VALVULAR HEART DISEASE

Aortic Stenosis

Definition

• Normal aortic valve area = 3-4 cm²

• Mild AS 1.5-3 cm² / Moderate AS 1.0-1.5 cm² / Severe AS <1.0 cm² / Critical AS < 0.5 cm²

Etiology

1. Congenital aortic stenosis

Usually is detected in pediatric patients but occasionally becomes apparent in early adulthood

2. Bicuspid aortic valve

A common congenital cardiac abnormality. The flow characteristics of the bicuspid valve are more turbulent than those of the normal valve, leading to valve injury, calcification, and stenosis in the fourth and fifth decades of life

3. Senile calcific aortic stenosis

Occurs when scarring and calcification of a tricuspid aortic valve lead to orifice narrowing in the sixth, seventh, and eighth decades of life

Although once considered a “degenerative” idiopathic disease, it is now clear that the pathology leading up to severe aortic stenosis is due to proliferative and inflammatory changes leading to calcification, similar to the development of the plaque in ASCAD

4. Rheumatic aortic stenosis

Never occurs alone and is always associated with Mitral valve disease

Pathophysiology

-Aortic valve stenosis → Pressure overload on the left ventricle (Due to the greater pressure that must be generated to force blood past the stenotic valve) → Compensatory left ventricular hypertrophy

Clinical features

A. Symptoms
-Asymptomatic patients with aortic stenosis are at little risk for sudden death. However, this risk increases dramatically when symptoms develop

-Clinical features of AS may present during exercise then at rest

1. Dyspnea

May lead to orthopnea and paroxysmal nocturnal dyspnea as the left ventricle fails

2. Angina

Occurs in 35%–50% of patients with aortic stenosis

Although the exact mechanism of angina is unknown, current data suggest that coronary blood flow reserve is impaired in the severely hypertrophied left ventricle. Impairment of the coronary blood flow reserve limits oxygen delivery to the myocardium and produces angina during exercise (the coronary arteries may be normal)

3.  Syncope

Occurs during exercise. When aortic stenosis is present, cardiac output across the stenotic aortic valve cannot increase during exercise. Because total peripheral resistance falls as the peripheral vessels dilate to supply skeletal muscles. This peripheral resistance normally compensated by an increase cardiac output. Since patients with severe AS cannot increase their cardiac output, the blood pressure falls and Syncope occurs

+Other causes syncope in aortic stenosis include:

-A reflex vasodepressor response to high intra-ventricular pressure, which causes a secondary peripheral vasodilation that, in turn, causes decreased blood flow to the brain resulting in loss of consciousness

-Atrial or ventricular arrhythmias

-Heart block as a result of conduction system calcification. The calcification in and around the aortic valve can progress and extend to involve the electrical conduction system of the heart

After syncope occurs in patients with aortic stenosis, expected survival is 2–3 years without valve replacement.

4. Heart failure

Heart failure occurs because the afterload placed on the myocardium becomes excessive. Both contractile dysfunction and diastolic muscle dysfunction occur when the myocardium is exposed to a prolonged, severe pressure overload.

5.   Systemic emboli

When Blood stasis and overload in left ventricle long enough it will leads to blood clot
B.  Physical Signs
1. Delayed carotid upstroke

In the presence of aortic stenosis, the carotid upstroke typically is delayed in timing and reduced in volume. This finding is the most reliable physical sign in gauging the severity of the disease

2. Systolic ejection murmur

A harsh, late-peaking systolic ejection murmur is heard in the aortic area and is transmitted to the carotid arteries. The murmur also may be reflected to the mitral area, producing the false impression that mitral regurgitation also is present (Gallavardin’s phenomenon)

3. Soft, single/Absent S2

Because the aortic valve is stenotic, its motion is severely impaired. The reduction in motion of the valve causes the aortic component (A2) of the S2 to be absent. Thus, the only component of the S 2 that is heard is the pulmonic component (P2), which is normally soft

4. S4

An S 4 usually is heard as a result of the reduced left ventricular compliance that occurs in left ventricular hypertrophy

5. Sustained, forceful apex beat

The point of maximal (PMI) cardiac impulse usually is not displaced unless heart failure has occurred. However, the impulse is sustained and forceful throughout systole

Diagnosis

1. Electrocardiography

The ECG usually shows evidence of left ventricular hypertrophy

! Patients who have aortic stenosis may present with angina, but an exercise test is absolutely contraindicated in patients who have severe aortic stenosis, because even the mildest exertion can cause syncope or sudden death. It is, therefore, crucial to examine every patient carefully before recommending an exercise ECC

2. Echocardiography

Can rule out significant aortic stenosis if valve motion is shown to be normal. However, Doppler examination of the aortic outflow tract during echocardiography can accurately measure the pressure gradient across the aortic valve and can be used to calculate the valve area

