Echophonocardiography

Echophonocardiography

Peter Mills and Ernest Craige

0 VER the past 10 yr, echocardiography has attained a preeminent position in the field

of noninvasive cardiac diagnosis. Among the outstanding advantages of echocardiography over previous graphic techniques are the abilities to quantitate chamber size, visualize abnormalities of valve motion, and differentiate structures that would appear homogenous on a chest x-ray. As clinical experience with the technique increases and diagnostic criteria are established and refined, the scope and precision of the method will no doubt continue to grow. This success should not, however, cause us to abandon other methods developed over the past 100 yr for the noninvasive assessment of abnormal cardiac structure and function. Phono- cardiography in isolation is often a weak diagnostic tool, but the addition of pulse tracings enhances the precision with which heart sounds may be identified. Unfortunately, the indirect carotid pulse, the most often used adjunct, is recorded with a transmission delay with respect to the phonocardiogram. Echocardiography, on the other hand, has no significant transmission delay and is therefore an ideal parameter with which to correlate intracardiac events, particularly heart sounds (Fig. 1).

For these reasons, and because of a long- standing interest in research into the origin of heart sounds, simultaneous echo and phonocardiograms have been recorded in our laboratory for a number of years. During the course of these studies, it has become apparent that the combination of the two techniques has a diagnostic value that may be lacking when they are employed either singly or serially. The combined echophonocardiographic study should always include the performance of a complete standard echocardiographic examination, which is subsequently interpreted independently. In addition, our routine recordings consist of carotid, venous, and precordial pulses, although, for the purposes of this paper, these techniques will not be considered in detail.

This review will be divided into four parts: (1) a brief description of the technique of echophonocardiography; (2) a summary of research into the origin of heart sounds; (3) echophonocardiography in the investigation of heart

disease; and (4) examples of the application of these techniques in solving clinical problems.

THE TECHNIQUE OF

ECHOPHONOCARDIOGRAPHY

There are a large number of possible combi- nations of phonomicrophone locations, echo beam directions, and pulsatile phenomena that may be recorded simultaneously. Therefore, for the optimal elucidation of a clinical problem by a combined noninvasive study, a preliminary protocol should be made on the basis of a stan-

dard bedside assessment. The performance of the echophonocardiogram requires a combination of both clinical and technical skills. One should be prepared to alter the direction of the procedure based on information that comes to light during the test. In some situations, especially children, difficulties arise from competi- tion in the placement of echo and phono transducers over the limited area available on the chest wall. Since a technically satisfactory echo recording is a sine qua non of a good echophonocardiographic examination, the placement of transducers requires some discrimina- tion and ability to weigh the relative value of the various techniques at one’s disposal.

Although a number of satisfactory transducer-amplifier-recorder systems are available, we have had the most experience with the Leatham filter system, with a microphone that can be attached to the chest wall by a suc- tion device, freeing the operator’s hands, and minimizing movement artefacts. Pulsatile tracings are taken with a hand-held transducer with a time constant of greater than 3 sec. A variety of ultrasound transducers are necessary for the different thicknesses of chest wall, size, age, etc. of subjects. We are most familiar with Aerotech Cardiac Ultrasound transducers. The Smith Kline Ultrasonoscope, interfaced with a

From lhe Division o/ Cardiology, Department of Medicine. University of North Carolina. Chapel Hill, N.C.

Reprint requests should be addressed IO Ernest Craige, M.D., Department of Medicine, Division of Cardiology, 338 Clinical Sciences Bldg. 2298. UNC School of Medicine, Chapel Hill. N.C. 27514.

G 1978 by Grune & Stratton, Inc.

0033~0620/78/2005-0006$02.00/O

Progress in Cardiovascular Diseases, Vol. XX, No. 5 (March/April). 1978 337

338 MILLS AND CRAIGE

contribution to sound genesis. The classrcal

I theory relates the principal elements of S, to mitral and tricuspid valve closure, respec-

I tively.‘-” The alternative hypothesis is that the

i two major high-frequency components of S, sound are generated by movement and acceleration of blood during early systole, the first component being related to left ventricular dP/dt and the second to ejection of blood into the root of the aorta.6p’z Both sides of this argu-

1 ment have been expounded at some length in recent years, 11.“1.‘4 and we shall review some of the contributions of echocardiography to this question.

,

I

Fig. 1. Echophonocardiogram of the aortic valve (AVE)

in a patient with mild aortic valve stenosis. The P-R interval

is long (0.18 sac), and therefore, the first heart sound (S, J is

soft. The loud sound recorded both at the pulmonary area

(PA) and mitral area (MA) is an aortic ejection sound

(AoEjXl, not S,, as would have been thought on ausculta-

tion. These findings are typical of a bicuspid aortic valve. Un-

less otherwise specified, recording speed is 100 mm/set,

time lines, 40 msec.

Cambridge Physiological Recorder or an Irex Recorder has been used in the illustrations in this article. More recently, a modification of the Irex equipment permits the use of two echo transducers simultaneously, so that two structures (valves, ventricular chambers, etc.) may be visualized at the same time as the ECG, phonocardiogram, and pulse tracings. Record- ings are made at 25,50, 100, or 200 mm/set, depending on the requirements, and are developed photographically for optimal clarity. Generally, phonocardiograms are recorded from two locations simultaneously, such as the second left in- terspace and apex, in order to demonstrate transmission or lack of transmission of sounds and murmurs over the precordium.

It is now generally agreed that the onset of the first high-frequency component of the first heart sound (S,) coincides with the moment of coaptation of the mitral valve leaflets seen echocardiographically.‘“-2’ The coincidence of echocardiographic tricuspid valve closure with the second high-frequency component of S, has been less frequently demonstrated as, in normal patients, tricuspid valve closure is often poorly defined echocardiographically. Furthermore, in normal patients, the time interval between the first and second high-frequency components of S, is short, and precise definition of the onset of the second component from the continuing vibrations of the first is frequently impossible. However, we have found that the start of the second high-frequency component of S, coincides with echocardiographic tricuspid valve closure in those patients in whom the two high- frequency components are clearly separated, and the point of echocardiographic tricuspid valve closure can be determined.

