Increased pressure in the left atrium increases pressure in the pulmonary veins and this in turn causes reflex contraction of the arterioles

Fig. 69. Changes in the intracardiac haemodynamics in mitral incompetence.

^—normal heart; 2—heart with mitral incompetence (the hypertrophied chambers are printed in red; normal

blood flow is shown by straight arrows, and the regurgitated flow is shown by the wavy arrow).

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in the lesser circulation (Kitaev's reflex) due to stimulation of barorecep-tors. Spasm in the arterioles increases significantly pressure in the pulmonary artery to intensify the load on the right ventricle which has to contract with a greater force in order to eject blood into the pulmonary trunk. The right ventricle can therefore also be hypertrophied during long­standing pronounced mitral incompetence.

Clinical picture. Most patients with mild or moderate mitral in­competence have no complaints for a long time and look very much like healthy subjects. As congestion in the lesser circulation develops, dyspnoea, palpitation of the heart, cyanosis, and other symptoms appear.

Palpation of the heart area reveals displacement of the apex beat to the left and sometimes inferiorly. The beat becomes diffuse, intensified, and resistant, which indicates hypertrophy of the left ventricle. Percussion reveals displacement of the heart's borders to the left and superiorly because of the enlarged left atrium and left ventricle. The configuration of the heart becomes mitral with an indistinct heart waist. The border of the heart shifts to the right in hypertrophy of the right ventricle. Auscultation of the heart reveals decreased first sound at the heart apex because the valves never close completely in this disease. Systolic murmur can be heard at the same point, which is the main sign of mitral incompetence. It arises during systole when the stream of blood passes a narrow slit leading from

Fig. 70. PCG in mitral incompetence. The amplitude of the first sound is decreased on a PCG taken at the heart apex; systolic murmur occupies the entire pause between the first and second

heart sounds.

the left ventricle to the left atrium. The systolic murmur is synchronous with the first sound. When the blood pressure rises in the lesser circulation, an accent of the second sound can be heard over the pulmonary trunk.

Auscultation findings are confirmed and verified by phonocar-diography (Fig. 70). The pulse and arterial pressure do not change in com-"pensated mitral incompetence. X-ray studies show a specific enlargement of the left atrium and the left ventricle detectable by enlargement (to the left, superiorly and posteriorly) of the heart silhouette. When blood pressure increases in the lesser circulation, the pulmoanry arch dilates. Signs of hypertrophy of the left atrium and the left ventricle can also be found on the ECG: it becomes the left type and the P waves become higher.

Echocardiography reveals distention of the left heart chambers (atrium and ventricle), movement of the mitral valve cusps in the opposite direc­tion, their thickening and the absence of full closure during systole.

Mitral incompetence may remain compensated for a long time. But a long-standing pronounced mitral incompetence and decreased myocardial contractility of the left atrium and the left ventricle cause venous conges­tion in the lesser circulation. Contractility of the right ventricle can later be affected with subsequent development of congestion in the greater circula­tion.

STENOSIS OF THE LEFT ATRIOVENTRICULAR ORIFICE

The left atrioventricular orifice usually narrows in a long-standing rheumatic endocarditis (stenosis ostii venosi sinistri). In very rare cases mitral stenosis may be congenital or secondary to septic endocarditis. The atrioventricular orifice narrows due to adhesion of the mitral cusps, their consolidation and thickening, and also shortening and thickening of the tendons. The valve thus becomes a diaphragm or a funnel with a slit in the middle. Cicatricial and inflammatory narrowing of the valvular ring is less important in genesis of mitral stenosis. The valve may be calcified in long­standing stenosis.

If stenosis is significant and the orifice is narrowed from the normal 4-6 cm² to 1.5 cm² and less, haemodynamics becomes affected con­siderably. During diastole, blood fails to pass from the left atrium to the left ventricle and the remaining blood is added to the blood delivered from the pulmonary veins. The left ventricle thus becomes overfilled with blood, the pressure in the ventricle increases. Excess pressure is first compensated for by intensified contraction of the atrium and its hypertrophy, but the force of the left atrial muscle is insufficient to compensate permanently for the pronounced narrowing of the mitral orifice and its contractile force soon weakens; the atrium becomes dilated, and the pressure inside it rises. This in turn increases pressure in the pulmonary veins, produces a reflex

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spasm in the arterioles of the lesser circulation and increases pressure in the pulmonary artery. All this requires intensified work of the right ventricle, which later also becomes hypertrophied. The left ventricle in mitral stenosis receives smaller volumes of blood and is therefore less active; its size slightly decreases (Fig. 71).

Clinical picture. When congestive changes occur in the lesser circula­tion, the patient develops dyspnoea and palpitation on physical exertion; he complains of pain in the heart, cough, and haemoptysis. Inspection reveals acrocyanosis and cyanotic blush on the face. If the disease develops in childhood, the patient's physical growth often slows down and infantilism may develop ("mitral nanism")- Visual examination of the heart region often reveals a cardiac beat consequent upon dilatation and hypertrophy of the right ventricle. The apex beat is not intensified; its palpation can reveal diastolic cat's purr (presystolic thrill). The broadening of cardiac dullness to the right and superiorly due to hypertrophy of the left atrium and right ventricle can be determined by percussion. The heart becomes "mitral" in configuration.

Fig. 71. Changes in the intracardiac haemodynamics in mitral stenosis. The wavy arrow in­dicates an obstructed passage of blood from the atrium to the ventricle (for designations see

Fig. 69).

In auscultation of the heart the first sound at the apex becomes loud and snapping because the left ventricle receives little blood and its contrac­tion is fast. An adventitious sound due to the opening of the mitral valve can be heard at the apex beat. It follows the second sound of the heart. The loud first sound, second sound, and the sound of mitral valve opening give a specific murmur which is characteristic of mitral stenosis. The second sound becomes accentuated over the pulmonary trunk when pressure in the lesser circulation increases. Diastolic murmur is characteristic of mitral stenosis because the passage from the left atrium to the ventricle during diastole is narrowed. This murmur can be heard to follow the mitral valve

opening sound (protodiastolic murmur) because the velocity of the blood flow in early diastole is higher due to the pressure difference in the atrium and the ventricle. The murmur disappears when the pressures equalize. If stenosis is not pronounced, the murmur can be heard only at the end of diastole, immediately before systole proper (presystolic murmur); it arises during acceleration of the blood flow at the end of ventricular diastole because of the early atrial systole. Diastolic murmur can be heard in mitral stenosis during the entire diastole. It increases before systole and joins the first snapping sound.

