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Eur J Cardiothorac Surg 2000;17:509-514
© 2000 Elsevier Science NL
Service de Chirurgie Cardiaque, Thoracique et Vasculaire, CHU Hôpital de la Cavale Blanche, 29609 Brest, France
Corresponding author. Tel.: +33-2-9834-7428; fax: +33-2-9834-7417
| Abstract |
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Key Words: Coronary artery surgery Coronary artery angioplasty Coronary artery endarterectomy Atheromatous plaque complications Coronary artery reconstruction Internal thoracic artery
| 1. Introduction |
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| 2. Material and methods |
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2.1. Operative technique
All patients underwent LAD bypass graft using pedicled ITA. CABG is the basis of the technique and CAR is a new way to make the anastomosis. A long arteriotomy is opened all along the diseased LAD; however, the LAD is not opened at the level of the first proximal significant lesion (Fig. 1) in order to avoid competitive flow between the native LAD and the ITA graft. The ITA is prepared to carry out the anastomosis. The length of the ITA longitudinal incision is the same as the length of the LAD arteriotomy (Fig. 1). Termino-lateral anastomosis between ITA and LAD is made in a such way as to reshape the LAD. The anastomosis part of the ITA is used as an arterial onlay patch (Fig. 1). Atheromatous plaques are excluded from LAD lumen and left outside the anastomosis (Fig. 2). It is not an endarterectomy because atheromatous plaques are put outside the lumen of the reconstructed LAD and are not removed nor withdrawn from the arterial wall. The arterial suture line settles the ITA patch inside the LAD so that the major part of the plaques are excluded from the LAD lumen. U-Stitch running sutures are used to achieve this plaque exclusion (Fig. 2). Finally, 75% of the new reconstructed LAD originate from the ITA wall and 25% from the native artery. This 25% of native LAD forms a posterior gutter which leads to the origins of septal and diagonal arteries. In this way, the need for long open endarterectomy is reduced. However, artery calcifications may prevent plaque exclusion because the needle cannot pass through calcified plaques. In this case a limited short endarterectomy is performed associated with intimal fixation at the proximal and distal edges of the endarterectomised area. The reconstruction consists in the exclusion of the major surface of the endarterectomised wall from the LAD lumen in such a fashion we have just described above. Thus the new reconstructed vessel is made of 75% good ITA wall and 25% LAD-endarterectomised wall.
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One hundred and ninety-four coronary artery bypass grafts (CABG) were performed and details of grafting are shown in Table 2. The Y-technique (re-implantation of the right ITA as a free graft in the left pedicled ITA) was used in bilateral ITA grafting. CAR involved 94 LAD. Short endarterectomy (less than 2 cm) was associated with CAR in 15 patients (16%). The length of the CAR was 3.5±1.7 cm, and ranged from 2 to12 cm. Twenty-seven patients underwent long CAR (>4 cm).
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| 3. Results |
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Follow-up data at 2 years included: clinical status (angina stage, MI, number of anti-anginal medicines per patient) and angiography. Thallium test was available when angiogram was refused by the patient. ITA and CAR patency was assessed as follows: (1) perfect patency, which means a diameter of the ITA greater than or equal to the diameter of the coronary artery without stenosis or anastomosis defect (acute angulation, folds or irregularities); (2) ITA or CAR occlusion (no opacification of the ITA or of the LAD); (3) thread-like artery (string sign) which means thin ITA with a diameter less than the diameter of the coronary vessel or less than 0.5 mm; (4) stenosis of the anastomosis at the level of the CAR.
Statistical analysis used Student's, Fischer and
2 tests.