CLINICAL INVESTIGATIONS OF THE ORIGINS

OF HEART SOUNDS

The First Heart Sound (S,)

The genesis of heart sounds, and particularly the origin of the first heart sound (S,), has been controversial since the early part of the 19th century.’ Discussion and experiments have centered around the question of whether or not the atrioventricular valves make a significant

Echocardiography is limited in its ability to define the complex sequence of events that occur in connection with atrioventricular valve closure. The moment at which the leaflets “coapt,” or are first in apposition, must occur shortly before the final tensing of the valve structure. The resolution of M-mode echocardiography is not adequate to distinguish between these two events. The coincidence of echocardiographic valve closure with the onset of sound does not necessarily imply a percussion note emanating from apposition of the delicate valve leaflets. Rather, it seems reasonable to suppose that as the valve structure reaches its elastic limits, high frequency vibrations are generated that fall in the acoustic range.

ECHOPHONOCAROlOGRAPHY

In sinus rhythm, the constant intensity of the sound and the temporal proximity as well as interdependence of valvular and ventricular events, make it difficult to resolve the questions of the relative importance of mitral valve closure and left ventricular dP/dt in the genesis of the first high-frequency component of S,. We have therefore studied clinical situations where beat-to-beat variations occur in the intensity of sound and to relate these variations in sound to velocity and amplitude of mitral valve closure.

Complete heart block provides such an op- portunity. It has been shown that the variation of intensity of S, in this condition is related to alterations in the position of the atrioventricular valves at the onset of ventricular systole and their subsequent closing velocity.‘5*‘7 Other dysrhythmias, such as atrial fibrillation, provide insight into physiologic and acoustic events because of alterations in the sequence of the cardiac cycle. Standard M-mode echocardiography, however, is limited in its ability to take advantage of these complex and fluctuating interrelationships because it displays only one intracardiac event at a time.

In order to clarify the relationship between sound intensity and mitral versus left ven- tricularraortic root events on a beat-to-beat basis, the ability to display two different intracardiac events at the same time as heart sounds would be invaluable. Therefore, we developed a

339

technique of dual echocardiography, which allows the simultaneous registration of two different valves, as well as the phonocardiogram. This technique has been employed in two patients with idiopathic atria1 fibrillation for the purpose of relating the variable intensity of S, to mitral valve motion and left ventricular function.

By simultaneously recording the aortic and mitral valves, we examined the effect on S, intensity of (1) the rate of anterior mitral leaflet closure and (2) left ventricular function as measured by the systolic time intervals derived from the aortic valve echocardiogram. An example of such a tracing is shown in Fig. 2, and analyses of 50 consecutive technically satisfactory beats from one of the patients are illustrated in Figs. 3 and 4. The relationship between the intensity of S, (r = 0.90) and the terminal rate of closure of the anterior mitral leaflet is statistically significant, whereas there is no consistent relationship between the ratio LVET/PEP and S, intensity. Similar results were obtained in the other patient, where an r value of 0.82 for the relationship between intensity of S, and rate of mitral valve closure was obtained. These studies suggest a cause and effect relationship between mitral valve closure and the first high-frequency component of S,, which can be appropriately designated “M,.” It should be noted, however, that the rate of ter-

Fig. 2. Dual echophonocardiogram of the aortic valve (AVE) in the upper part of the tracing and the mitral valve (MVE) in the lower part. from a patient with atrial fibrillation but no mitral stenosis. Seats 1, 2, and 3 show progressive increases in the intensity of the first high-frequency component of S, (M,). Atrial fibrillation allows the terminal closing velocity of the anterior mitral valve leaflet to be measured free from any effect of atrial systole. The closing velocity increases on beats l-3 in parallel with the increasing intensity of M,. Recording speed, 200 mm/set: time lines, 10 msec.

MILLS AND CRAIGE

50

-G

+ [ .

‘_E 40 ^,. % >

k’&y , ,

100 200 300 400 500 600

RATE OF MV CLOSURE (mmhec)

Fig. 3. Plot of M, intensity versus terminal rate of closure of the anterior leaflet of the mitral valve on 50 beats obtained from the patient in Fig. 2.

minal mitral leaflet closure in atria1 fibrillation is determined to a major extent by left ventricular isovolumic contraction. Clearly, the left ventricle will therefore exert some influence on the intensity of M,;24 we suggest that this influence is mediated by its effect on mitral valve closure.

The second high-frequency component of S, may be studied using similar techniques. In right bundle branch block, the first heart sound is usually widely split, the two components coin- ciding with mitral and tricuspid valve closure. In a patient showing this phenomenon, we found that following right ventricular pacing, which causes the right ventricle to depolarize before the left, tricuspid valve closure preceded mitral closure and high-frequency sounds are still associated with each event.22 In a number of

5Or

I I , 16 14 12 IO 08 06 04 02 0

PEP /LVET - increasing strength of ventricular contraction

Fig. 4. Plot of M, intensity versus PEP/LVET on the same beats as Fig. 3. The systolic time intervals were derived from the aortic valve echocardiogram. The variation in MI intensity cannot be accounted for by changes in ventricular function as measured by PEP/LVET.

other instances, a clear association between tricuspid valve closure and the second component of S, could be demonstrated to the exclusion of aortic root events. Recent studies with high-fidelity catheters and intracardiac phonocardiography,2” suggest that the second high-frequency component of S, originates in the right heart from the tricuspid valve.

Therefore, echophonocardiographic studies present strong evidence that the two high-frequency components of the first heart sound are related to closure of the mitral and tricuspid valves, respectively. Ventricular function is clearly of importance in the final completion of valve closure, but its effect on the intensity of S, seems to be of secondary importance compared with valvular events.

