Aortic Stenosis

Physical Examination

• General examination:

  • Shortness of breath at rest or on exertion

  • Cyanosis, particularly central cyanosis

  • Signs of IE

  • Pulse: low volume, slow rising

  • BP: narrow pulse pressure

  • Ankle oedema

  • Elevated jugular venous pressure (JVP)

• Precordial inspection:

  • Visible apical impulse

• Palpation:

  • Apex beat shifted laterally and downward, may be sustained or forceful

  • Palpable systolic thrill at the right upper sternal border or over the aortic area

  • Left Parasternal heave indicating right ventricular hypertrophy

• Auscultation:

  • Harsh ejection systolic murmur, best heard in the aortic area (right upper sternal border) and radiating to the carotids, louder during expiration

  • Soft or absent second heart sound (A2), particularly if the stenosis is severe

  • Presence of an S4 gallop, indicating a stiff left ventricle

  • Additional diastolic murmur of aortic regurgitation may be present in mixed aortic valve disease

Investigations

• Laboratory tests:

  • Complete blood count, renal function tests, electrolytes

  • Cardiac biomarkers: Rule out concurrent myocardial injury or ischemia

  • B-type natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP): Evaluate heart failure or severity of symptoms

  • C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR): Rule out infective endocarditis if suspicion arises

  • Blood cultures: If infective endocarditis is suspected

• Electrocardiogram (ECG): Detect left ventricular hypertrophy, atrial fibrillation, or ischemic changes

• Imaging studies:

  • Chest X-ray: Assess for cardiomegaly, pulmonary congestion, or aortic calcification

  • Transthoracic echocardiography (TTE): Confirm diagnosis, assess valve morphology, measure peak and mean pressure gradients, and calculate aortic valve area; evaluate left ventricular size, function, and wall thickness

  • Transesophageal echocardiography (TEE): Obtain better visualisation of the aortic valve, especially in cases of poor TTE image quality or suspicion of endocarditis

  • Cardiac magnetic resonance imaging (MRI): Evaluate aortic valve anatomy and left ventricular function if echocardiography is inconclusive

• Invasive tests:

  • Coronary angiogram: Assess coronary artery disease prior to valve intervention, particularly in patients with angina or risk factors for coronary artery disease

• Other tests:

  • Exercise stress test or stress echocardiography: Assess functional capacity and symptom severity in patients with low-gradient, low-flow aortic stenosis or equivocal symptoms

  • Cardiopulmonary exercise testing: Evaluate functional capacity and identify factors limiting exercise tolerance

Management

• General management:

  • Multidisciplinary team approach for optimal management, including cardiology, cardiothoracic surgery, and primary care

  • Monitor and optimise blood pressure control

  • Manage coexisting cardiovascular risk factors (e.g., diabetes, hyperlipidemia, smoking)

  • Encourage a heart-healthy diet and regular exercise as tolerated

  • Educate the patient about the condition and the importance of regular follow-up

• Medical management:

  • No medical treatments have been proven to delay progression of aortic valve disease or to improve survival

  • Good dental hygiene and regular follow up

  • Anticoagulants: Indicated for patients with atrial fibrillation or other risk factors for thromboembolism

• Surgical management:

  • Aortic valve replacement (AVR): Gold standard treatment for severe symptomatic aortic stenosis or asymptomatic patients with left ventricular dysfunction; options include surgical AVR (SAVR) with a mechanical or bioprosthetic valve or transcatheter aortic valve implementation (TAVI) for high-risk patients or those who are not surgical candidates

  • Balloon aortic valvuloplasty: Temporary measure to alleviate symptoms in patients who are not candidates for AVR or as a bridge to surgery.

Causes of Aortic Stenosis

• Degenerative calcification

• Congenital bicuspid aortic valve

• Rheumatic heart disease

Causes of Ejection systolic murmur

• Aortic stenosis: The most common cause of ESMs, resulting from the narrowing of the aortic valve, which obstructs blood flow from the left ventricle to the aorta. It can be due to degenerative calcification, congenital bicuspid aortic valve, or rheumatic heart disease.

