**3.9 Pathophysiology**

There is 0 gradient exists across the standard aortic valve during the cardiac cycle. The cross-sectional area of a normal aortic valve is >2 cm2 . While reductions in the valve area to 1.5–2.0 leads to minimal pressure gradient, further narrowing produces dramatic increases in the mean pressure gradient [34]. In AS, progressive obstruction of outflow tract increases afterload ventricular, and wall stress of the left ventricle leads to high left ventricular systolic and diastolic pressures, decreased aortic pressure, and prolonged left ventricular ejection time.

**23**

of the heart.

*Aortic Valve Disease: State of the Art*

ejection fraction [35].

coronary artery disease.

**3.10 Clinical features**

*3.10.1.1 Symptoms*

*3.10.1 Clinical presentation*

*3.10.1.2 Physical findings*

tion or calcified, inelastic arteries.

*DOI: http://dx.doi.org/10.5772/intechopen.93311*

Obstruction to flow usually develops slowly allowing the LV to adapt by concentric thickening hypertrophy serves to reduce wall tension (the law of Laplace describes wall tension is proportional to pressure and radius and adversely proportional to thickness). As long as the process of muscular wall thickening keeps pace with narrowing of the aortic orifice, the 'wall tension' is maintained. Gradually, this results in compensatory concentric left ventricular hypertrophy (LVH) to maintain

The stability comes at a price, now the hypertrophied walls are less compliant and LV less able to fill rapidly. Satisfactory end-diastolic volume becomes heavily reliant upon atrial contraction. Atrial fibrillation often precipitates dramatic acute congestive heart failure in patients with severe AS. The concentric hypertrophy increases myocardial oxygen requirement coupled with reduced coronary flow due to deviated diastole and low diastolic pressures, which aggravates subendocardial ischemia in the presence of normal coronary artery ventricular arrhythmias are common as well. The compensatory mechanism may become insufficient in patients with chronic severe AS, resulting in thinning and dilation of the left ventricle, lead-

Exertional syncope may develop resulting from peripheral vasodilation induced by exercise with the background of a fixed cardiac output. Blood pressure drop may reduce cerebral perfusion, below the minimum required for consciousness [37]. A negative balance between oxygen supply and demand is the norm in AS. LVH increased afterload, and the long systole increases myocardial oxygen demand. The high filling pressure and longer systolic time decrease myocardial oxygen supply by reducing myocardial perfusion time. Myocardial ischemia in patients with AS is due to the alteration in myocardial oxygen supply and demand even in the absence of

Patients with, mild or moderate AS are usually asymptomatic unless they have the coexisting cardiopulmonary disease or infective endocarditis. Patients often remain asymptomatic until the ventricle begins to fail. At this initially, they usually develop fatigue followed by cardinal symptoms of angina, syncope, and dyspnea expected survival following the onset of these symptoms is 2, 3, and 5 years, respectively [38]. In rare instances, sudden tragic death is the first manifestation of the disease. Patients may be sedentary; it unclear whether they are inactive by choice or have gradually restricted their activity to avoid symptoms. A treadmill stress test under

The classic finding in the assessment of peripheral pulses is a delayed and slowly

rising wave contour pulsus parvus et tardus. However, it may be absent patients with associated aortic regurgitation or in patients with associated aortic regurgita-

Precordial palpation may reveal a sustained and laterally displaced cardiac impulse. Because the hypertrophied LV is noncompliant, the critical contribution to filling provided by atrial contraction severe thrill is often palpable at the base

close medical supervision may help in their assessment.

ing to a decrease in ejection fraction and congestive heart failure [36].

### *Aortic Valve Disease: State of the Art DOI: http://dx.doi.org/10.5772/intechopen.93311*

*Advances in Complex Valvular Disease*

role in mitral, and occasionally, aortic stenosis.

remains to be determined.

*Echocardiogram assessment of aortic valve.*

**3.8 Epidemiology and aetiology**

younger patients (>65) [33].

**3.9 Pathophysiology**

**3.7 Aortic stenosis**

**Figure 3.**

Occasionally, balloon valvotomy serves an important therapeutic and diagnostic

Positron emission tomography (PET) is an emerging imaging technique which allows improved resolution more flexibility than SPECT, including the possibility of imaging metabolic substrates and neural transmitters. In light of its expense and dependency mostly cyclotron-produced isotopes, its role in valvular heart disease

Aortic stenosis (AS) may be to congenital or acquired, and the congenital form could be above (supra), below (subvalvular) or at the valve level. A supravalvular is a rare form of long and tubular narrowing is associated with, (William's Syndrome) hypercalcemia, mental retardation, and peripheral pulmonic stenosis. Subvalvular stenosis may be caused by the septum extending into the outflow tract, a cylindrical constriction of the outflow tract or, in hypertrophic cardiomyopathy the obstruction caused by the anterior movement of the mitral valve leaflets. In some patients, this is present only at diminished ventricular (LV) volumes recreated in the echo-

Isolated aortic stenosis (AS) is more frequent in men and is found in 2% of people 65 years of age and older. The most frequent causes of AS include agerelated calcific degeneration, bicuspid aortic valve, and rheumatic aortic valve. The distribution of these causes diverges across age groups and geographic regions. Age-related degeneration is the commonest cause of AS in elderly patients. In comparison, bicuspid aortic valve calcification accounts for most surgical cases in

There is 0 gradient exists across the standard aortic valve during the cardiac

in the valve area to 1.5–2.0 leads to minimal pressure gradient, further narrowing produces dramatic increases in the mean pressure gradient [34]. In AS, progressive obstruction of outflow tract increases afterload ventricular, and wall stress of the left ventricle leads to high left ventricular systolic and diastolic pressures, decreased

. While reductions

cycle. The cross-sectional area of a normal aortic valve is >2 cm2

aortic pressure, and prolonged left ventricular ejection time.

cardiography laboratory by Valsalva cause aortic regurgitation [32].

**22**

Obstruction to flow usually develops slowly allowing the LV to adapt by concentric thickening hypertrophy serves to reduce wall tension (the law of Laplace describes wall tension is proportional to pressure and radius and adversely proportional to thickness). As long as the process of muscular wall thickening keeps pace with narrowing of the aortic orifice, the 'wall tension' is maintained. Gradually, this results in compensatory concentric left ventricular hypertrophy (LVH) to maintain ejection fraction [35].

The stability comes at a price, now the hypertrophied walls are less compliant and LV less able to fill rapidly. Satisfactory end-diastolic volume becomes heavily reliant upon atrial contraction. Atrial fibrillation often precipitates dramatic acute congestive heart failure in patients with severe AS. The concentric hypertrophy increases myocardial oxygen requirement coupled with reduced coronary flow due to deviated diastole and low diastolic pressures, which aggravates subendocardial ischemia in the presence of normal coronary artery ventricular arrhythmias are common as well. The compensatory mechanism may become insufficient in patients with chronic severe AS, resulting in thinning and dilation of the left ventricle, leading to a decrease in ejection fraction and congestive heart failure [36].

Exertional syncope may develop resulting from peripheral vasodilation induced by exercise with the background of a fixed cardiac output. Blood pressure drop may reduce cerebral perfusion, below the minimum required for consciousness [37].

A negative balance between oxygen supply and demand is the norm in AS. LVH increased afterload, and the long systole increases myocardial oxygen demand. The high filling pressure and longer systolic time decrease myocardial oxygen supply by reducing myocardial perfusion time. Myocardial ischemia in patients with AS is due to the alteration in myocardial oxygen supply and demand even in the absence of coronary artery disease.