The pulse in mitral stenosis may be different on the left and right arms. In considerable hypertrophy of the left atrium, the left subclavian artery is compressed and the pulse on the left arm becomes smaller (pulsus dif-ferens). If the left ventricle is not filled completely and the stroke volume is decreased, the pulse becomes small (pulsus parvus). Mitral stenosis is often complicated by atrial fibrillation, and the pulse becomes arrhythmic. Arterial pressure usually remains normal; the systolic pressure sometimes slightly decreases and diastolic pressure increases. X-ray patterns of the heart show the specific enlargement of the left atrium, which leads to disappearance of the heart waist and "mitral" configuration appears (Fig. 72a). Enlargement of the left atrium is determined in the first oblique position by the degree of displacement of the oesophagus which becomes especially vivid with barium sulphate suspension (Fig. lib). If pressure in the lesser circulation increases, X-rays show swelling of the pulmonary arch and hypertrophy of the right ventricle. X-ray pictures sometimes show calcification of the mitral valve. Pneumosclerosis develops during long­standing hypertension of the lesser circulation; it may also be revealed dur­ing X-ray examination.

The ECG of the heart with mitral stenosis shows hypertrophy of the left atrium and the right ventricle: the amplitude and duration of the P wave in­crease, especially in the first and second standard leads; the electrical axis of the heart deviates to the right, a high R wave appears in the right chest leads and a pronounced S wave in the left chest leads.

A phonocardiogram taken at the apex shows the high amplitude of the first sound; the second sound is followed by the mitral valve opening sound and diastolic murmur; the amplitude of the second sound over the pulmonary artery increases compared with that over the aorta (Fig. 73). If PCG and ECG are taken synchronously, attention should be paid to the length of the interval Q-\ sound (from the beginning of the Q wave on the ECG to the first sound on the PCG) and the second sound—OS interval. Echocardiograms in mitral stenosis are characterized by the following:

1. The A wave, describing the maximum opening of the valve during atrial systole either decreases or disappears altogether.

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Fig. 72. X-ray of a heart with mitral stenosis.

a—mitral heart; b—deviation of the contrasted oesophagus by the small radius arc in the right anterior ob­lique position.

Fig. 73. PCG in mitral stenosis. The PCG taken at the heart apex shows increased amplitude of the first sound, diastolic (presystolic) murmur, and the sound of the mitral valve opening

(OS).

2. The speed of diastolic closure of the anterior mitral cusps decreases to decrease the E-F slope.

3. Movements of the cusps change. The cusps of a normal mitral valve move in the opposite direction to set apart during diastole: the anterior cusp moves toward the anterior wall while the posterior cusp to the posterior wall. In stenosis, these movements become unidirectional because the more massive anterior wall pulls the posterior one by adhesion. The movement of the valve is represented on the echocardiogram in the form of a square wave. Enlargement of the left atrium and changes in the cusps (fibrosis, calcinosis) can also be detected by echocardiography.

Mitral stenosis soon becomes attended by congestion in the lesser cir­culation which requires greater work of the right ventricle. Decreased con­tractility of the right ventricle and venous congestion in the greater circula­tion develop therefore in mitral stenosis earlier and more often than in mitral incompetence.

. Dilatation of the right ventricle and weakening of its myocardium are sometimes attended by relative tricuspid insufficiency. Moreover, long-

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standing venous congestion in the lesser circulation in mitral stenosis causes, with time, sclerosis of the vessels and growth of connective tissue in the lungs. Another obstacle to the blood flow is thus created in the lesser circulation and this adds to the difficulties in the work of the right ven­tricle.

AORTIC INCOMPETENCE

Aortic incompetence (aortic insufficiency) is the failure of the aortic valve to close completely during ventricular diastole; blood thus leaks back into the left ventricle. Aortic incompetence is usually secondary to rheumatic endocarditis, and less frequently bacterial (septic) endocarditis, syphilitic affection of the aorta, or atherosclerosis. Inflammatory and sclerotic changes occurring in the base of the cusps during rheumatic en­docarditis make them shrink and shorten. Atherosclerosis and syphilis can affect only the aorta (to distend it), while the valve cusps are only shorten­ed. The cicatricial changes may extend onto the cusps to disfigure them. Parts of the valve disintegrate in ulcerous endocarditis associated with sep­sis and the cusps are affected with their subsequent cicatrization and shortening.

Fig. 74. Changes in the intracardiac haemodynamics in aortic incompetence. The hyper-trophied chambers are printed in red (for designations see Fig. 69).

Haemodynamics. During diastole, blood is delivered into the left ven­tricle not only from the left atrium but also from the aorta due to regurgita-tion, which overfills and distends the left ventricle during diastole. During systole, the left ventricle has to contract with a greater force in order to ex-pell the larger blood volume into the aorta. Intensified work of the left ven­tricle causes its hypertrophy, while the increased systolic volume in the aor­ta causes its dilatation (Fig. 74).

Aortic incompetence is characterized by a marked variation in the blood pressure in the aorta during systole and diastole. An increased volume of blood in the aorta during systole increases systolic pressure and since part of blood is returned during diastole into the ventricle, the diastolic pressure quickly drops.

Clinical picture. Subjective condition of patients with aortic in­competence may remain good for a long time because the defect is compen­sated for by harder work of the powerful left ventricle. Pain in the heart (anginal in character) may sometimes be felt; it is due to relative coronary insufficiency because of pronounced hypertrophy of the myocardium and inadequate filling of the coronary arteries under low diastolic pressure in the aorta. The patient may sometimes complain of giddiness which is the result of deranged blood supply to the brain (which is also due to low diastolic pressure).

If contractility of the left-ventricular myocardium is impaired, conges­tion in the lesser circulation develops and the patient complains of dyspnoea, tachycardia, weakness, etc. The skin of the patient is pallid due to insufficient filling of the arterial system during diastole. Marked varia­tions in the pressure in the arterial system during systole and diastole ac­count for the appearance of some signs, such as pulsation of the peripheral arteries, the carotids (carotid shudder), subclavian, brachial, temporal, and other arteries; rhythmical movements of the head synchronous with the pulse (Musset's sign), rhythmical change in the colour of the nail bed under a slight pressure on the nail end, the so-called capillary pulse (Quin-cke'sjpulse), rhythmical reddening of the skin after rubbing, etc.

The apex beat is almost always enlarged and shifted to the left and in-feriorly. Sometimes, along with the elevation of the apex beat, a slight depression in the neighbouring intercostal spaces can be observed. The apex beat is palpable in the sixth and sometimes seventh hypochondrium, anteriorly of the midclavicular line. The apex beat is diffuse, intense, and rising like a dome. This indicates significant enlargement of the left ventri­cle. The border of cardiac dullness can be found (by percussion) to shift to the left; the heart becomes "aortic" (with pronounced waist of the heart).

