Echocardiography of the aortic and pulmonary valves

Echocardiography of the aortic and pulmonary valves

Echocardiography of the Aortic Pravin M. Shah (with technical assistance E CHOCARDIOGRAPHIC detection of the semilunar valves lagged considerably...

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Echocardiography

of the Aortic

Pravin M. Shah (with technical

assistance

E

CHOCARDIOGRAPHIC detection of the semilunar valves lagged considerably behind the examination of atrioventricular valves. The first documentation of aortic valve and aortic root recordings were reported by Gramiak and Shah.‘.* Ultrasonic detection of pulmonary valve was first reported by Gramiak, Nanda, and Shah.3 This article will describe’ current applications of these areas of clinical echocardiography. TECHNIQUE

AND

in Cardiovascular

Vol. XX.

No. 6 (May/June).

of Linda J. Sylvester)

NORMAL

AORTIC ROOT AND ECHOGRAM

VALVE

The two aortic walls move, nearly synchronously, anterior in systole and posterior in diastole (Fig. 2). The anterior motion begins following the first heart sound (mitral valve closure point C) and reaches a peak 80-100 msec after the aortic component of the second heart sound. This latter point, termed “0,” is generally coincident with early mitral valve opening to its E point or the mitral opening snap when present. The posterior movement of the aortic wall is generally a two-step motion. At slower heart rates (less than 90 beats/min) the early more rapid posterior movement to a point “R” is followed by a relatively flat appearance during the period of diastasis. A further posterior displacement (A) is observed following atria1 contraction. At more rapid heart rates, the early rapid posterior movement merges smoothly with the atria1 wave with loss of the intermediate phase of diastasis. The internal dimension of the aortic root expands in endsystole, but only by a few millimeters. The mechanism of the characteristic aortic wall motion has been recently clarified by the work of Strunk and associates9 to represent left atria1 filling and emptying events. These authors proposed that the posterior aortic wall in the echocardiogram also represents the anterior left atria1 wall and its movement through systole reflects left atria1 distension with its filling. Following mitral valve opening, an early rapid emptying of the atrium results in reduc-

NORMAL ECHO ANATOMY (FIGURE 1)

Diseases,

Valves

the junction of the right ventricular infundibulum and the main pulmonary artery. Behind are strong echoes, presumably arising from the aorto pulmonary sulcus with a portion of the left atria1 cavity seen still posteriorly.

A 2.25 mHz pulsed-echo transducer is suitable for most patients, with the exception of small children in whom a 3.5 mHz transducer is more adequate. A standard procedure is to place the transducer in the third or the fourth left interspace directed posteriorly so as to identify a characteristic motion pattern of the mitral valve, either in A- or M-mode display. The transducer is then directed medially and cephalad by about 15” until the typical parallel anterior and posterior aortic wall echoes are identified. A gradual transducer angulation demonstrates that normally the anterior mitral leaflet is at the same depth as the posterior aortic wall. Having identified the two parallel strong echoes emanating from the aortic walls, appropriate gain adjustment will permit visualization of the central aortic cusps. The latter appear somewhat centrally in diastole and move rapidly out to the aortic walls in early systole. The space in front of the aorta is the right ventricle near its infundibulum and behind is the left atrium. In order to obtain a recording of the pulmonary valve, it is often necessary to move the transducer one interspace higher from the aortic position and angle it posteriorly and slightly superiorly either pointing directly posterior or slightly to the left. With appropriate attenuation of the near field, an anterior space about 2-5 cm from the chest wall is visualized. The posterior leaflet of the pulmonary valve is generally recognized occupying a central position in this space in diastole and moving posteriorly in early systole. The space represents Progress

and Pulmonary

From the Cardiology Unit. Department of Medicine, University of Rochester School of Medicine, Rochester, N. Y. Reprint requests should be addressed to Pravin M. Shah, M.D.. Chief. Cardiology Division, Wadsworth VA Hospital. Sawtelle and Wilshire Blvds., Los Angeles, CaliJ 90073. o 1978 by Grune & Stratton, Inc. 0033~0620/78/2006-0011$02.00/O 1978

