1 https://jamanetwork.com/journals/jama/fullarticle/2825540?utm_source=openevidence&utm_medium=referral
- ↑ https://pubmed.ncbi.nlm.nih.gov/32828787/
- ↑ https://jamanetwork.com/journals/jamacardiology/article-abstract/2824468?utm_source=openevidence&utm_medium=referra
- ↑ 15.0 15.1 15.2 https://jamanetwork.com/journals/jama/article-abstract/2781245?utm_source=openevidence&utm_medium=referral
- ↑ 16.0 16.1 https://www.aafp.org/pubs/afp/issues/2026/0200/infective-endocarditis.html