Aortic valve stenosis (AS) is the commonest indication for valvular surgery in the developed world. Severe AS affects approximately 2% of patients aged 65 years old, and 4% of patients aged 85 years old. The disease can have significant impact on health of patients, with a spectrum of consequences. Surgical valve replacement remains the gold standard for improving life quality and expectancy. These factors mean that it is an important pathology to understand, as it can commonly be encountered within daily clinical practice, as well as the need to manage the care of these patients during specialised cardiac surgery.
The common causes of aortic stenosis are:
Aortic sclerosis (most common)
Bicuspid aortic valve
Aortic sclerosis is the most common cause of AS in elderly patients. It may also be called degenerative or calcific AS. The process is similar to atherosclerosis and has similar risk factors. There is deposition of lipoproteins in the valve leaflets with subsequent inflammation, fibrosis and calcification. Over several years, this process can result in AS, with the calcification of the valve progressively impairing valve opening.
Congenital bicuspid aortic valve (i.e. there are only 2 valves leaflets) is a less common cause of AS, but the most common cause in young patients (under 70 years old). This is found in approximately 0.5% of births and affects men more than women. Other congenital valvular forms exist e.g. unicuspid aortic valve, but these more commonly cause problems in infancy and childhood.
Rheumatic fever remains the leading cause of AS in developing countries. Here there is progressive fibrosis of the valve with some commissural fusion and retraction of the valve leaflets. As such there often a combination of regurgitation and stenosis. There may also be mitral valve disease.
Supravalvular AS is also a possible cause of AS. This is the result of a sporadic membrane or constriction above the level of the valve. It is associated with certain congenital conditions e.g. Williams syndrome.
Rare causes of AS include:
The aortic stenosis will often remain asymptomatic and not cause problems for many years (often 10 to 20 years). As the disease progresses, there is increased narrowing of the valvular area, and thus increased obstruction to the flow of blood from the left ventricle. There is therefore an increased pressure gradient between the aorta and LV. To counteract this increased afterload, there is hypertrophy of the LV. In the initial stages, this preserves normal function and preserves cardiac output, although the hypertrophy does reduce diastolic compliance. This means that the ventricle requires higher filling pressures, and the action of atrial filling becomes much more important than in a normal heart. The increased myocardium muscle mass, and the raised diastolic pressures (coronary blood flow occurs in diastole) mean that coronary blood flow to the myocardium is impaired. This can result in impaired flow, particularly in the subendocardium, resulting in myocardial ischaemia. These factors contribute to the impaired exercise tolerance of the heart, even if it is able to cope at rest. Eventually the progressive diastolic dysfunction can progress with fibrosis and ischemia of the myocardium leading to systolic dysfunction and heart failure. These changes lead to a risk of sudden cardiac death.
Signs & Symptoms
The presentation of aortic stenosis will often be late in the disease process, as there will often be no consequences of the initial disease. Similarly the development of symptoms is generally gradual, and usually related to the diastolic dysfunction phase.
The most common features are:
The exertional breathlessness is the most common feature. This relates to the inability of heart to meet the cardiovascular demands of exercise. This may be so notable, that the cardiac output during exercise isn’t enough to maintain cerebral perfusion, leading to dizziness or syncope. Similarly, as the myocardial oxygen demands increase during exertion (due to increased muscle mass) and yet flow is inhibited by the increased diastolic pressures, angina can develop. This may even be in the presence of healthy coronary arteries.
Other causes of syncope may be transient arrhythmias (atrial fibrillation or ventricular tachycardia).
There are no visible signs of AS, instead being found on more detailed clinical examination. The degree of AS may produce differing consequences which may also manifest as clinical signs e.g. signs of congestive cardiac failure.
Reduced in amplitude and delayed compared to LV contraction (pulsus parvus et tardus)
Pulsus alternans may occur is systolic dysfunction is present
The palpable apex beat may include a systolic thrill.
The apex beat is often not displaced until systolic dysfunction develops
Classically a ejection systolic murmur (crescendo-decrescendo)
Best heard over left upper sternal border
Radiates to both carotids
Can be augmented by increased preload (e.g. passive leg raise) and reduced by reducing it (e.g. Valsalva maneuver).
The aortic component of S2 can be reduced
An S4 may be present.
The diagnosis is usually suspected clinically, and is confirmed with echocardiography. Echocardiography will assess:
Aortic valve area
Aortic valve pressure gradient
Other valvular lesions (including any AR)
Assessment of LV function
Other investigations include:
ECG - to provide information on conduction abnormalities and signs of ischaemia
CXR - to look for features of cardiac failure and other chest disease.
Bloods - serum electrolytes and full blood count.
Coronary angiography is commonly performed in patients if surgery is being planned to assess for any disease (CABG may be considered simultaneously).
The severity of the disease can be classified based on the echocardiography findings:
Valve Area (cm^2):
Normal : 3-4
Peak gradient (mmHg):
Other methods for describing severity include:
Valve area adjusted for body surface area
Aortic jet velocity
There is no medical option that improves outcome in AS. The definitive option is aortic valve replacement (AVR). The timing of this, and the different forms that it can take, is determined based on the severity of the disease and the symptoms.
General advice for patients with AS relates to avoiding significant exertion, which can precipitate deterioration (including sudden death). As there is significant overlap between the risk factors for atherosclerotic disease and AS, the management of these is an important consideration. This may include:
Patients with hypertension should have antihypertensive therapy introduced very carefully because of the risk of adverse effects on cardiovascular status.