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452

SHAH

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of a normal aortic valve is likely to peak dP/dt of left ventricular

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aortic

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in our laboratory.’ in Table I

endsystole centricity

si-

anterior

held open in position at its

of ejection.

physic;LI \,alvc

measured reproduced

Fig. 2. Aortic root and valve echogram with multaneous phonocardiogram IPCG) and electrocardiogram (ECG). RVO, right ventricular outflow: AW. anterior and posterior walls of aortic root: AoV, aortic valve cusps; left atrium. The letters R and N in the echogram of represent right and noncoronary cusps. The letters 0, R. A denote motion of PW. which also forms the anterior of the left atrium.

the cusp

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SYLVESTER

volume

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lateral

Fig. 1. A schematic of the beam directions and the echographic outlines as the transducer is directed to (Al aortic root. (B) mitral valve. and (Cl left ventricular cavity. Note pulmonary valve (D) is generally obtained by placing the transducer one interspace higher. The beam through the aortic root as well as the pulmonary artery exit through left atrium posteriorly.

atrinl

cardiac

resting

mediastinal rellccted 01‘

left

the

AND

of veof the

opening

vc-

to be repressure

ECHOCARDIOGRAPHY

Table

OF AORTIC

AND

for Aortlc Root 1. Values in Normal Subjects

PULMONARY

and

Valve

Mean* Aortic

SD

Root

End-diastolic dimension (mm) End-systolic dimension (mm) Total amplitude of motion (mm) Aortic Valve Amplitude Amplitude

of opening of closing

Rate of opening

motion motion

movement

(mm) (mm) (mm/set)

33.7

f 4.4

35.0 10.4

f 4.2 f 5.8

10.3 f 7.2 f 369.0

1.5 1.4

f 83.6

rise and may serve as an index of contractility. Clinically, it is observed that patients with congestive cardiomyopathy tend to have more leisurely rates of valve opening. Similarly, valve closing velocity is likely to be influenced by the rate of ventricular relaxation and the level of aortic pressure. Clinical

Applications

A number of clinical applications of the echocardiographic examination of the aortic root and valve has been reported. Potential usefulness of the technique may be broadly described in the following categories: (A) congenital and acquired structural abnormalities of the aortic valve and/or root, and (B) functional abnormalities of the aortic valve and/or root. Structural Aortic

453

VALVES

Abnormalities

Valve Disease

Aortic stenosis in the adult. Symptomatic aortic valve stenosis, either from a congenital or acquired etiology, is generally observed beyond the fourth decade. Some degree of cusp calcification is almost uniformly present.2 The aortic’ root echocardiogram demonstrates a presence of calcification with multiple thick echoes replacing the normal cusp architecture (Fig. 3). Little or no cusp motion is generally observed, although in some patients, one cusp may retain relatively normal motion. Although cusp calcification does not necessarily indicate significant valve stenosis, especially in the elderly, its absence can be used, with rare exceptions, to virtually exclude such a diagnosis. In women under 60 yr of age, valve calcification assumes a greater diagnostic significance and is indicative of a severe lesion. In the presence of strong

Fig. 3. valve (AV) or no cusp

Cal&c aortic stenosis. Note the normal aortic is replaced by thick multiteared echoes with little motion. Other abbreviations as in Fig. 2.

echoes emanating from the calcified actual orifice size cannot be evaluated. Congenital adolescence.

aortic

stenosis

cusps,

in childhood

or

The stenotic valve in this age group is congenitally deformed but not thickened or calcified. The cusp mobility is preserved, and despite the narrowed opening, the echo of the aortic valve fails to show significant abnormality. A likely explanation for the apparently normal valve opening may be related to echo beam reflections from the base of the stenotic but domed aortic valve cusps. Therefore, this examination cannot be used to diagnose or exclude significant congenital aortic valve stenosis in the younger patients. Commonly, however, echocardiographic features of bicuspid aortic valve may be observed (vide infra). Aortic regurgitation. Rheumatic or calcific aortic valve disease with regurgitation is associated with thickening and/or calcification of the aortic cusps. This can be visualized with the echo examination and may simulate the appearance noted in the aortic stenosis in adults. Systolic cusp opening movement is, however, preserved in patients with dominant valve regurgitation. The aortic root dimension may be increased, indicating dilatation of the aortic root, often seen with valve incompetence. The aortic dilatation is often out of proportion in patients with cystic medial necrosis or Marfan’s syndrome. In addition, mitral valve echocardio-

