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Fig. 3. Short-axis views at the left ventricular level in diastole (A) and in systole (B and C). The aneurysm is a well-demonstrated outpouching of the ventricular wall (arrows). The opening of the aneurysm in the left ventricular cavity is almost occluded in systole (B and C). LV = left ventricle.
congenital muscle defect in an infant. Report of a case with discussion of pathogenesis of associated endocardial fibroelastosis. Am J Cardiol 1963;12:721-9. 4. Ruttenberg HD, Jue KL, Elliott LP, Anderson RC, Edwards JE. Cardiac myopathy, probably of congenital origin. A case simulating anomalous origin of the left coronary artery from the pulmonary trunk. Circulation 1964;29:768-76. 5. Mardini MK. Congenital diverticulum of the left ventricle. Report of two unusual cases. Br Heart J 1984;51:321-6. 6. Gueron M, Hirsch M, Opschitzer I, Mogel P. Left ventricular diverticulum and mitral incompetence in asymptomatic children. Circulation 1976:53:181-6.
Successful surgery for atfioventricular reentrant tachycardia in a small child Christopher L. Case, MD, Fred A. Crawford, MD, Paul C. Gillette, MD, Bertrand A. Ross, MD, and Vicki L. Zeigler, RN. Charleston, SC. Most supraventricular tachycardia (SVT) may now be successfully treated surgically in adults as well as infants and children. Surgical treatment for atrioventricular (AV) nodal reentrant tachycardia is now becoming a viable option in adults. This surgery was spurred by case reports of “accidental” preservation of AV conduction while attempting to ablate the nodal reentrant circuit by operative dissection of the AV junction.’ Ross et a1.2 have reported the largest series of AV nodal reentrant tachycarFrom South Reprint Carolina, 29425.
South Carolina Carolina.
Children’s
requests: Christopher Dept. of Pediatric
Heart
L. Case, Cardiology,
Center, MD, Medical 171 Ashley
Medical
University
of
University of South Ave., Charleston, SC
dia successfully treated surgically. Cox3 has also reported success in four patients with the use of a cryosurgical procedure. The youngest patient reported in either series is 10 years old. We would like to describe a successful outcome in what we believe is the smallest child operated on for incessant AV nodal reentrant tachycardia. The patient is a 4X-year-old 15 kg white girl who had SVT first documented at 15 months of age. Digoxin was first used for tachycardia control. She experienced multiple breakthroughs, so propranolol was added to her regimen. This combination resulted in first-degree and second-degree AV block with sinus and nodal bradycardia of 30 to 35 beats/min. Physical examination was unremarkable and the ECG in her native rhythm while she was taking no medication was normal sinus rhythm. A four-catheter electrophysiology study was performed preoperatively. Normal basic intervals with a cycle length of 750 msec were recorded when the patient was in sinus rhythm. Corrected sinus node recovery time was mildly abnormal at a maximum of 380 msec. Two-to-one AV block was recorded at a 285 msec atria1 paced cycle length. ‘There was evidence for dual AV node pathways with the A,-H, interval increasing more than 65 msec when the atrial prematurity pacing interval was decreased 20 msec. The SVT of 300 cycle length was induced with premature atrial stimulation. During the tachycardia, not only was there a normal septal sequence of retrograde atria1 conduction, but also this atria1 activation clearly preceded ventricular activation, showing evidence for an AV nodal reentrant mechanism (Fig. 1). Due to failure of medication to control the patient’s tachyarrhythmia and also because of significant side effects of her medical regimen, surgical therapy was thought to be a logical alternative. A median sternotomy approach was employed. Pacing and reference electrodes were placed on the right atrium and ventricle. During normothermic cardiopulmonary
American
July 1986 Heart Journal
Fig. 1. Intracardiac electrograms of patient in AV nodal reentrant tachycardia. Note septal sequence of atria1 retrograde activation with low septal right atria1 depolarization preceding V. From top to bottom: ECG, (composite electrocardiogram), lead I, AV,, V,, high right atrium electrogram (HRA), distal coronary sinus electrogram (DCS), coronary sinus electrograms (CS,, CS3, C&, CS&, His bundle electrograms (HBE,, HBE,), right ventricular apex electrogram (RVA), and femoral artery pressure (FAP). H = His depolarization; V = ventricular depolarization; LSRA = low septal right atria1 depolarization.