3. Cardiac catheterization

Diagnosis and evaluation of the severity of aortic stenosis may be confirmed by cardiac catheterization, during which the pressure gradient across the valve is measured and the degree of stenosis is calculated

Mitral Stenosis 

Etiology

• Rheumatic heart disease

• Almost all cases of mitral stenosis in adults are secondary to rheumatic heart disease

Pathophysiology

1. Mitral valve stenosis impedes left ventricular filling, thereby increasing left atrial pressure as a pressure gradient develops across the mitral valve

Elevated left atrial pressure is referred to the lungs, where it produces pulmonary congestion

As the stenosis becomes more severe, it may significantly reduce forward cardiac output

2. The burden of propelling blood across the stenotic mitral valve is borne by the right ventricle. The overload on the right ventricle may be increased further when secondary pulmonary vasoconstriction occurs (The mechanism of which is explained by Jordan’s hypothesis). Thus, the right ventricle must generate enough force both to overcome the resistance offered by the stenotic valve and to propel blood through constricted pulmonary arteries. Consequently, pulmonary arterial pressure may increase to three to five times normal, eventually resulting in right ventricular failure

Clinical features

A. Symptoms

1. Left-sided failure

Dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea occur as a result of reduced left ventricular output and increased left atrial pressure (Pulmonary hypertension or pulmonary oedema). In mitral stenosis, the symptoms of left ventricular failure usually are not attributable to left ventricular dysfunction but, rather, to the mitral stenosis itself

2. Right-sided failure

When pulmonary hypertension is severe, the chance of developing pulmonary oedema decreases and symptoms of right heart failure dominates the clinical picture; producing edema, ascites, hepatomegaly

3. Hemoptysis

The high left atrial pressure produced in mitral stenosis may lead to rupture of small bronchial veins, producing hemoptysis

4. Systemic embolism

Stagnation of blood in the enlarged left atrium and left atrial appendage occurs in mitral stenosis, particularly if atrial fibrillation is present. Under these circumstances, a thrombus may form in the left atrium and can become a source of systemic embolism

5. Palpitations

Atrial fibrillation is common in this condition (due to enlargement of the left atrium) and may cause palpitations, which are often accompanied by a sudden worsening in the dyspnoea because the loss of the atrial contraction

+Symptoms that are secondary to effects of left atrial enlargement include:

• Hoarseness due to stretching of the recurrent laryngeal nerve.

• Dysphagia due to oesophageal compression.

• Left lung collapse due to compression of the left main bronchus.

B. Physical Signs

1.  Pulmonary rales

Bilateral pulmonary rales occur secondary to elevated left atrial and pulmonary venous pressures

2.  Increased intensity of the S1

The S1 usually increases in intensity because the transmitral gradient delays diastolic mitral valve

closure. Thus, the mitral valve remains open until ventricular systole closes it forcibly, resulting

in an increase in S 1 intensity. Late in the course of the disease, the valve may become so stenotic

that it no longer opens or closes, reducing the intensity of S1

3.  Increased intensity of the P2

The P2 component of the S2 is usually increased in intensity if pulmonary hypertension has

developed

4.  Opening snap

An opening snap is heard following the S 2 as the stenotic valve is forced open in diastole by the

high left atrial filling pressure. The higher the pressure, the sooner does the mitral valve open

5.  Diastolic rumble

The murmur of mitral stenosis is a low-pitched apical rumble, which begins after the opening

snap. If the patient is in sinus rhythm, atrial systole produces a presystolic accentuation of this

murmur

6.  Sternal lift

Enlargement of the right ventricle as a result of pulmonary hypertension produces a systolic lift of

the sternum

7.  Other symptoms

Neck vein distention, edema, hepatic enlargement, and ascites may be present if right ventricular

failure occurs

Diagnosis

1. Electrocardiography

The ECG may show atrial fi brillation, as well as signs of left atrial enlargement and right ventricular

hypertrophy

2. Chest radiography

• Straightening of the left heart border and a double density along the right heart border (formed by the right and left atria) occur as a result of left atrial enlargement

•Signs of pulmonary venous hypertension, including an increase in pulmonary vascular markings and Kerley’s lines, are likely to be present

• When pulmonary hypertension leads to right ventricular enlargement, the lateral view shows a loss of the retrosternal airspace

3. Echocardiography

• The echocardiogram shows reduction in the excursion of the valve leaflets and thickening of the valve. Two-dimensional echocardiography can be used to visualize and measure the residual mitral valve orifice. Invariably, left atrial enlargement is present.

• Doppler examination of the mitral valve may also help to quantify the severity of the stenosis.