454

SHAH

gram will show diastolic flutter, a highly characteristic finding. Aortic valve endocarditis. Bacterial or fungal endocarditis are associated with vegetations of varying size on the surface of the aortic cusps. These vegetations may reflect prominent echoes so as to fill the aortic root in diastole with confluent “fuzzy” echoes’,’ (Fig. 4). The cusp opening in systole may be normally preserved. This appearance is somewhat typical and can be used to suggest the diagnosis. Since healed vegetations may also produce similar echoes, it is not possible to gauge the activity of the endocarditis from an echocardiographic examination. Endocarditis may result in cusp perforation or avulsion. The cusp prolapse may be detected by demonstration of diastolic cusp echoes in the

* .

.

.

.

.

.

*

l

*

.

Fig. 4. Bacterial endocarditis. The aortic valve (AoV) echo has a shaggy. fuzzy appearance most prominent in diastole. S, and S2 denote first and second heart sounds and DM is the diastolic murmur of acute aortic regurgitation. (Reproduced by permission.“)

AND

SYLVESTER

left ventricular outflow space in the mitral valve recordings or mitral ~aortic transition. Cusp perforation may result in prominent diastolic cusp flutter. These findings are not specific, since a tear in a myxomatous valve may also exhibit similar flutter. Hemodynamic significance of a structurally deformed valve may be inferred from the demonstration of enlarged left ventricular cavitary diameter and/or increase in wall thickness. Parameters of ventricular performance. such as ejection fraction. may be derived. Acute or subacute aortic regurgitation, if severe, may result in mitral valve preclosure in late diastole. These findings in patients with aortic valve disease are of practical significance and are described elsewhere in greater detail. Congenital bicuspid aortic valve. Nanda and associates first reported diastolic eccentricity of the aortic valve cusps as a sign of congenitally bicuspid aortic valve.” Normally, the returning echoes from the aortic valve in diastole are located centrally within the aortic root. Significant eccentricity is defined as a ratio of the distances between the cusp echo and the far aortic wall over the cusp echo and the near aortic wall exceeding 2: I. Appropriate transducer angulation may be necessary to demonstrate this finding, since its presence in one section suggests the diagnosis despite its absence in other recordings (Fig. 5). Some difficulty in measurement of eccentricity index may be experienced when multiple linear echoes are seen in the place of l- 2 normal cusp echoes. The multiple linear echoes are thought to represent redundant valve leaflets, often found with the congenital bicuspid valves. Sensitivity and specificity of either finding remain to be established, although early experience is encouraging. Multiple confluent echoes resulting from a calcified aortic valve should not be mistaken for multilayering. It must be emphasized that echocardiographic diagnosis of bicuspid valve cannot be made in presence of calcific aortic stenosis. Lack of a “gold standard,” short of anatomic proof at surgery or autopsy, makes it difficult to confirm the diagnostic accuracy of these echocardiographic signs. It is an important area of potentially useful application, since a diagnosis of bicuspid valve underscores a

ECHOCARDIOGRAPHY

OF AORTIC

Fig. 5. Bicuspid aortic the cuso is neerlv central aortic root; LA, left atrium;

AND

PULMONARY

valve (AV) in right panel and in a normal valve but eccentric ECG, electrocardiogram.

455

VALVES

normal with

need for antibiotic prophylaxis against bacterial endocarditis. Clinically, this diagnosis may be suspected in the presence of aortic ejection sound with or without an associated flow murmur.

