1970, Br. J. Radiol.

, 43, 673-684
VOLUME 43 NUMBER 514

OCTOBER 1970

The British Journal of Radiology

Review article
An evaluation of conventional radiography in acquired heart disease
By Ronald G. Grainger, M.D., M.R.C.P., F.F.R.
Department of Radiology, The Royal Hospital, Sheffield 1, and The Northern General Hospital, Sheffield 5

There can be no dispute that simple conventional

radiographic techniques have an important role in
the radiological assessment of the structure and
function of the heart. There is, however, an increasing controversy as to the value of these simple
methods, now that it is important to provide confident and unequivocal radiological evidence on
which may well depend the decision to undertake
cardiac surgery, and the nature of the surgical intervention.
Sophisticated methods of selective angiocardiography will almost always provide the radiological
information which is required. These sophisticated
angiocardiographic techniques are available in most
large medical centres and there is an increasing
tendency to ignore the simple radiographic techniques and to proceed to angiocardiography at an
early stage in the diagnostic evaluation. This tendency is to be deprecated: selective angiocardiography is a very safe technique in experienced hands,
but it is always rather uncomfortable for the patient
and occasionally leads to complications. It has always been the author's opinion that an essential
criterion before angiography is undertaken should
be that there is a real prospect that the outcome will
influence the management of that particular patient
(Grainger, 1965).
The precision of angiocardiographic diagnosis
has exposed some of the fallacies and the unmerited
confidence of those enthusiastic radiologists and
cardiologists who claim to be able to analyse in considerable detail the intra-cardiac anatomy in almost
every diagnostic problem.
In this review, the author will present some personal views on the value of conventional radiographic
Based on a lecture delivered at the British Institute of Radiology, February 19,1970

techniques in acquired heart disease. No attempt will

be made to cover the whole of this extensive subject,
but some points of personal interestespecially the
controversial oneswill be emphasised.
FLUOROSCOPY

The art of fluoroscopy is rapidly being lost.

Instead of utilising modern techniques, such as
closed-circuit television, image amplification, videotape and cine-radiography as invaluable aids for the
teaching of fluoroscopy, this useful investigation is
being delegated to junior trainee staff, often without
direct experienced supervision. The method is
therefore down-graded: its results become unreliable.
Modern techniquesespecially selective angiocardiographyhave exposed some of the fallacies
of the enthusiastic fluoroscopists of the previous
generation, but there can be no doubt that image
intensification and closed-circuit television greatly
enhance the value of fluoroscopy. The method provides evidence which no other technique can produce so readily.
(A) Heart size
The heart of an infant lies transversely, the diaphragms are high. Even an experienced radiographer may have great difficulty in obtaining a chest
radiograph of an infant in full inspiration. Without
such a film, radiological assessment of infantile
heart size may be quite impossible: the diaphragms
may lie as high as the 4th intercostal space, the thymus may completely fill the upper third of the chest.
The normal heart then appears to fill the thoracic
cavity and may look grossly enlarged, particularly to
those inexperienced in paediatric radiology.
A few seconds of fluoroscopy will resolve this

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problem. The child is encouraged to take a full