bypass, a right atriotomy was performed. With the use of a hand-held probe for mapping, the earliest site of atria1 endocardial activation during tachycardia was identified just anterior to the AV node. With the patient in sinus rhythm, a series of 12 3 to 4 mm cryolesions at -70’ C for 120 seconds each were placed around the AV node, utilizing the boundaries of the triangle of Koch as described by Cox. The PR interval was prolonged from 120 to 220 msec after ablation. Transient second-degree AV block occurred several times and the probe was quickly rewarmed. Ventricular pacing was performed that showed no retrograde conduction, giving evidence that the retrograde limb of the circuit had been ablated. The child tolerated the procedure without difficulty. In the perioperative period, the patient exhibited a rapid recovery. Her PR interval, which was 100 msec preoperatively, varied between 120 and 150 msec postoperatively. She exhibited normal sinus rhythm without any second-degree block, third-degree block, or tachycardia. An electrophysiology study with temporary pacing wires on postoperative day 4 revealed the reappearance of retrograde 1:l conduction. No tachycardia could be indllced.
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SVT 6 months post-surgery. Surgical treatment of cardiac dysrhythmias in children has been firmly established.* Most pediatric experience in ablative procedures has been acquired in the treatment of
patients with accessory connections. These have been performed on children as small as 7.5 kg at our institution. Treatment of posterior septal accessory connection, very close to the AV node, has also been performed. It has recently been recognized that AV nodal reentrant SVT may also be surgically treated without major postoperative conduction disturbances. Experience in these techniques is more limited. As a consequence, age and weight criteria that predict successful, complication-free surgical outcome are less well established. Patient size criteria would seem to be a more important factor in peri-AV nodal surgery, where the complication of injury to the node is more likely. We describe a successful case of AV node reentrant surgery in a 15 kg, 4*/2-year-old girl. Further size limitations of the therapeutic modality await definition.
REFERENCES
1. Pritchet ELC, Anderson RW, Bendett DG, Kasell J, Harrison L, Wallace AG, Sealy WC, Gallager JJ. Reentry within the atrioventricular node: surgical care with preservation of atrioventricular conduction. Circulation 1979;60:440-6. 2. Ross DL, Johnson DC, Denniss AR, Cooper MJ, Richards DA, Uther JB. Curative surgery for atrioventricular (“av nodal”) reentrant tachycardia. J Am Co11 Cardiol 1985;6:1383-92. 3. Cox JL. The status of surgery for cardiac arrhythmias. Circulation 1985;71:413-17.
Volume Number
116 1, Part 1
Brief
4. Ott DA, Gillette PC, Garson A, Co&y DA, Reul GJ, McNamara DG. Surgical management of refractory supraventricular tachycardia in infants and children. J Am Co11 Cardiol 1985;5:124-9.
Intracardiac right-to-left cardiac surgery
shunting
following
James I. Klepper, MD, Frank Seifert, MD, William E. Lawson, MD, George I. Mallis, MD, John P. Dervan, MD, Gerald Smaldone, MD, PhD, and Edward J. Brown, Jr., MD. Stony Brook, N.Y.