AV in left panel. Note the diastolic a bicuspid AV. Some multilayering

closure point and position of the cusps is also seen.

of Ao,

Aortic Root Dissection

phasized that a diagnosis of dissection cannot be made in presence of calcification within the aortic root, since the resulting multilayered echoes make it impossible to assess the wall width. Although the echocardiographic signs of dissection are often useful in the appropriate clinical setting, their false positive and false

Aortic dissection extending to the aortic root results in separation of intima from the external layers of the aortic wall, and the actual wall width is increased. Echocardiographically, this separation is diagnosed by observing widening of the aortic wall at the root7 (Fig. 6). Normal echocardiographic aortic wall thickness rarely exceeds 10 mm. In some cases, apparent reduplication of strong aortic echoes may yield a wall of up to 15mm thickness. Hence, a diagnosis of aortic dissection may only be made when the wall thickness exceeds 15 mm. Identifications of the inner wall echo as reflected from intima is made by demonstrating that the aortic valve excursion in systole is limited to the inner echo. When clinical suspicion of aortic dissection is present, these findings provide additional support. Absence of these findings cannot be used to exclude aortic dissection above the level of the root. Occasionally, the apparent aortic wall width on echo may be increased in absence of any clinically evident dissection. This is thought to result from a beam angulation through the sinus of valsalva. Aortic root echoes from a slightly varied transducer location will generally avoid the confusion. It must be em-

Fig. 6. Aortic root widening of the anterior The cusp opening in margin. Abbreviations mission’9

dissection. Note the characteristic aortic wall (AWI exceeding 15 mm. systole reaches up to the intimal as in Fig. 2. (Reproduced by per-

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SHAH

negative rates remain to be established. The diagnostic accuracy of this entity at present does not permit this technique to yield definitive information. However, when aortic dissection is suspected or confirmed by angiographic means, repeated echocardiographic examinations may be indicated to detect development of aortic regurgitation from mitral valve futter and to diagnose dissection into the pericardial space. Congenital

Malpositiwt

01 the .-lot-tic, Root

Fullot’.r trtralog~~. Aortic override forms a component of this entity. and the degree of override may be variable. The aortic root straddles the interventricular septum and appears anatomically related to both the ventricles. This anatomic anomaly can be detected on a slou echocardiographic sweep from the mitral valve to the aortic root. The normal relationships on such a sweep demonstrate the inverventricular septum being contiguous with and at the level of anterior aortic wall and the mitral leaflet with the posterior aortic wall. In the presence of aortic override, the anterior aortic wall is markedly anterior to and often discontiguous with the interventricular septum. The echocardiographic contiguity is subject to technical artefact resulting from beam width or echo dropouts. A more anterior orientation of the aorta in relation to the interventricular septum may also be observed in hypertrophic subaortic stenosis (IHSS) or other disorders with septal hypertrophy. Importantly, in the clinical setting of a congenital cyanotic heart disease. the echocardiographic demonstration of the aortic override is useful. Transportation of’greut \‘e.s.seI.\. This term includes a variety of anatomic malformations with the aortic root being anatomically discontiguous from the mitral valve. M-mode echocardiography is useful mostly in the classic D transpositions, where the aorta is anterior and to the right and the pulmonary artery posterior and to the left. Attention to transducer angulation will demonstrate that the anterior great vessel is directed rightward and the posterior leftward, a circumstance that is just the opposite of the normal.’ Two-dimensional echocardiography is distinctly superior in geometric orientation of

AND

SYLVESTER

anatomy and will be found more useful than Mmode technique in congenital malformations involving origin of great vessels. Functional Abnormalities of the Aortlc Valve and/or Root Besides the structural abnormalities involving the aortic root. characteristic functional abnormalities are observed in the presence of other disease states. They are important to consider. since these changes may draw attention to the correct diagnosis.