Auscultation reveals decreased first sound at the apex, since during left-ventricular systole the period when the valves are closed is absent. The se­cond sound on the aorta is also weak, and if the valve is damaged significantly, it can be inaudible. The second sound can be quite loud in atherosclerotic affection of the aorta. Diastolic murmur heard over the aorta and at the Botkin-Erb listening point is characteristic. This is a low blowing protodiastolic murmur which weakens by the end of diastole as the blood pressure in the aorta drops and the blood-flow rate decreases. The described changes in the sounds and murmurs are clearly visible on

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Fig. 75. 5CG in aortic incompetence. The amplitude of the heart sounds and diastolic murmur are decreased on the ECG taken over the aorta.

phonocardiograms (Fig. 75). Murmurs of functional aetiology can also be heard in aortic incompetence at the heart apex. If the left ventricle is markedly dilated, relative mitral incompetence develops and systolic mur­mur can be heard at the heart apex. Diastolic murmur (presystolic or Austin Flint murmur) can sometimes be heard. It arises due to an intense regurgitation of the blood that moves aside the mitral valve cusp to account for functional mitral stenosis. Doubled sound (Traube double sound) and doubled Vinogradov-Duroziez murmur can sometimes be heard over the femoral artery in this disease.

The pulse in aortic incompetence is fast, full, and high, which is due to high pulse pressure and increased volume of blood delivered into the aorta during systole. Arterial pressure constantly varies: the systolic pressure rises and diastolic falls, and the pulse pressure is therefore high.

X-ray studies show an enlarged left ventricle with a distinct waist of the heart (Fig. 76) and dilatation of the aorta; pulsation of the aorta is intense.

The ECG also reveals various signs of hypertrophy of the left ventricle (Fig. 77): the electrical axis is deviated to the left, the S waves in the right chest leads are deep and the amplitude of the R wave is higher in the left chest leads; these signs often combine with signs of overstrain in the left ventricle and relative coronary insufficiency (changes in the terminal part

of the ventricular complex, displacement of the S-T interval, and the negative T wave).

Echocardiograms taken from patients with aortic failure show flutter of the anterior mitral cusp during diastole caused by the thrust of the blood regurgitated from the aorta into the ventricle.

Aortic incompetence can for a long time be compensated for by inten­sified work of the hypertrophied left ventricle. When its contractile force decreases, congestion in the lesser circulation develops. Acute weakness of the left ventricle sometimes develops and is manifested by an attack of car­diac asthma. Dilatation of the weakened left ventricle can cause relative mitral incompetence. This increases venous congestion in the lesser circula­tion associated with decompensated aortic incompetence and adds to the load on the right ventricle. This is mitralization of aortic incompetence, which may become the cause of venous congestion in the greater circula­tion.

Fig. 76. X-ray in aortic incompetence. The heart's configuration is aortic; the left ventricle is dilated and hypertrophied, the ascending aorta is dilated.

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Fig. 77. ECG in aortic incompetence. AORTIC STENOSIS

The narrowing of the aortic orifice (aortic stenosis) interferes with ex­pulsion of blood into the aorta during contraction of the left ventricle. Aortic stenosis is usually caused by rheumatic endocarditis; less frequently

ll

it develops due to bacterial endocarditis, atherosclerosis, or it may be con­genital. Stenosis results from adhered aortic valve cusps or develops due to cicatricial narrowing of the aortic orifice.

Haemodynamics. During systole, the left ventricle is not emptied com­pletely because part of blood fails to pass the narrowed orifice into the aor­ta. A new normal portion of blood delivered during diastole from the left atrium is mixed with the residual volume and the ventricle becomes over­filled. The pressure inside it thus rises. This disorder is compensated for by an intensified activity of the left ventricle to cause its hypertrophy (Fig. 78).

Clinical picture. Aortic stenosis can remain compensated for years and would not cause any unpleasant subjective sensations (even during intense physical exertion). If obstruction of the aortic orifice is considerable, insuf­ficient blood ejection into the arterial system upsets normal blood supply to the hypertrophied myocardium and the patient feels pain in the heart (angina pectoris-type pain). Disordered blood supply to the brain is manifested by giddiness, headache, and tendency to fainting. These symp­toms like pain in the heart would more likely occur during physical exercise and emotional stress.

The skin of the patient is pallid due to insufficient blood supply to the arterial system. The apex beat is displaced to the left, less frequently in-feriorly; it is diffuse, high, and resistant. Systolic thrill (cat's purr) can be palpated in the region of the heart. Percussion reveals displacement of the left border; the heart is "aortic" due to hypertrophy of the left ventricle. Auscultation of the heart at its apex reveals diminished first sound due to overfilling of the left ventricle and prolongation of systole. The second sound is diminished over the aorta. If the aortic cusps adhere and are im-

Fig. 78. Upset intracardiac haemodynamics in stenosed aortic orifice (for designations see

Fig. 69).

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L /C

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(1 m ft m

Fig. 79. PCG and sphygmogram in aortic stenosis. The PCG taken over the aorta shows crescendo-decrescendo (diamond-shaped) systolic murmur; the peak of the sphygmogram is

serrated like a cock's comb.

mobile, the second sound can be inaudible. Rough systolic murmur over the aorta is characteristic. This murmur is generated by the blood flow through the narrowed orifice. It is conducted by the blood onto the carotids and can sometimes be heard in the interscapular space. The pulse is small, slow, and rare, since the blood slowly passes into the aorta and its volume is decreased. Systolic arterial pressure is usually diminished, while diastolic remains normal or increases. The pulse pressure is therefore decreased.

X-ray examination shows hypertrophied left ventricle, "aortic" con­figuration of the heart, and dilatation of the ascending aorta (post-stenotic); the cusps of the aortic valve are often calcified.

The ECG usually shows signs of hypertrophy of the left ventricle and sometimes of coronary insufficiency. The phonocardiogram shows the specific changes in the heart sounds: diminished amplitudes of the first sound at the heart apex and of the second sound over the aorta. Systolic murmur over the aorta is typical; its oscillations are recorded in the form of specific diamond-shaped figures (Fig. 79).

Sphygmograms of the carotids reveal slowed ascent and descent of the pulse wave (slow pulse), small amplitude of the pulse waves, and specific serrated pattern of their peaks (sphygmograms in the form of a cock's comb) showing oscillations associated with conduction of systolic murmur onto the neck vessels.

Echocardiograms show decreased opening of the aortic valve during systole. Echoes from the cusps become more intense and signs of hyper­trophy of the left ventricle appear.

Aortic stenosis remains compensated for a long time. Circulatory insuf­ficiency develops in diminished contractility of the left ventricle and it is manifested as in aortic incompetence.

TRICUSPID INCOMPETENCE

Insufficiency of the tricuspid valve can be functional (relative) and organic (permanent). Organic tricuspid incompetence occurs in rare cases, mainly due to rheumatic endocarditis. Tricuspid incompetence usually combines with affections of other heart valves; as an independent disease, it occurs in exceptionally rare cases.

