Ann Thorac Surg 2005;79:348-351
© 2005 The Society of Thoracic Surgeons
Case report
Can An Early Peri-Anastomotic LITA Stenosis Be Reversible?
Calin Ivascau, MDa,
Dimitrios Buklas, MDa,
Massimo Massetti, MD*,a,
Remy Sabatier, MDb,
Olivier LePage, MDa,
Eugenio Neri, MDc,
Gerard Babatasi, MDa,
Andrè Khayat, MDa
a Department of Thoracic and Cardiovascular Surgery, Caen, France
b Department of Cardiology, University Hospital Center, Caen, France
c Dipartimento di Chirurgia, Unità Operative di Chirurgia dell'Aorta Toracica e Chirurgia Vascolare, Università degli Studi di Siena, Siena, Italy
Accepted for publication August 15, 2003.
* Address reprint requests to Dr Massetti, Thoracic and Cardiovascular Surgery Department, CHU Ave de la "Cote de Nacre," Caen 14033, France
massetti-m{at}chu-caen.fr
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Abstract
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Peri-anastomotic graft stenosis is a possible complication of coronary artery bypass graft operations. Early failure of myocardial revascularization may result from graft stenosis with inherent difficulties in perioperative diagnosis and subsequent management. We report the case of a 58-year-old man who experienced early preanastomotic left internal thoracic artery bypass stenosis that progressively resolved during a 2-year period without reoperation or interventional angioplasty. Although the mechanisms underlying graft stenosis remain unclear, this case emphasizes the role of repeated coronary angiography in the choice of treatment.
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Introduction
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Peri-anastomotic graft stenosis is a possible complication of coronary artery bypass graft operations performed either with off pump or conventional on pump procedures. Resulting early failure of myocardial revascularization carries inherent difficulties in perioperative diagnosis and subsequent management.
We report the case of a 58-year-old man who experienced early preanastomotic left internal thoracic artery bypass stenosis after standard off pump coronary artery bypass procedure with postprocedural recurrence of angina symptoms.
In August 2000, a 58-year-old man presented to Caen University Hospital with severe substernal chest pain that had started 2 hours earlier and was partially relieved with sublingual nitroglycerine. Seventeen years earlier, the patient had experienced an inferior wall myocardial infarction. He underwent urgent coronary angiography that showed right coronary artery (RCA) occlusion; no indication for surgery was given when that occurred and the patient underwent standard medical treatment with no recurrence of symptoms.
His electrocardiogram on admission revealed myocardial ischemia in leads V1 to V5 with an ST-T segment depression of 2 mm. Ischemic changes were further exacerbated by mild exercise.
The patient underwent cardiac catheterization, which showed an already known 100% occlusion of the right coronary artery and a severe stenosis of the midsegment of the left anterior descending coronary artery (LAD). Symptoms resolved with medical treatment (ie, heparin, beta blocker), and the patient was scheduled for elective coronary artery bypass graft surgery in October 2000. The procedure consisted of a single left internal thoracic artery (LITA) to LAD bypass with off pump coronary artery bypass technique. The operation was performed using a standard median sternotomy approach, the LITA was harvested, pedicled, and prepared in standard fashion (using electrical scalpel and hemostatic clips to divide collaterals); no intraluminal papaverine was administered. At inspection the conduit quality appeared adequate and its flow (after distal transection) was satisfactory. Heparin (200 IU/kg) was administered. Heart exposure and stabilization was achieved using the Cohn immobilizer device (Genzyme Corp, Cambridge, WA). A bloodless field was obtained using two polytetrafluoroethylene vessel loops passed proximal and distal to the anastomosis site. The LITA was then clamped proximally with a standard soft Diethrich-type bulldog clamp (1/2 force surgical spring clip, Applied Medical, Rancho Santa Margarita, CA). The medium segment of LAD was incised and the anastomosis was performed using a continuous 8-0 Prolene suture (Ethicon, Somerville, NJ). No additional sutures were applied. At routine inspection, the surgical result was considered optimal with an excellent LITA pulse assessed by finger palpation. The intervention was completed without any complication. During the third postoperative day, the patient presented with recurrence of mild effort angina symptoms; therefore urgent coronary angiography examination was immediately performed. The selective LITA angiogram showed a patent anastomosis to the LAD. In addition, the LITA presented a regular caliber along its course, as yet, about 1 cm before the anastomotic site, and it presented a stenotic aspect. During the examination the patient was hemodynamically stable with trivial electrocardiogram modifications, and the LAD presented a satisfactory distal perfusion. There where no significant electrocardiogram or enzyme (CPKMB and troponin) modifications.
