Catheterization and Cardiovascular Diagnosis 28:228-230 (1993)

Patent Ductus Arteriosus Presenting in Old Age

Chi-ling Hang, MD, and Jo Thompson Sullebarger, MD
This re~ort ~escribes an unusual case of patent ductus arteriosus, presenting in oid age.
~he patient IS the oldest living female with patent ductus reported thus far in the medical
literature [1,2]. She initially presented with chest pressure and dyspnea, and subse-
quently developed subacute bacterial endocarditis and typical angina pectoris with ECG
changes, but with normal coronary anatomy. © 1993 Wiley-liss, Inc.

Key words: asthma, dyspnea, cardiac catheterization, closure

CASE DESCRIPTION lier. The blood pressure was 160/90, the heart rate was
84, and she was afebrile. There was no jugular venous
A 74-year-old white woman with a three year history
distension. The lungs were clear. The cardiac examina-
of orthopnea, exertional dyspnea, and chest tightness
tion revealed a 2/6 continuous murmur, best heard at the
was admitted when these symptoms became acutely
left upper sternal border, which did not change with hand
,,:o.rse over a 2 week period. Her past history was sig-
~rip or Val~alva maneuver. There were no subconjunc-
mflcant for a mild chronic normochromic normocytic
tIval petechiae, Osler's nodes, Janeway lesions, or lym-
anemia, but was otherwise unremarkable. Her blood
phadenopathy. The white cell count was 11,000, with
pressure was 130170 mm Hg, and her heart rate was 76.
72% neutrophils, 9% lymphocytes, 15% monocytes, and
There was no jugular venous distension. Diffuse expira-
3% eosinophils. All five sets of blood cultures isolated
tory wheezes and bilateral basal rales were heard on lung
streptococcus sanguis. Pulsed Doppler echocardiography
exam, and the cardiac exam showed a 2-3/6 systolic
demons.trated continuous flow in the pulmonary artery,
murmur along the left sternal border. There was trace
suggestIve of a moderate sized patent ductus arteriosus.
edema. The chest X ray showed mild cardiomegaly, and
No valvular disease or vegetations were seen. She was
the ECG showed an inverted T wave in AVL, but was
treated with intravenous penicillin G for a total of 30
otherwise normal. Her admitting diagnosis was heart
days, and recovered. During her hospital stay she had
failure, and she improved with diuretic treatment. How-
two episodes of chest tightness, associated with new T
ever, echocardiography showed normal left ventricular
wave inversion in leads V2-V3. Myocardial infarction
wall.motion and valves, and the left ventricular ejection
was ruled out by cardiac enzymes.
fr~ctlOn was 70% by MUGA scan. Spirometry revealed
After discharge, she continued to have cxertional dys-
mlld obstructive lung disease. On the basis of these stud-
pnea, wheezing, orthopnea, and paroxysmal nocturnal
ies the diagnosis was changed to asthma, and treatment
dyspneain in spite of treatment for asthma. She was ad-
was changed to prednisone, albuterol, and theophylline.
mitted twice at age 86 with chest tightness similar to her
Two years later, she developed worsening exertional
and paroxysmal dyspnea, orthopnea, and bipedal edema, previ?us episodes: which was accompanied by deeper
antenor T wave mversion. Myocardial infarction was
and was eventually readmitted in respiratory failure. The
again ruled out by cardiac enzymes. A cardiac catheter-
blood pressure was 102/60 and the heart rate was 98.
ization was performed (Table I). Oximetry demonstrated
!he~e was no jugular venous distension. On lung exam-
a step-up in oxygen saturation from the right ventricle to
matIon, there were diffuse rhonchi, wheezes, and bilat-
the pulmonary artery (Fig. 1). There was mild pulmo-
eral basal rales. An S3 gallop was noted, and there was
nary hyp~rtension, and a calculated pulmonic to systemic
2 + bipedal edema. The ECG was unchanged. The chest
flow ratIO of 1. 5: 1 by oximetry. Early appearance of
X ray showed pulmonary congestion. She responded
contrast in the pulmonary artery was noted on 30 degree
well to intravenous diuretics, and therapy for asthma.
Pulm~nary congestion was thought to be due to respira-
tory dIstress syndrome, which was attributed to noncom- From the University of Rochester, New York.
pliance with asthma medications.
Later that year, she was readmitted with two weeks of Received June 4, 1992; revision accepted September 1, 1992.
intem:ittent high grade fevers, shaking chills, and ar-
Address reprint requests to Dr. Chi-Ling Hang, University of Roch-
thralglas. She had undergone root canal work and drain- ester, Cardiology Unit, Box 679, 601 Elmwood Avenue, Rochester
age of a dental abscess approximately two months ear- NY 14642. '

© 1993 Wiley-liss, Inc.