3.1. Peri-operative results
Cardiopulmonary bypass weaning was difficult in 12 patients (11%). Operative mortality was 3.5% (three patients). Post-operative MI rate was 6.6% (six MI in non-CAR grafted area): five MI occurred when myocardial protection was crystalloid cardioplegia (mortality:13%) and only one when retrograde cold blood cardioplegia was used (mortality:1.7%) (P<0.05). Operative complications were: low cardiac output in two patients requiring intra-aortic balloon assistance (2.2%); seven respiratory infections (7.7%); three sternal wound infections (3.3%); one phrenic nerve paralysis; four strokes (4.4%) only one of which was definitive; three oesophagitis (3.3%); one acute renal failure (1.1%). No post-operative haemorrhage was noted. Sixty-four patients had no post-operative complications.
3.2. Results at 2 years
Follow-up was 29±10 months. Two patients were lost for follow-up, two patients had left ventricular failure, one patient underwent cardiac transplantation and one patient died from stroke. Three patients had moderate angina. In the follow-up two patients presented an MI of the posterior wall of the left ventricle in the non-grafted area (2.3%). Eighty-one patients (95%) were free from cardiac event. Anti-anginal medicines were as follows: one medicine in 50 patients (58%), two medicines in five patients (6%) and no medicine in 31 patients (36%). The number of anti-anginal medicines per patient was 0.7±0.6. (P<0.01 versus pre-operation).
Angiographic control was performed at 26±10 months in 60 patients (70% of the surviving patients). This control was not possible in seven patients (6%) for medical reasons: aorto-bi-femoral vascular prosthesis (two patients), stroke (two patients), peripheral neurologic degeneration (one patient), and cancer (two patients). Nineteen patients refused this angiographic control; all these patients were free from angina. Fifteen thallium tests were available in these patients. There was one defect in the venous graft area and one defect in the non-grafted area.
One hundred and twenty-five coronary grafts were controlled angiographically (Table 3). ITA patency was superior to venous graft patency: P<0.05. Sixty LAD coronary reconstructions were angiographically controlled. CAR patency was perfect in 56 patients (95%); there were two thread-like artery ITA due to competitive flow with the native LAD (3%); one CAR was occluded (2%). Details of CAR patency are shown in Table 4. Left ventricular ejection fraction was 69±11%.
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| 4. Discussion |
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In 25% of the cases CAR was indicated according to pre-operative angiographic findings. In 38% of the patients the distal bed of the LAD was not angiographically normal (40%<stenosis<70%) and intraoperatively CAR was required because LAD lesions were more important than shown on the pre-operative angiogram. In 20% of the cases, LAD distal bed seemed angiographically normal but significant stenotic plaques or plaque at risk were discovered at surgery. In this study CAR corresponds to 6% of the patients operated on for coronary surgery in the same period. In our institution at present the cardiologists are well aware of the capabilities of CAR, and more patients are proposed for CAR in addition to CABG (20% of the coronary surgical population).
In our series aortic cross-clamping time was long and overall MI rate was 6.6%. Operative mortality in our study is similar to other series of coronary surgery on diffuse lesions (2.510%) [10,11] but slightly higher than the mortality we previously reported in classical coronary surgery on non-diffuse lesions [12]. This increased total operative mortality is due to the complexity of surgery on very severe coronary artery lesions with long aortic cross-clamping time. However, the use of retrograde cold blood cardioplegia improved significantly the occurrence of post-operative MI (1.7% with retrograde cold blood cardioplegia versus 13% with antegrade crystalloid cardioplegia in our series, P<0.05). This improvement allows more ambitious surgery with more safety, which is encouraging for this complex surgery.
