Aortic valve stenosis: causes, pathophysiology, symptoms, severity, diagnosis and treatment
Table of Contents
Aortic valve stenosis (AVS) is a heart condition in which the aortic valve is narrowed and prevents the normal flow of blood from the left ventricle.
Epidemiology
Aortic valve stenosis occupies the leading position in the structure of morbidity of all valve pathologies of the heart. The prevalence of AAC increases significantly with age: in the age group over 75 years the prevalence of AAC can reach 12-13%, and the critical stage of aortic stenosis is observed in 3-4% of elderly patients.
Men are more susceptible to SAC than women.
In high-income countries with a developed health care system, the disease is diagnosed more frequently, which is associated with a higher level of medical care and accessibility of diagnostic procedures. In developing countries, data on the prevalence of SAC are limited, which may be due to inadequate diagnosis and shorter life expectancy of the population.
In the past, the main cause of aortic stenosis was rheumatic fever leading to deformation and fusion of the valve flaps. With the development of medicine and the decreasing incidence of rheumatism in developed countries, the structure of etiologic factors has changed. Currently, the leading cause of aortic stenosis is age-related degenerative changes of the valve, such as calcification and fibrosis of the flaps. In addition, the role of atherosclerosis in the development of the disease has increased.
The tendency to increase the number of patients with SAC in the modern world is primarily due to the factor of population aging, decreasing mortality from other diseases, as well as due to the improvement of diagnostic methods and their availability.
Etiology
- Degenerative changes: age-related calcification of aortic valve flaps, leading to their thickening and decreased mobility.
- Congenital anomalies: bicuspid aortic valve, which predisposes to earlier development of calcification and hence SAC.
- Rheumatic fever: leads to valve leaflet fusion and deformity.
Less commonly, SAC may be associated with conditions such as chronic renal failure, carcinoid syndrome, Paget’s disease, and systemic lupus erythematosus.
Pathophysiology
Valve narrowing increases the resistance to blood ejection, which leads to increased systolic pressure in the left ventricle, resulting in its concentric hypertrophy – wall thickening without significant cavity enlargement.
Hypertrophy leads to decreased compliance (distensibility) of the left ventricle, which impairs its ability to relax in diastole. The increase in diastolic pressure in the left ventricle is transmitted to the left atrium, causing its hypertrophy and dilatation. However, these compensatory mechanisms are not able to fully offset the increasing venous pressure in the pulmonary vessels, which leads to blood stasis in the small circle of blood circulation, which can provoke the appearance of signs of heart failure.
In the early stages of SAC, cardiac output is maintained due to the Frank-Starling mechanism, according to which the force of myocardial contraction increases with increasing myocardial stretch. However, with prolonged pressure overload and progression of hypertrophy, myocardial reserve capacity is depleted, which leads to a decrease in contractile function and development of systolic dysfunction.
Left ventricular wall hypertrophy leads to increased myocardial oxygen demand, while increased diastolic pressure limits blood supply to coronary arteries, reducing the efficiency of their perfusion, which can lead to myocardial ischemia even in the absence of coronary atherosclerosis.
Decompensated defect leads to dilatation of the left ventricular cavity and left atrioventricular ring with the development of mitral insufficiency.
Clinical manifestations
It may remain asymptomatic for a long time. Over time, the combination of the above changes leads to the appearance of the characteristic symptoms of aortic stenosis SAC: dyspnea, angina pectoris and syncope.
- Shortness of breath occurs due to blood stasis in the pulmonary veins.
- Angina pectoris – due to ischemia of hypertrophied myocardium.
- Fainting – due to decreased cardiac output and insufficient cerebral blood flow.
The appearance of these symptoms indicates an unfavorable prognosis and the need to consider surgical treatment. The appearance of cardiac asthma, edema of the lower extremities, liver enlargement indicates the transition of the disease to the decompensation stage and requires immediate medical intervention.
Diagnosis
Echocardiography (echocardiography) is the main method for the diagnosis of SAC. It assesses aortic valve anatomy, degree of calcification, orifice area, pressure gradient, and left ventricular (LV) function and size. A transthoracic echocardiogram (TTE) is recommended for initial evaluation. In cases where TTE does not provide sufficient information, transesophageal echoCG (TSE) is indicated.
Classification of degrees of aortic stenosis according to echocardiographic criteria (echocardiography)
| Parameter | Light SAC | Moderate SAC | Severe SAC | Critical SAC |
| Peak speed (m/s) | <3.0 | 3.0-3.9 | ≥4.0 | ≥5.0 |
| Average gradient (mmHg) | <20 | 20-39 | ≥40 | ≥60 |
| Valve area ( cm²) | >1.5 | 1.0-1.5 | ≤1.0 | ≤0.6 |
| Valve area index ( cm²/m²) | >0.85 | 0.6-0.85 | ≤0.6 | ≤0.4 |
The following parameters are used to assess the severity of SAC:
- Peak blood flow velocity through the aortic valve (Vmax): a value of ≥4.0 m/s indicates severe SAC;
- Mean pressure gradient across the valve (ΔPm): a value ≥40 mmHg indicates severe SAC;
- Aortic valve orifice area (AAV): a value ≤1.0 cm² or ≤0.6 cm²/m² body surface area indicates severe SAC.