inspiration, if necessary by making him cry. After
the forced expiration of crying, the child will take
a full inspiration: at that moment the diaphragm
descends, the true size of the thoracic cavity is
revealed and the true heart size can be readily assessed and recorded on film.
If the thymus obscures the upper mediastinum,
rotation of the child a few degrees to the right and
then to the left during fiuoroscopy, will permit evaluation of the upper mediastinal shadows.
In the adult, the more radiolucent apical pad
of fat can usually be distinguished from the heart
on well-penetrated chest radiographs. Sometimes
this is not possible and the apical fat pad may make
the heart appear to be enlarged when it is really of
normal size. If there is any doubt, a few seconds of
fiuoroscopy will always resolve this problem. The
patient is asked to take a full inspiration, the fluotoscopic shutters are coned down to a small field over
the apex of the heart. The true rounded cardiac
apex can always be readily identified with its intrinsic pulsation as it rises off the diaphragm with each
systole. The apical pad of fat is clearly defined: it is
much more radiolucent than the heart and moves
passively (sometimes it is almost immobile) with
each beat. Fluoroscopic diagnosis is far easier than
radiography when the apical fat pad presents a diagnostic problem.
(B) Pulsation
Evaluation of cardiac pulsation is an essential
part of the art of fiuoroscopy; for example the
vigorous, over-active pulsation of the left ventricle
alternating with diastolic contractions of the ascending aorta is a useful diagnostic feature in aortic incompetence. The timing of the pulsation of the
right atrium is a diagnostic feature in tricuspid valve
disease: in tricuspid incompetence, the right atrium
distends markedly during ventricular systole; in
tricuspid stenosis, the right atrium contracts vigorously immediately before ventricular systole.
Most observers find the assessment of the pulsation
of the left atrium to be very difficult in the differentiation of mitral stenosis and incompetence, but
Dunne (1967), after a most careful analysis, considers that a fluoroscopic distinction can be made.
The vigour of ventricular pulsation may be
impaired over a localised segment of heart wall. This
sign of previous myocardial infarction must be carefully pursued by analysing the pulsation of the ventricular silhouette as the patient is slowly rotated.
Generalised weakness of cardiac pulsation is
seen with a large, failing heart and the fluoroscopic

appearances may be identical with pericardial

effusion.
(c) Chamber identification
With careful, well-coned fluoroscopy, the atrioventricular groove can usually be identified (particularly in the R.A.O. projection) as a thin radiolucent
stripe which moves downwards and forwards during
each ventricular systole. Any doubts that this stripe
is the A-V groove can be resolved if left ventriculography or coronary angiography is being performed.
The inter-ventricular groove can sometimes be
identified on fluoroscopy in L.A.O. projection, separating the right ventricle in the front from the left
ventricle behind.
The epicardiac line of fat can sometimes be identified by careful T.V. fluoroscopy, using a small
field of view. It represents the visceral pericardium,
and therefore any extensive "cardiac" shadow external to it usually indicates pericardial fluid. The
associated poor pulsation of the "cardiac silhouette"
is a confirmatory sign.
(d) Calcification
Image intensification with closed-circuit television is the most effective method of detecting cardiac
calcification. Two or three minutes of careful, skilled fluoroscopy using a small field is far more
valuable than any number of radiographs or tomographs. It is essential to use a small viewing field,
the optimum fluoroscopic and television factors and
to search diligently in the regions where calcification
may be anticipated.
(i) Valvular calcification may occur in the valve
cusps, in the valve ring or in the subvalvar angle.
Standard text-books describe the typical appearance,
pulsation and situation of valvular calcification.
Kirk and Russell (1969) have recently shown by
autopsy stroboscopic tomography that calcification
in the mitral area in the elderly patient is nearly always situated in the angle between the valve cusp
attachment (to the valve ring) and the ventricular
endocardium. This mitral sub-valvar calcification
has a characteristic appearance, C-shaped with the
open segment situated anteriorly at the attachment
of the anterior leaflet of the mitral valve. This characteristic shape is due to the absence of the ventricular wall in the open segment which is, of course,
the border of both the mitral and aortic valve orifices. Calcification of the left heart valves is very
frequent. Calcification of the right heart valves is
very unusual. Congenital aortic valve stenosis (often
bicuspid) very commonly exhibits extensive calci-