Relative (functional) insufficiency of the tricuspid valve occurs more often. It is due to dilatation of the right ventricle and distention of the right-atrioventricular orifice. Tricuspid incompetence often combines with mitral diseases because the right ventricle has to perform greater work due to the high pressure in the lesser circulation. This causes overstrain and distention of the right ventricle.

Haemodynamics. Due to incomplete closure of the tricuspid valve dur­ing right-ventricular systole, part of blood is regurgitated into the right atrium, where it is mixed with the normal volume of blood delivered from the venae cavae. The atrium thus becomes distended and hypertrophied. During diastole, a larger volume of blood is delivered into the right ventri­cle from the right atrium because the portion of blood that was regurgitated into the atrium during systole is added to the normal volume of blood delivered. This causes dilatation and hypertrophy of the right ven­tricle (Fig. 80). Compensation in this disease is attained by intensified work of the right atrium and the right ventricle whose compensatory power is not great and congestion in the greater circulation therefore soon develops.

Clinical picture. Pronounced venous congestion in the greater circula­tion in the presence of tricuspid incompetence causes oedema, ascites, feel­ing of heaviness and right hypochondriac pain (due to enlargement of the liver). The skin becomes cyanotic, sometimes with a yellowish tint. The neck veins swell and pulsate; the positive venous pulse and pulsation of the liver are also observed. These pulsations are explained by the regurgitation

20*

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of blood from the ventricle to the atrium through an incompletely closed atrioventricular orifice, owing to which pressure increases in the atrium and emptying of the neck and liver veins is made difficult. Tricuspid in­competence is characterized by extensive hepatic pulsation: the liver is displaced anteriorly and swells. This can be felt by trying to hold the liver by both hands: the pulsating liver sets the hands apart during the pulse wave.

Inspection of the patient reveals pronounced pulsation in the region of the right ventricle. As distinct from the heart beat in mitral stenosis, this pulsation is characterized by systolic retraction and diastolic protrusion of the chest.

Systolic retraction of the chest in the region of the right ventricle is ex­plained by pronounced diminution of its volume because much blood is delivered at that moment to the hepatic veins. Systolic retraction of the chest corresponds to the systolic swelling of the liver, and vice versa, diastolic overfilling of the right ventricle and protrusion of the chest in the ventricular region combine with diastolic diminution of the liver volume. Therefore, if the examiner places one hand on the region of the right ven­tricle and the other hand over the liver, he can feel specific rolling movements of the hands. The apex beat is as a rule not pronounced because the left ventricle is displaced posteriorly by the hypertrophied right ventricle. Percussion reveals marked displacement of the heart border to the right due to hypertrophy of the right atrium and right ventricle.

Wg. 80. Changes in intracardiac haemodynamics in tricuspid incompetence (for designations :,■;.-• see Fig. 69).

Auscultation at the base of the xiphoid process reveals diminished first sound; systolic murmur can be heard at the same listening point and also at the 3rd and 4th interspaces, to the right of the sternum; this murmur in-

I

creases when the patient keeps his breath at the height of inspiration. Since pressure in the lesser circulation decreases in tricuspid incompetence, the second sound over the pulmonary trunk decreases in its clearness.

Pulse does not change significantly or it becomes small and fast, because serious heart failure often occurs in tricuspid incompetence. Arterial pressure usually decreases. The venous pressure increases mar­kedly.

Signs of hypertrophy of the right heart's chambers can be detected roentgenographically. Electrocardiography also shows hypertrophy. Phonocardiography records systolic murmur at the base of the xiphoid process and at the 3rd and 4th intercostal spaces, to the right of the ster­num; the systolic murmur has a decreasing character. When a phonocar-diogram is taken at the height of inspiration, the vibration amplitude in­creases.

A phlebogram of the jugular vein reveals a high positive a wave which is connected with the intensified activity of the hypertrophied right atrium, or the wave has the form characteristic of the positive venous pulse.

Echocardiography of the tricuspid valve is more difficult than that of the mitral or the aortic valve. Echocardiograms can reveal paradoxical movements of the interventricular septum in overloading of the right ven­tricle associated with tricuspid insufficiency.

Tricuspid incompetence usually combines with grave circulatory insuf­ficiency. Long-standing congestion in the greater circulation upsets the function of many organs, such as the liver, kidneys, or the gastro-intestinal tract. The liver is especially affected: prolonged congestion in the liver is at­tended by growth of connective tissue to provoke the development of the so-called cardiac fibrosis of the liver. This, in turn, even more interferes with the normal function of the organ and causes severe metabolic disorders.

COMBINED AND CONCOMITANT HEART DISEASES

Acquired diseases of the heart, rheumatic in particular, often occur as combined affections of the valves, i.e. valve incompetence and stenosis of the orifice occur simultaneously. Moreover, concomitant affection of two, and sometimes three valves (mitral, aortic, and tricuspid) may occur simultaneously.

Mitral incompetence is most common. It usually concurs with stenosis of the left venous orifice. Signs of both heart diseases are then found but one sign dominates as a rule; less frequently, signs of valvular in­competence and stenosis are equally pronounced.

Dyspnoea and cyanosis are early symptoms of the mitral disease. The

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heart expands to the left, superiorly, and to the right, because both ven­tricles and the left atrium are hypertrophied. Intensity of the first sound at the apex depends on the prevalent disease: if mitral incompetence is the leading syndrome, the first heart sound diminishes; if mitral stenosis dominates, the first sound increases and becomes squelching. Two sounds are heard at the apex: systolic due to valvular insufficiency, and diastolic due to stenosed orifice.

Pulse and arterial pressure do not change in prevalence of mitral in­competence, while if mitral stenosis dominates, systolic arterial pressure may decrease and diastolic pressure increase; the pulse becomes small.

Combined aortic incompetence is usually secondary to rheumatic en­docarditis. Both systolic and diastolic murmurs are characteristic; these sounds can be heard over the aorta. Vascular pulsation and high pulse pressure are typical of aortic incompetence; they are not so pronounced in combined aortic affection. At the same time, slow and small pulse, and low pulse pressure that are typical of aortic stenosis, are also less pronounced in combined aortic incompetence.

Detailed clinico-instrumental examination of patients with concomitant affections of several valves reveals signs typical of each particular disease. It is necessary in such cases to conclude on the gravity of each disease and the prevalence of one of them. This is especially important for prognostic conclusions and for prospective surgical treatment.