H! pertrophic hubaortic stenosis (IHSS) or hbpertrophic obstructive cardiomyopathy (HOCM) ma! be associated with a dynamic outllou obstruction in the left ventricle. manifested echocardiographically by 54 stolic anterior movement (SAM) of the mitral valve. The mid-systolic obstruction is associated with increased velocity of aortic tlo\+ in the first third of \! stole and deceleration of Ilow in mid-to-late s~stole. The aortic val\,e cusps may t>picull! shol+ mid-s! stolic closure of one or two cuxps with ;I reopening movement in late systole. This linding is noted in ;I minorit! of patients with IHSS. ;I coarse systolic tlutter of the anrtic \alc e being ;I more frequent tinding (Fig. 7). The latter. however. is not ;I specific finding, mhilc mid-systolic closure is especially characteristic.

l:arll s> stolic aortic preclosure is observed in presence of severe discrete subaortic stenosis resulting from :I membrane in the left ventricular outflow (Fig. 8). This is probably caused h> :I venturi efTect from the high velocity jet through the narrow membranous opening. The \,cnturi etrect is directly related to the velocit! of tlow. which in turn is related to theorifce si/e as well as the rate of ejection. .Although pronounced degrees of precloxure generalI> retlect severe degrees of obstruction, a direct simple relationship does not exist.

The posterior aortic root wall proximity to the left atrial anterior

is in direct wall, and its

ECHOCARDIOGRAPHY

OF AORTIC

AND

PULMONARY

VALVES

457

Fig. 7. Aortic valve in hypertrophic subaortic stenosis (IHSS). Note the normal box-like pattern of the aortic valve is replaced by coarse flutter of the cusps in the presence of outflow obstruction. The systolic cluster of echoes in the left atrium (LA) are spontaneous intracardiac echoes and probably represent mitral regurgitation.

motion is influenced by changes in the atria1 size by its filling and emptying. Diastolic movement of the posterior aortic wall is dampened by severe mitral stenosis where the rate of emptying is reduced. Strunk and associates have

developed an atria1 emptying index,Y,‘o which is expressed as a ratio of posterior displacement of the aortic wall in the first one-third of diastole as compared to complete diastole prior to the atria1 wave. A ratio less than 0.5 was associated with severe stenosis, 0.5-0.65 with moderate stenosis, and 0.65-0.85 with mild stenosis. The authors recommend getting aortic root records at higher amplification and more rapid paper speed to enable more accurate measurements. Confirmation of these results in subsequent studies will add to the clinical applications of M-mode echocardiography, since the diastolic mitral valve slope is not too useful a parameter for quantification of mitral stenosis. Low Cardiac Output

Fig. 8. Discrete subaortic stenosis. Aortic echogram shows an early systolic preclosure coronary cusp. The arrow points to the maximum with subsequent gradual reopening. SM, svstolic

valve (AV) of the right preclosure murmur.

Amplitude of aortic cusp opening is decreased in the presence of low output states. The aortic root motion is also decreased. As yet, no reliable quantitative information of stroke volume has been demonstrated from the aortic echo. However, these features of reduced aortic cusp and root motion should point to a reduction in stroke volume. It might be speculated that important quantitative information on left ventricular contractile properties may be obtained from analysis of the velocity of aortic

458

SHAH

cusp opening. No correlative been reported. THE

PULMONARY Normal

Echo

Its Physiologic

studies have as yet

VALVE

ECHOGRAM

Appearance

and

Correlates

Unlike the aortic root, the walls of the pulmonary artery are not recorded in the echogram because the beam traverses through the right ventricular outflow space anteriorly and exits through the posterior aortopulmonary sulcus and the left atrium. The posterior cusp of the pulmonary valve is the one commonly seen, especially in adults. Two cusps may be visualized in small children. The dynamics of a normal pulmonary valve appearance, particularly during ventricular diastole, is poorly understood. The normal motion of this cusp through cardiac cycle is shown in Fig. 9. Atria1 systole is associated with a partial opening of the pulmonic valve (“a” dip). In some normal subjects, a full opening movement may also be observed following a deep inspiratory effort. The mechanism of this motion is thought to represent increase in right ventricular end-diastolic pressure with right atria1 contraction and the resultant doming or opening of the pulmonary valve, since the normal pulmonary arterial right ventricular enddiastolic gradient is small. Following the onset of ventricular systole, the valve begins to open initially at a slower rate and subsequently at a more rapid rate of motion reaching point C. The open cusp is held in this position until end-