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fication, but congenital pulmonary valve stenosis
almost never calcifies.
Pulmonary valve calcification should suggest the
possibility of previous bacterial endocarditis affecting this valve.
Artificial valves of the Starr-Edwards type can
be easily seen on fluoroscopy or conventional radiography, as the cage is made of metal. In the posteroanterior view, the mitral and aortic valves are
projected very close together and the identification
of the valve may be impossible from the position of
the prostheses on the postero-anterior radiograph
or antero-posterior fluoroscopy. The direction of
blood flow through the valve can, however, always be
decided because the closed end of the metal cage is
the distal pole of the valve or the exit port: if the
closed end points downwards and to the left, it is a
mitral valve replacement (Fig. 1).
Fluoroscopy demonstrates a regular up and down
movement of the prosthesis "en-masse" in line with
the movement of the valve ring. If the stitching of
the seating of the valve has broken down, the valve
may be seen to rock or tilt during each beat, in
addition to its mass movement.
The ball of the Starr valve was originally radiolucent, but the more recent valves have radio-

FIG. 1.
Starr-Edwards mitral valve replacement. It is not possible
from this radiograph to decide, from the position of the
valve, whether it is a mitral or aortic valve replacement. The
thick collar (->) of the valve indicates the inflow and therefore this is a mitral valve.

opaque balls. In a well-functioning valve, the ball

retains its exact spherical shape and it moves regularly up and down within its metal cage (Fig. 2).
These features are well seen during fluoroscopy. If
the ball becomes deformed, it may become obviously
ovoid and its movement may be irregular, or it
may stick within the cage.
(ii) Calcification of the coronary arteries can be
readily identified during careful fluoroscopy. By
rotating the patient, the calcium may be sky-lined
and its position in the A-V or interventricular groove
confirmed, thereby identifying the nature of the
calcification. As expected, coronary artery calcification is frequent in coronary atheroma and ischaemic heart disease.
(iii) Endocardial calcification is seen occasionally in mitral valve disease as a curvilinear lining of
the enlarged left atrium. It is best seen on wellpenetrated lateral radiographs (Fig. 3) and on careful fluoroscopy.
(iv) Myocardial calcification may follow necrosis
after myocardial infarction. It may be "missed" on
the conventional postero-anterior radiograph, but is
readily observed on fluoroscopy and lateral or oblique
radiographs. The cardiac contour may remain normal
despite the calcification: alternatively, the ischaemic
myocardium may bulge like an aneurysm (usually of
the left ventricle) (Fig. 4). Fluoroscopy often
demonstrates abnormal pulsation over the calcified
zone whether or not the cardiac silhouette is deformed. The pulsation may be diminished or paradoxical over the diseased myocardium.
(v) Pericardiac calcification may be quite invisible on a good quality postero-anterior radiograph,
but is usually clearly seen on lateral or oblique films
or on fluoroscopy during rotation of the patient.
It is most important to avoid diagnosing the
absence of significant cardiac calcification on the
basis of postero-anterior chest radiographs, however
good their quality. Even when supplemented by
good quality lateral and oblique films, significant
valve calcification and coronary artery calcification
may not be visible. Careful fluoroscopy, using a
small field and optimal radiographic and television
factors, is far more effective in the search for cardiac
calcification. Do not delegate the choice of factors to
the radiographerby trial and error for each individual case, the radiologist will rapidly be able to
select factors for optimum fluoroscopic vision.

CHAMBER ASSESSMENT

The assessment of the size of each of the four

heart chambers and their main vascular connections

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LV

FIG. 2.
Aortic Starr-Edwards valve. Radio-opaque ball within a metal cage. The perforated collar is sewn to the aortic valve ring,
and is the inflow of the valve.
(A) The valve is closed in ventricular diastole as the ball is seated firmly and closes the collar.
(B) The valve is open in ventricular systole and blood passes through the aperture of the collar into the aorta.
(LV = left ventricle. Ao = ascending aorta.)