Prognosis and treatment of heart diseases. The course of heart diseases and their prognosis depend on many factors. Mild changes in the heart valves, in the absence of marked affections of the myocardium, can remain non-manifest for a long time without impairing the work capacity of the patient. Aortic insufficiency is compensated for a long time but when decompensation develops, the patient soon dies. Mitral stenosis has a worse prognosis because the disease is compensated by a weaker left atrium. Congestion soon develops in the lesser circulation, which is follow­ed by incompetence of the right heart chambers, and the greater circulation soon becomes affected by congestion. Repeated rheumatic attacks have an adverse effect on the course of the disease: the valvular apparatus of the heart is progressively impaired and the myocardium is affected. These disorders provoke circulatory insufficiency. Moreover, any infection, poisoning, physical or nervous overstrain, pregnancy and labour may give an impetus to the development of heart failure.

Restitution prognosis depends on the general condition and physical fitness of the patient. In the absence of symptoms of circulatory insuffi­ciency, the patient may return to his usual occupation; in the presence of signs of decompensation, the patient should be recommended to change his occupation. Work capacity can be preserved in a patient with heart disease

provided he fulfills special recommendations for his work and rest, if he abstains from overeating, smoking, or drinking. Remedial exercises can be prescribed to strengthen the myocardium in the absence of cardiac insuffi­ciency.

Prophylaxis of heart diseases consists mainly in prevention of rheumatism, sepsis and syphilis. Prophylaxis also implies sanation of infec­tious foci, strengthening of the body, and exercises.

Conservative treatment of patients with heart diseases consists in pro­phylaxis and treatment of heart failure. Mitral stenosis is often corrected surgically (mitral comissurotomy). The adhered cusps are disjoined and the atrioventricular orifice is widened. This operation removes severe haemodynamic disorders. Aortic comissurotomy is performed in stenosed aortic orifice, but this operation is much more complicated. Surgical treat­ment of mitral and aortic incompetence consists in replacement of the destroyed valve by an artificial one.

Patients with rheumatic heart disease should be regularly observed in out-patient conditions.

Myocarditis

Myocarditis is inflammation of the myocardium. The disease affects both men and women at any age. Acute, subacute, and chronic myocarditis are differentiated. The disease may be local or diffuse.

Aetiology and pathogenesis. Aetiological factors responsible for the development of myocarditis are various bacterial and virus infections. The most common cause of myocarditis is rheumatism, next come sepsis, diphtheria, rickettsiosis, scarlet fever, and virus infections. Myocarditis may develop in sensitization to some medicinal preparations (allergic myocarditis). Inflammatory changes in the myocardium caused by various infections are the result of allergic reaction of the body sensitized by certain microbes. The microbe antigen or its toxin act on the myocardium to cause formation of tissue antigens (auto-antigens) in it. As a result, auto-antibodies are formed which account for the vast changes in the myocar­dium.

Pathological anatomy. Dystrophic processes in the muscle fibres are characteristic. Predominant exudative or proliferative processes are also observed in the interstitial tissue (in­terstitial myocarditis). The outcome of the inflammatory changes is cardiosclerosis.

Clinical picture. This includes signs of decreased contractility of the myocardium and upset cardiac rhythm. The patient complains of dyspnoea in physical exertion, extreme weakness, palpitation, intermissions, dull and boring pain, or attacks of pain in the heart (like in angina pectoris).

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The skin is pallid, sometimes with a slight cyanotic shade. In pronounc­ed heart failure the neck veins become swollen. The pulse is small, soft, sometimes arrhythmical and accelerated: it may however be slowed down too. Extrasystole and, less frequently, paroxysmal fibrillation develop in deranged excitation function and automaticity.

Decreased diffuse apex beat, which is displaced anteriorly, is revealed on examination of the heart. Percussion can detect displacement of the heart to the left. Auscultation reveals a markedly decreased first sound at the early systole (due to decreased rate of rise in the intraventricular pressure). The second sound is either unchanged or diminished due to hypotension. Gallop rhythm can be heard in significantly decreased myocardial contractility. Systolic murmur can often be heard over the heart apex. It arises due to relative mitral incompetence. Arterial pressure, especially systolic, decreases and the pulse pressure falls accordingly.

ECG changes in myocarditis are quite varied and transient. Sinus tachycardia, sinus arrhythmia, and extrasystole (in the form of separate or group atrial or ventricular extrasystoles) can most frequently be found on electrocardiograms. Conduction is deranged according to incomplete or complete atrioventricular block. Diffuse affections of the myocardium are shown on ECG as diminished and split P wave, changed QRS complex (decreased voltage of the waves and their splitting), decreased S-T interval, the presence of two phases and inversion of the decreased T wave.

The blood counts show moderate neutrophilic leucocytosis with shift to the left, increased ESR, and hyperglobulinaemia (mainly due to a₂- and 7-globulins).

Course. The course of myocarditis is usually favourable and ends with recovery. Sclerosis of the myocardium develops in some patients (myocar­dial cardiosclerosis).

Treatment. Myocarditis patients are prescribed strict bed-rest. The main cause that provokes the disease is treated by antibiotics, desensitizing preparations, and hormones. Cardiac glycosides and diuretics are given in the presence of heart failure. In order to improve metabolism in the myocardium, carboxylase, ATP, vitamins, and potassium preparations are prescribed. Deranged cardiac rhythm can be restored by appropriate preparations.

Cardiomyopathy

Cardiomyopathy includes diseases of unknown aetiology characterized by affections of the heart muscle attended by enlargement of the heart and its insufficiency.

The following three types of cardiomyopathy would be usually dif-

ferentiated: (1) congestive or dilatation; (2) hypertrophic; and (3) restric­tive cardiomyopathy.

Congestive cardiomyopathy is characterized by dilatation of the heart chambers with pronounced heart failure. The patients develop dyspnoea during slightest physical exertion and even at rest, attacks of suffocation and cardiac pain which cannot be removed by nitroglycerin; heart palpita­tion and intermissions are also characteristic. As circulatory insufficiency progresses, the liver becomes .enlarged and oedema and hydrops of the cavities develop. The borders of the heart are markedly displaced to the right, upwards, and to the left. The heart sounds at the apex are dulled, the second sound over the pulmonary trunk is accentuated, gallop rhythm often develops along with systolic murmur at the apex due to developing relative mitral insufficiency. The pulse is small and fast, sometimes ar­rhythmical. The arterial pressure is usually decreased.

ECG in congestive cardiomyopathy shows various changes in the myocardium; signs of overloading of the heart chambers and focal changes develop along with rhythm and conduction disorders.

Echocardiography reveals marked dilatation of the heart chambers and decreased contractility of the myocardium.

Hypertrophic cardiomyopathy is characterized by the primary hyper­trophy of the myocardium with subsequently developing cardiac insuffi­ciency which differs but little from congestive cardiomyopathy by its symp­toms.