Consideration for surgery Patients will be recommended for surgery if they have:
Severe AS and symptoms
Severe AS and LVEF <50% (if asymptomatic)
They may also be considered for surgery if the have asymptomatic severe AS without LV dysfunction, but:
An abnormal response to exercise
Risk factors for rapid progression
Surgery is felt to be low risk
Sometimes surgery may be considered in patients with just moderate AS but who have indications for other cardiac surgery e.g. CABG.
For patients without these criteria there may be a period of close monitoring with repeated clinical and echocardiographic assessment.
Surgical procedures for AS may include:
Aortic valve replacement
Transcatheter aortic valve implantation (TAVI)
Aortic Valve Replacement
AVR refers to the surgical replacement of the aortic valve. There is removal of the valve tissue, and replacement with an artificial valve - this may be mechanical or tissue in design. This will usually be done, as with much open heart surgery, via a sternotomy with the patient on cardiopulmonary bypass. If there is coexisting coronary artery disease, CABG procedures will often be performed at the same time.
The choice of valve type will be dependent on the expected longevity of the patient, and the potential consequences of anticoagulation. Tissue valves generally have a lower lifespan that mechanical valves, which may necessitate a repeat operation if the replacement valve fails. However, mechanical valves mandate significant lifelong anticoagulation.
The TAVI approach to treating AS is an alternative for patients with severe comorbidities who may struggle with the extent of the surgery for a standard AVR. It is a percutaneous approach to replacing the aortic valve, often using femoral artery access. A transapical approach, using a similar technique through a mini-thoracostomy incision, is also possible. It is only recommended for AS.
The procedure can be done under general anaesthesia or local anaesthesia with sedation. There is continuous fluoroscopic and echocardiogram guidance. The technician performs balloon valvuloplasty of the aortic valve, before placing a collapsed valve replacement using the inserted guidewire. To make the process easier, the heart is often rapidly paced at around 200 bpm.
The procedure has different risks associated with it compared with open AVR. However, it is clearly better than conservative management in patients who are not candidates for AVR. Peri-procedure complications include:
Stroke (higher risk than with open AVR at approx 5%)
Vascular complications (10-15%)
Post-op valvular dysfunction
This is essential a palliative procedure for patients who are unsuitable for surgery. It involves a similar endovascular approach as with the TAVI. A balloon is inflated to improve the opening of the aortic valve. There can be an improvement of symptoms, however, restenosis can occur within 6 to 12 months. It is often considered if the patient’s life expectancy is under 1 year.
The anaesthetic procedure for valve replacement will be as for sternotomy with CPB. A full, careful preoperative assessment should be undertaken, evaluating some of the features discussed above.
Perioperative management Full monitoring as per patients undergoing cardiac surgery. This effectively mandates an awake arterial line. Central venous access may be considered whilst awake depending on the clinical state of the patient. Defibrillator pads should be attached in case rapid cardioversion is needed (external chest compression are likely to achieve little if there is significant AS).
Heart rate management is important for these patients. Tachycardia is poorly tolerated as it further impairs coronary perfusion, which is often already physiologically strained. However, excess bradycardia can also cause decompensation. A rate of 60 - 80 bpm is optimal.
Sinus rhythm is also important. The loss of atrial kick to ventricular filling can be a cause of decompensation. DC cardioversion may be needed for any arrhythmia if there is cardiovascular compromise, and this could include AF.
Maintaining afterload is very important in these patients, as they may be very dependent on the diastolic pressure for coronary perfusion. Any factors that can affect this (probably the most notable being induction of anaesthesia) must be done very carefully. A heavily opioid based anesthesia may be used to try and reduce the impact of general anaesthetic agents in this way. The use of vasopressors e.g. metaraminol infusion, should be used to offset the impact of anaesthesia on cardiovascular tone. Inotropic agents may still be needed to assist a struggling LV.
Adequate preload is also important to allow good filling of a potentially stiff LV. An appropriate choice of assessment of fluid status should probably be used - some clinicians will use a pulmonary artery catheter for this.
Good cardioplegia of a hypertrophied heart is important to ensure damage does not occur during CPB.
This can be challenging if there is significant hypertrophy, and may necessitate direct coronary cannulation or retrograde cardioplegia.
Post-op Continued attention to the aforementioned cardiovascular parameters remains important. Pacing may be required post bypass/surgery and sequential A-V pacing may be useful simulate the atrial kick for ventricular filling. Of note, a SBP of around 100 mmHg is the target, to provide some protection to the aortic root stitches.
The outcomes after surgical AVR are generally very good, though impacted on by coexisting disease. Isolated AVR in hospital and 30-day mortality is quoted as around 3%. It is closer to 5% when combined with CABG. Following surgical AVR, mortality returns to close to that of the general population, demonstrating the very beneficial impact of surgery.
The outcomes after TAVI are comparible. 30 day mortality is quoted as <5%. As noted, the complication rate (particularly stroke) is possibly higher. The concept of TAVI as a procedure is constantly evolving and thus this may change.
Untreated AS has a poor prognosis. Asymptomatic patients with severe AS have a 2 year mortality of 50%. This would appear to be worse in symptomatic patients. These patients are at particular risk of sudden cardiac death, as noted above.
What are the causes of aortic stenosis?
Describe the pathophysiology of aortic stenosis.
What are the common symptoms of aortic stenosis?
What are the clinical signs associated with aortic stenosis?
How can the severity of aortic stenosis be classified?
What are the management options for aortic stenosis?
What are the key anaesthetic aspects for patients with aortic stenosis?
Links & References
Beers, M et al (eds). Aortic Stenosis. The Merck Manual (18th ed). 2006