FIG. 3.
Calcification of left atrial wallmitral stenosis. Curvilinear
calcification (<) outlining a moderately enlarged left atrium.
The calcium is probably deposited in a layer of clot lining
the atrial endothelium.

forms the basis of the (conventional) radiological

evaluation of cardiac disease.
Unfortunately, conventional radiological assessment of individual chamber size may be very difficult or impossible. The classic radiological signs of
enlargement of each of four heart chambers are well
described and illustrated in many standard textbooks, but the application of these signs in any given
cardiac problem may be fraught with difficulty.
There can be no doubt that many of these
radiological signs are quite valid and yield important
diagnostic information. What is challenged is the
frequency with which the classic text-book signs can
be realistically applied and a confident interpretation
deduced.
Every effort should be made to assess individual
chamber size from conventional radiographs,
fluoroscopy and barium swallow. The radiological
evidence must be analysed and a radiological
assessment of each chamber made and reported.
In many clinical situations, however, the radiological evidence is equivocal and a confident cardiac
chamber assessment cannot therefore be made with
assurity. Clinical evaluation and ECG will often be
more reliable in these patients than conventional
radiography.
The left atrium is the easiest of the four heart

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An evaluation of conventional radiography in acquired heart disease

A
FIG. 4.
Calcification following myocardial infarction.
(A) A band of calcification (*) over the apex of the left ventricle. No aneurysm. No change in cardiac contour. Note pad of
fat at cardiac apex.
(B) Another patient. A large calcified aneurysm (<-) of left ventricle distorting cardiac contour.

chambers to assess, because its upper border lies

within the angle of the carina and its posterior surface is in contact with the anterior wall of the oesophagus immediately below the carina. Splaying of
the carina, elevation, posterior displacement and
narrowing of the left main bronchus and posterolateral displacement of the mid-oesophagus are
most important radiological signs of left atrial
enlargement (Fig. 5). On well-penetrated posteroanterior films, the outline of the left atrium can often
be clearly discerned.
Ventricular assessment poses the main radiodiagnostic problem, for while the classic signs of
ventricular enlargement are very useful, they are
frequently unselective or equivocal.
Left ventricular enlargement (Fig. 6) displaces
the cardiac apex to the left, backwards and downwards, sometimes below the dome of the diaphragm.

Right ventricular enlargement classically displaces

the apex to the left but not downwards, so that the
apex is square or elevated (Fig. 7).
A more reliable and practical feature is the size
of the arteries which receive ventricular blood.
Enlargement of the pulmonary conus and main
pulmonary artery is almost invariable if the right
ventricle is enlarged (Fig. 7). The only exception of
importance is in congenital heart disease with pulmonary infundibular stenosis as, for example Fallot's
tetralogy.
Enlargement of the ascending aorta is frequently
seen when the left ventricle is enlarged (Fig. 6),
and its absence should be carefully considered before
diagnosing left ventricular enlargement.
Attention to the size of the ascending aorta and
the main pulmonary artery, together with assessment of the position and curvature of the cardiac

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FIG. 5.
Giant left atrium. Note marked splaying of the carina with
elevation of both right and left main bronchi.

apex, will often permit a confident, soundly based

assessment of (right or left) ventricular predominance
on the postero-anterior film alone.
Radiological signs of pulmonary venous congestion and oedema indicate a lesion on the left side
of the heart but do not imply left ventricular enlargement or failure. There may be marked pulmonary venous congestion in pure mitral stenosis:
the left ventricle is normal in size but the right ventricle may be considerably enlarged, particularly if
there is secondary pulmonary arterial hypertension.
The right ventricle lies immediately behind the
sternum, anterior to the left ventricle (Fig. 8). When
the right ventricle enlarges, it tends to enlarge forwards and upwards, inceasing its area of contact
with the sternum. When the left ventricle enlarges,
it tends to enlarge backwards and downwards and to
the left, towards and eventually overlapping the
left border of the lower dorsal spine.
Traditional diagrams and descriptions of lateral
and L.A.O. radiographs amplify the above basic
facts and one could be forgiven for believing that the
differential diagnosis of right or left ventricular enlargement is easy and unequivocal. Unfortunately,

FIG. 6.
FIG. 7.
FIG. 6. Left ventricular enlargement. The apex is displaced outwards and downwards almost to the left chest wall. The
aorta is slightly enlarged. No enlargement of the pulmonary conus or main pulmonary arteries. Moderate enlargement
of left atrium (just visible at right heart border). The patient has stenosis and incompetence of both mitral and aortic
valves.
FIG. 7. Right ventricular enlargement. The cardiac apex is flattened and almost vertical. The pulmonary conus is verylarge and both main pulmonary arteries are prominent. Normal aorta. The patient has cor pulmonale.