The special form of hypertrophic cardiomyopathy is obstructive cardiomyopathy, which is also known as idiopathic hypertrophic subaortic stenosis. This cardiomyopathy is characterized by asymmetric hypertrophy of the interventricular septum in the region of blood outflow from the left ventricle. The cavity of the left ventricle diminishes. A circular ridge of the hypertrophied myocardium is formed beneath the aortic valve. The ridge interferes with blood ejection into the aorta. This form of myocardiopathy is first manifested by symptoms characteristic for aortic stenosis: the pa­tient develops headache, giddiness, faints, and heart pain (like in angina pectoris). Palpation and percussion of the heart reveals hypertrophy of the left ventricle; auscultation reveals coarse systolic murmur which is best heard at the 3rd or 4th intercostal space at the left edge of the sternum. The pulse is small and slow. Symptoms of circulatory insufficiency soon ap­pear.

Echocardiography is most important among additional methods used to diagnose hypertrophic subaortic stenosis. It reveals asymmetrical hyper­trophy of the interventricular septum, narrowing of the left ventricle and systolic deflection of the mitral valve cusp in the direction of the interven­tricular septum.

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Hypertrophic cardiomyopathy can be familial, inherited by the autosome-dominant type.

Restrictive cardiomyopathy is associated with disordered distensibility of the myocardium due to endocardial and subendocardial fibrosis. The diastolic function of the myocardium becomes upset and heart failure (without marked hypertrophy of the myocardium or dilatation of the heart chambers) develops.

Pericarditis

Pericarditis is inflammation of the pericardium.

Aetiology and pathogenesis. In most cases pericarditis develops in the presence of rheumatism or tuberculosis. Rheumatic pericarditis usually concurs with affection of the myocardium and endocardium. Rheumatic, and mostly tuberculous pericarditis are manifestations of infectious allergic process. In certain cases, tuberculous pericarditis depends on the spread of infection from the foci in the lungs and tracheobronchial lymph nodes (via the lymph ducts to the pericardium). Pericarditis can develop in other infections as well (e.g. scarlet fever, measles, influenza, or sepsis). Sometimes it develops due to the transition of inflammation from the adja­cent organs in pleurisy, pneumonia, myocardial infarction, and also in in­juries to the heart and in uraemia.

Pathological anatomy. Dry (fibrinous) pericarditis and pericarditis with effusion are distinguished. Depending on the character of effusion, pericarditis may be serous, serofibrinous, purulent, or haemorrhagic. Serous effusion and small masses of fibrinous ex-udate may be fully resorbed. Fibrinous and purulent effusions undergo organization to thicken the pericardium membranes and cause commissures. Pericardium layers sometimes become adherent and the pericardial sac disappears (concretio pericardii). This condition is known as adherent (adhesive) pericarditis. Calcium is often deposited in the affected pericar­dium and the heart becomes enclosed in a rigid case. The dense fibrous thickening of the pericardium compresses the heart. This condition is known as constrictive pericarditis.

DRY PERICARDITIS

Clinical picture. Pain in the heart is often the only complaint of patients with dry pericarditis. The pain varies in character from discomfort and pressure to strong torturing pain with radiation to the left part of the neck and the shoulder blade.

Inspection and percussion of the heart do not reveal any changes unless myocarditis or other heart diseases concur. The most important, and sometimes the only sign of dry pericarditis is the sound of pericardial fric­tion. Dry pericarditis ends with complete recovery in 2—3 weeks; or the disease may convert into pericarditis with effusion or adhesive pericarditis.

. PERICARDITIS WITH EFFUSION

Clinical picture. Patients complain of the pressing sensation in the chest and pain in the heart. As effusion is accumulated, dyspnoea develops. Dysphagia develops in compression of the oesophagus and hiccup when the phrenic nerve is compressed. Fever is an almost obligatory symptom.

The appearance of the patient is characteristic: the face is oedematous and the skin is cyanotic and pallid. The neck veins are swollen due to an obstructed blood flow to the heart via the superior vena cava. Compression of this vein accounts for the oedematous appearance of the face, neck, and the anterior surface of the chest (Stokes' collar). The neck veins may sometimes swell only during expiration. If much exudate is collected in the pericardial sac, the patient assumes a characteristic posture: he sits in bed and inclines forward, his hands resting against the pillow lying on his knees. The feeling of heaviness in the heart is thus lessened and respiration made easier.

Inspection of the heart region reveals levelling of the interspaces. The apex beat is absent; if it is palpable, it appears to be displaced superiorly or medially of the left border. Percussion shows considerable enlargement of the cardiac dullness in all directions, absolute and relative dullness being almost undistinguishable. The area of dullness resembles a trapezium or a triangle: the right cardiohepatic angle becomes obtuse. If much exudate is accumulated, dullness extends to the left to diminish the tympany zone of Traube's space. Heart sounds are markedly decreased. The pulse is ac­celerated, small, and sometimes paradoxical. Arterial pressure is normal or decreased. Venous pressure is elevated. Palpation of the abdomen reveals marked enlargement of the liver due to congestion of blood in it. X-ray study shows enlarged heart silhouette in the transverse direction and superiorly; the waste of the heart is absent, the pulsation is markedly weak, which is especially vivid on the X-ray picture.

The ECG shows low voltage of all waves and also changes in the S-T in­terval and the T wave in all standard leads. The S-T interval is first located above the isoelectric line and then below it. The T wave is first low and then becomes negative. The ECG changes are like those observed in myocardial infarction except that they are equally pronounced in all leads (concordant), and that the Q wave remains unchanged.

Echocardiography is very important in the diagnosis of pericarditis with effusion. Echocardiography reveals the space between the pericar­dium and epicardium which is filled with fluid that does not return the pro­bing ultrasound pulses. If effusion is small, the echo-free space can only be revealed between the pericardium and the posterior wall of the heart in a

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patient in the supine position. In the presence of a large effusion, this space can be revealed in the region of the anterior wall of the heart.

Course. Purulent pericarditis is a grave danger to the patient's life unless urgent treatment is given. Serous pericarditis may end in complete recovery. Adhesive pericarditis produces persistent pathology because operative separation of the pleural layers is not sufficiently effective.

Treatment. Treatment depends on the cause of pathology. Rheumatic pericarditis is treated as rheumatism, and tuberculous pericarditis as tuber­culosis. Various cardiacs and stimulants should be given in the presence of cardiac insufficiency. If effusion is large, the pericardium is punctured and the fluid withdrawn.

Essential Hypertension

Essential hypertension (morbus hypertonicus) is the condition in which elevated arterial pressure is the leading symptom. The disease is provoked by nervous and functional disorders in the regulation of the vascular tone. Men and women, mostly over 40, are equally attacked by the disease.

Essential hypertension should accurately be differentiated from symp­tomatic hypertension in which arterial pressure rises as a symptom of some other disease, this symptom being far from the leading one. Symptomatic hypertension occurs in aortic coarctation, atherosclerosis of the aorta and its large branches, in endocrine dysfunction (e.g. Itsenko-Cushing disease, phaeochromocytoma, primary aldosteronism, or the Conn syndrome), af­fection of the renal parenchyma, occlusive affection of the main renal arteries, and in some other diseases.

