Heart Valvular Diseases

Stable pathological changes in the structure of the heart are called Heart diseases.
We distinguish 2 types of them:
Congenital heart disease (lower incidence)
Acquired heart disease (higher incidence)
Congenital HD arise due to abnormal development of the heart and the great vessels
during the intrauterine growth of the fetus. Examples:
- preservation of the ductus arteriosus (Botallos duct)
- stenosis of the great vessels
- congenital defects of the valves
- preservation of foramen ovale
- preservation of intraventricular foramen
Acquired HD may be caused by several diseases:
- infectious endocarditis
- acute rheumatic fever
- sepsis
- syphilis
- injuries
- arteriosclerosis
All these diseases will cause inflammatory processes in the valve cusps and often
end in their sclerosis. The sclerosis will end in 2 ways:
- deformation and shortening of the valves; the valve will not be able to
close completely valve incompetence;
- the cusps of the valves may adhere to one another and to narrow the orifice
they close valve stenosis.
Mitral regurgitation (incompetence)
Mitral (bicuspid) valve regurgitation is an incomplete closing of the left
atrioventricular orifice during ventricular systole. As a result, the blood is returned back
(regurgitated) from the left ventricle to the left atrium. MVI may be:
- organic (caused by diseases, usually rheumatic endocarditis)
- functional (when the mitral valve is not affected, but the mitral orifice is
enlarged and the cusps fail to close completely. It can happen because of
dilatation of the left ventricle and weakening of the circular muscle fibers
of the atrioventricular orifice in pronounced hypertrophy, myocarditis).
Haemodynamics. Because the mitral valve fails to close completely during
systole of the left ventricle (LV), part of the blood is regurgitated into the left atrium
(LA). Systole by systole in left atrium the blood pressure increases, because to the

blood, that comes from the pulmonary veins, is added the regurgitated portion of the
blood. The atrium is dilated and after a period of time becomes hypertrophied.
The greater amount of blood that is delivered from the overfilled LA during
diastole to the LV exceeds a normal one, and the LV becomes hypertrophied.
Intensified work of the LV compensates for the mitral incompetence during a long
time. When the LV weakens, diastolic pressure in it increases and this increases the
pressure in the LA.
Increased pressure in LA increases pressure in the pulmonary veins and this
causes reflex contraction of the arterioles in the lesser circulation (Kitaevs reflex).
Spasm of arterioles increases pressure in pulmonary artery the Right ventricle (RV)
has to contract with a greater force to eject the blood; so after a period of time RV can
be hypertrophied.
Clinical picture. Most patients with mild or moderate mitral regurgitation have
no complaints for a long time and look like healthy persons.
When the pressure in lesser circulation develops, appear dyspnea, palpitation, dry
cough, orthopnea and others. Cyanosis is often met.
Palpation of the heart area reveals changes of characteristics of the apex beat:
- its replacement to the left and sometimes dawn;
- becomes diffuse, intensified, resistant (because of hypertrophy of the LV).
Percussion reveals displacement of the heart borders to left (because of
hypertrophy of the LV) and superiorly (because of hypertrophy of the LA). The
configuration of the heart becomes mitral with an indistinct heart waist. If happens the
hypertrophy of RV, the heart borders are moved to the right also.
Auscultation of the heart reveals:
1st sound decreased at the heart apex (because of the diminishing of the valve
component mitral valves never close completely);
Systolic murmur, synchronous with the 1st sound, at the heart apex (blood stream
in systole passes from LV to LA through a narrow slit because of incomplete
closed valves); it is transmitted to the axillary area,
Accent of the 2nd sound over the pulmonary trunk (because of the increased
pressure in lesser circulation.
Over the apex:
The pulse and arterial pressure do not change in mitral incompetence.
Instrumental explorations:
X-ray studies show the enlargement of LA and LV- to the left, superiorly and
posteriorly; pulmonary arch may be dilated; mitral configuration;
ECG: signs of hypertrophy of LA and LV; may be of the RV also;
EchoCG: distension of the left chambers, movement of the mitral valve cusps
in the opposite direction, their thickening, absence of the full closure during
systole.
Phonocardiography.

