Mitral and aortic heart defects. Hemodynamic disorders. Diagnostics, clinical pattern.
The acquired valvular heart disease (valvular heart defects, lat. – vitium cordis) is observed approximately in 0,5-1 % of the population, combining approximately 20-25 % of all heart diseases and occupy the third place among the most wide-spread heart diseases after hypertonic and ischemic diseases. Acquired and congenital heart defects are distinguished. The incidence of acquired heart defects is much higer.
Congenital heart defects occur due to abnormal development of the heart and big vessels during the intrauterine growth of the foetus with preservation of residual elements of fetal circulation after birth.
Between the causes of acquired valvular heart disease (AVHD) the main part belong to rheumatic disease, sepsis, atherosclerosis; lues, lesions ets. are the rare causes of this disease. In adolescent patients /in the age of 10-20 years / heart lesions by rheumatic etiology occupy more than 4/5 of all cases of AVHD.
The valvular heart disease is the stable pathological changes in the structures of the heart that interfere with its normal function.
In according to datas by V.A.Tchernogubov the main cause of acquired valvular defects is rheumatic fever; it occupies for about 90 % of all cases of AVHD.
Acquired valvular heart defectts are divided on some groups:
1.. Defects of the mitral valve.
П. Defects of the aortic valve.
Ш. Defects of the trycuspid valve.
ІV. Defects of the pulmonic valve.
The inflammatory process in the leaflets of the affected valve quite often is resulting in their sclerosis with deformation or shortening. Such valve does not obtures completely atrio-ventricular aperture, thus its incompletence develops.
If the leaflets of the valve are adhered on its edges, the orifice they obtured is narrowed. Such state is termed as the stenosis of the orifice.
The mitral heart defects are as follows: the stenosis of the left atrio-ventricular aperture or the mitral stenosis (lat. – stenosis valvulae mitalis) and incompletence of the mitral aperture or the mitral incompletence (lat. – insufficientia valvulae mitralis).
THE MITRAL INCOMPLETENCE. The mitral incompletence is the result of congenital or acquired abnormality in mitral leaflets, supporting structures of the mitral valve, the mitral valve annulus, or left ventricular myocardium. When one or more of these structures are abnormal, the valve may become incompetent, resulting in a systolic blood back-flow to the left atrium (regurgitation).
Etiology: there are organic and relative mitral defects. The organic defect more often is a result of rheumatic endocarditis. Rheumatic process produses development of of connecting tissue in the leaflets of the mitral valve, shriveling and shortening of valve’s leaflets as well as chordae tendinous, connected with leaflets. As a result the ability of the valve to close fails. During systole the edges of the leaflets don’t meet completely each with other and the slit between leaflets occurs. Blood stream come through that slit from the left ventricle to the left atrium.
At the case of relative incompletence the mitral valve is not altered, however due to widening of the left atrio-ventricular aperture casps of the valve fail to close it completly in systole.
The relative mitral incompletence develops due to following causes:
a / dilatation of the left ventricle chamber becouse of uncomplete obturation of enlarged aperture with leaflets;
b/ leaflets of the mitral valve during systole of the left ventricle can bend to left atrium’s cavity (prolapsed mitral valve);
c / dysfunction of papillary muscles due to their ischemia, cardiosclerosis;
d / breakage of chordas tendinous connecting valve with papillary muscles;
e/ due to calcification of valvular fibrous annulus, when mitral valve narrowing during ventricular systole occurs.
Clinical pattern.
The natural history and symptomatic course of a patient with mitral incompetence are related to the degree of mitral regurgitation, the rapidity with which it develops, and the status of the underlying left atrial and ventricular function. Patients with insidious onset and gradual progression of mitral regurgitation, as occurs in chronic rheumatic mitral incompetence, have a prolonged asymptomatic interval of up to 20 years or more after the initiating event, and symptoms first appear in middle age or beyond. In most cases, left atrium compliances and its size increases to accommodate the regurgitant volume and effectively protect against marked increase in pulmonary vascular pressures. Consequently, symptoms of pulmonary congestion are less prominent and occur late in the course of the disease.