Aetiology and pathogenesis. Overstrain of the central nervous system, caused by prolonged and strong emotional stress and also mental overstrain, are believed to be the main cause of the disease. In some cases essential hypertension develops after brain concussion (concussion-commotion form). The importance of neurogenic factors was emphasized by Lang in 1922; later this hypothesis was confirmed by the Soviet physi­cians during World War II: the incidence of essential hypertension increas­ed significantly in the sieged Leningrad.

Development of the disease greatly depends on occupation: it occurs mostly in subjects whose occupation is associated with nervous and mental overstrain, e.g. in scientific workers, engineers, physicians, drivers, etc. Familial predispostion is another important factor.

The early stage of essential hypertension is characterized by nervous-functional disorder in regulation of the vascular tone. Vegetative-endocrine disorders and changes in the renal regulation of the vascular tone are later steps of the pathological process. Overstrain of the higher nervous

activity causes vasopressor adrenal reaction by which arterioles, mainly the arterioles of the internal organs and especially of the kidneys, are narrow­ed. Ischaemia of the renal tissue develops as a result. This in turn stimulates production of renin by the juxtaglomerular cells of the kidneys. Renin stimulates formation of angiotensin-II which in turn causes a pro­nounced pressor effect and stimulates secretion of aldosterone (sodium-retaining hormone) by the adrenal cortex. Aldosterone promotes transition of sodium from the extracellular fluid into the intracellular fluid to in­crease the sodium content of the vascular wall. This causes oedematous swelling of the wall and narrowing of the vessel, which in turn promotes elevation of arterial pressure.

There is a system of depressor factors in the body whose dysfunction plays an important role in the pathogenesis of essential hypertension. Bradykinin and angiotensin, which produce a depressive effect, have been isolated. It is believed that the depressor system becomes altered by some unknown reason during essential hypertension.

Pathological anatomy. Essential hypertension gradually affects permeability of vascular walls and their protein content. At late or grave forms of the disease, this causes sclerosis or necrosis of small arteries and secondary changes in the tissues of organs. Walls of large vessels are usually affected by atherosclerotic changes. The extent of vascular affection differs in various organs and various clinicoanatomical variants of the disease therefore arise, with a prevalent affection of the vessels of the heart, brain, or kidneys (primary cirrhosis of the kidneys thus develops).

Clinical picture. During the early stage of the disease, the patient would usually complain of neurotic disorders: general weakness, impaired work capacity, inability to concentrate during work, deranged sleep, transient headache, a feeling of heaviness in the head, vertigo, noise in the ears, and sometimes palpitation. Exertional dyspnoea (ascending upstairs, running) develops later.

The main objective sign of the disease is elevated systolic pressure (over 140-160 mm Hg) and diastolic pressure (over 90 mm Hg). Arterial pressure is very liable during the early stage of the disease, but later it stabilizes. Examination of the heart reveals signs of hypertrophy of the left ventricle: expanding apex beat, and displacement of the cardiac dullness to the left. The second sound is accentuated over the aorta. The_/ pulse becomes firm and tense.

X-rays reveal "aortic" silhouette of the heart. The aorta is elongated, consolidated, and dilated.

The ECG is of the left type with displaced S-T segment, low, negative, or two-phase T wave in the 1st and 2nd standard chest leads (V₅-Vg).

Coronary atherosclerosis concurs not infrequently. This may cause angina pectoris and myocardial infarction. In the late period of the disease,

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heart failure may develop due to fatigue of the heart muscle as a result of increased arterial pressure. Heart failure is often manifested by acute at­tacks of cardiac asthma or oedema of the lungs; or chronic circulatory in­sufficiency may develop.

Vision may be deteriorated in grave cases. Examination of the fundus oculi reveals its general pallidness; the arteries are narrow and tortuous, the veins are mildly dilated; haemorrhage into the retina (angiospastic retinitis) is sometimes observed.

High arterial pressure in the affected cerebral vessels can derange cerebral circulation. This can cause paralysis, disorders in sensitivity, and sometimes death of the patient. Cerebral circulation is deranged due to spasms of the vessels, their thrombotic obstruction, haemorrhage due to rupture of the vessel, or diapedetic discharge of erythrocytes.

The affected kidneys become unable to concentrate urine (nicturia or isohyposthenuria develops). Metabolites (otherwise excreted with urine) are retained to provoke uraemia.

Essential hypertension is characterized by periodically recurring tran­sient elevations of arterial pressure (hypertensive crisis). Development of such crises is preceded by psychic traumas, nervous overstrain, variations in atmospheric pressure, etc.

Hypertensive crisis develops with a sudden elevation of the arterial pressure that can persist from a few hours to several days. The crisis is at­tended by sharp headache, feeling of heat, perspiration, palpitation, gid­diness, piercing pain in the heart, sometimes by deranged vision, nausea, and vomiting. In severe crisis, the patient may lose consciousness. The pa­tient is excited, haunted by fears, or is indifferent, somnolent, and in­hibited. Auscultation of the heart reveals accentuated second sound over the aorta, and also tachycardia. The pulse is accelerated but can remain un­changed or even decelerated; its tension increases. Arterial pressure in­creases significantly. ECG shows decreased S-T interval and flattening of the T wave. In the late stages of the disease, with organic changes in the vessels, cerebral circulation may be deranged during crisis; myocardial in­farction and acute left-ventricular failure may also develop.

Classification. According to Myasnikov, three stages of the disease are classified; each stage is further divided into two phases, A and B.

The A phase of the first stage is latent; it is characterized by elevated arterial pressure during a psychic stress, while under normal conditions arterial pressure is normal. The B phase is transient (transitory hyperten­sion); arterial pressure increases only occasionally and under certain condi­tions; objective changes are absent.

In the second stage, arterial pressure is elevated permanently and more significantly. Phase A is characterized by permanent but unstable

hypertension. Subjective sensations are pronounced; hypertensive crises are possible; spasms of the cerebral and coronary arteries are likely to oc­cur as well. Signs of hypertrophy of the left ventricle develop. Phase B is characterized by a significant and stable elevation of the arterial pressure. Hypertensive crises are frequent. Paroxysms of angina pectoris and derangement of cerebral circulation of the angiospastic character occur. Changes in the fundus oculi and pronounced signs of hypertrophy of the left ventricle can be revealed.

During the third stage, sclerotic changes in the organs and tissues are /t!iti/^observed along with stable and marked elevation of the arterial pressure. A is compensated. Arteriosclerosis of the kidneys is observed, but

renal function is not upset significantly. Cardiosclerotic changes do not stable heart failure; and sclerosis of cerebral vessels is not attend­ed by pronounced disorders in the cerebral circulation. Phase B is decompensated, with grave dysfunction of various organs and with renal insufficiency; cerebral circulation is disordered and hypertensive retinopathy is observed. In this stage of the disease, the arterial pressure may normalize after infarction or apoplectic stroke.