In cases of low cardiac output and reduced LV ejection fraction (<50%), stress echoCG with dobutamine is recommended to differentiate true severe CAD from pseudo-severe CAD.
MRI/CT: can be used as an additional method of investigation, including the choice of operative access.
CTA is the gold standard for imaging prior to TAVI. It allows assessment of the anatomy of the aortic root and ascending aorta, the extent and prevalence of valve and vessel calcification, the risk of coronary artery obstruction, and the possibilities of vascular access.
MRI can detect and quantify myocardial fibrosis, which is a sign of decompensation of aortic valve stenosis.
Determination of brain natriuretic peptide (BNP) or its precursor (NT-proBNP) levels may be useful for risk stratification in patients with SAC. Elevated levels of these markers are associated with a worse prognosis and may provide an additional argument in favor of intervention in asymptomatic patients.
Treatment of aortic stenosis
Modification of risk factors helps to slow the progression of SAC and reduce the likelihood of complications: control of blood pressure, maintenance of normal blood lipid levels through diet and hypolipidemic drugs, complete cessation of tobacco smoking, strict control of blood glucose levels, maintenance of a healthy weight through a balanced diet and regular physical activity.
Drug therapy
There are currently no medications that can slow the progression of SAC. However, drug therapy may be useful in the management of symptoms and comorbid conditions: diuretics (to reduce pulmonary congestion in the presence of heart failure), beta-blockers (to control HR and BP, especially in the presence of concomitant CHD), angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers (in the presence of heart failure or hypertension). It is important to note that the use of these drugs requires caution, as excessive reduction of BP may worsen organ perfusion in patients with severe SAC.
Aortic valve replacement is indicated in the following cases when:
- Symptomatic severe SAC;
- Asymptomatic severe CAD in the presence of: LV systolic dysfunction (EF <50%) positive exercise test;
- Very severe SAC (mean gradient ≥60 mm Hg or peak velocity >5.0 m/s);
- A rapid deterioration of the patient’s condition or a sudden increase in the BNP concentration in the blood.
Transcatheter aortic valve implantation (TAVI) is a minimally invasive technique for aortic valve replacement. Transfemoral arterial access is most commonly used. However, in cases when the femoral arteries are too narrow, tortuous or affected by atherosclerosis, alternative ways of catheter insertion may be used: transapical access – through the LV apex, transaortic access – through the ascending aorta, transclavicular access – through the subclavian artery. Balloon-expandable and self-expandable valves are used.
TAVI should be preferred in patients aged ≥75 years and/or at high surgical risk (EuroSCORE II >8%) and/or when open surgery is not possible due to comorbidities.
Contraindications to TAVI:
- Inability to access the aortic valve through the vessels (in case of severe atherosclerosis or small arterial diameter);
- Unfavorable valve or aortic anatomy making the procedure technically unfeasible;
- Life expectancy of less than 1 year or no improvement in quality of life after the procedure.
Surgical prosthetic aortic valve replacement (SPAR)
Open surgical aortic valve replacement remains the standard of care for many patients. Implantation of mechanical or biological valves can be performed. The operation is performed under conditions of artificial circulation. Depending on the anatomical features, it can be performed from a complete sternotomy, mininotomy, right-sided anterior minithoracotomy.
Contraindications to CPAC: high surgical risk or presence of comorbidities that make surgery unsafe.
FAQ
1. Why does aortic valve stenosis occur?
2. Which auscultation findings are characteristic of aortic valve stenosis?
3. How does hemodynamics change in aortic valve stenosis?
4. Which complaints are characteristic of patients with aortic valve stenosis?
5. What is the difference between TAVI and surgery?
List of Sources
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Burden of valvular heart disease, 1990-2017: Results from the Global Burden of Disease Study 2017. Chen J, et al. J Glob Health. Sep 8;10(2):020404. doi: 10.7189/jogh.10.020404.
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Pathophysiology of Aortic Stenosis and Future Perspectives for Medical Therapy. Zheng KH, Tzolos E, Dweck MR. Cardiol Clin. 2020 Feb;38(1):1-12. doi: 10.1016/j.ccl.2019.09.010.
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Management of Patients With Aortic Valve Stenosis. Kanwar A, Thaden JJ, Nkomo VT. Mayo Clin Proc. 2018 Apr;93(4):488-508. doi: 10.1016/j.mayocp.2018.01.020.
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TAVI and the future of aortic valve replacement. Howard C, Jullian L, Joshi M, Noshirwani A, Bashir M, Harky A. J Card Surg. 2019 Dec;34(12):1577-1590. doi: 10.1111/jocs.14226.
