Large left ventricle, paradoxically split second heart sound, and a continuous murmur.
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 [cm.sup.2] 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 [less than or equal to] 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 coils (5) 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 the pulmonary arterial side, we achieved complete PDA occlusion with no residual shunt as judged by angiography and echocardiography (Figure 3).
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(1.) Marquis RM. Persistence of the ductus arteriosus. In: Watson H (editor). Paediatric Cardiology. St. Louis: C.V. Mosby;1968:242-285.
(2.) Gibson GA. Diseases of the Heart and Aorta. Edinburgh: Young J. Pentland;1898:161.
(3.) Campbell M. Patent ductus arteriosus. Some notes on prognosis and pulmonary hypertension. Brit Heart J 1955;17:511-533.
(4.) Gross RE, Hubbard JP. Surgical ligation of a patent ductus arteriosus. Report of first successful case. JAMA 1939;112:729-731.
(5.) 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.
(6.) 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.
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
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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|Title Annotation:||ECG of the Month|
|Author:||Ilie, C. Carmen; Quintal, Roberto E.; Jain, Neeraj; Ali, Murtuza J.; Daniels, Christopher; Helmcke,|
|Publication:||The Journal of the Louisiana State Medical Society|
|Article Type:||Case study|
|Date:||Jul 1, 2011|
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