Selective catheter injection of nitrates and calcium antagonist was then considered in the suspect of a spasm, but resulted in no appreciable modification of the caliber at the level of the stenosis. This made the hypothesis of localized conduit wall edema (Fig 1) more consistent as the cause of the stenosis affecting the last segment of the LITA. We decided, in presence of patient clinical stability and on the basis of the causal hypothesis of a localized wall edema, to proceed only with the medical treatment (ß-blockade) and to reevaluate the lesion at short term. The patient had an uneventful subsequent postoperative course with no recurrence of symptoms. In January 2001, after a 3-month period, a coronary angiogram control was scheduled, which demonstrated reduction of the grade of the stenosis (Fig 2) with distal perfusion of the LAD that remained satisfactory. The most recent (July 2002) coronary angiography control showed the complete resolution of the preanastomotic stenosis (Fig 3).
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Fig 1. Coronary angiogram performed on postoperative day 3 in October 2000, after the recurrence of angina symptoms. Illustration of the left internal thoracic artery and left anterior descending coronary artery graft with a severe (80%) stenosis 1 cm prior to the anastomosis.
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Fig 2. Illustration of the left internal thoracic artery and left anterior descending coronary artery graft 3 months after the operation in January 2001; the stenosis, although still present, is not significant.
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Fig 3. Coronary angiogram performed 21 months postoperatively in July 2002, demonstrating the complete absence of the perianastomotic stenosis.
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Comment
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After myocardial revascularization, localized preanastomotic or peri-anastomotic stenoses can occur regardless of the surgical technique used [1]; such abnormalities can remain completely asymptomatic or can determine a recurrence of angina symptoms. In the case of stenoses affecting the conduits used for revascularization, in particular the arterial conduits, there are two main mechanisms that are advocated: (1) a localized spasm or (2) local edema affecting the vessel wall [1, 2]. The spasm is a phenomenon that can be resolved by the use of nitrates, calcium antagonists, or other drugs like steroids or prostaglandins [3]. Local edema is mainly attributable to the manipulation and consequential trauma of the conduits during their harvest, especially in the case of skeletonized internal thoracic arteries. Both mechanisms may severely compromise graft patency and function, exposing myocardial viability at risk. Special care must be made during surgical manipulations, such as control of collaterals, vessel preparation, and needle penetration during anastomosis. Minimal adventitial trauma can be responsible for localized swelling, hematomas, or even dissection, thus making mandatory the routine inspection of the conduits along their entire length either before or after the anastomosis. In the presented case, the first postoperative angiogram confirmed the overall good quality of LITA and excluded technical problems affecting the LITA and LAD anastomosis. The detected stenosis, not responding to selective drug administration, led us to consider local edema as the most likely mechanism for the stenosis. Under these circumstances the decision making process can be difficult [4]. Our observations emphasize the importance of an early angiogram either for differential diagnosis or for immediate clinical management. This enabled us to exclude any anastomosis technical failure, to assess the adequacy of LAD flow, and it provided us the direct demonstration of the stenosis irreversibility after local vasodilators administration. Only at the light of these controls could we confidently choose a conservative approach for the patient. Other instrumental investigations such as intraoperative transit-time flowmetry or LITA Doppler ultrasound have been proposed; although they provide quite reliable information about graft and anastomosis function, they have important practical limitations [4, 5], and thus far they have less accuracy of coronary angiography [6, 7]. When early postoperative ischemia occurs, all potential mechanisms need to be rapidly elucidated, especially when graft stenosis is suspected and myocardial viability is at risk. Under these circumstances, early intervention is mandatory. In this perspective, cardiac catheterization enables both optimal diagnosis and prompt treatment. Previous reports indicate that local edema can resolve spontaneously [4]; nevertheless angioplasty or reoperation may be required [1, 4] in the event of severe graft patency compromise associated with myocardial dysfunction or jeopardy. According to Wiklund and colleagues [4], the majority of stenosis visualized at the early coronary angiography could not be seen at a later coronary angiography. For stenosis seen by angiograph in the early postoperative period, in the absence of ischemic symptoms and with an acceptable intraoperative flow measurement, immediate reoperation is not advisable. The presented case confirms that a conservative approach can be a valid alternative in stable patients in whom preanastomotic stenosis, sustained by local edema, does not compromise graft function.
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References
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Abstract
Introduction
