Diagnostic Shelf

Pulmonic Insufficiency Versus Aortic

Insufficiency in a Patient with
Mitral Stenosis*
ALDO A. LUISADA, M.D., F.A.C.C. and JAN SZATKOWSKI, M.D

Chicago, Illinois

T
HE PATIENT was a thirty-eight year old white by an opening snap. The first sound was
man who, at the age of thirteen years, loud and snapping at the apex. There was a
had had an episode of rheumatic fever ac- grade 2 systolic murmur, followed by a very
companied by polyarthritis which left a heart loud (grade 5), rumbling and prolonged early-
murmur. diastolic murmur in the second and third left
History: The patient was asymptomatic interspaces, well transmitted across the sternum
until the age of twenty-eight, when he started toward the fourth and fifth right interspaces,
suffering from exertional dyspnea, occasional poorly along the left sternal line and not at all
palpitation and easy fatigability. Within four toward the aortic area or the apex. This
years he became almost completely invalided murmur was not increased by inspiration.
and presented the clinical picture of cardiac There was a grade 2, harsh systolic murmur
failure. He was then hospitalized (1954) over the aortic area followed by a weak second
and underwent mitral commissurotomy. Following sound.
this the patient had numerous episodes of There was evident venous collateral cir-
pneumonia and pulmonary infarctions and culation on the abdominal wall. The lower
his condition continued to become progressively margin of the liver was palpable 5 finger-
worse. He was hospitalized on a few occasions breadths below the right costal border. There
and was treated with digitalis, diuretics, was a shifting dullness, suggesting ascites.
antibiotics and low salt diet. The femoral and pedal pulses were weak and
Physical Examination: The patient was mod- there was marked pedal edema.
erately cyanotic and dyspneic, sitting in a semi- The clinical diagnosis was mitral stenosis and
recumbent position. The jugular veins were possible insufficiency; pulmonary hypertension;
distended and pulsating. The pulse was pulmonic insufficiency (Graham Steel1 mur-
72 per minute, regular; respirations were mur?) .
36 and blood pressure was 120/70 mm. Hg. Laboratory Studies: Blood culture on repeated
There was dullness and absence of fremitus at occasions was negative. Radioactive iodine
the right base and fine crepitant rales above the thyroid tracer study was within the normal
area of dullness. range. Hemoglobin was 12.2 gm. ; blood urea
The maximal apical impulse was palpated nitrogen was 29 mg. ; creatinine, 1 mg. ; bili-
in the sixth intercostal space at the anterior rubin, total: 3.1 mg. per cent; direct: 0.95
axillary line. There was a prominent forward mg. per cent; cholesterol, 174 mg. per cent.
thrust at the epigastrium and the whole pre- Serum enzymes were within normal limits.
cordial area was shaken by a heaving pulsation. Urinalysis showed a trace of protein, a few red
There were no thrills. Auscultation revealed a blood cells and granular casts in the sediment.
grade 2 diastolic rumble at the apex preceded Electrocardiogram: There was severe right
* From the Chicago Medical School, Division of Cardiology, Chicago, Illinois.

JULY 1961 155

156 Luisada and Szatkowski

1 2*DD d
.I, I - , , ! , ,.-

FIG. 1. Phonocardiogram in the second left interspace. The large diastolic

murmur (DDd) was attributed to pulmonic insufficiency.

PA RV

FIG. 2. Pullback of the catheter from pulmonary artery (PA) to right ventricle
(RV). (X) marks the crossing of the valve. The diastolic pressure of the
artery (100/31 mm. Hg) is very low when compared to that of the ventricle
(104/l 9), confirming pulmonic insufficiency.

axis shift (+115); atria1 fibrillation with ings. There was a normal pattern, except for
slow ventricular response; depressed S-T in lack of the a wave; there was no evidence of
leads II, III, aVF and VZ to Va; elevated S-T in tricuspid insufficiency.
aVR, aVL and Vi. A QR complex was present X-ray Examination: Extreme enlargement of
in V, and a qRS complex in V, (right bundle the cardiac shadow was noted, chiefly of the left
branch block pattern). atrium and the right ventricle. The left ven-
Phonocardiogram and Pulse Tracings: Apex. tricle was less markedly enlarged than the other
There was an opening snap 0.08 second after chambers. There was a severely enlarged pul-
the aortic component of the second sound, monary artery. A calcified mitral valve was
followed by a diastolic rumble. The Q-l inter- visible. Kerley lines were present in both lower
val measured 0.08 second. Third left interspace. lung fields. Fluoroscopy revealed a hilar dance
A large series of vibrations were seen in dia- and large pulsations of the main pulmonary ar-
stole, starting with the second sound, first in- tery; the pulsations of the aortic knob were small.
creasing, then decreasing and lasting until the Right Heart Catheterization: (October 29, 1958;
next first sound. Similar tracings were recorded Illinois Research Hospital). No evidence of
at the first and third left interspace (Fig. 1). left to right shunt was found. Systemic
Aortic area. A minimal systolic murmur, mini- arterial oxygen saturation was 85.2 per cent;
mal early diastolic murmur and a weak second right atria1 mean pressure was 15 mm. Hg ; right
sound were noted. Hepatogram and jugular trac- ventricular pressure, 94/l 5 ; pulmonary artery

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 157

FIG. 3. Intracardiac phonocardiogram from pulmonary artery (above); prcs-

sure pulse of the artery (center) ; electrocardiogram (below). The large diastolic
murmur within the artery (DDd) is caused by pulmonic insufficiency. The
collapse of the pulse is rapid, there is no appreciable dicrotic wave and there.
are multiple vibrations in the diastolic section of the pulse curve.