Treatment. Complex therapy is required; Reasonable work should be alternated with rest, sufficient sleep, and remedial exercises. Sedatives should be given to improve sleep and to normalize excitation and inhibition processes. Hypotensive preparations (rauwolfia, ganglioblocking prepara­tions, magnesium sulphate) are prescribed to inhibit the increased activity of the vasomotor centres and the synthesis of nor adrenaline. Diuretics (saluretics) are given to decrease intracellular sodium; aldosterone blocking agents (spironolactone) and other preparations are also given.

Atherosclerosis

Atherosclerosis is a chronic disease characterized by systemic affection of arteries due to metabolic disorders in the vascular wall. Atherosclerosis is one of the most common diseases and the most frequent cause of disability and premature death. It usually attacks people over 40-45 but sometimes occurs in younger patients. The incidence of atherosclerosis in men is 3-4 times higher than in women.

Aetiology. The aetiology of the disease is uncertain. It has been established that atherosclerosis occurs in subjects who undergo long ner­vous and psychic overstrain, hypodynamia, who suffer from overeating (taking much food rich in animal fats) and obesity, and diabetes mellitus, or myxoedema. The pathogenesis of the disease is complicated and not clear. It is believed that the function of a complicated neurohumoral ap­paratus regulating metabolism becomes upset by some causal factors. As a

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result, biochemical, physico-chemical, and morphological composition of the blood is affected along with impairment of the blood coagulation system, disorders of structure, biochemistry and function of the arteries, and of their permeability. Hereditary predisposition to atherosclerosis is important in some cases.

Pathological anatomy. The changes are localized in large elastic arteries, i.e. in the aorta, the coronary, cerebral, renal arteries and the large arteries of the limbs.

The atherosclerotic process occurs in stages. First, lipids are deposited in the arterial in-tima to form fat spots and strips, which do not rise above the surface of the intima. Later, connective tissue grows in the region of lipid accumulation to form a fibrous atherosclerotic plaque which rises above the intima surface to narrow the lumen of the vessel. The lipid-protein complex inside the plaque can decompose to ulcerate its surface and to form an atheromatous ulcer. The ulcerated plaques can become the cause of thrombosis of the vessel and calcification of the fibrous plaques, which causes even greater changes in the arterial walls.

Clinical picture. The disease may be asymptomatic for years (pre-clinical period). Study of the blood during this period shows increased cholesterol or beta-lipoprotein content. The further picture of the disease depends on the affection of particular vessels (aorta, coronary arteries of the heart, cerebral vessels, renal arteries, and the limb arteries). This is the clinical period of the disease, which is divided into three stages, namely the ischaemic stage, during which ischaemic changes occur in the organs (e.g. angina pectoris attacks occur in atherosclerosis of the coronary arteries); the second or thrombonecrotic stage, characterized by thrombosis in the changed arteries (myocardial infarction may occur at this stage); and the third, fibrous stage, characterized by the development of connective tissue in the organs (e.g. cardiosclerosis).

Atherosclerosis of the coronary arteries (see "Angina Pectoris", "Myocardial Infarction" and "Cardiosclerosis").

Aortic atherosclerosis usually occurs in individuals aged over 40, but even its grave forms can sometimes be asymptomatic. Atherosclerosis of the ascending aorta and its arch occurs more frequently. The patient feels pressing or burning pain in the retrosternal region which radiates in both arms, the neck, the back, and the upper abdomen. As distinct from pain in angina pectoris this pain is more persistent; it can continue for hours and even days, with periodic weakening and strengthening. The elastic proper­ties of the aorta decrease and the heart has to perform greater work, which causes hypertrophy of the left-ventricular myocardium. Inspection of the heart reveals increased apex beat and its displacement to the left; on per­cussion, the borders of dullness of the vascular bundle are expanded. Retrosternal pulsation can be palpated in the jugular fossa because of the high standing of aortic arch (due to its elongation). The first heart sound is

as a rule dull, the second sound is heard over the aorta; systolic murmur is also found which appears or becomes intensified when the patient raises his arms (Sirotinin-Kukoverov symptom). Systolic murmur is due to both sclerotic narrowing of the aortic orifice and roughness of the inner surface of the aorta. Maximum arterial pressure increases, while minimum pressure either remains unchanged or slightly falls. X-ray study reveals straightened, dilated, and elongated aorta. Atherosclerosis of the ab­dominal aorta is rarely diagnosed during life.

Atherosclerosis of the mesenteric arteries impairs blood supply to the intestine and may cause attacks of angina abdominis: the patient suddenly feels (3-6 hours after meals) piercing pain in the upper abdomen or in the umbilical region, which persists from 2 or 20 minutes to 1-2 hours. The pain is attended by the swelling of the abdomen, regurgitation, constipa­tion, palpitation, and increased arterial pressure. In thrombosis of mesenteric arteries, the intestinal loops begin necrotizing, which is manifested by haemorrhage and paralytic intestinal obstruction.

Atherosclerosis of the renal arteries causes vascular nephrosclerosis, which is manifested by hypertension and isohyposthenuria.

Atherosclerosis of the cerebral arteries is manifested by decreased work capacity (mental in particular), impaired memory, decreased active concen­tration, and rapid fatigue. The patient complains of insomnia and gid­diness. The behaviour of the patient with pronounced atherosclerosis of the cerebral arteries changes: he becomes fussy, selfish, fidgety, and cap­tious; his mental power decreases. Atherosclerosis of the cerebral arteries is complicated by disturbed cerebral circulation (haemorrhage, thrombosis).

Atherosclerosis of the limb arteries. Clinical signs of this disease are pain in the gastrocnemius muscles during walking. The pain is very severe and the patient has to stop for a while, but as he proceeds with walking, the pain soon develops again (intermittent claudication). The patient feels chill and cold in the legs. Examination of the legs reveals the absense of pulse (or weak pulse) on the dorsalis pedis artery and the posterior tibial artery. Dry gangrene of the lower extremities develops in grave cases due to local circulatory disorder. Angiography of the affected vessels reveals deforma­tion, tortuosity, narrowing of the lumen, and microaneurysms.

Treatment. Combined therapy is aimed at removal of nervous effects, normalization of metabolic processes by prescribing rational diet and ap­propriate medicinal preparations to control the lipid content (lecithin, vitamin C, nicotinic acid, miscleron—2—3 capsules a day per os for several months, in courses, etc.).

Rational diet, correct alternation of work and rest, regular exercise, quiet at home and at work are important conditions for prophylaxis of atherosclerosis. , - ...,■.. ........ ,.,,..,

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