7th March 2024

Aortic stenosis

Any disorder involving the aortic valve will generate pressure/volume overload on the left ventricle. Over time, this will affect the left atrium. An aortic murmur will be heard loudest over the aortic area.

Aortic stenosis (AS) is characterised by an ejection systolic murmur radiating to the carotids. The pathology is due to a stenosed aortic valve causing blood to be squeezed past the narrowed valve opening. Causes of AS include:

• Degenerative calcification. The most common cause in patients > 65 years
• Bicuspid aortic valve. This is the most common cause in patients < 65 years
• Congenital e.g. William’s syndrome where there is supra valvular stenosis
• Post rheumatic fever
• Sub valvular e.g. HOCM

Clinical manifestations

AS can vary from asymptomatic to low cardiac output symptoms which includes chest pain, dyspnoea, syncope and pulmonary oedema. The severity of the stenosis can manifest in symptoms ranging from reduced exercise tolerance to sudden cardiac death (SCD).  The classical symptoms are only in 30-40% of individuals with AS. When symptoms appear, survival without surgery is, on average, 2-3 years. SCD occurs in 1-2% of asymptomatic AS patients per year. Symptoms of severe AS include: 

• Narrow pulse pressure and small volume pulse due to little blood escaping the ventricle
• Slow rising pulse due to a narrow outflow
• Soft or absent S2 due to a narrow pulse pressure and restricted leaflet motion.
• Displaced apex beat due to left ventricular hypertrophy.
• Delayed ejection systolic murmur
• Paradoxical split S2 and palpable thrill

Diagnosis

While AS may be clinically silent in many cases, a broad range of symptoms, as outlined above, can lead to a suspicion of disease. 

• Chest x-ray may show cardiomegaly due to left ventricular hypertrophy and detect abnormalities of aortic contour or size.  
• Echocardiography is key to confirming the diagnosis and severity of aortic stenosis, assessing valve calcification, LV function and wall thickness. It can also detect other valve pathologies and provide prognostic information. 
• Transoesophageal echocardiography is used when images on a transthoracic echo prove insufficient. A pressure gradient of over 40mmHg is diagnostic of severe aortic stenosis and is an indication for surgery. Aortography done as part of a coronary angiogram may also support a finding of AS. 
• Exercise testing may unmask symptoms and is recommended for risk stratification of asymptomatic patients with severe aortic stenosis. Exercise echocardiography provides additional prognostic information by assessing the increase in mean pressure gradient and change in LV function. Although the severity of valvular calcification is prognostically important in an asymptomatic patient, the most important predictor is LV function. 
• Coronary angiography is essential prior to transarterial valve implantation (TAVI) and surgical AV valve replacement (SAVR) to determine the potential need for concomitant revascularisation. 
• Cardiac CT (CCT) provides information on calcium score, anatomy of the aortic root and ascending aorta, and feasibility of vascular access. 
• Myocardial fibrosis (due to amyloidosis, for example) is a major driver of LV decompensation in aortic stenosis. This can be detected and quantified using cardiac magnetic resonance (CMR). 
• Natriuretic peptides predict symptom-free survival and outcome in normal and low-flow severe aortic stenosis. They can be used to arbitrate the source of symptoms in patients with multiple potential causes and identify those with high-risk asymptomatic aortic stenosis who may benefit from early intervention.

Management 

This depends on the symptoms and severity of AS. 

• Early intervention is recommended for all patients with symptomatic severe aortic stenosis. The only exception is for those in whom intervention is unlikely to improve quality of life or survival. Symptomatic patients without severe AS can be managed medically with conventional heart failure therapy. It is important to note that angiotensin-converting enzyme inhibitors (ACEI) are safe in AS, provided that BP is monitored carefully. They provide beneficial myocardial effects before the onset of symptoms and after TAVI and SAVR but are not generally recommended. 
• Coexisting hypertension should be treated to avoid additional afterload, although medication (particularly vasodilators) should be titrated to avoid symptomatic hypotension. 
• Replacement should also be considered in asymptomatic patients with a valvular gradient > 40 mmHg with features of LVSD. 
• Asymptomatic patients without severe aortic stenosis or evidence of LV dysfunction are managed with watchful waiting and prompt intervention at symptoms onset. Intervention such as TAVI or SAVR is recommended in symptomatic patients with high-gradient AS, regardless of LVEF. 
• Balloon valvuloplasty is reserved for patients with critical AS who are not fit for valve replacement and has a high rate of recurrence.