OCTOBER 1970

An evaluation of conventional radiography in acquired heart disease

FIG. 8.
FIG. 9.
FIG. 8. Relationship of ventricles. The right ventricle (R.V.) lies directly anterior to left ventricle (L.V.) They communicate via a V.S.D. (j). S. = Sternum. (From Cardiac Catheterization and Angiocardiography, by Verel and Grainger.
Livingstone Ltd.)
FIG. 9. Enlarged left ventricle. Left anterior oblique projection. Note curve of posterior inferior aspect of left ventricle
with an increased line of diaphragmatic contact (see text). The dotted line would be a typical curve for right ventricular
enlargement. (Same patient as Fig. 6).

when the right ventricle enlarges it pushes the left

ventricle backwards towards the spine: the lateral
and L.A.O. films may then very closely simulate
radiographs of isolated left ventricular enlargement.
Some differentiating criteria may still be present.
True left ventricular enlargement bulges downwards
and backwards as a short arc of a large circle: the
postero-inferior curvature of the heart (as seen on
the lateral or L.A.O. radiograph) bulges low down,
just above the diaphragm: the line of ventricular
contact with the diaphragm on the lateral or L.A.O.
film is increased (Fig. 9).
In right ventricular enlargement, the left ventricle may be lifted off the diaphragm and tilted upwards as well as being displaced backwards. These
features may be well seen on the lateral or L.A.O.
projection, where the lower posterior heart border
may be a long arc of a smaller circle, the posteroinferior bulge of the heart is lifted well off the diaphragm and the line of ventricular contact with the
diaphragm is not increased as it is in left ventricular
enlargement (Fig. 9).
When the above signs are well marked, the
radiological differentiation of right and left ventricular enlargement may be made with considerable

confidence. Unfortunately, these signs are occasionally misleading: more often these features are
not distinctive enough to be of differential diagnostic value.
Radiological assessment of left ventricular size
can be facilitated by noting the relationship of the
posterior border of the inferior vena cava (I.V.C.)
on the lateral radiograph.
The posterior border of I.V.C. can usually be
identified on the lateral radiograph as a vertical,
almost straight line, extending upwards from about
the mid-point of the diagrammatic cupola (Fig. 10).
This identification is readily confirmed by selective
inferior vena cavography or right atrial injection
(Fig. 10). The posterior border of the left ventricle
bulges about 15-20 mm behind this line in the
normal lateral radiograph (Fig. 11).
If the left ventricle is enlarged and the right heart
is not enlarged (e.g. aortic valve disease), the posterior margin of the left ventricle bulges backwards
to a greater extent, often more than 20 mm behind
the I.V.C. line at its farthest point (Hoffman and
Rigler (1965) suggest more precise mensuration.)
This is in contrast to the situation when the right
heart is enlarged and displaces the left ventricle back-

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FIG. 10.
FIG. 11.
FIG. 10. Identification of the inferior vena cava (or right atrial) line. Lateral projection. Injection into right atrium (ra)
identifies its straight posterior wall. Behind this line, the left atrium can be faintly seen (la). The posterior border of the
inferior vena cava (<) is a downward continuation of the posterior border of the right atrium.
FIG. 11. Relationship of line of I.V.C. and left ventricle. Note the left ventricle (-<) bulges behind the line of I.V.C. (>).
Normally this distance is no more than 15-20 mm.