The Second Heart Sound (S2)

The classical concept of the origin of the two components of the second heart sound relates these vibrations to the closure of the aortic and pulmonary valves, respectively,3 these sounds being referred to as A, and P,. Recently, Shaver and his coworkers have evolved the concept of “hangout” to explain physiologic splitting of S,.2”.26 The importance of valve closure in the genesis of S, has been supported by the routine coincidence of the onset of A, and echocardiographic aortic valve closure observed in a number of noninvasive laboratories.13.“0.“7 This view has been recently challenged,2x*2g and it has been suggested that aortic valve closure preceded A, by a period of 5-25 msec (mean, 12 msec), the high-frequency sound being attributed to the recoil of the mass of blood in the root of the aorta. These observations are compatible with earlier studies that suggested that A2 results from the deceleration of blood in the aorta, which in turn is caused by valve closure.3”.3’

In defense of the classic view, two observations need be cited. (1) The echophonocardiographic studies showing a time lag between aortic valve closure and A, measured the sound at its peak amplitude rather than at the very onset of the vibrations. We have found that the onset of the vibrations of high-frequency heart sounds occurs at completion of opening or closing of valve motion recorded echocardiographically. (2) In some patients, the onset of AZ recorded at the mitral area preceded the

ECHOPHONOCARDIOGRAPHY 341

Fig. 5. Phonocardiogram IPCG) of the aortic component of the second heart sound (A,) recorded at pulmonary (PA) and mitral (MA) areas. The inset shows the delav in onset of the high-frequency vibrations of about 10 msec.

onset of the sound recorded at the pulmonary area by about 10 msec (Fig. 5). A similar phenomenon has been noted with regard to S,.32

A recent investigation by Hirschfield et al.“” utilizes high-fidelity aortic root pressure tracings in conjunction with echocardiography and phonocardiography. The simultaneous occurrence of aortic valve closure, the onset of A,, and the incisura on the pressure record rein- forces the classical concept of the role of the aortic valve in the genesis of A,. Similar studies in our own laboratory confirm these results.

A parallel controversy exists with respect to

Fig. 6. Echophonocardiogram of the pulmonary valve (PVEI in a patient with pulmonary hvpertension and an aortic prosthesis. Two components of Sp cannot be clearly separated. The inset shows the relative delay in “closure” of the anterior cusp of the pulmonary valve compared with the posterior cusp. The explanation for this echocardiographic observation is unclear. However, the point of coaptation of both leaflets is compatible with the hypothesis that Py results from this event.

the pulmonary component of the second sound (Pp). Technical factors make this a more difficult question, since the moment of coaptation of the pulmonary valve leaflets was not recorded in the two studies that showed a delay between “valve closure” and P,. Generally, only the posterior leaflet of the pulmonary valve is recorded echocardiographically. In cases where we have also recorded the anterior leaflet, the posterior leaflet is seen to reach a “closed” position prior to the arrival of the anterior leaflet, and so actual coaptation may occur later (Fig. 6). The posterior leaflet alone is therefore inadequate by itself as a marker of pulmonary valve closure.

Echophonocardiographic studies of the second heart sound are compatible with the concept that A, is generated by tensing of the closed aortic cusps that act as a membrane. In this respect, the sound may be considered “valvular” in origin although as with the first heart sound, this does not imply the sound is produced by “clapping” together of the closing leaflets or cusps.

Ejection Sounds and Opening Snaps

Although some of the details of these studies of the first and second heart sounds may seem merely “academic,” the principles involved are of considerable clinical importance, especially in the echophonocardiographic recognition of opening snaps and ejection sounds. These sounds have their onset at the time of maximal opening of the atrioventricular or semilunar


valves, whereas the first and second heart sounds occur at complete closure of the respec- tive valves.‘s Recognition of these relationships allows echophonocardiography to determine the presence or absence of ejection sounds and opening snaps with considerably more precision

Fig. 8. Echophonocardiogram in a patient with a history of previous malignant hvpertension. The high-frequency ejection sound fAoHtX) occurs at full opening of the aortic valve-a similar relationship as seen in the patient with aortic valve stenosis in Fig. 1. The hypertensive aortic ejection sound is well recorded at the aortic area-a feature not usually found with other ejection sounds. It is poorly transmitted to the mitral araa, and in some cases, cannot be recorded at this location.

than has been previously possible with phonocardiography alone.

Early systolic ejection sounds classically occur with deformities of the semilunar valves, as in congenital aortic34-“” (Fig. I), pulmonary stenosis,““.37 (Fig. 7) or a bicuspid aortic valve.“,“’ They are also found in some patients with hypertension of the systemic”“.4o (Fig. 8) or pulmonary circulation’“.“5.4’ (Fig. 9), pulmonary atresia or tetralogy of Fallot.35*4’ The sounds have been called “valvular” when found in association with abnormal valves and “vascular” in the other pathologies.““,4” In either case, it can be shown by echophonocardiography that the high-frequency ejection sound starts at the moment of full opening of the pulmonary or aortic valve, and we recently observed that this moment always occurs on the upstroke of the high-fidelity pressure curve in the aorta or pulmonary artery. Although it is generally accepted that the “valvular” ejection sound is caused by the halting of the “doming” valve,44 the origin of the “vascular” sounds is not clear and their presence is by no means in- variable in systemic and pulmonary hypertension. It may be that vascular ejection sounds do in fact originate from the semilunar valve cusps that have undergone changes in structure in response to the increased pressures.

Opening snaps of the mitral and tricuspid


Fig. 9. Echophonocardiogram of the pul-

monary valve in a patient with pulmonary hyper-

tension. The onset of the ejection sound

(PulmHytX) coincides with the moment of full opening of the pulmonary cusp.

valves are analogous to the semilunar valve ejection sounds. The exact coincidence of the opening snap of mitral stenosis with the achieve- ment of a fully open position by the mitral valve (E point) is clearly demonstrable by echophonocardiography’8.‘“-47 (Fig. 10). This point follows the left atrial-left ventricular pressure crossover.“’ An opening snap is characteristic of a stenotic valve, 4q but is also seen in circumstances characterized by a swift opening ve-

locity of a nonstenotic valve”” (Fig. 11). Condi- tions favoring such a mechanism include mitral regurgitation, tricuspid atresis (high-velocity flow through mitral valve), complete heart block, and thyrotoxicosis.