Mitral valve stenosis

Etiology rheumatic or septic endocarditis.
The atrioventricular orifice narrows due to adhesion (sticking together) of the
mitral cusps, their thickening. The valve becomes like a funnel with a slit in the middle.
If stenosis is significant and the orifice is narrowed (from the normal 46 cm) to
1-2 cm and less, haemodynamics becomes affected considerable. During diastole blood
passes with difficulty from the LA to LV and a portion of it remains in the LA. To this
remaining blood a new portion of it is added from the pulmonary veins in ventricle
systole. The LA becomes overfilled with blood, excess pressure is first compensated for
by intensified contraction of LA and its hypertrophy; but the force of LA muscle is
insufficient and soon weakens; the LA becomes dilated, the pressure inside it rises.
This increases pressure in the pulmonary veins, produces reflex spasm of the
arterioles in the lesser circulation (Kitaevs reflex) and increases pressure in pulmonary
artery and the Right ventricle. Later RV can be hypertrophied. The LV in mitral stenosis
receives smaller volumes of blood and is therefore less active; its size may decrease.
Clinical picture. In this valve disease the pressure in lesser circulation becomes
increased after a short period of compensation. When the pressure in lesser circulation
develops, appear complaints on dyspnea, palpitation, dry cough (often with
haemoptysis), pain in heart, orthopnea and cyanosis. Both mitral valve diseases mitral
incompetence and mitral stenosis are called blue diseases, because of cyanosis often
met in them.
Inspection reveals:
Acrocyanosis,
Cyanotic blush on the face (mitral face).
Mitral nanism is a lower physical developing of a person because of
congenital mitral stenosis.
Presence of the cardiac beat (because of hypertrophy of RV).
Palpation reveals:
Diastolic cats purr over the apex
Cardiac beat
Percussion:
- displacement of the cardiac border to right and up (hypertrophy of LA and
RV)
- mitral configuration
Auscultation gives the most information over the apex - the area of mitral valve
auscultation:
1st sound is loud and snapping (the LV receives less blood than in normal conditions;
its contraction is fast)
Immediately after the normal second sound appears an adventitious sound due to the
loud opening of the mitral valve - sound of the mitral valve opening;
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 The loud 1st sound + second sound + sound of the mitral valve opening give a
specific triple rhythm, characteristic for mitral stenosis.
Diastolic murmur - is appears because the passage from the LA to LV is narrowed; it
follows the sound of the mitral valve opening (protodiastolic murmur). It is usually
rough, pronounced.
Arterial Pulse may be different (pulsus differens) in the case of pronounced
hypertrophy of the LA, which can compress the left subclavian artery and the pulse on
the left arm becomes smaller. Mitral stenosis is often complicated by atrial fibrillation,
and the pulse becomes arrhythmic (unequal pulse).
Arterial pressure usually remains normal; systolic pressure may be slightly
decreased.
Instrumental explorations:
X-ray studies show the enlargement of LA superiorly (determinated by the
degree of displacement of the oesophagus), appears mitral configuration
(disappearance of the heart waist); pulmonary arch may be dilated; RV may be
hypertrophied;
ECG: signs of hypertrophy of LA and RV;
EchoCG: distension of the left atrium, A-wave disappears; movement of the
mitral valve cusps change they move in the same direction; their thickening,
fibrosis and calcinosis of the cusps. May be appreciated dilatation of the RV.
Phonocardiography.

Aortic regurgitation (incompetence)

Aortic regurgitation is the failure of the aortic valve to close completely during
ventricular diastole; so the blood leaks back from aorta into the LV.
Etiology: rheumatic endocarditis, septic endocarditis; syphilitic affection of the
aorta ; atherosclerosis; trauma.
Inflammatory and sclerotic changes occur in the base of the cusps make them
shrink and shorten (rheumatic endocarditis). Atherosclerosis and syphilitic disease can
affect only aorta to distend it, while aortic valve cusps are only shortened. Trauma can
lead to rupture of the valve cusps.
Haemodynamics. During diastole, blood is delivered into the LV not only
from the LA, but also from aorta due to regurgitation. LV is overfilled and distended. In
systole LV has to contract with a greater force in order to expel the larger blood volume
into aorta. Intensified work of LV causes its hypertrophy and aortic dilatation. The
strong muscle of LV can compensate the disease for a long time 10-20 years.
Arterial blood pressure is characterized by marked variation in aorta during
systole and diastole Systolic Pressure in much increased, while Diastolic Pressure
quickly drops to level of 40 20 mmHg. Examples:
- 160 / 40mmHg;
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- 170 / 20 mmHg/
Arterial pulse is quick and high (pulsus celer et altus).
Clinical picture. Subjective condition of patients with aortic regurgitation may
remain good for a long time. First signs:
- Pain in chest in the heart region (anginal character), because of the relative
coronary insufficiency due to pronounced hypertrophy of LV.
- Giddiness, syncope (a result of deranged blood supply to the brain due to
low diastolic pressure).
- Dyspnea, weakness, palpitation (in the stage of congestion in the lesser
circulation).
Inspection. Skin is pallid due to insufficient filling of the arterial system during
diastole. Marked variation in the blood pressure in the arterial system during systole and
diastole causes the appearance of some signs, such as - pulsation of all the peripheral
arteries:
Pulsation of the carotids arteries (carotid shudder)
Pulsation of the temporal, subclavian arteries
Rhythmical movements of the head synchronous with the pulse (Mussets
sign)
Rhythmical change in the color of the nail bed under a slight pressure on
the nail end (capillary pulse; Quinckes pulse)
Rhythmical reddening of the skin after rubbing.
Palpation reveals:
- Apex beat (apical impulse) is enlarged, elevated, diffuse and intense (due
to enlargement of LV).
- Apex beat is shifted to the left and inferiorly (sometimes may be
determined in the 6th or 7th intercostals spaces, on anterior axillary line.
Percussion:
- displacement of the left cardiac border to left (hypertrophy and dilatation
of LV).
- aortic configuration (with pronounced heart waist).
Auscultation on the aorta:
2nd sound is decreased, sometimes inaudible (due to absence of the period
when aortic valve cusps are completely closed);
Diastolic murmur, transmitted dawn and heard also at the Erb-point, which
weakens by the end of diastole
Auscultation on the apex:
1st sound is decreased (overfilling of the LV with blood);
Murmurs of functional etiology can be heard in aortic incompetence at the heart
apex:
Systolic murmur (if the LV is markedly dilated, it can lead to relative mitral
regurgitation (so-called mitralization of aortic regurgitation); because of
the dilated mitral orifice, mitral valve cant close complete the slit);