wards. Enlargement of the right ventricle or of the

right atrium will displace the I.V.C. line backwards
to the same extent as they displace the left ventricle
backwards. Therefore in right heart enlargement,
the I.V.C.-left ventricle distance remains normal as
both are displaced backwards to the same degree.
Measurement of the I.V.C.-left ventricle distance
on the lateral radiograph is therefore a useful differentiating feature between right and left ventricular
enlargement.
However, as with all radiological signs, it must be
interpreted with full knowledge of the fallacies to
which it is subject. The film must be taken in full
inspiration: the presence of barium in the lower
oesophagus often prevents visualisation of the posterior border of the left ventricle (Fig. 12).
An even more critical factor is that the X-ray
beam must be exactly in the coronal plane {i.e.
perpendicular to the patient's sagittal plane) and
centred to the mid-coronal plane. This alignment of
the central ray with the mid-coronal plane is critical
because the two landmarks are separated by several
centimetres in the coronal plane (the I.V.C. lies to
the right of the mid-line: the posterior border of the
left ventricle lies to the left of the mid-line). Because

of this spatial separation, a slight angulation between

the central X-ray beam and the true coronal plane
will cause a considerable variation in the I.V.C.-left
ventricle distance as measured on the lateral radiograph and will completely invalidate this useful
method (Fig. 13).
PATHOLOGICAL CORRELATION

Having assessed the size of the individual heart

chambers, and the lung fields (see later), the radiologist must then relate his findings to the clinical
information (if any) he has been given, and then
suggest the probable structural and functional derangement of the heart.
Heart chambers enlarge under three possible
conditions:
(1) Pressure overload.
(2) Volume overload.
(3) Weakened heart wall.
(1) Pressure overload occurs whenever a heart
chamber has to generate a greater pressure in order to overcome an obstruction at its outlet, e.g.
left ventricular pressure overload in aortic valve
stenosis, co-arctation, systemic hypertension. The
pressure overload occurs in systole; the left ventri-

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FIG. 12.
Left ventricle obscured by the oesophagus. Barium in the lower oesophagus obscures the posterior border of left ventricle
(black line). The I.V.C.-L.V. distance cannot be measured. I.V.C. indicated by <-: L.V. indicated by black line. Patient
has aortic incompetence with large L.V.

FIG. 13.
The influence of rotation on the I.V.C. sign, same patient in (A) and (B). Note the marked difference in the I.V.C.-L.V.
distance (> -<-) when the X-ray beam is not in the mid-coronal plane. In (A) the I.V.C.-L.V. distance is much less than
normal: in (B) the distance is greatly increased. Both radiographs are "reasonable" laterals, but the geometry of the sign
is very sensitive to the smallest rotation (see text).

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cular myocardium hypertrophies. The stroke volume

is not increased and therefore dilatation of the left
ventricular cavity does not occur until the muscle
begins to fail. Thus in pressure or systolic overload,
hypertrophy of the chamber muscle and not dilatation of its cavity is the result. This is reflected on
the radiograph, for the left ventricular contours are
rounded and not significantly enlarged when that
chamber is subjected to an increasing pressure load.
In known aortic valve disease, a left ventricle which
is only slightly enlarged suggests aortic stenosis
rather than incompetence.
When the pressure overload overwhelms the left
ventricular myocardium, the chamber dilates, fails
and causes pulmonary venous congestion.
(2) Volume overload occurs whenever a chamber
receives a larger inflow of blood than normal, e.g.
due to a shunt in septal defects, or due to valve incompetence. In these circumstances the receiving
chamber must dilate to accommodate the extra inflow and to ensure an increased stroke volume.
Cavity dilatation is therefore a feature of volume
overload, but as no obstruction to outflow is present,
the pressure generated during systole is not increased and muscle hypertrophy is not a feature.
As the inflow of blood into the chamber occurs in
diastole, volume overload may be regarded as diastolic overload in distinction to the systolic pressure
overload of outflow obstruction.
Thus a large left ventricle in a patient with
known valvular disease will suggest aortic or mitral
incompetence (volume overload) rather than aortic
stenosis (pressure overload) or mitral stenosis (no
L.V. overload).
If, however, there is radiological evidence of
pulmonary venous congestion or oedema, the above
concept must be modified, for left heart failure is
now present and an enlarged left ventricle may be the
result of a failed attempt to cope with a previous
pressure overload (e.g. aortic stenosis).
MITRAL VALVE DISEASE