• Pulmonary stenosis: This is the narrowing of the pulmonary valve, leading to the obstruction of blood flow from the right ventricle to the pulmonary artery. It can be congenital or secondary to conditions like carcinoid syndrome or rheumatic heart disease.

• Hypertrophic cardiomyopathy (HCM): This genetic condition is characterised by an abnormally thickened interventricular septum or ventricular wall, causing obstruction to the left ventricular outflow tract during systole, leading to an ESM.

• Aortic sclerosis: A less severe form of aortic stenosis, characterised by mild calcification and thickening of the aortic valve leaflets without significant obstruction to blood flow. It typically produces a softer ESM.

• Flow murmurs: These are benign ESMs caused by increased blood flow across the aortic or pulmonary valves during systole, often seen in conditions like anaemia, fever, or hyperthyroidism.

Difference between Aortic Stenosis and Aortic Sclerosis

• Auscultation:

  • Aortic stenosis: A harsh ejection systolic murmur is typically heard best at the upper right sternal border or second intercostal space, radiating to the carotid arteries. The murmur may also be accompanied by a soft second heart sound (S2) or paradoxically split S2.

  • Aortic sclerosis: A softer ejection systolic murmur without radiation to the carotids is characteristic. The murmur may be heard at the same location as in aortic stenosis, but it is generally less intense and has a more localised sound.

• Carotid pulse:

  • Aortic stenosis: The carotid pulse is weak and delayed due to the obstruction of blood flow across the aortic valve. This finding can be palpated by placing two fingers on the carotid artery and noting a diminished and slow-rising pulse.

  • Aortic sclerosis: The carotid pulse is typically normal, as there is no significant obstruction to blood flow.

• Pulse Pressure

  • Pulse pressure is typically narrowed or reduced in patients with significant aortic stenosis due to the obstruction of blood flow across the aortic valve. This leads to a decrease in systolic blood pressure, while diastolic blood pressure remains relatively unchanged.

• Apical impulse:

  • Aortic stenosis: A sustained and forceful apical impulse may be palpable due to left ventricular hypertrophy resulting from increased afterload.

  • Aortic sclerosis: The apical impulse is usually normal, as there is no significant obstruction to blood flow or increased afterload.

• Presence of other signs:

  • Aortic stenosis: In severe cases, you may observe signs of heart failure, such as peripheral oedema, jugular venous distension, or pulmonary crackles on auscultation.

  • Aortic sclerosis: As it is generally a benign condition, these additional signs are typically absent.

Complications of Aortic Stenosis

• Left ventricular hypertrophy: Increased pressure gradient across the stenotic aortic valve results in increased afterload on the left ventricle, causing it to thicken and hypertrophy over time.

• Heart failure: Progressive left ventricular hypertrophy, and increased afterload can eventually lead to systolic and diastolic dysfunction, resulting in heart failure. This may manifest as exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and peripheral oedema.

• Atrial fibrillation: Left ventricular hypertrophy and diastolic dysfunction can cause left atrial enlargement, increasing the risk of atrial fibrillation. Atrial fibrillation can further exacerbate heart failure symptoms and increase the risk of thromboembolic events.

• Angina: Reduced coronary blood flow due to the increased oxygen demand from the hypertrophied left ventricle and decreased aortic diastolic pressure can lead to angina, even in the absence of coronary artery disease.

• Syncope: Decreased cerebral perfusion caused by a sudden drop in blood pressure, often during exertion or stress, can result in syncope.

• Sudden cardiac death: Severe aortic stenosis, particularly in patients with hypertrophic cardiomyopathy, can predispose to fatal arrhythmias, leading to sudden cardiac death.

• Infective endocarditis: The damaged aortic valve is more susceptible to infection, increasing the risk of infective endocarditis.

• Stroke: Atrial fibrillation or infective endocarditis-related emboli can lead to stroke in patients with aortic stenosis.

Severity of AS

• Low volume pulse, slow rising pulse

• Narrow pulse pressure

• Heaving apex beat

• Reversed splitting of second heart sound

• Fourth heart sound

• Signs of pulmonary hypertension

• Signs of left ventricular failure