As congestion in pulmonary circulation occurs, dyspnea, palpitation of the geart, cyanosis and other symptoms develop. When left ventricular function deteriorates, dyspnea, orthopnea, and paroxysmal nocturnal dyspnea become more prominent as well as a couph (dry or with small expectoration of sputum, sometimes with admixions of blood (haemoptoe)/ Quite often patients can feel pain in the heart area by various character: dull ache, strabbing or pressing pain of different intensity, which is not correspond th degree of overload. Palpitation, cyanosis may be revealed in such patients at rest or after physical examination. Peripheral edema may be apparent in patients with end-stage mitral incompetence/
Palpation. the apical impulce is displaced to the left and downwards. It is resistent, brief. and somewhat diffuse. Despite its brevity, it’s amplitude is increased. Not infrequently, an abnormal left parasternal systolic impulse may be observed or palpated. The apical thrill may be present and usually indicates severe mitral incompetence.
Blood pressure an arterial pulse. Blood pressure is usually normal. The peripheral arterial pulse is ofteormal but may be of small amplitude.
Percussion – displacement of heart borders upwards and leftwards may be revealed (so-called “mitral heart configuration” with indistinct heart waist) becouse of the enlarged left atrium and ventricle. At hypertrophy of the right ventricle the right heart border is displaced rightwards due to hypertrophy of the right ventricle.
Auscultation. In chronic mitral incompetence, the first heart sound usually is decreased in intensity. The weakening of the first heart sound occures because of absence of period of closured valves. . In uncomplicated mitral insufficiency the first sound is either faint or inaudible. The second heart sound usually is normal Accent of the second heart sound above the pulmonary artery is caused by increased blood pressure in pulmonary veins.
The third heart sound heard at the apex with the bell of the stethoscope is common (protodiastolic gallop). It tends to occur especially in moderate or severe mitral incompetence, because of the high diastolic flow into the ventricle, and therefore does not necessarily imply significant left ventricular dysfunction or left ventricular filling pressures. It generally occurs 120 to 240 msec after the second heart sound.
The auscultatory hallmark of the mitral incompetence is a sytolic murmur that typically is holosystolic, starts with the first heart sound and remains at constant intensity throughout systole, ending at or after the aortic component of the second heart sound. Usually the murmur is medium to high pitched, soft, blowing in quality. The intensity of the murmur does not correlate well with the severity of regurgitant flow. The murmur is best heard with the diaphragm of the stethoscope placed firmly over the apex. Although in some patients the murmur may be located to one point, most frequently the apical murmur transmisses to the axilla. This murmur is usually transmitted to the left and toward the posterior axillary line.The murmur may be notably short, soft, or absent in acute severe mitral incompetence.
The systolic murmur is better heared if the patient lies down on his left side and stops breathing.
The datas revealed during auscultation have to be improved and confirmed by fonocardiogram (FCG).
On X-ray film the enlargement of heart sillhouette leftwards, upwards and downwards is observed. True cardiomegaly with left ventricular and left atrial enlargement is a common finding in significant chronic mitral incompetence. Left atrial enlargement may be recognized by straightening of the left heart border, by a characteristic right-sided double density (right and left atrial borders are superimposed), and, occasionally, by elevation of the left main-stem bronchus.
The radiographic size the left atrium provides a rough guide to the severity and duration of the mitral incompetence. The atrium generally is more enlarged in mitral incompetence than in mitral stenosis; it may be gigantic if both lesions are present.
In patients with mitral incompetence, the pulmonary vasculature is usually normal until late in the disease when significant venous pulmonary hypertension develops. When increased blood pressure in pulmonary circulation persists –dilatation of pulmonary arteria arch, hypertrophy, dilatation of the right ventricle are detected. The resulting redistribution of blood flow to the upper lobes and interstitial edema causes Kerley B lines.
On ECG – hypertrophy of the left atrium may be revealed. About 75% of patients with moderate to severe mitral incompetence have atrial fibrillation, consistent with the presence of significantly enlarged left atrium. Patients with normal sinus rhythm nearly always have evidence of left atrial enlargement i.e., P mitrale configuration (broad notched P waves in lead II and biphasic P waves in lead V1). Left ventricular hypertrophy with leftward or normal axis has been said to be characteristic of mitral incompetence, but the QRS complex and axis usually are normal and associated with nonspecific ST-segment and T-wave alterations. Right ventricular hypertrophy is notably uncommon, and its presence indicates significant pulmonary hypertension.