Acquired intracardiac right-to-left shunts are not commonly encountered in clinical practice. There have been reports describing acquired right-to-left shunting across a patent foramen ovale, but most of these have been described in patients with underlying pulmonary disease.“g We encountered a patient who, 2 months after coronary bypass surgery, developed a clinically significant right-to-left shunt across a patent foramen ovale. We believe this was precipitated by a localized right atria1 pericardial tamponade that led to an elevated right atria1 pressure and subsequent shunting of blood from the right atrium to the left atrium across a patent foramen ovale. Described in this report is the clinical course and treatment of this patient. A 73-year-old man was admitted 8 weeks after aortic valve replacement with a chief complaint of increasing dyspnea for 1 week and upper abdominal pleuritic pain for 3 days. Ten years prior to admission, the patient was diagnosed as having aortic insufficiency. He remained asymptomatic until 4 years prior to admission, when he first began experiencing chest pain and dyspnea on exertion. His symptoms progressed, and 6 months prior to admission he underwent cardiac catheterization. Findings included moderate to severe aortic insufficiency, trace mitral insufficiency, and a dilated left ventricle with an ejection fraction of 42 571.There was a 60% stenosis in the proximal left anterior descending coronary artery. Right atria1 and pulmonary artery oxygen sat.urations were equal and were 69%. The arterial oxygen saturation was 96.5% on room air. The patient underwent aortic valve replacement with a porcine bioprosthesis and received a saphenous vein bypass graft to the left anterior descending coronary artery. The operation and postoperative course were uneventful. However, 1 week following hospital discharge, the patient was readmitted with pleuritic chest pain and an elevated sedimentation rate of 29
From the Cardiovascular and Pulmonary Divisions, Department of Meditine and the Cardiac Surgery Division, Department of Surgery, State IJniversity of New York, Stony Brook Health Sciences Center. Reorint Sciences
reouests: C&r
Edward J. Brown. Jr., MD. T17, Rm. 020, SUNY Stony
Cardioloev Division. Brook, I-v%’ 11794.
Health
Communications
189
mm/hr. A diagnosis of postpericardiotomy syndrome was made and the patient became asymptomatic with indomethacin therapy. Following therapy, the sedimentation rate normalized to 12 mm&. Two months after cardiac surgery, the patient developed dyspnea at rest and pleuritic upper abdominal pain, and was admitted to the hosptial. He was tachypneic, with a blood pressure of 180/100 mm Hg and a pulse of 90 beats/min. He was afebrile. There was no jugular venous distension and his lungs were clear. He had a 216 systolic ejection murmur best heard at the left upper sternal border and a three-component pericardial friction rub. There was mild right upper quadrant abdominal tenderness. No leg swelling was present and Homans’ sign was negative. His cardiac silhouette was enlarged with clear lung fields seen on chest x-ray film. His ECG demonstrated normal sinus rhythm and left ventricular hypertrophy. His white blood cell count was 7300 cells/mm3, and the sedimentation rate was 11 mm/hr. The arterial blood gases demonstrated a pH of 7.44 with a Pco2 of 38 mm Hg and a PO, of 46 mm Hg. With a 100% oxygen facemask, the pH was 7.41, the Pcop was 38 mm Hg, and the PO, was 62 mm Hg. A technetium-99m perfusion lung scan was negative. A balloon-tipped pulmonary artery catheter was inserted. The mean right atria1 pressure was 12 mm Hg, the right ventricular pressure was 23/6 mm Hg, the pulmonary artery pressure was 23/11 mm Hg, and the mean pulmonary capillary wedge pressure was 6 mm Hg. A two-dimensional echocardiogram revealed a dilated left ventricle with global hypokinesis and a small posterior pericardial effusion. There was a 2 to 3 cm echo-free space surrounding and indenting the free wall of the right atrium (Fig. 1). Saline contrast injection into the antecubital vein demonstrated a right-to-left shunt across the interatrial septum at the level of the foramen ovale (Fig. 2). The patient was started on prednisone, 60 mg per day. Over the next 48 hours, he began to improve with disappearance of his abdominal pain, less dyspnea, and an increasing PO, on arterial blood gas determinations. After 5 days of steroid therapy, a left and right heart cardiac catheterization was performed. The mean right atria1 pressure was 7 mm Hg, the right ventricular pressure was 32/8 mm Hg, the pulmonary artery pressure was 32/16 mm Hg, the mean pulmonary capillary wedge pressure was 8 mm Hg, and the mean left atria1 pressure was 7 mm Hg. An oximetry run was normal with no evidence of intracardiac shunting. With the patient breathing room air, an arterial oxygen saturation value was 95 7%. A patent foramen ovale was easily crossed with a 1 cm flotation balloon catheter. After 8 days of corticosteroid therapy, a repeat contrast echocardiogram showed resolution of the rightto-left shunt. The patient was asymptomatic and was discharged taking prednisone, 20 mg per day, which was continued for 1 month. A repeat echocardiogram demonstrated disappearance of the loculated pericardial effusion. Arterial oxygen saturations were 94% in both the supine and standing positions. Six months after surgery, the patient remained asymptomatic with an arterial oxygen saturation of 94%.