 Patent Ductus Arteriosus in Old Age 229

TABLE I. Results From Cardiac Catheterization

Pressures
Right atrium (a/v/mean) 7/6/5
Right ventricle 40114
Pulmonary artery 40/15/27
Pulmonary wedge (alv/mean) 15/25/15
Left ventricle 160/20
Aorta 160/50/90
Cardiac output
Heart rate 66
O 2 consumption index 115
Cardiac output/index (systemic) 4.8/3.1
Cardiac output/index (pulmonary) 7.5/4.8
Q/Qs 1.5: 1

RAO ventriculography, and aortography in the 50 degree

LAO view revealed a small patent ductus arteriosus, with
a contrast jet streaming into the pulmonary artery (Fig.
2). The coronary arteries, left ventricular wall motion,
and ejection fraction were normal. Her hospital stay was
uneventful, and she was discharged home on isosorbide
dinitrate, diltiazem, and furosemide. Percutaneous clo-
sure of the ductus with a Rashkind occluder was consid-
ered, but the patient refused.
DISCUSSION
Patent ductus arteriosus is noted in about 1 in 200 live
births, making it the third most common congenital car-
diac malformation [3,4]. It is more prevalent in females
than in males (2.6:1) [5], and is not usually associated
with other anomalies. The clinical presentation of patent
ductus is dependent upon the size of the defect. Large
shunts tend to cause congestive heart failure early in life,
and are associated with high mortality if untreated.
Smaller shunts are compatible with long survival. In
adults, the common presenting complaints are dyspnea
and exercise intolerance (60%), left chest pain (25%),
palpitations (15%), cough (12.5%), angina (7.5%), he-
moptysis (5%), and lassitude (5%) [6]. In one series,
30% of patients were asymptomatic [6]. In most adults
with patent ductus, the shunt is small, pulmonary pres-
sures are often normal, and shunt from the aorta to the
pulmonary artery persists throughout the cardiac cycle,
resulting in a characteristic thrill and continuous machin-
ery murmur with a late systolic accentuation at the upper
left sternal edge.
The patient presented here had a clinical picture con-
sistent with pulmonary congestion at age 74. The diag-
nosis of patent ductus arteriosus was initially missed,
because the continuous murmur was obscured by wheez-
ing. When the patient later returned with bacterial en-
docarditis, the murmur was noted, and the diagnosis was
confirmed by Doppler echocardiography, and later by
cardiac catheterization.
Fig. 1. Oximetry results. There is a saturation step-up at the
level of the pulmonary artery. Left atrial saturation drawn from
wedge position.
As in this patient, the majority of long-lived patients
with patent ductus arteriosus have relatively small left to
right shunts, of borderline hemodynamic significance
[7]. Some patients may undergo a spontaneous reduction
in the dimension of the shunt, as evidenced by a spon-
taneous closure rate of 0.6% per year [8].
Now rare among adults with patent ductus, bacterial
endocarditis was once a common cause of death. Of 57
patients reported in the pre-antibiotic era, 40% died of
bacterial endocarditis and 28% died of congestive heart
failure [6]. In a more recent review, the incidence of
subacute bacterial endocarditis was only 10% (0.4% per
annum) and congestive heart failure occurred in only
7.5% of cases [9]. Infection typically develops on the
ductus walls at the pulmonary end, and produces a clin-
ical syndrome of fever and continuous bacteremia. Our
patient presented with a two week history of intermittent
high grade fevers, shaking chills, arthralgia, recent den-
tal work, a cardiac murmur, and positive blood cultures.
While the echocardiogram did not show a vegetation,
endocarditis is still the most likely diagnosis. Echocar-
diography can identify vegetations in most cases of val-
vular endocarditis, but may be less sensitive in patent
ductus.
Chest pain is a fairly common presentation of patent
ductus arteriosus despite the presence of normal coronary
arteries, and it may be relieved by surgical interruption
230 Hang and Sullebarger
...A
Fig. 2. A: Left ventriculography in the 30-degree RAO view, demonstrating the early appearance of contrast in
the pulmonary artery. B: Aortography in the 50-degree LAO view, demonstrating a small patent ductus and
contrast in the pulmonary artery.
of the patent ductus. Our patient not only presented with
chest pain typical of exertional angina pectoris with nor-
mal coronaries, but also had significant ECG changes
consistent with ischemia. She was found to have a wide
pulse pressure (160/50) during catheterization. The eti-
ology of the angina may be similar to the mechanism
seen in aortic insufficiency [6]. The combination of sys-
temic arterial runoff through the patent ductus and left
ventricular diastolic overload/left ventricular hypertro-
phy may result in subendocardial hypoperfusion during
physical exertion.
In premature infants, a patent ductus may be closed
pharmacologically with indomethicin. Surgical closure is
required in infants unresponsive to indomethicin, and
may be accomplished at low risk in infants, children, and
young adults. In adults, the risk of the operation may be
increased by pulmonary hypertension and atherosclerotic
changes in the great vessels. Erdman et al. [10] and
Bell-Thomson et al. [11] have each described a simple
surgical technique. Closure may also be performed per-
cutaneously, using a plug [12] or an umbrella occluder
via an arterial [13] or transvenous [14,15] approach. Our
patient, who has just celebrated her 87th birthday, re-
cently returned for follow-up without signs or symptoms
of heart failure, and only rare episodes of chest pain. She
does not wish closure of the defect, but will consider
transvenous catheter closure if her symptoms progress.
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