Download Large Left Ventricle, Paradoxically Split Second Heart Sound, and a

Journal of the Louisiana State Medical Society
ECG OF THE MONTH
Large Left Ventricle, Paradoxically Split Second
Heart Sound, and a Continuous Murmur
C. Carmen Ilie, MD; Roberto E. Quintal, MD; Neeraj Jain, MD; Murtuza J. Ali, MD;
Christopher Daniels, MD; Frederick R. Helmcke, MD; and D. Luke Glancy, MD
An asymptomatic, muscular, 41-year-old man came to the clinic because of a swishing sound in his ears at
night. On exam his neck veins were normal; pulses were full and brisk; and a large and dynamic left ventricular
impulse was felt just outside the left anterior axillary line in the sixth intercostal space. The second heart
sound was paradoxically split, and both components were loud. A prominent third heart sound was heard
at the cardiac apex, and a grade 4/6 continuous murmur was best heard in the second left intercostal space.
An electrocardiogram was recorded (Figure 1).
Figure 1. Electrocardiogram recorded at one-half standard, where 5 mm = 1mV, of a 41-year-old man with a continuous murmur. See
text for explication.
What is your diagnosis?
Explication is on page 228.
226 J La State Med Soc VOL 163 July/August 2011
Journal of the Louisiana State Medical Society
ECG of the Month
Presentation is on page 226.
DIAGNOSIS: Sinus bradycardia, left bundle branch block, and
QRS voltage of left ventricular enlargement.
The paradoxically split second heart sound predicts
left bundle branch block (LBBB). The commonest cause
of LBBB is left ventricular enlargement, which here is
documented by the size and position of the left ventricular
impulse and is emphasized by the QRS voltage. There are
many causes of continuous murmurs.1 A good rule is that if
it is maximal between the left second intercostal space and
the left clavicle and peaks at the second heart sound, the
continuous murmur, known as Gibson’s murmur,2 is due to
a patent ductus arteriosus (PDA), whereas if the continuous
murmur is maximal elsewhere it is probably due to some
other cause – coronary arteriovenous fistula, ruptured sinus
of Valsalva aneurysm, etc. Thus, the location of this patient’s
murmur indicates a PDA.
Undiagnosed patent ductus arteriosus is rare in
adults of developed countries, but less so in immigrant
laborers such as this man. The diagnosis was confirmed
by echo-Doppler examination and computed tomographic
angiography which showed a ductus 7 mm in diameter, ie, ~
0.4 cm2 in cross-sectional area, with continuous flow through
it into the left pulmonary artery just beyond its origin from
the pulmonary trunk (Figure 2). A ductus this size results
in a large left-to-right shunt with the extra workload being
borne almost entirely by the left ventricle, which accounts
for that chamber’s huge internal diameter (8.5 cm in diastole)
in this patient. The left ventricle in such patients eventually
fails,3 and the ejection fraction of only 40% suggests that this
will occur soon rather than later in this patient. Pulmonary
arterial systolic pressure is estimated to be 35-45 mm Hg
(reference ≤ 30); there is mild pulmonic regurgitation; and
the right ventricle has normal size and function.
Patent ductus arteriosus is a mechanical problem that
lends itself to a mechanical solution, ie, closure of the ductus.
Robert Gross first accomplished this surgically over 70 years
ago.4 Initially this was performed by simple ligation, but
because of a significant recurrence rate with that procedure,
suture-ligation and division of the ductus became the
method of choice. More recently, catheter-based closure of
the ductus, initially done with coils5 and subsequently with
the Amplatzer duct occluder,6 has become the procedure
of choice.
The Amplatzer Duct Occluder, frequently used for
closure of moderate to large PDAs, has two important
features: a relatively small delivery system (5-7 Fr) and the
ability to be retrieved and repositioned prior to detachment.
A lateral angiogram with contrast injection in the descending
aorta (Figure 2) is helpful in selecting the diameter of
the device: at least 2 mm larger than the narrowest PDA
diameter (5.9 mm in our case). Using a device 10 mm
in diameter on the aortic side and 8 mm in diameter on
Figure 2. Preclosure images of the patent ductus arteriosus (PDA). A. Color Doppler demonstrating flow from descending aorta (DAo)
into pulmonary artery (PA) through the PDA. RV – right ventricle. B. Computed tomographic angiogram, axial view, showing the
communication between the DAo and PA. AAo – ascending aorta. C. Aortogram, left lateral view, demonstrating contrast filling the PA
through the PDA back to the pulmonary valve (black arrows).
228 J La State Med Soc VOL 163 July/August 2011
Figure 3. Postclosure images of the ductus arteriosus. A. Color
Doppler showing the Amplatzer Duct Occluder (ADO) and the
absence of residual shunt. RV – right ventricle, PA – pulmonary
artery, DAo – descending aorta. B. Aortogram, left lateral view
demonstrating the absence of residual shunt.
the pulmonary arterial side, we achieved complete PDA
occlusion with no residual shunt as judged by angiography
and echocardiography (Figure 3).
REFERENCES
1.
2.
3.
4.
5.
6.
Marquis RM. Persistence of the ductus arteriosus. In: Watson H
(editor). Paediatric Cardiology. St. Louis: C.V. Mosby;1968:242-285.
Gibson GA. Diseases of the Heart and Aorta. Edinburgh: Young J.
Pentland;1898:161.
Campbell M. Patent ductus arteriosus. Some notes on prognosis
and pulmonary hypertension. Brit Heart J 1955;17:511-533.
Gross RE, Hubbard JP. Surgical ligation of a patent ductus
arteriosus. Report of first successful case. JAMA 1939;112:729-731.
Alwi M, Kang LM, Samion H, et al. Transcatheter occlusion of
native patent ductus arteriosus using conventional Gianturco
coils. Am J Cardiol 1997;79:1430-1432.
Masura J, Walsh KP, Thanopoulous B, et al. Catheter closure of
moderate-to-large-sized patent ductus arteriosus using the new
Amplatzer duct occluder: immediate and short-term results. J Am
Coll Cardiol 1998;31:878-882.
Dr. Ilie is an interventional fellow in the Section of Cardiology,
Department of Medicine, Louisiana State University Health Sciences
Center, New Orleans (LSUHSC-NO). Dr. Quintal is a clinical professor
of medicine in the Section of Cardiology, Department of Medicine,
LSUHSC-NO. Drs. Jain and Ali are assistant professors of clinical
medicine in the Section of Cardiology, Department of Medicine,
LSUHSC-NO. Dr. Daniels is an interventional fellow in the Section
of Cardiology, Department of Medicine, LSUHSC-NO. Dr. Helmcke
is an assistant professor of clinical medicine in the Section of Cardiology,
Department of Medicine, LSUHSC-NO. Dr. Glancy is a professor in
the Section of Cardiology, Department of Medicine, LSUHSC-NO.
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