The nature of the volume overload is important

for the left ventricle can tolerate mitral incompetence to a much better extent than aortic incompetence producing an equivalent volume overload.
Braunwald has investigated this feature experimentally and offers an explanation based on myocardial mechanics (Braunwald, 1969). Because of this,
considerable mitral incompetence may be present
without significant left ventricular dilatationthis
observation has been made many times during left
ventriculography. An equivalent volume overload
due to aortic incompetence will always produce left

ventricular dilatation which can usually be detected

radiologically.
The volume overload of the left atrium due to a
significant mitral incompetence always results in
left atrial enlargement. Occasionally the left atrium
may become aneurysmal, reaching the right chest
wall and grossly deforming the carina (Fig. 5). In
contrast, pure mitral stenosis causes a pressure
overload on the left atrium which hypertrophies,
often without much dilatation. Thus, severe mitral
stenosis may be present without detectable left atrial
enlargementindeed the cardiac silhouette and
fluoroscopic examination may be normal. The radiologist should therefore never deny the possibility
of mitral stenosisclinical examination is more
accurate in these patients.
In mitral stenosis, the left atrium is often only
modestly enlarged, and therefore does not bulge
beyond the right border of the right atrium. Quite
frequently the right border of the enlarged left
atrium coincides exactly with the right border of
the right atrium on the postero-anterior radiograph
(Fig. 14)this is probably because the restraining
influence of the pericardium tends to limit left atrial
enlargement to lie within the general confines of the
heart silhouette. If enlargement of the left atrium
progresses, it will stretch the pericardium and bulge
beyond the previous heart contours (Fig. 5).
Severe mitral stenosis may exist without radiologically diagnosable enlargement of the left atrium: the
increase in left atrial pressure may be sufficiently
marked to cause radiologically evident pulmonary
venous congestion and oedema. The consequent
strain on the right ventricle may be increased by
reactive pulmonary arterial hypertension: the right
ventricle hypertrophies due to pressure overload
and may then fail and dilate. This dilatation of the
failing right ventricle may stretch the tricuspid ring
sufficiently to produce functional tricuspid incompetence, even through an undamaged tricuspid valve.
The resulting volume overload on the right atrium
causes dilatation of that chamber, which may become aneurysmal and almost fill the right hemithorax (Fig. 16). Thus the paradoxical situation is
established of aneurysmal dilatation of the right
atrium and undetectable (or absent) enlargement of
the left atrium, resulting from severe mitral stenosis.
This situation has been seen by us on several
occasions, but has apparently not been reported until
1970 (Roberts, Humphries and Morrow). It can be
diagnosed with confidence from careful radiological
analysis of conventional radiographs (Fig. 15).
Unfortunately the films are frequently misinterpreted as a giant left (instead of right) atriumand

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FIG. 14.
Enlarged Left Atrium.
(A) Note the extreme limit of the right border of the left atrium (-) coincides exactly with right border of right atrium (>)
This coincidence is probably due to the pericardium (see Text).
(B) Simultaneous lateral angiogram. Marked mitral incompetence demonstrated by left ventriculogram which shows gross
reflux into the enlarged left atrium (LA).