AND

SYLVESTER

systole. when at point “d“ it executes a somewhat gradual valve closure movement. In early diastole, the most anterior point, “e,” is reached soon after closure. The valve then executes a rapid early diastolic posterior movement to point “f.” often followed by a relatively flat mid-diastolic motion. Atria1 systole initiates the “a” dip. The diastolic motion occurs in two components with slower heart rates (less than 90 beats/min). The flat mid-diastolic motion is no longer seen at rapid heart rates. When the anterior cusp is recorded. its motion pattern is in the opposite direction. Although the mechanisms of the valve opening motion with atria) and ventricular systole and of the valve closure at end-systole are ascribed to instantaneous pressure relationships between the right ventricle and the pulmonary artery, the early and mid-diastolic motion pattern is poorly understood. .A recent study in our laboratory has shown that the amplitudes as well as slopes of earl! and mid-diastolic motion of the pulmonary valve cusp are nearly identical to that of the posterior aortic wall in normal subjects as well as in a variety of pathologic states.” It has been pointed out in an earlier section of discussion on the aortic root motion, that the posterior aortic wsall motion accurately reflects changes in left atrial volume during the phases of cardiac cycle. This is due to the proximate relationship of the aortic root on the anterior left atria1 wall. The observation that the pulmonary valve motion is identical, and therefore represents changes in left atria1 volume, can be readily explained on

Fig. 9. The normal pulmonary valve (PV) echogram of the posterior cusp. Following atrial systole a small opening motion, “a,” is seen. The ventricular systole results in full opening to point “c.” At end-systole, the movement “d” to “e” is executed. Early diastolic posterior motion “8” to “f” is noted. APS, aorta pulmonary sulcus.

ECHOCARDIOGRAPHY

OF AORTIC

EXPIRATION

AND

NORMAL 1

PULMONARY

459

VALVES

INSPIRATION

contraction. The classic explanations on the right heart pressure dependence often provide physiologically useful correlates in normal and pathologic states, but do not tell the entire story. The critical pressure differences influencing the pulmonary valve motion are schematized in the accompanying illustrations (Fig. 10). Normal Values

ECG PCG ST1 PV

-

Fig. 10. A schematic to show normal pulmonary arterial (PA) and right ventricular (RV) pressures during expiration and inspiration. Simultaneous electrocardiogram (ECG). phonocardiogram (PCG). and systolic time intervals of the right heart ($11) and the pulmonary valve echogram are shown. Note that valve fully opens in presystole following inspiration, while showing a small “a” dip on expiration. The diastolic pressure gradients are shown by the stippled areas.

noting the anatomic relations of the two structures. The pulmonary artery also lies in front of the superior portion of the left atrium. The conclusion is reached that the hitherto unexplained early and mid-diastolic motion of the pulmonic valve is a passive motion transmitted from the left atrium. The “a” dip is a complex motion partially dependent on the right ventricle-pulmonary arterial pressure difference following right atria1 contraction and also on the left atria1 emptying with left atria1

Fig. 11. Pulmonary valve (PV) in pulmonary hypertension. Note the absence of “a” dip despite sinus rhythm and prominent midsystolic notching.

The normal values for cusp deflection amplitudes have been reported. The “a” dip, in the presence of sinus rhythm, normally exceeds 2 mm and, in one study, averaged 3.7 f 1.2 mm. The amplitude of leaflet opening in systole varies from 10 to 15 mm. The diastolic e-f slope averaged 36.9 f 25 mm (range 6-115 mm/sec).12 The right ventricular systolic time intervals, namely pre-ejection period (RPEP) and ejection time (RVET), are influenced by heart rate and age. However, the RPEP/RVET ratio was not significantly altered by heart rate or age, and the mean value in one study was 0.24 (range0. 16-1.30).13 Clinical Applications

The current clinical applications can best be described in three categories (A) pulmonary hypertension, (B) pulmonary valve stenosis, and (C) miscellaneous conditions. Pulmonary

Hypertension

The pulmonary valve echo is significantly abnormal in pulmonary hypertension, be it primary or secondaryI (Fig. 11). The

460

prominant features include (I ) “a” dip attenuution. (2) mid-systolic notching, (3) llut early and mid-diastolic waveform (E F slope). and (4) abnormal right ventricular pre-ejection period (RPEP) and ejection time (RVET).