 Diastolic murmur Austin Flint murmur arises due to an intense

regurgitation of the blood that moves aside the mitral valve cusp and
appears as functional mitral stenosis.
Auscultation of vessels:
- Double sound (Traube double sound) on femoral artery
- Double murmur Duroziez over femoral artery
Arterial pulse in aortic incompetence is fast, full and high.
Arterial pressure constantly varies: systolic one rises and diastolic one falls; pulse
pressure is always high.
Instrumental explorations:
X-ray studies show the enlargement of LV; appears aortic configuration
(with a distinct heart waist); dilatation of aorta; pulsation of aorta;
ECG: signs of hypertrophy of LV; may be signs of coronary insufficiency
(changes in ST interval and T wave);
EchoCG: flutter of the anterior mitral cusp during diastole; Doppler EchoCG
can appreciate the degree of aortic incompetence.
Phonocardiography.

Aortic valve stenosis

The narrowing of the aortic orifice makes an interference for the expulsion of
blood into aorta during systole of ventricles. Stenosis results from adhered aortic valve
cusps or from cicatrisation of the aortic orifice.
Etiology: rheumatic endocarditis, septic endocarditis; atherosclerosis.
Haemodynamics. During systole the LV is not emptied completely, because
part of blood fails to pass the narrowed aortic orifice. A new normal portion of blood
delivered from LA in diastole is mixed with remaining volume of blood, and the LV
becomes overfilled, the pressure inside it increases; after a period of time the LV
becomes hypertrophied.
Clinical picture. Subjective condition of patients with aortic incompetence may
remain good for a long time. First signs:
- Pain in chest in the heart region (anginal character), because of the relative
coronary insufficiency due to pronounced hypertrophy of LV; most
frequently appears during physical exercises;
- Giddiness, syncope, headache (a result of deranged blood supply to the
brain due to low arterial pressure).
- Dyspnea, weakness, palpitation (in the stage of congestion in the lesser
circulation).
Inspection. Skin is pallid due to insufficient filling of the arterial system with
blood. Both aortic valve diseases are called pallid valve diseases.
Palpation reveals:
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- Apex beat (apical impulse) is enlarged, diffuse, high, resistant (due to

enlargement of LV).
- Apex beat is shifted to the left and inferiorly (sometimes may be
determined in the 6th or 7th intercostals spaces, on anterior axillary line.
- Systolic cats purr on the aorta.
Percussion:
- displacement of the left cardiac border to left (hypertrophy and dilatation
of LV).
- aortic configuration (with pronounced heart waist).
Auscultation on the aorta:
2nd sound is decreased (due to immobilization of the aortic valves that are
adhered);
Systolic murmur, a very rough one; it is conducted by the blood to the
carotids, sometimes can be heard also in the interscapular space. It is
generated by the blood flow through the narrowed orifice.
Auscultation on the apex:
1st sound is decreased (overfilling of the LV with blood); prolongation of
systole.
Arterial pulse in aortic valve stenosis is small, slow and rare, since the blood
slowly passes into aorta and its volume is decreased.
Arterial pressure: systolic pressure is usually decreased; while diastolic pressure
remains normal; pulse pressure is decreased.
Instrumental explorations:
X-ray studies show the enlargement of LV; appears aortic configuration
(with a distinct heart waist); may be poststenotic dilatation of aorta;
ECG: signs of hypertrophy of LV; may be signs of coronary insufficiency
(changes in ST interval and T wave);
EchoCG: decreased opening of the aortic valve during systole; Doppler
EchoCG can appreciate the degree of aortic valve stenosis; signs of
hypertrophy of LV.
Phonocardiography.