Surgical Treatment of Aortic Valve Disease

Epidemiology and Etiology

Isolated aortic stenosis (AS) is more common in men than in women and is found in 2% of people 65 years of age and older. The most common causes of AS include age-related calcific degeneration, bicuspid aortic valve, and rheumatic aortic valve. The distribution of these causes varies across age groups and geographic regions. Age-related degeneration is the most common cause of AS in patients older than 70 years. In contrast, bicuspid aortic valve calcification accounts for most surgical cases in patients younger than 70 years.

Pathophysiology

No appreciable gradient exists across the normal aortic valve during systole. In AS, gradual obstruction of the left ventricular outflow leads to an increased left ventricular afterload and left ventricular wall stress, elevated left ventricular systolic and diastolic pressures, decreased aortic pressure, and prolonged left ventricular ejection time. Over time, this results in compensatory concentric left ventricular hypertrophy (LVH) to maintain ejection fraction. In patients with chronic severe AS, this compensatory mechanism may become insufficient, leading to gradual dilation and thinning of the left ventricle, and result in a decrease in ejection fraction and in congestive heart failure.

Myocardial oxygen supply and demand is also altered in AS. LVH, increased systolic pressure, and prolonged ejection time result in increased myocardial oxygen demand. Increased diastolic pressure and prolonged systolic ejection time result in decreased diastolic and myocardial perfusion time and hence myocardial oxygen supply. The alteration in myocardial oxygen supply and demand is the underlying mechanism behind myocardial ischemia in patients with AS, even in the absence of coronary artery disease.

Clinical Features

The classic symptoms of AS are angina, exertional syncope, and symptoms of congestive heart failure such as shortness of breath. The mechanisms for angina and congestive heart failure are explained in the previous section. The mechanism for syncope is likely related to the blunting of exercise-induced augmentation in stroke volume as a result of outflow obstruction coupled with exercise-induced peripheral vasodilation. These changes cause a drop in systemic blood pressure leading to cerebral hypoperfusion and syncope.

The classic physical finding is a crescendo-decrescendo systolic ejection murmur heard best at the second right intercostal space, which may variably radiate to the carotid arteries. A palpable thrill may be present in severe cases of AS. Palpation of the arterial pulse may reveal a weak and delayed pulse known as pulsus parvus et tardus .

Diagnosis and Grading

Two-dimensional transthoracic echocardiography is the most common modality for the diagnosis and grading of AS ( Table 77-1 ). In most patients, this modality can reliably establish aortic jet velocity, aortic valve peak and mean gradients, and aortic valve area.

Natural History

Without intervention, symptomatic AS has dismal outcomes. Multiple studies consistently reported survivals of 3 years for angina and syncope and 1.5 to 2 years for dyspnea and heart failure. These findings have driven recommendations for early surgical intervention in patients with symptomatic AS. One third of asymptomatic patients with severe AS will become symptomatic in 2 years with an estimated cardiac death of less than 1% each year to 5% each year. Patients with higher grades of AS severity seem to progress at a faster rate than lower grades of AS. After AS becomes moderate, aortic valve area decreases on average by 0.1 cm ² per year, the pressure gradient across the valve rises on average by 7 mm Hg per year, and the jet velocity increases by 0.3 m/sec per year.

Indications for Surgery

The class I recommendations for aortic valve replacement (AVR) in patients with AS according to the American College of Cardiology (ACC) and the American Heart Association (AHA) are the following:

• 1

  Symptomatic patients with severe AS

• 2

  Patients with severe AS undergoing concomitant coronary artery bypass graft (CABG) surgery, heart valve surgery, or aortic surgery

• 3

  Patients with severe AS and left ventricular systolic dysfunction (ejection fraction < 50%)

The class IIa recommendations for AVR are the following:

• 1

  Asymptomatic patients with very severe AS (aortic jet velocity ≥ 5.0 m/sec or mean pressure gradient ≥ 60 mm Hg) and low surgical risk

• 2

  Apparently asymptomatic patients with severe AS and an exercise test demonstrating decreased exercise tolerance or a fall in systolic blood pressure

• 3

  Symptomatic patients with low-flow/low-gradient severe AS with reduced LVEF (resting valve area ≤ 1.0 cm ² , aortic jet velocity < 4.0 m/sec or mean pressure gradient < 40 mm Hg, LVEF < 50%, and low-dose dobutamine stress study showing an aortic jet velocity ≥ 4.0 m/sec mean pressure gradient ≥ 40 mm Hg with a valve area ≤ 1.0 cm ² )

• 4

  Symptomatic patients with low-flow/low-gradient severe AS with an LVEF ≥ 50%, a calcified aortic valve with significantly reduced leaflet motion, and a valve area ≤ 1.0 cm ² only if clinical, hemodynamic, and anatomic data support valve obstruction as the most likely cause of symptoms and data recorded when the patient is normotensive (systolic blood pressure < 140 mm Hg) indicate an aortic jet velocity < 4.0 m/sec or mean pressure gradient < 40 mm Hg, and a stroke volume index < 35 mL/m ² , and an indexed valve area ≤ 0.6 cm ² /m ² .

• 5

  Patients with moderate AS who are undergoing cardiac surgery for another indication.

The class IIb recommendation for AVR is the following:

• 1

  Asymptomatic patients with severe AS if the patient is at low surgical risk and serial testing shows an increase in aortic velocity of ≥ 0.3 m/sec per year.