tricuspid incompetence is not considered by the

radiologist. Roberts et al. (1970) claim to report the
first three documented patients with this picture;
they attribute the limited enlargement of the left
atrium to thickening of its wall by mural thrombus,
which may be calcified.
Mitral incompetence may be due to several causes
other than rheumatic damage to the valve, viz.
hypertrophic obstructive cardiomyopathy, enlarged
left ventricle, ruptured papillary muscle, ruptured
chordae tendinae. The latter two mechanisms involve
acute mitral valve dysfunctionthe papillary muscle
rupture is usually due to myocardial infarction; the
chordae usually are damaged by bacterial endocarditis. In both of these varieties of acute dysruption of
the mitral valve, acute and severe mitral incompetence may result and the patient may develop fatal
pulmonary oedema from the resultant left heart
failure. Despite the severity of the acute mitral
incompetence, the left atrium may be only slightly
enlarged. The radiologist should consider these
causes of pulmonary oedema (even in the absence
of left atrial enlargement) when it develops during
or following an acute cardiac episode. Radiological
confirmation may be obtained by left ventriculography. These diagnoses are not merely academic
exercises, as an increasing number of patients are

benefiting from valve replacement of a ruptured

mitral valve mechanism.
THE LUNG FIELDS

The lungs are the only organs of the body whose

vasculature can be visualised radiologically without
the use of contrast media. The air in the lungs forms
a natural contrast medium and the radiologist must
use this fortunate circumstance to full advantage.
The lungs receive the total output of the right heart;
the lungs are the only blood supply to the left heart.
It is therefore to be expected that because of the air
contrast medium, radiological examination of the
lung fields is a most valuable method of assessment
of the function of both the left and the right side
of the heart.
The relevent radiological features are very well
documented (Grainger, 1958; Simon, 1963; Steiner,
1958); they are generally accepted and not controversial. The reader is referred to these standard
publications.
Suffice it to say that radiological evidence of left
heart failurepulmonary venous congestion and
oedema (both interstitial and alveolar)can be detectted by the careful radiologist well before it can be
detected by the clinician. The careful radiological
assessment of the lung vascularity, its interstitial

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43, No. 514

Ronald G. Grainger

FIG. 15.
Giant right atrium in mitral stenosis.
(A) Large right atrium causing marked convexity of right heart border. The angle which it makes with the diaphragm
suggests right rather than left atrium. Note distended azygos vein (>) due to right heart failure.
(B) Penetrated antero-posterior film of same patient. Note outline of modestly enlarged left atrium (<-) which is far
smaller than the giant R.A. seen in (A). Note absence of displacement of oesophagus. If the large chamber seen in (A) were
L.A. it would displace the oesophagus, usually to the right but occasionally to the left. The carina cannot be seen in this
print, but it was not splayed and this also excludes a giant left atrium.

framework, the alveoli and the pleura must never be

neglected in any evaluation of conventional radiography in the diagnosis of suspected cardiac disease.

assessment of ventricular dominance, for the classic descriptions are frequently not applicable, nor sufficiently selective, for the individual patient under consideration.
REFERENCES
BRAUNWALD, E., 1969, New Engl.J. Med., 281, 425.

ACKNOWLEDGMENTS

My sincere thanks are given to the radiographic and

photographic staffs of The Royal Hospital and The Northern General Hospital, Sheffield.

DUNNE, E. F., 1967, Cardiac Radiology, 18 (Kimpton,

London).

ABSTRACT

HOFFMAN, R. B., and RIGLER, L. G., 1965, Radiology, 85,

The author has concentrated on a few aspects in which

simple conventional radiographic techniques may play a
considerable role in the assessment of cardiac structure and
function. These comments are by no means comprehensive
and the standard works of reference should be consulted,
but the author would again advise that the radiologist
must beware of the temptation to over-confidence in

GRAINGER, R. G., 1958, Br. J. Radio!., 31, 200;

1965,

ibid., 38, 201.

93.
KIRK, R. S., and RUSSELL, J. G. B., 1969,

Br. Heart. J.,

31, 684.
ROBERTS, W. C , HUMPHRIES, J. O., and MORROW, A.

1970, Am. Heart. J., 79,28.

SIMON, M., 1963, Radio!, din. N. Amer., 1, 363.
STEINER, R. E., 1958, Br.J. Radio!., 31, 188.

Reprints of this Review may be obtained from the

Editorial Office, The British Journal of Radiology,
32 Welbeck Street, London, W1M 7PG. Price: 7s.
(35p) or SI.00 post free.

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