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J Thorac Cardiovasc Surg 1995;109:1259-1262
© 1995 Mosby, Inc.
LETTERS TO THE EDITOR |
Department of Cardiac Surgerya
Department of Cardiologyb
University of Pisa
Pisa, Italy
To the Editor:
In a recent letter Dr. Bucsenez and colleagues
1 described the management of anomalous origin of the left coronary artery from the right sinus of Valsalva. We read it with interest, because the reported case was among a few others showing the clinical relevance of an anomalous origin of the left coronary artery that involved the vessel coursing between the pulmonary artery and the aorta.
Myocardial ischemia and sudden death 2-4 have been reported as common sequelae to the various types of solitary coronary ostium. A clear surgical indication was evident in the reported case, in which a myocardial infarction was the consequence of an anomalous origin of the left coronary artery from the right sinus of Valsalva and of its course between the pulmonary artery and the aorta. Less predictable is the natural history of the patients with similar anomalies not showing such dramatic consequences. When the effect on overall survival of patients with an isolated single coronary artery is evaluated, their prognosis is usually unaffected by this anomaly, even if a minority (15%) of patients have severe cardiac problems before the age of 40 years. 5
The surgical indication is then not so well defined when such an anomaly is found on a coronary angiogram performed because of a different cardiac disease. This situation was observed in a patient who had angina and dyspnea on exertion because of an acquired aortic stenosis and was found to have a solitary coronary ostium.
This association has not been previously reported. In this situation the myocardial ischemia may be caused by both the anomaly and the acquired disease. The indication for surgical treatment may therefore be controversial. The absence of any fixed or dynamic stenosis that could be demonstrated by coronary angiograms prompted us to choose an isolated valve replacement in our case. The consequence of this decision will be reported.
A 68-years-old woman with a calcified aortic stenosis, who had dyspnea and angina pectoris on exertion, was admitted to our institution. Echocardiographic findings showed good left ventricular function and a transvalvular gradient of 100 mm Hg. The age and the symptoms of the patient induced us to perform a coronary artery angiogram. A single coronary ostium in the aorta, which gave origin to three vessels, was observed. The left anterior descending coronary artery (LADCA) had a leftward direction, forming a loop that was caused by its coursing between the pulmonary artery and the ascending aorta (Fig. 1). The left circumflex coronary artery (LCCA) had a separate origin inside the common ostium, and its initial course was similar to that of the LADCA (Fig. 2). The right coronary artery was normal.
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Cardiopulmonary bypass was initiated, the aorta was crossclamped, and cardiac arrest was induced through the injection of blood cardioplegic solution into the aortic root. A transverse aortotomy confirmed the presence of a solitary right coronary ostium, but it was not possible to assess the paths of the initial tracts of the LADCA and LCCA, which, according to their origins, to the angiogram, and to their visible courses, were supposed to pass between the aortic and pulmonary anuli. The aortic valve, which was extensively calcified, was resected and a 21 mm St. Jude Medical prosthesis (St. Jude Medical, Inc., St. Paul, Minn.) was implanted. The sutures were passed through the aortic anulus with the greatest care, as superficially as possible, with the aim to avoid damage to the left coronary arteries. Cardioplegic solution was infused retrogradely in the coronary sinus 20 minutes after aortic crossclamping, avoiding the difficulties related to the injection into the large single coronary ostium. The aortotomy was closed with a double running suture and the aortic crossclamp released.
Recovery of cardiac function was not good; the electrocardiogram showed a left bundle branch block and the left ventricle was dyskinetic. The cardiac movement disorder was more severe when weaning from cardiopulmonary bypass was attempted and high cardiac filling pressures were reached. Retrograde coronary sinus perfusion was used to eliminate a possible gaseous coronary embolus, but it was ineffective. Then we decided to replace the valve prosthesis with a smaller one, to reduce a hypothetical compression of the LADCA and LCCA. When the prosthesis was removed no signs of possible damage or obstruction of the coronary arteries was observed. Blood cardioplegic solution was injected antegradely into the solitary coronary ostium, but no hematoma was visible at the level of the previous sutures. A new 19 mm St. Jude Medical aortic prosthesis was implanted. Unfortunately the situation remained unchanged; weaning from bypass was again unsuccessful because of severe depression of the left ventricle, which remained dyskinetic. Acting on the hypothesis that even the smaller prosthesis, because of its rigid anulus, compressed the anomalous left coronary arteries, we decided at this time to perform a double saphenous bypass graft procedure on the LADCA and the marginal artery of the LCCA. This procedure resolved the situation. Satisfactory cardiac function was soon obtained, even though pharmacologic inotropic support was needed, and the patient was weaned from bypass. Cardiac function quickly improved and the inotropic support was suspended on the first postoperative day. The postoperative recovery was slow as a consequence of the long bypass time, but the patient was discharged from the hospital 3 weeks after the operation. At the 6-month postoperative follow-up examination she was in class I of the New York Heart Association classification, and an echocardiographic assessment revealed normal cardiac function.
In our opinion this case supports the hypothesis that the pathophysiologic mechanism of sudden myocardial ischemia is related to the course of the left coronary artery. When the coronaries arise from the anterior sinus of Valsalva and the left coronary artery passes obliquely between the aorta and the pulmonary artery, an acute angle is formed that can occlude the artery if extrinsic compression is applied. Increased expansion of the aorta and the pulmonary artery during exercise can produce this compression, and sudden death almost always occurs during or immediately after physical activity. In the case of our patient, who had a normal life until the symptoms of the aortic stenosis developed, the rigid prosthetic valvular anulus assumed a relevant part in the described mechanism. Different anatomic relationships between the coronary arteries and the contiguous structures can explain the different outcomes of patients having a similar anomaly. More sophisticated diagnostic tools that could assess exactly this relationship could probably facilitate the choice of a safe operative strategy when the surgical indication is not clear. In the absence of such an opportunity, only the experience of prior cases can be of help to determine the best treatment for such dramatic situations.
12/8/60694
References
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