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a Division of Cardiothoracic Surgery, Department of Surgery, Thomas Jefferson University, Philadelphia, Pennsylvania
b Department of Cardiothoracic Surgery, Drexel University College of Medicine, Philadelphia, Pennsylvania
c Department of Pediatric Cardiology, Drexel University College of Medicine, Philadelphia, Pennsylvania
Accepted for publication July 29, 2008.
* Address correspondence to Dr Youdelman, Division of Cardiothoracic Surgery, Department of Surgery, Thomas Jefferson University, 1025 Walnut St, Suite 607, Philadelphia, PA 19107 (Email: benjamin.youdelman{at}jefferson.edu).
| Two videos of this procedure can be viewed on the Internet at: http://ats.ctsnetjournals.org/content/vol87/issue4/images/data/1292/DC1/youdelman1.mpg and http://ats.ctsnetjournals.org/content/vol87/issue4/images/data/1292/DC1/youdelman2.mpg.
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Abstract |
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Anomalous aortic origin of a coronary artery (AAOCA) has been associated with signs and symptoms of myocardial ischemia, and may be a cause for sudden death in children and young adults [1, 2].
Anatomic variations include the left main coronary artery arising from the right sinus of Valsalva, and the right coronary artery arising from the left sinus. Theories to explain the mechanism for myocardial ischemia are varied. They include stenosis or distortion of the coronary ostium, compression of an intramural coronary segment subjected to high aortic wall tension, kinking at the acute angle of the proximal anomalous coronary during hyperdynamic conditions, or compression of the coronary artery between the aortic and pulmonary roots during effort-related expansion of these vessels [3]. With the pathophysiology imprecise, it follows that the surgical approached to AAOCA has been varied.
Numerous operations have been proposed to treat this condition including coronary artery bypass surgery (CABG) with arterial or venous conduits, reimplantation of the coronary artery into the appropriate sinus of Valsalva [4], and coronary ostial enlargement with or without unroofing of an intramural segment [5]. Currently there is no consensus for surgical treatment.
Risk of sudden death in a patient with AAOCA is believed to be reduced by creating durable, unobstructed coronary artery flow. The recommendation for surgery in adolescents or young adults is generally made when signs or symptoms of myocardial ischemia are present, but are less well-defined when the coronary anomaly is discovered incidentally in asymptomatic infants or young children.
We report a 9-year-old boy who presented with syncope preceded by palpitations, dizziness, and diaphoresis. Similar symptoms occurred 4 years earlier, and palpitations are reported with exercise.
His electocardiogram showed sinus arrhythmia, a prolonged Q-T interval of 461 msec, but no ischemia. He underwent echocardiography that revealed anomalous origin of the left coronary artery from the right coronary sinus of Valsalva. Computerized tomographic angiography and cardiac catheterization demonstrated the left coronary artery coursing between the aorta and pulmonary trunk. No intramural course was identified.
Coronary artery bypass grafting surgery using the left internal mammary artery (LIMA) pedicle graft connected to the left anterior descending coronary artery was performed. After separation from cardiopulmonary bypass, the hemodynamics were good. However, when the chest retractor was removed, diffuse ST segment elevation occurred and the patient had ventricular tachycardia. The graft was inspected and found to have a palpable pulse. Echocardiography showed normal cardiac function without segmental wall motion abnormalities. The patient was transported to the cardiac catheterization laboratory for emergent angiography.
Initial injection into the left subclavian artery showed poor filling of the LIMA graft; however, direct injection into the LIMA filled the entire coronary circulation. Injection into the right sinus of Valsalva uniformly filled both right and left coronary systems, but retrograde flow from the left anterior descending coronary artery through the LIMA and into left subclavian artery demonstrated a steal circuit diverting blood from the left anterior descending coronary artery territory (Fig 1; video 1 viewable at http://ats.ctsnetjournals.org/content/vol87/issue4/images/data/1292/DC1/youdelman1.mpg). The patient returned to the operating room for surgical revision.
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The aortic root was explored and a single coronary ostium was identified. The right coronary artery arose from the ostium and traveled in its usual course. The left coronary artery exited from within the single ostium in an oblique fashion. No intramural course was identified. The obliquity of the left coronary origin seemed to create a point of coronary stenosis, and this opening was enlarged by incising it into the aortic media and then repairing it.
The patient was weaned from circulatory support with good hemodynamics and no ischemic changes on electrocardiogram. However, again with removal of the chest retractor, the ischemic phenomenon recurred even with the LIMA graft occluded.
We hypothesized that transferring the LIMA to the ascending aorta would increase the perfusion pressure enough to improve flow through the LIMA graft and relieve the steal syndrome. After completion of the LIMA to the aorta proximal anastomosis, when the chest retractor was removed this time, there was less pronounced ST elevation in the lateral electrocardiogram leads and only rare premature ventricular complexes (PVC). The electrocardiographic measurements showed that normal sinus rhythm remained and the mild ST elevations improved in time.
The day after surgery, transthoracic echocardiography was normal. A repeat angiogram showed the left coronary ostial repair to be patent with unobstructed antegrade flow. The flow in the distal LIMA graft was biphasic. Injection in the ascending aorta showed antegrade flow into the LAD from the LIMA graft (Fig 2; video 2 viewable at http://ats.ctsnetjournals.org/content/vol87/issue4/images/data/1292/DC1/youdelman2.mpg). The coronary steal was no longer present.
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Comment |
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Internal mammary artery steal syndrome after coronary bypass operations is rare in adults and is usually associated with subclavian artery stenosis [8]. Steal syndrome associate with internal mammary artery grafting in children has not previously been reported.
In this case, we hypothesize that ischemia after CABG using a pedicle LIMA graft occurred when impingement on the left subclavian artery or proximal LIMA graft was relieved by removal of the chest retractor. Without the obstruction to flow, runoff through the LIMA into the left subclavian artery, away from the coronary circulation occurred, producing a steal phenomenon. That occlusion of the LIMA graft on return to the operating room did not completely resolve the ischemic changes on electrocardiogram and may be a consequence of the myocardium having been ischemic for several hours and not having had adequate recovery time.
Although CABG for surgical treatment of AAOCA has been advocated by some, the experience with this patient demonstrates a shortfall of this approach. Internal mammary artery steal for a LIMA pedicle graft is a real phenomenon that can be created when two patent vessels supply blood flow to a common end artery. Relative resistances of the vascular beds at either end of the LIMA will determine flow through this graft. It would be unlikely to predict a case of steal syndrome using a LIMA graft without the presence of proximal left subclavian artery stenosis, which has been seen in adults [8]. Based on this experience, we recommend caution in choosing CABG using a LIMA pedicle graft for the treatment of AAOCA.
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