Echocardiography reveales the enlargement of the left heart chambers, movement of the mitral valve cusps in the opposite direction, their thikening and the absence of full closure during systole. By Doppler mode turbulent blood stream into the cavity of the left atrium in the expressed cases of incompletence is recorded, that is the indirect sign of mitral incompletence.
STENOSIS OF THE LEFT ATRIOVENTRICULAR APERTURE (lat. – stenosis of the left atrioventricular aperture, stenosis ostii venosi sinisti). The rheumatic endocarditis occupies a leading place in it’s etiology. Each 500-800 persons among 100000 in the population have mitral stenosis. Clinical and auscultatoly findings of the mitral stenosis become evident earlie than in incopmletence. Thay sometimes allow a precise diagnosis and semiquantitation of the severity of the defect at the bedside. Duroziez is credited with being the first to describe the crescendo presystolic murmur of mitral stenosis.
Three degrees of the mitral stenosis are distinguished:
1 ) severe mitral stenosis ( the square of mitral orifice is 0,5 cm2 or less);
2) the moderate one / the square of mitral orifice is about 1-0,6 cm2),
3) mild stenosis (the square of a mitral orifice is 1,5-1,1 cm2).
In the advanced stages of the mitral stenosis pulmonary venous hypertension leads to progressive pulmonary arteriolar constriction associated with intimal and medial hyperplasia. Its development protects the pulmonary capillaries from excessive pressure which would result in transudation of fluid into the interstitial tissues and alveoli of the lung. However, it leads to pulmonary arterial hypertension with resultant right ventricular hypertrophy and eventually to right ventricular failure with tricuspid incompetence, hepatic congestion, visceral congestion, ascites, and edema.
In mitral stenosis the less volume of blood enters into the left ventricle, that is why the loading on it dcreases, that resulting in dimension of its sizes.
Clinical pattren.
Many patients with mitral stenosis have a classic history of acute rheumatic fever or a histoty of recurrent streptococcal tonsillitis or pharyngitis, suggesting that a smoldering type of rheumatic fever may have occurred.
When lung congestion drveelops, patients complain on evolving types of dyspnea, paroxysmal nocturnal dyspnea, orthopnea, as well as recumbent cough and hemoptysis that may be associated with rupture of bronchial veins during bronchitis or later be the frothy, bloody sputum or pulmonary edema. Effort fatigue predominates early, followed by symptoms related to the hepatic and visceral congestion.
The symptoms tend to progress gradually, but there will be brief periods of increased severity of symptoms due to respiratory infections, unusual physical or emotional stress, paroxysmal atrial fibrillation, pregnancy, or pulmonary embolism.
Inspection reveiles acrocyanosis or cyanosis of cheeks, tip of the nose and the area above the bridge, the malar erythrocyanosis may be noted (lat. – “facies mitrale”). Visual examination of the heart region often reveales a cardiac beat consequent upon dilatation and hypertrophy of the right ventricle (lat. – gibbus cardiacus).
The arterial pulse is usually normal, ex¬cept that in patients with a low cardiac output and atrial fibrillation it will be reduced.
If the defeat develops in childchood – patient’s growth slows down, infantilism develops /lat. – “mitral nanism”/.
In the case of severe left atrial enlargement the last one presses on the nervus larynageus (its ramus recurens), therefore paresis of phonatory bands develops and the patient loses voice /aphonia/.
Palpation: The left ventricular impulse is normal and somewhat diffi¬cult to detect except in the left lateral decubitus position. In presence of significant pulmonary hypertension, a hypertrophied right ventricle will produce an outward impulse that can be seen and palpated along the left sternal edge.
The diastolic (presystolic) trill /lat. – fremissement cataire/ best of all is determined in the position of the patient on the left side at maximal expiration. It is caused by transit of blood through reduced apertura from the left atrium to the left ventricle.
The pulse in mitral stenosis can be unequal on right and left arms. At considerable hypertrophy of the left atrium the left subclavial artery is pressed by the left ventricle and pulse filling on the left diminishes, (lat. – pulsus differens). If the left ventricle is not filled completely and the stroke volume is decreased, the pulse become small lat. – (pulsus parvus). At the case of arrhythmia pulse is atthythmic.
Blood pressure is normal, sometimes systolic pressure slightly decreases and diastolic one – increases.
Percussion: displasement of heart’s borders upwards and leftwards resulting in hypertrophy of the left atrium and right ventricle. Thus the heart is of “mitral” configuration.
