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J Thorac Cardiovasc Surg 1996;111:901-902
© 1996 Mosby, Inc.


LETTERS TO THE EDITOR

Anomalous origin of the left coronary artery from the pulmonary artery: Is reconstruction of a double coronary artery system always necessary?

S. Sivasubramanian, MS, S. M. R. G. Krishnamurthy, MCh, P. Thirumalai, DM, R. Alagesan, DM, S. Viswakumar, MCh, A. Sukumar, MCh, D. Muthukumar, DM, G. Karthikeyan, MD

Department of Cardiothoracic Surgery
Department of Cardiology
Madras Medical College and Government General Hospital
Madras 600 003, India

To the Editor:

In their article on anomalous origin of the left main coronary artery from the pulmonary artery (J Thorac Cardiovasc Surg 1995;109:393-4), Chan, Hare, and Buxton rightly state that the optimal surgical strategy for correction of this malformation, especially in the older patient, is still not resolved.

They also highlight what we believe is an important point, namely, the role of noncoronary collateral blood flow to the left coronary artery (LCA). The pathophysiology of anomalous left coronary artery from the pulmonary artery (ALCAPA) depends on the extent of development of routes of blood supply to the left ventricle and the alterations in pulmonary vascular resistance. Although many earlier reports mention development of collaterals between the right and left coronary systems (intercoronary collaterals) as being responsible for survival into adulthood, the possibility of other systemic blood vessels feeding the LCA in ALCAPA has not been reported. These vessels also enlarge enough to maintain antegrade flow into the LCA, especially in the subgroup of patients surviving into the second or third decade without symptoms.

Recently we operated on a 15-year-old symptom-free boy who was being examined because of a continuous murmur in the left third and fourth intercostal spaces parasternally, detected by his physician on a routine examination. The patient had no evidence of ischemia, ventricular hypertrophy, or left ventricular dysfunction on electrocardiography or echocardiography. Echocardiography suggested, and cardiac catheterization and angiocardiography confirmed, the diagnosis of ALCAPA with a large left-to-right shunt and the patient underwent surgical treatment.

After establishing moderate hypothermic cardiopulmonary bypass with crystalloid cardioplegic arrest, we opened the pulmonary artery with the intention of performing an intrapulmonary tunnel (Takeuchi) procedure. However, we were surprised by a brisk backflow of arterial blood into the pulmonary artery from the LCA ostium. Electrical activity of the heart returned within a couple of minutes of administration of cardioplegic solution.

Suspecting an improperly applied aortic crossclamp to be the cause of backflow, we inspected the clamp and found it to be properly positioned. Because the profuse arterial return from the LCA persisted and a repeat dose of cardioplegic solution was similarly ineffective, we closed the LCA ostium from within the pulmonary artery with 5-0 Prolene sutures (Ethicon, Inc., Somerville, N.J.). Cardiopulmonary bypass was discontinued without problems and the patient made an uneventful postoperative recovery. There was no evidence of ischemia on a postoperative stress electrocardiogram or residual shunt on an echocardiogram.

Regarding the optimal surgical management, simple ligation of the anomalous LCA is a viable proposition in dealing with ALCAPA when enough collaterals from the right coronary artery exist to supply the left coronary system adequately.Go 1 However, as cardiac surgical technique evolved and systemic-coronary connections could be surgically created with safety, the reconstruction of a double coronary system began to be advocated widely.

The disadvantage claimed with simple LCA ligation is that the entire myocardium is left at the mercy of a single coronary artery. This risk is reduced if a systemic artery is connected to the LCA. Although theoretically attractive, no long-term comparative study with patients who have undergone the two-coronary system of reconstruction followed up for an equal period of time has been published to support this contention. The two widely quoted studiesGo Go 2,3 to condemn LCA ligation because of its high operative mortality and risk of sudden death after surgery have included observations on patients operated on in infancy also, usually as last resort procedures in desperately ill patients. Because these patients may not have had well-developed intercoronary collaterals at the time of the operation, LCA ligation is bound to produce sudden left ventricular ischemia and a poor outcome. Conclusions drawn from such a patient population cannot be extrapolated to the group with well-developed collateral flow and no ischaemia. In fact, other workersGo Go 4,5 have reported good results after LCA ligation in patients of this type.

Again, theoretically, any surgical conduit to the LCA, constructed as it is very early in the life of the patient, is subject to the same hemodynamic stresses and probably has an equal chance of atherosclerotic obstruction with aging as the right coronary artery. In fact, in all forms of two-coronary reconstructions, long-term patency of the grafts has varied on the basis on the choice of conduit. If grafts are patent for at least 18 months, the size of the right coronary artery collaterals return to normal. Should late occlusion occur, these young patients may be left with the equivalent of left main trunk disease!

In their case, Chan, Hare, and Buxton had to provide an alternate channel because of the preoperative features of left ventricular ischemia, and their actions were proved right by the postoperative improvement in these parameters.

Our contention, however, is that, in a patient such as ours, who has no symptoms, has no features of reduced myocardial perfusion, and has apparently excellent collateral blood supply to the anomalous LCA, there is no need at present for surgically creating an alternate conduit to the LCA. The fact that it is possible to do so safely does not justify its need or indicate that it should be done.

Only periodic follow-up of our patient with investigations to detect later development of left ventricular ischemia will determine whether we are correct.

References

  1. Sabiston DC, Floyd WL, McIntosh HD. Anomalous origin of the left coronary artery from the pulmonary artery in adults: surgical management. Arch Surg 1968;97:963-8.[Medline]
  2. Bunton R, Jonas RA, Lang P, Rein JJT, Castaneda AR. Anomalous origin of left coroanary artery from pulmonary artery: ligation versus establishment of a two coronary artery system. J THORAC CARDIOVASC SURG 1987;93:103-8.[Abstract]
  3. Wilson CL, Dlabal PW, McGuire SA. Surgical treatment of anomalous left coronary artery from pulmonary artery: follow up in teenagers and adults. Am Heart J 1979;98:440-6.[Medline]
  4. Wright NL, Baue AE, Baum S, Zinnser HF. Coronary artery steal due to an anomalous left coronary artery originating from the pulmonary artery. J THORAC CARDIOVASC SURG 1970;59:461.[Medline]
  5. Arciniegas E, Farooki ZQ, Hakimi M, Green EW. Management of anomalous left coronary artery from the pulmonary artery. Circulation 1980;62(Suppl):I180-9.



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