The amplitude of the “a” dip is related to the presystolic gradient between the pulmonary artery and the right ventricle which, when increased from a rise in pulmonary arterial diastolic pressure, results in attenuation of the “a” dip. Generally, pulmonary arterial mean pressures between Xl and 40 mm Hg are associated with an “a” dip of less than r! mm and higher pressures with absence of “a” dip. This is especially so if the right ventricular enddiastolic pressure is normal. However, when right ventricular decompensution sets in. the gradient between pulmonary arterial and right ventricular end-diastolic pressure may be reduced. and a normal “a” dip ma> return. The usefulness of the return of “a” dip to indicate right ventricular decompensation in ;I patient with pulmonary hypertension has not been examined prospectively. The estimations of pulmonary hypertension based on the “a” dip magnitude are inconsistent in JO’,; 759 ot patients. This discrepancy may be explained bq the effects of left atrial dynamics mentioned earlier.

A mid-systolic notching has been observed in patients with pulmonary hypertension. The basis for this finding remains obscure. Its sensitivity is also not determined, although when present, it appears to be a somewhat specific finding.

The flat E F slope. observed in earlier studies with pulmonary hypertension, is neither a reliable nor a consistent observation. It is more an indication of a reduced rate of left atrial emptying, as in mitral stenosis or in low output state especially when left atrium is enlarged. It is suggested that flat E-F slope no longer be considered as a sign of pulmonary hypertension.

SHAH

AND

SYLVESTER

,\bnormal prolongation of right ventricular prc-ejection period (RPEP) and abbreviation 01 ejection time (RVET) results such that the RPEP/RVET ratio in excess of 0.3 has hecn reported to be associated with pulmonary hypertension. The time intervals tend to bc atfected by preload as well as by inotropl in addition to afterloud (i.e.. pulmonary hypertension), and exceptions to the above observation\ are to be expected and do occur. However. when present. the abnormal ratio may provide t’urther evidence ol’ the presence of significant pulmonar\: hkpcrtension. Pulmonary

Stenosis

Significant obstruction across the pulmonary valve results in elevations of right ventricular systolic pressure and a decrease in pulmonar> artcri:tl pressure.” The chronic pressure oterload results in right ventricular hypertroph\. \\hich in turn renders thu \ entriclc lea5 distensible. necessitating ;I prominent “:I” wave due to ;I I~)rccl‘uI right atrial contraction. The resulting elevation 01’ right ventricular end-diast~~lic prt:s\urc \vith arbociated reduction in pulmonary arterial prehsure niaq result in val\,e prior to onset of systole. :\Ithough this finding of pre\-stolic opening of the pulmonary valve has been described with sei’crc pulmonary valve stenosis. it is not a sutticientll sensitive sign. Presystolic pulmonar, I alcc opening may occur normall\ following an cxaggcrated inspiratory effort: however, such an occurrcnce in expiration ix distinctly abnormal. Severe pulmonary valve stenosis ma! hc associated with presq stolic ~,alve opening throughout both phases of respiration and ma> provide a mechanism lhr preh>>tolic ejection click iTa(Fig. II!). Pulmonary infundibular stenosis, on the other hand. is not associated with a discernable abnormality in the “a” dip and demonstrates irregular systolic fluttering of the pulmonar> valve cusp.“’ The latter probably results from the normal leallets being in a turbulent jet distal to infundibular obstruction. Neither sensitivitk