The diagnosis of tricuspid stenosis can be difficult, and the presence of an opening snap occurring at full opening of the tricuspid valve, characteristically later than full mitral opening, is a very useful finding.

Fig. 10. Echophonocardiographic relationships in

mild mitral stenosis. Comparing this tracing with Fig. 1, the analogous relationships of mitral valve opening and

the opening snap (OS) with aortic valve opening and the aortic ejection sound may be seen. Indeed. it has been

suggested that the latter be called “aortic opening

snaps”:‘” ‘J The coincidence of mitral valve closure and the onset of S , is shown here.

Fig. 11. A nonstenotic tricuspid valve opening snap (TOS). This echophonocardiogram. recorded from a patient with anomalous venous return. shows an opening snap coin- cident with full opening of a normal tricuspid valve (TVE). This is anelogous with the finding of nonstenotic mitral opening snaps. Tricuspid opening snaps may also be found in patients with rheumatic tricuspid stenosis or Ebstein’s anomaly.

Third and Fourth Heart Sounds

In contrast with S,, S.‘, ejection sounds, and opening snaps, which are dominantly of high frequency, the third and fourth (atrial) heart sounds are of low frequency. The third heart sound may be associated with a change in slope of the E--F portion of mitral valve closure, but this probably reflects a change in the pattern of ventricular filling, rather than being indicative of a direct causative relationship. The onset of the third heart sound has been reported to bear a close relationship to halting of the rapid posterior motion of the left ventricular wall in early diastole,5’ although others have questioned this relationship. 52 The left-sided fourth heart sound occurs during the phase of atria1 reopening of the mitral valves and is temporally closely related to the “A” point of mitral valve motion. No consistent relationship to ventricular wall motion has yet been demonstrated, and in clinical practice, a fourth heart sound is best detected by combined phono and apex cardiography.

Concepts of the Genesis of the Heart Sounds

In summary, we would like to offer the following hypotheses to explain the origin of

MILLS AND CRAIGE

heart sounds that may be divided into high- and low-frequency categories. Of the high-frequency sounds, the first and second heart sounds are causally related to completed closure of the atrioventricular and semilunar valves, respectively. High-frequency sounds may occur at the time of complete opening of the semilunar and atrioventricular valves and are recognized as ejection sounds or opening snaps. The majority and possibly all of these sounds are valvular in origin. In contrast, low- frequency sounds are probably related to alterations in patterns of ventricular filling, which may in turn cause alterations in motion of the atrioventricular valves. Thus, the high-frequency sounds may be regarded as “valvular,” the low-frequency as “ventricular.”

EVALUATION OF CARDIAC DISEASE

In the preceding section we have discussed the role of echophonocardiography in the elucidation of the genesis of individual heart sounds. In the following section, the application of the principles developed from these studies and the uses of echophonocardiography in routine cardiac practice will be discussed.

Obstruction to Left Ventricular Outflow

Ejection systolic murmurs are characteristically found in patients with outflow tract obstruction, and echophonocardiographic studies are particularly useful in determining the nature of the underlying pathology in these cases. An accurate noninvasive anatomic diagnosis allows appropriate planning of cardiac catheterization when this is indicated. In patients in whom the degree of obstruction is obviously not critical, the appropriate prognosis and follow-up can be determined from the echophonocardiographic findings alone.

Congenital Aortir Valve Stenosis

Although M-mode echocardiography is relatively insensitive in detecting congenital aortic stenosis,“” we have found that the presence of an aortic ejection sound defined by echophonocardiographic studies is frequently associated with this abnormality. The aortic valve echocardiogram may show multiple diastolic echoes, suggesting thickening of the cusps, but this finding is of limited diagnostic value as it depends to

ECHOPHONOCARDlOGRAPHY

some extent upon the echocardiographic gain settings and transducer angulation. Assessment of the severity of the stenosis is best accom- plished by considering the carotid upstroke contour, the configuration of the murmur that moves later in systole with increasing stenosis, as well as the echocardiographic and electrocardiographic evidence of left ventricular hypertrophy.

Recent studies38 suggest that an aortic ejection sound, unaccompanied by other evidence of aortic stenosis, originates from a nonstenotic bicuspid aortic valve. The presence of eccentric closure of the aortic cusps is valuable additional evidence of a bicuspid valve,“4.55 but the closure line may be central when a bicuspid valve is present. A useful additional test is to record the aortic valve from the apex when the persistence of visualization of the cusps during systole3’ (Fig. 12) suggests a bicuspid or “doming” valve. This technique helps to distinguish valvular ejection sounds from systemic hypertensive sounds. The ejection sound often heard in patients with coarctation of the aorta is usually associated with marked eccentricity of the aortic valve echo, suggesting that the sound originates from a nonstenotic bicuspid valve, rather than from the aortic root.

Establishing the diagnosis of a bicuspid aortic valve offers new possibilities in preventive cardiology, as this congenital lesion underlies many cases of isolated calcific aortic stenosis. While specific recommendations for preventing the calcification of such valves are not yet available, patients should be advised to take antibiotic prophylaxis against bacterial endocarditis. It is of practical importance, therefore, to differentiate between an aortic ejection sound, a split first heart sound, a fourth heart sound, or an early systolic click associated with mitral valve prolapse. Generally, careful echophonocardiographic studies directed towards the accurate recording of the sound in question with the mitral, tricuspid, aortic, and if necessary, the pulmonary valves will resolve the question. Echophonocardiography has demonstrated that aortic ejection sounds may occur in patients with rheumatic valvular disease (Fig. 13), although previously this had not been thought to occur.56 This finding suggests involvement of the aortic valve commisures by the rheumatic process; in such patients, the possibilities of fu-

Fig. 12. The typical appearance of a bicuspid aortic valve

recorded with the echo transducer at the cardiac apex. The

diagnosis in this patient had been established elsewhere by

angiography. The aortic cusp is seen throughout systole. presumably because it is unable to fold against the walls of the

aorta during ejection, being bicuspid rather than tricuspid.