pressure W/28 (mean, 52), pulmonary wedge deteriorate rapidly and he died on May 19,
pressure, 32 mm. Hg ; cardiac index, 1.5. 1960.
Right Heart Catheterization: (April 8, 1960; Autopsy Findings (Dr. Krainer): The heart was
Mount Sinai Hospital). There was no evidence huge and weighed 600 gm. The apex was
of left to right shunt. Arterial blood oxygen formed by the right ventricle. The pericardial
saturation was 82.5 per cent. Mean right sac was obliterated by widespread adhesions.
atria1 pressure was 20 mm. Hg. There was The tricuspid valve was dilated (120 mm.
severe right ventricular and pulmonary hyper- circumference). The right ventricle was dilated
tension with right ventricular pressure of 104/19 and hypertrophied (11 mm. thick). The
and pulmonary artery pressure of 100/31 pulmonic valve was delicate and of normal
(mean, 66). The low diastolic gradient be- appearance. The pulmonic ring measured 85
tween the pulmonary artery and right ventricle mm. (normal, 71 mm.; average for a 600 gm.
was interpreted as evidence of pulmonic heart, 82 mm.). The left atrium was enor-
insufficiency (Fig. 2). The wedge pressure mously dilated. The mitral valve was extremely
tracing was not reliable. Intracardiac phono- stenotic and had fibrotic and calcified leaflets
cardiography revealed a large diastolic murmur reducing the opening to less than 1 cm.2 A
within the pulmonary artery (Fig. 3). brown line corresponded to the surgical frac-
Course: Upon admission to the Mount Sinai ture. The left ventricle was slightly dilated;
Hospital, the patient was given Aldactone and its wall was not hypertrophied (10 mm. thick).
chlorothiazide. The response in sodium excre- The aortic valve showed some cusp fusion at the
tion was satisfactory but the urinary output did commissures with thickening, retraction and
not increase to any significant degree. The calcification. Its ring measured 55 mm.
digitalis and antibiotic therapy was continued. The pulmonary arteries showed severe athero-
Thoracentesis and paracentesis were performed sclerotic thickening with multiple plaques.
in order to give the patient some symptomatic The liver weighed 650 gm. and had an increased
relief from the extreme dyspnea at rest. How- consistency.
ever, the patients condition continued to Conclusion: Findings were: severe mitral

JULY 1961
158 Luisada and Szatkowski

stenosis with slight insufficiency; slight calcific ing types: (1) congenital (rare) ; (2) rheu-
aortic stenosis with possible minimal insuf- matic (extremely rare); (3) bacterial (rare) ;
ficiency; adhesive pericarditis; severe athero- or (4) that due to pulmonary hypertension
sclerosis of pulmonary arteries. with dilatation of the valvular ring (a well-
known form is that causing the Graham Steell
COMMENTS
murmur, even though this is usually soft, faint,
The clinical picture of this case clearly and variable). (5) It may be due to fibrosis of
revealed that there still was severe mitral the pulmonic leaflets as a result of long lasting
stenosis, in spite of the previous commissurotomy. pulmonic hypertension (a similar explanation
It was impossible to decide whether this was was given by Luisada and Wolff for the diastolic
due to restenosis or incomplete commissurotomy. murmur of their three cases, although un-
The extreme pulmonary hypertension was fortunately without autopsy evidence). The
attributed to both mitral stenosis and arterio- present case was interpreted as having a
sclerosis of the pulmonary arterioles, confirmed pulmonic insufficiency of type (4) or (5), and
by autopsy. catheterization confirmed it.
The extremely loud and rumbling diastolic Postmortem examination revealed a moderate
murmur over the second and third left inter- aortic stenosis which had escaped clinical
spaces resembled that of a patent ductus. The detection, possibly with a minimal aortic insuffi-
loudness and roughness of this murmur; its ciency ; a severe mitral stenosis; arteriosclerosis
transmission toward the lower right precordium ; of the pulmonary arterioles; and a minimally
the lack of a similar murmur over the second dilated pulmonic ostium with delicate leaflets.
right interspace ; the fluoroscopic evidence of It is unfortunate that no attempt was made to
hilar dance while there was a small, poorly submit the pulmonary artery to a pressure of
pulsating aortic knob and there was no increase of 100 mm. Hg and to measure the ostium in
the systemic pulse pressure, led to the diagnosis of such a state.
pulmonic insuficiency. This was confirmed by In view of the catheterization data, the
right heart catheterization. In addition to character and loudness of the murmur, the
severe right ventricular and pulmonary hyper- x-ray data and the lack of increase in pulse
tension, catheterization revealed right ven- pressure in the systemic circulation, the final
tricular failure. It also showed a large pulmonic conclusion was that the murmur was pro-
pulse pressure and a low pulmonic diastolic duced by pulmonic insufficiency, relative in
pressure, so that although systolic pulmonic type and caused by pulmonary hypertension.
pressure was 100 mm Hg, diastolic pulmonic Whether the murmur should or should not be
pressure was 31 mm. Hg, only 12 mm. above called a Graham Steel1 murmur is a purely
the diastolic pressure of the left ventricle. The semantic problem. However, in view of the
recording of the diastolic murmur within the peculiar characteristics of this murmur, we
pulmonary artery further confirmed the in- would prefer not to use this term.
terpretation.
The downhill course of the patient advised REFERENCE
against left heart catheterization and a new 1. LUISADA, A. A. and WOLFF, L. Significance of pul-
surgical commissurotomy. monary diastolic murmur in cases of mitral
Pulmonic insuficiency can be of one of the follow- stenosis. Am. J. M. SC., 209: 204, 1945.

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