ECHOCARDIOGRAPHY

OF AORTIC

AND

PULMONARY

VALVES

461

pulmonary valve (shown by broken line) during expiration lexp) *s well as inspiration (insp). A presystolic ejection click was present coincident with the full opening of the valve.

nor specificity of this finding is known, and a quantitation of the degree of infundibular stenosis is generally not possible. Miscellaneous

Conditions

A variety of conditions in which the right ventricular end-diastolic pressure exceeds pulmonary arterial pressure may result in presystolic valve opening. This has been described with acute volume overload with ele-

vations in right ventricular diastolic pressures, e.g., ruptured sinus of Valsalva aneurysm” in right atrium or right ventricle with severe restriction to right ventricular filling, as in advanced constrictive pericarditis. These observations suggest that presystolic pulmonary valve opening may occur in conditions other than pulmonary valve stenosis and depend to a considerable degree on an interplay between instantaneous right ventricular and pulmonary arterial pressuresin late diastole.

REFERENCES I. Gramiak R, Shah PM: Echocardiography of the aortic root. Invest Radio1 3:356, 1968 2. Gramiak R, Shah PM: Echocardiography of the normal and diseased aortic valve. Radiology 96: 1, 1970 3. Gramiak R, Nanda NC, Shah PM: Echocardiographic detection of pulmonary valve. Radiology 102:153, 1972 4. Dillon JC, Feigenbaum H, Konecke LL, et al: Echocardiographic manifestations of valvular vegetations. Am Heart J 86:698, 1973 5. Roy P, Tajik AJ, Giuliani ER, et al: Spectrum of echocardiographic findings in bacterial endocarditis. Circulation 53:474, 1976 6. Nanda NC, Gramiak R, Manning J, et al: Echocar-

diographic recognition of the congenital bicuspid aortic valve. Circulation 49:870, 1974 7. Nanda NC, Gramiak R, Shah PM: Diagnosis of aortic root dissection by echocardiography. Circulation 48:506, 1973 8. Gramiak R, Chung KJ, Nanda NC, et al: Echocardiographic diagnosis of transposition of the great vessels. Radiology 106:187, 1973 9. Strunk BL, Fitzgerald JW, Lipton M, et al: The posterior aortic wall echocardiogram, its relationship to left atrial volume change. Circulation 56:744, 1977 10. Strunk BL, London EJ, Fitzgerald J, et al: The assessment of mitral stenosis and prosthetic mitral valve

462 obstruction using the posterior aortic wall echocardiogram. Circulation 55:885, 1977 11. Pocoski DJ. Shah PM, Sylvester LJ: Physiologic correlates of the echocardiographic pulmonary valve motion in diastole. (submitted for publication) 12. Weyman AE, Dillon JC, Feigenbaum H. et al: Echocardiographic patterns of pulmonic valve motion in pulmonic stenosis. Am J Cardiol 33:178, 1974 13. Hirshfeld S, Meyer R. Schwartz DC, et al: The echocardiographic assessment of pulmonary artery pressure and pulmonary vascular resistance. Circulation 52~642, 1975 14. Nanda NC, Gramiak R, Robinson TI, et al: Echocardiographic evaluation of pulmonary hypertension. Circulation 50:575. 1974

SHAH

AND

SYLVESTER

15. Flanagan WH, Shah PM: Echocardiographic correlate of presystolic pulmonary ejection sound in congenital valvular pulmonic stenosis. Am Heart J 94:633 636. 1977 16. Weyman kchocardiographic vular pulmonary

AE.

Dillon JC, Feigenbaum H, et al: differentiation of infundibular for valstenosis. Am J Cardiol 36:21. 1975

17. Weyman AE. Dillon JC. Feigenbaum H, et al: Premature pulmonic valve opening following sinus of valsalva aneurysm rupture with the right atrium. Circulation 51:556. 1975 IX. Shah PM. Sylvester LJ: Echocardiograph) Hortic and pulmonary valve. in Practical Cardiology. New York. Medical Publishers, 1977, pp 21 30

ut‘ the vol. 3.