The ejection sound recorded at the left sternal edge (LSE) is

preceded by the first heart sound, and its onset coincides

with the full opening excursion of the valve. Note that in this

view. the aortic valve motion is similar to that of the pulmonary valve recorded from the conventional anterior

chest wall site. This technique is useful in differentiating

aortic ejection sounds of valvular origin from aortic

hypertensive ejection sounds where the aortic cusps are not

seen during systole. Recording speed, 200 mm/set.

ture valve stiffening and calcification are important.

CalciJic Aortic Stenosis

Calcific aortic stenosis is characterized by the absence of an ejection sound, reflecting loss of mobility of the valve CUSPS.~~ The ejection systolic murmur cannot always easily be differentiated from a “flow” murmur, but the echocardiographic finding of a dense band of echoes in the aortic root obscuring the valve cusps is suggestive of calcific aortic stenosis. It may be difficult to determine whether these findings represent aortic stenosis (obstruction to outflow) or aortic sclerosis (cusp calcification without obstruction). The contour of the carotid pulse and duration of ejection time, as well as the presence of an S, and A wave on the phono and apex cardiograms, are helpful in establishing the physiologic alterations accompanying such a murmur.

346 346 MILLS AND CRAIGE

Hypertrophic Cardiomyopathy

The presence or absence of left ventricular outflow obstruction in patients with hypertrophic cardiomyopathy was an early stimulus to the correlation of echo and phonocardiographic abnormalities.“7-5g It is now well established that systolic anterior motion of the mitral valve and a systolic murmur are found in patients with obstruction to the left ventricular outflow and are usually absent in patients without obstruction. Similarly a mid-systolic closing motion of the aortic leaflets occurs with the start of the systolic murmur and with a re- duction of blood flow in the aorta, all these being due to the onset of obstruction.60 These relationships can be demonstrated within the same patient by using amyl nitrate to provoke the obstruction.

The question of ejection sounds in hypertrophic cardiomyopathy”’ has recently been clarified by the echophonocardiographic studies from Shah’s laboratory.6’ Discrete systolic sounds do occur in patients with obstruct- ing hypertrophic cardiomyopathy, and these sounds coincide with halting of systolic anterior motion of the mitral valve during systole. These “pseudoejection” sounds tend to occur in patients with significant obstruction, and they may be caused by the anterior mitral valve leaflet hitting the interventricular septum. The intermittent presence of these sounds, apparently depending on the abruptness of halting of the SAM, explains previous uncertainty about their existence and significance.

Fig. 13. Echophonocardiogram of a patient with rheumatic mitral and aortic valve disease. The rhythm is atrial fibrillation. Notice the reciprocal relationship between the intensity of the ejection sound (loudest after long R-R intervals) and the first heart

sounds (loudest after short R-R intervals). This is similar to the findings shown in Fig. 2. The ejection sound is softest after a short R-R interval (beat

3). reflecting reduced ventricular

i I performance following a shortened filling period.

In a number of patients with hypertrophic cardiomyopathy, it is not possible to obtain echocardiograms of diagnostic quality. This ap- plies particularly to the right ventricular aspect of the interventricular septum, preventing accurate measurement of septal thickness. In these cases, the contours of the carotid and apex pulses, the presence of a fourth heart sound, and provocation of a systolic murmur with amyl nitrate may be diagnostically helpful.

Fibrous Subaortic Stenosis

In contrast to congenital aortic valve stenosis, fibrous subaortic stenosis is characterized by the absence of an ejection sound occurring at full aortic valve opening (Fig. 14). The ejection systolic murmur in this condition has no specific features, and hence, employing phonocardiography alone is diagnostically unhelpful. The classical echocardiographic features of subaortic stenosis consist of early partial closure of the aortic valve cusps and high-frequency vibrations of the cusps during systole.““-66 However, cases arise in which the degree of early systolic closure and fluttering of the cusps may be difficult to differentiate from the minor degree of these features some- times seen in normals. In such cases, the ejection systolic murmur and the absence of an ejection sound are useful in clarifying the diagnosis.

Obstruction to Right Ventricular Outflow

The physiologic principles underlying the echophonocardiographic findings in obstruction

ECHOPHONOCAROlOGRAPHY 347

PCG-PA

Fig. 14. Typical echophonocardiagraphic features of discrete subaortic stenosis. The ejection systolic murmur is not accompanied by an ejection sound. Early systolic closure and fluttering of the aortic cusps is seen. These findings clearlv contrast with those of aortic valve stenosis.

to left ventricular outflow also apply in the right heart. On the right side, however, the effects of inspiration in augmenting right ventricular filling is an additional factor.

Pulmonary Valve Stenosis

A pulmonary ejection sound is usually found in patients with pulmonary valve stenosis, provided the valve is mobile. The ejection sound occurs at full opening of the valve. When the stenosis is severe, this event and tricuspid valve closure occur close together. However, the characteristic decrease of intensity of pulmonary ejection sound with inspiration allows it to be distinguished from T,, which is usually augmented by inspiration. The respira- tory variation in intensity of the pulmonary valve ejection sound and the echocardiographic pattern of the pulmonary valve in pulmonary stenosis37.“7.“X have a similar explanation. With inspiration, there is increased right ventricular diastolic filling, and if there is reduced com- pliance due to right ventricular hypertrophy, the right ventricular end-diastolic pressure may exceed the pulmonary artery diastolic pressure, and the pulmonary cusps will tend to open. This phenomenon is accentuated by atria1 systole.

Thus, with inspiration, the pulmonary cusps are “half open” at the onset of ventricular systole, their excursion is less, and the ejection sound is of reduced intensity.

In further support of this hypothesis, we have observed echocardiographic pulmonary valve opening prior to the simultaneously recorded high-fidelity pulmonary pressure upstroke. This was found in a patient who had undergone successful pulmonary valvotomy for severe pulmonary stenosis but had a large residual A wave on the right ventricular pressure tracing. Similar echocardiographic findings have been noted,6g and Leatham’O has reported a pulmonary ejection sound that preceded the QRS complex in a patient with severe pulmonary stenosis.