Auscultation: The cardinal auscultatory features of initial stenosis consist of accentuation of the first heart sound, early diastolic opening snap, and early, middiastolic crescendo-descendo murmur with presystolic accentuation. Mitral stenosis in its early or milder form is often unrecognized unless the physician listens carefully at the apex, with the patient in the left lateral decubitus position, and uses the bell of the stethoscope to detect the low-frequency diastolic murmurs. The patient should be examined both at rest and with exercise in order to estimate the severity of the stenosis property.
The first heart sound characteristically is very loud, it is the result of two factors: (1) thickened chordae which are less elastic thaormal and therefore cause a more abrupt termination of valve motion, and (2) the mitral valve is close to being maximally open at the onset of systole. Due to delay in mitral valve closure the left ventricle is not completly filled with blood and heart contraction descends promptly. The 1 sound sometimesn resembles the hue of the “sound in the empty pot”.
An adventitious sound due to opening of the mitral valve can be heard at the apex beat – so-called an opening snap sound which is an important auscultatory sign of mitral stenosis. This sound is heard between 30 and 120 msec after the aortic valve component of the second sound and occurs when left ventricular pressure drops below left atrial pressure in early diastole.
It is a brief, high-pitched sound with wide transmission. It is caused by the “tambourine effect” of the valve with fused commissures .snapping into the ventricle rather than opening to allow free flow of blood. It is best heard at the point of maximal apical impulse; it also is heard easily along the left sternal border with the patient in the recumbent position. In addition to the implication of disease of the mitral valve, almost always rheumatic, the relationship of this sound to the aortic valve component of the second sound is helpful in assessing the severity of the mitral valve stenosis.
The II sound normally occurs within 50 msec of the onset of the QRS. Because of the delay in mitral valve closure, the mitral component of the II sound is delayed. In mitral stenosis, it is usually delayed 70 msec or more. The delay of the II sound depends on the duration of the preceding cycle.
The intensity of the second heart sound usually is normal in patients with mitral stenosis. However, one have to separate it from the opening snap before one can reliably define the qualities of its components. With severe mitral stenosis and the appearance of pulmonary hypertension, the pulmonary component of the second sound will increase in intensity (accentuation of the second heart sound above pulmonic artery). The loud first sound, second sound, and the sound of mitral valve opening give a specific murmur which is characteristic of mitral stenosis and resembles the song of a quail.
A formula for estimating of the severity of the mitral stenosis is devised based on the delay in the first sound and the interval between the second sound and the opening snap of the mitral valve: the more severe the is stenosis, the greater the Q-to-first sound interval and the shoner the second sound-Q-to-opening snap interval. In calcific mitral stenosis, the first sound may be softer thaormal, and then the opening snap is usually absent.
Murmurs. The characteristic murmur of the mitral stenosis is a low-pitched diastolic creschendo- deschendo murmur heard best with the bell applied lightly to the skin over the heart apex. The murmur varies in length and may be only presystolic, middiastolic, or holodiastolic, can be heared during all diastole, strengthening before a systole (presystolic accentuation) and immediately merging with clapping first sound.: A holodiastolic murmur during long diastolic periods indicates a persisting gradient and hence severe stenosis. In the milder form of mitral stenosis it may be difficult to hear, and often the patient must exercise before it is clearly audible. The most characteristic murmur of mitral stenosis is one that begins immediately after the opening snap of the mitral valve, extends throughout diastole with presystolic accentuation, and ends with a loud first sound.
Finally, in the presence of pulmonary hypertension com¬plicating mitral stenosis, pulmonary valve incompetence will develop. Trills is associated with a high-pitched decrescendo diastolic murmur heared best along the left sternal border (Graham Steele murmur). When this murmur is present, it is associated with a. loud pulmonary component of the second sound that usually is palpable and implies severe mitral stenosis.
In the case of calcification of the mitral valve rasping systolic murmur gains “irony” shade and sometimes a high “murmur-squeak” may be revealed. In the case of appearance of ciliary arrhythmia in patients with mitral stenosis heart sounds become absolutely inordinate. S.P.Botkin compared them with “a forge hum”.