Echophonocardiography distinguishes the pulmonary valve ejection sound of pulmonary stenosis, which is associated with a systolic murmur in the pulmonary area, and a delayed P, from a pulmonary hypertensive ejection sound, which is usually seen with the “W” pattern of pulmonary valve motion, and absence of a systolic murmur (Figs. 7 and 9).

Injiindibular Stenosis

In patients with pure infundibular stenosis, no ejection sound accompanies the ejection systolic murmur. However, as might be anticipated, the pattern of motion of the pulmonary valve is abnormal, being characterized by mid-systolic partial closure and fluttering of the cusps” (Fig. 15). This pattern has some similarity to that seen in pulmonary hypertension,72.73 but the presence of the murmur serves to distinguish the two diagnoses. As with subaortic stenosis, the echocardiographically abnormal cusp motion is a reflection of the turbulent flow caused by obstruction proximal to the valve.

Mitral Stenosis

Echophonocardiography has contributed significantly to our understanding of the genesis of the characteristic murmur of mitral stenosis. This murmur, called “presystolic” by long- standing custom, was shown by Criley”’ to be actually dependent on ventricular rather than atria1 systole for its distinctive crescendo immediately before S,. Recently, application of echophonocardiographic techniques has em- phasized that the crescendo phase of the

MILLS AND CRAIGE

Fig. 15. Echophonocardiogrsphic findings in a 25-yr-old with a gradient of 120 mm Hg due to pure infundibular stenosis. P, is late and was variable in intensity. The systolic murmur runs through A* There is no ejection sound, and the pulmonary valve partially closes and flutters during systole.

murmur is related to the swift closing movement of the stenotic mitral apparatus. Atria1 systole may initiate the murmur, but the final crescendo phase, which is quite brief, occurs during left ventricular isovolumic contraction. The secondary role of atria1 systole is em- phasized by the occurrence of a presystolic crescendo murmur following short diastoles with severe mitral stenosis and atria1 fibrillation.75 In these circumstances, there is a high gradient across the valve, and the murmur can be attributed to upward motion of the stenotic mitral apparatus against the flow of blood from atrium to ventricle.

The opening snap (OS), one of the most useful diagnostic features of mitral stenosis, can usually be separated from the second heart sound by auscultation. However, with increasing severity of stenosis, the high left atria1 pressure results in an abbreviation of left ventricular isovolumic relaxation and, therefore, earlier opening of the mitral valve relative to aortic valve closure. This observation forms the basis for measurement of the A,--OS time, a widely used phonocardiographic index of the severity of mitral stenosis. When the left atria1 pressure is very high, the opening snap is so early-O.04 or 0.05 set from AZ-that it may be difficult to distinguish it from P,. Under these circumstances, echophonocardiography can identify the opening snap precisely and provide evidence of the hemodynamic severity of the stenosis as well as the mobility of the valve (Fig. 10). In patients in whom calcification has

resulted in loss of the opening snap, echophonocardiography allows the time from A2 to full mitral valve opening to be determined.

A recent study76 points out that isovolumic relaxation is from A, to the start of mitral valve opening, and this time interval may turn out to correlate more accurately with left atria1 pressure than does the conventional A2 OS time.

Mitral Valve Prostheses

The applications of echophonocardiography in mitral stenosis have been extrapolated to the assessment of malfunction of prosthetic valves in the mitral position. ii,‘* Patients with a mitral valve prosthesis may deteriorate for a number of reasons, including paravalvular leak, thrombosis around the cage of the prosthesis, or left ventricular dysfunction. These will result in an increase in left atria1 pressure, and therefore, analysis of the A2 to prosthetic valve opening time should be diagnostically useful. Since some of the valves in current use open silently, echophonoc~rdiography provides a means of measuring the A-, to prosthesis opening time. With most prostheses, the normal A, to opening time is about 0.10 set, and abbreviation to 0.04-0.06 set suggests a high left atria1 pressure. Both a paravalvular leak or a thrombus causing obstruction may therefore lead to shortening of isovolumic relaxation, and consequently, a narrow AX-prosthesis opening interval. The key to separation of these two complications-thrombosis or regurgitation-is


Fig. 16. Pm- and postoperative echophono-

cardiographic studies in a patient shown to have a severe paraprosthetic mitral valve leak. Panel 1

shows hyperdynamic left ventricular walls with normal septal motion. Panel 2 demonstrates the shortened (0.04 set) time interval from A? to opening of the malfunctioning prosthesis-a porcine heterograft. Following successful reoperation (panel 3) the A, to opening time had returned to normal-O.1 1 sec.

I. PRE-OP 2. PRE-OP 3. POST-OP

provided by an echocardiographic examination of the left ventricle (Fig. 16). Thrombosis of the prosthesis, like mitral stenosis, is associated with a small left ventricular dimension with wall motion that is not exaggerated. With a paravalvular leak, however, the ventricle may be dilated, its walls hyperdynamic, and the movements of the septum apparently normal in contrast with the expected hypokinesis or frankly paradoxical septal movement that is expected following successful mitral valve replacement. 7g Where left ventricular dysfunction is responsible for a poor result following mitral prosthetic surgery, the isovolumic relaxation time is variable. This is because the increased left atria1 pressure tends to shorten isovolumic relaxation, but the reduced negative dP/dt lengthens this time interval. However, the echocardiogram of the left ventricle is diagnostic, showing the dilated chamber and poor wall motion resembling that of congestive cardiomyopathy.

Left Atrial Myxoma

Although echocardiography has revolu- tionized the diagnosis of left atria1 myxoma, establishing this diagnosis still requires sufficient clinical suspicion for an echocardiogram to be requested. Echophonocardiographic studies em-

, PCG-MA

phasize the way in which a myxoma mimics mitral stenosis, causing not only a very loud first heart sound but also a diastolic sound, the “tumor plop,” which occurs very close to the time that a mitral opening snap might be expected (Fig. 17). These physical signs appear to be typical of left atria1 myxomata,*O and their recognition is an important pointer in selecting patients in whom a myxoma needs to be “ruled out.”