On the chest roentgenogram –shows a specific enlargement of the left atrium, which leads to disappearance of the heart waist /the mitral heart configuration/ are detected. On the lateral film (the first oblique position) enlargement of the left atgrium is determined by the degree of displacement of the esophagus which is good visible after the patient have drunk baric suspension. The chest roentgenogram is helpful in both confirming the diagnosis and assessing the severity of the stenosis. A large left atrial sillhouette, dilated upper lobe veins, and evidence of alveolar or interstitial edema with 1- to 3-cm horizontal lines in the costophrenic angles (Kerley B lines) all are consistent with severe mitral stenosis.
In presence of pulmonary hypertension, the swelling of pulmonary artery arch and hypertrophy of the right ventricle are watched.The central pulmonary arteries are prominent, and there will be a sudden decrease in the vascular markings in the peripheral lung fields associated with right ventricular enlarge¬ment that will be seen best in the lateral film. Valvular calcification is visible on roentgenogram. At pulmonary prolonged hypertension pneumosclerosis develops.
The electrocardiogram in mitral stenosis maps signs of hypertrophy of the left atrium and left ventricle: deviation of heart electrical axis rightwards, high and prolonged waves Р in the right thoracic leads and expressed waves f in the left thoracic leads may be detected. The ECG may be ofteormal except for a prolonged, bifid P wave in lead 2 and a prominent late negative deflection in V1 related to left atrial enlargement. Atrial fibrillation is the most common abnormal rhythm. Despite severe degrees of right ventricular hypertrophy, the ECG commonly will disclose only right axis deviation with S waves in leads 1 and V6 and an rSr in lead V1.
On the phonocardiogram taken from the apex high voltage of the I heart sound is often detected; the second sound is often followed with the opening snup and diastolic murmur, the last one is better heard above the pulmonary artery; voltage of the П sound is enlarged in comparing with those above the aorta. The interval Q-to-I sound is enlarged.
Echocardiography Pertinent information obtainable from echocardiographic examination of a patient with mitral stenosis includes extent of calcification and fibrosis of the mitral valve, presence of atrial thrombi, enlargement of chambers in size and disorders of contractility, presence of other valvular abnormalities.The hypertrophy and augmentation of the left atrium, change of the mitral valve leaflets /induration, adhesion, calcification) may be revealed, the locomotion of leaflets becomes undirectional, gains the П-similar form.
As the surgical treatment of the acquired heart valvular disease is successful now, it is necessity to precise diagnostics of degree of narrowing or degree of the valvular failure and detection of prevalence of one of them.
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.
Clinical picture. Subjective condition of patients with aortic sncompetence 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 diastolic pressure).
If contractility of the left-ventricular myocardium is impaired, congestion in the lesser circulation develops and the patient complaints 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 count for the appearance of some signs, such as pulsation of the perphieral 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 (Quincke’s pulse), rhythmical reddening of the skin after rubbing, etc.
The apex beat is almost always enlarged and shifted to the left and inferiorly. 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 intercostal space laterally of the midclavicular line. The apex beat is diffuse, intense, rising like a dome. This indicates significant enlargement of the left ventracle. The border of cardiac dullness can be found (by percussion) to shift to the left; the heart becomes “aortic” (with pronounced waist of the herat.
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 oer 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 sa 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 phonocardiogram. 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 apex. Diastolic murmur (presystolic or Austin-Flint murmur) can sometimes be heard. It arises due to an intence regurgitation of the blood that moves aside the mitral valve cusp to account for functional mitral stenosis. Doubled sound (Traube souble sound) nd doubled Vinogradov-Durozierz murmur can sometimes be heard over the femoral artery in this disease.
The pulse is fast, full, and high, which is due to high pulse pressure and increased volume of blood deliverred 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 and dilatation of the aorta; pulsation of the aorta is intense.
The ECG also reveals various signs of hypertrophy of the left ventricle: 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.
AORTIC STENOSIS
The narroving 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 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.
Clinical picture. Aortic stenosis can remain compensated for years and would not cause any unpleasant sublective sensations (even during intense physical exertion). If obstruction of the aortic orifice is considerable, infufficient 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 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 ineriorly; 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 heart 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 immobile, 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 (poststenotic); 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.
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 insuf¬ficiency develops in diminished contractility of the left ventricle and it is manifested as in aortic incompetence.
Treatment. Conservative treatment means management of heart failure. Operative treatment – implantation of artificial prostesis in incompetence or comissuritomy in stenosis.