Mitral Regurgitation

Combined echo and phonocardiographic studies are particularly important in assessing patients with mitral regurgitation. While the noninvasive diagnosis is made by the presence of the characteristic pansystolic murmur, neither the etiology nor the hemodynamic importance of the condition are usually apparent from the phonocardiographic findings alone. The echocardiographic features of mitral regurgitation are nonspecific, but a useful index of the severity of the regurgitation is provided by the hyperdynamic left ventricular wall motion, increased left ventricular cavity dimensions, and left atria1 enlargement. Thus, while auscultation and phonocardiography establish the diagnosis, the role of echocardiography is to

MILLS AND CRAIGE

assess the severity of the regurgitation and, on occasion, its pathogenesis.

Rheumatic Heart Disease

The echocardiographic appearance of rheumatic mitral regurgitation comprises a spectrum of mitral valve motion ranging from an apparently normal pattern to one in which the features of mitral stenosis are prominent. The combination of a pansystolic murmur and an echocardiogram consistent with mitral stenosis indicates the presence of mitral regurgitation on a rheumatic basis.

Mitral Valve Prolapse

The characteristic echocardiographic features of mitral valve prolapse have been described in a number of recent articles.*‘-“” The systolic click and late systolic murmur often coincide with the prolapse movement detected echocardiographically. The increased amplitude and rate of mitral valve closure tend to be reflected in the phonocardiogram by an unusually loud first heart sound, a diagnostic point that may be useful in separating prolapse from rheumatic mitral regurgitation where a soft S, is to be expected.88 Establishing the etiology of mitral regurgitation has important therapeutic and prognostic implications. Pe-

Fig. 17. Echophonocar- diographic findings in left atrial myxoma. S, is very loud, and the tumor plop can be seen as the myoxma appears to halt its downward motion between the mitral valve cusps.

nicillin prophylaxis against rheumatic fever is not required in patients with mitral valve prolapse, whereas it is indicated in rheumatic valvular disease. In a recent study on the prognosis of mitral valve prolapse, we found that the outlook for patients with a late systolic murmur was less benign than for those in whom a mid- systolic click was the only phonocardiographic manifestation of the abnormal valve.“’

Mitral Regurgitation Secondary to Cardiomvopathjl

Another important differential diagnosis is between primary valvular disease and mitral regurgitation secondary to left ventricular dysfunction. In the latter situation, the typical findings of a congestive cardiomyopathy are apparent on the echocardiographic study. The therapeutic implications are very important, since insertion of a prosthetic mitral valve does little to alter the prognosis for these patients despite the presence of impressive auscultatory and phonocardiographic evidence of mitral regurgitation.

Acute Mitral Regurgitation

This variant requires special consideration since the truncation of the murmur in late systole may lead to a failure to recognize the

ECHOPHONOCARDIOGRAPHY

presence of this very important hemodynamic lesion that may masquerade as an ejection systolic murmur.88.8g A further potentially mislead- ing feature is that the left ventricular wall motion may not show the anticipated hyperdynamic wall motion.g0 Exaggerated motion of the aorta, possibly reflecting an increased left atria1 stroke volume, may prove to be the key echocardiographic feature of this diagnosis.g’ The recording of a parasternal impulse with the characteristics of a large left atria1 V wave rather than a ventricular pressure waveform, is often a useful pointer to the correct diagnosis.92.93

Aortic Regurgitation

In 1861, the great American clinician Austin Flint provided a remarkably futuristic analysis of the physiologic disturbances responsible for the apical diastolic rumble in pure aortic regurgitation.ga He ascribed the low-pitched apical murmur to a functional mitral stenosis resulting

351

from the cascade of blood from the aortic leak impinging on the anterior mitral leaflet. Where pressure in the left ventricle in late diastole reaches very high levels (40-50 mm Hg), so as to equilibrate with aortic diastolic pressure, a reverse gradient is created across the mitral valve.g5 It therefore closes in mid to late diastole. The auscultatory and phonocardiographic consequences of this hemodynamic situation include a premature cessation of the Flint murmur in mid to late diastole and extinc- tion of the mitral component of S, (Fig. 18). These conditions are most apt to occur in acute aortic regurgitation where the ventricle has not dilated and therefore responds to a massive aortic leak with extreme elevation of end- diastolic pressure. An understanding of this physiologic derangement and its bedside as well as echophonocardiographic manifestations is important for optimal management of acute aortic regurgitation, which is usually caused by infective endocarditis.“6

Fig. 18. Dual echophonocardiogram of the aortic and mitral valves showing all the cardinal features of acute aortic regurgitation. The first heart sound is absent because the mitral valve has closed in mid-diastole. There is fluttering of the anterior leaflets of the mitral valve. The diastolic murmur does not run throughout diastole because of equalization of the aortic and left ventricular pressures. The cause of this hemodynamic situation was bacterial endocarditis. which had resulted in vegetations on the aortic valve and a flail cusp (found at surgery). The patient underwent an aortogram primarily to determine the presence or absence of additional mitral regurgitation (which was found to be trivial). Because of the risk of embolization, the aortic valve was not crossed. The patient underwent successful aortic valve replacement for severe aortic regurgitation.

352

Fig. 19. Echophonocardiographic features of ASD. These patients regularly show a loud high-frequency sound IT,) at the time of tricuspid valve closure fvertical line). Both leaflets of the tricuspid valve are well recorded. Ai and Pr are widely split.

MILLS AND CRAIGE

CASE HISTORIES

The following cases serve to illustrate some of the uses of echophonocardiography in clinical practice.

Case 1

The diagnosis of an atria1 septal defect can be supported from the fixed splitting of Sp, and the typical electrocardiographic and radiographic abnormalities. Figure 19 illustrates some of the echophonocardiographic findings in an atria1 septal defect. The echocardiogram shows both leaflets of the tricuspid valve clearly recorded. Paradoxical septal motion and right ventricular volume overload were also present but are not illustrated. All of these may also be found with anomalous venous return or other causes of right ventricular volume overload, but the wide, relatively fixed splitting of S, (Fig. 19) is characteristic of an atria1 septal defect. Echo- phonocardiographic study (Fig. 19) shows that the loud high-frequency sound at the left sternal edge coincides with tricuspid valve closure. When the P-R interval is normal, this is in- variably seen in atria1 septal defect and is a valuable diagnostic sign.“7.“X

Fig. 20. Echophonocardiographic findings in Ebstein’s anomaly. The mid-systolic sound, which might be mistaken for a systolic click associated with mitral valve prolapse, coincides with delayed closure of the tricuspid valve.

ECHOPHONOCAROlOGRAPHY 353

Fig. 21. The chest x-ray in case 3. There is a “shell” of

calcification seen at the cardiac apex. Careful inspection revealed a gap in this shell, indicated by the two arrows. (Re-

produced by permission.‘“‘)

Case 2

Another cause for a loud tricuspid closure sound is Ebstein’s anomaly (Fig. 20). Again, combined echophonocardiography is useful as the isolated echocardiographic features are nonspecific and may be difficult to distinguish from severe right ventricular volume overload. However, the identification of a loud late T, or “sail sound” is pathognomonic of Ebstein’s anomaly.““~‘oo

Case 3

We recently studied a young man who presented with a history of nonspecific chest pain, a loud apical systolic murmur, and cardiomegaly on chest x-ray with calcification at the cardiac apex (Fig. 21).

Timing of the murmur with mitral and aortic valve echocardiograms established that the murmur started at the time of mitral valve closure and before aortic valve opening-the characteristics of a “pansystolic” murmur (Figs. 22 and 23). However, the murmur also finished well before AZ, suggestive of an “ejection” murmur (Fig. 23). Possible causes for a murmur with this configuration include acute mitral regurgitation and a muscular ventricular septal defect. However, the left ventricular

Fig. 22. Mitral valve echophonocardiogram of case 3.

The systolic murmur starts immediately after mitral valve closure, indicating flow into a recipient chamber whose

pressure is lower than the aortic diastolic pressure.

(Reproduced bY permission. ‘W 1

echocardiographic scan in this patient showed a relatively echo-free space behind the posterior left ventricular wall, and possible explanations for this finding include a posterior pericardial effusion, pleural effusion, or mediastinal cyst.

Fig. 23. Aortic valve echophonocardiogram from case 3 illustrating that the murmur is fully developed at the time of

complete aortic valve opening. It is at this time that “ejec-

tion” systolic murmurs begin. Yet, in this patient, the

murmur had ceased well before aortic valve closure-a characteristic of ejection murmurs. (Reproduced by per-

mission. “” )

Fig. 24. Left ventricular angiogram explaining the findings in Figs. 21-23. During systols there is flow from the left ventricular cavity through a narrow neck (white arrows) into a pseudoaneurysm. Thus, the murmur starts with the onset of ventricular systole but ceases when there is equilibration of pressure between the left ventricle and the pseudoaneurysm. (Reproduced by permission.“*I

We have also encountered a large coronary artery-coronary sinus fistula causing a similar appearance. A posterior echo-free space has, however, been reported in one case of left ventricular pseudoaneurysm,10’ and this diagnosis would be compatible with the configuration of the systolic murmur, with flow starting at the

MILLS AND CAAIGE

onset of ventricular systole and being halted by filling of the stiff-walled noncompliant pseudoaneurysm in late systole.

Careful examination of the chest x-ray revealed a gap in the calcified “shell” at the cardiac apex (Fig. 21), and left ventricular angiography confirmed that this was a narrow communication between the left ventricular cavity and the pseudoaneurysm (Fig. 24). In this patient, integration of all the noninvasive findings was necessary before deciding on the most likely diagnosis.

Case 4

The absence of echocardiographic abnormalities in the presence of other noninvasive findings may often be valuable. A 40-yr-old woman with typical symptoms of hypertrophic cardiomyopathy was found to have an ejection systolic murmur. This was much louder in the pulmonary area than at the cardiac apex-and unusual for a murmur at this location-becom- ing more intense during expiration. These observations were noted on auscultation and confirmed phonocardiographically (Fig. 25). Echocardiography revealed asymmetric septal hypertrophy (Fig. 26), but despite a careful search, no systolic anterior motion of the mitral valve was detected, and the aortic valve motion was normal with no mid-systolic closure.

Fii. 25. Phonocardiogram from case 4 showing an ejection systolic murmur in the pulmonary area that is louder with expiration end softer with inspiration-the converse of moat murmurs due to obstruction to right ventricular outffow.


Fig. 26. Echocardiogram from case 4 showing asymmetric septal hypertrophy (ratio of IVS to free wall l-8:1). Re- cording speed, 50 mm/set.

This suggested that the patient did indeed have hypertrophic cardiomyopathy, but that there was obstruction to right ventricular rather than left ventricular outflow. The effect of sud- denly increasing venous return by elevation of the legs was therefore studied. The augmenta- tion in intensity of the murmur with this ma- neuver was consistent with the hypothesis of a dynamic obstruction to right ventricular outflow. This was confirmed at cardiac catheterization, where a 15-mm gradient was found between the right ventricular cavity and the pulmonary artery, and no gradient could be detected across the left ventricular outflow despite appropriate provocative maneuvers.

The rest of the study confirmed the noninvasive diagnosis of hypertrophic cardiomyopathy with obstruction to right ventricular outflow.

CONCLUSION

Although great advances have been made with M-mode echocardiography, doubts have been expressed concerning the further expan- sion of the diagnostic capabilities of the method. While this may be true with respect to echocardiography in isolation, it is our belief that with the addition of already established methods, the combination of techniques described above is capable of increasing the scope of noninvasive methods in cardiology.

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Echophonocardiography

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