When coronary arteries are diffusely and extensively diseased, open endarterectomy covered with venous patch have been reported [57]. Myofibro-intimal proliferation is a major drawback of this technique [8,9,11]. One of the aims of CAR is to decrease the need of long open endarterectomy as much as possible. Non-calcified atheromatous plaques are excluded from the lumen of the new reconstructed vessel. This new reconstructed LAD is composed of 75% ITA and 25% native diseased LAD. Theoretically, one of the advantages of CAR with plaque exclusion is to stop the growth of plaques excluded from the lumen of the LAD. The diameter of the new LAD is greater than the native one. Although progressive disease may develop in the 25% remaining atheromatous wall, this greater diameter and the percentage of ITA wall in contact with the arterial blood should prevent relapse of myocardial ischemia. In our series there was no re-stenosis of CAR at 2 years. The other advantage of plaque exclusion is to diminish the risks of plaque complications. CAR excludes significant plaques that narrow the distal bed but also some atheromatous plaques which are very fragile, with a lipid core and low proportion of fibrosis. This kind of plaque may not reduce significantly the coronary vessel lumen (range 4069%). These plaques are frequently associated with significant lesions in extensively diseased LAD. The risk of rupture of this plaque is great, leading to thrombosis and MI [13]. Our patients were operated on for significant extensive lesions but CAR allows the exclusion of plaques at risk. This does not mean that non-significant lesions are an indication for CAR, CABG or PTCA when there is not a significant proximal lesion. We excluded these plaques at risk in the run of surgery indicated for proximal significant lesions. Perhaps this possibility of exclusion of plaques and particularly plaques at risk is an explanation for the very low rate of MI in areas revascularised with CAR during the 2 years of follow-up in our series.
When endarterectomy was needed in calcified plaques, a short endarterectomy associated with the exclusion of a great part of the endarterectomised wall is performed in order to decrease the risk of post-operative myofibro-intimal proliferation. It has been proved that incomplete endothelial covering of the endarterectomised arterial wall enhances myofibrocyte proliferation and this proliferation leads to endothelial cellular growth inhibition [1416]. It is a true vicious circle. On the contrary, myofibro-intimal proliferation is stopped when endothelial covering is complete [1416], so quick re-endothelialisation reduces intimal proliferation. In our technique 75% of the endarterectomised coronary arterial wall is excluded from the LAD lumen, and as endarterectomised area in contact with blood is reduced the complete endothelial covering should be achieved relatively rapidly, so that the intimal proliferation period is reduced. This may be an explanation for the very low rate of re-stenosis in our series despite the rate of 16% endarterectomy.
The survival rate of patients with diffuse coronary artery disease is 8090% at 1 year and 4080% at 5 years [17,18]. In our series there are no cardiac deaths at 2 years follow-up. The quality of life has been improved in this study: 95% of the patients are free from cardiac events and the number of anti-anginal medicines per patient has been significantly lowered.
The good clinical results of this study have been confirmed by the post-operative coronary angiography at 2 years follow-up.
In the literature, the patency rate at 1 year of the venous graft with endarterectomy is between 56 and 90% [1012].When an ITA is anastomosed to the venous patch, the patency rate increases and ranges from 81 to 98% [6,7]. In our study perfect ITA patency of CAR with or without endarterectomy is 95%. It is difficult to compare our results with the results of other series from the literature because thread-like arteries (string sign) are considered as graft failure in our study, which is not always the case in reported series. In our series ITA patency is similar to the ITA patency we reported in surgery for non-diffuse coronary artery lesions [12]. CAR does not increase the rate of ITA graft failure despite the diffuse and extensive coronary lesions.
| 5. Conclusion |
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| Footnotes |
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| Appendix A Conference discussion |
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Dr Barra: First question, all the anterior walls of the left ventricle were functional in this series. The second question is?
Dr Dion: About your stitch, how do you place your stitch?
Dr Barra: When we perform a limited endarterectomy, we fix the plaque at the edge of the endarterectomy with an 8 or 9-0 suture.
Dr Dion: Do you use a mattress suture?
Dr Barra: No, no, running suture.
Dr Dion: And when your needle cannot go through the calcium, what are you doing?
Dr Barra: The calcium has been removed. We remove only the calcified plaque, and at the edge of the endarterectomy we suture the intima to the endarterectomised wall. But a lot of this endarterectomised wall, maybe more than 75%, is excluded from the suture.
Dr D. Javidi (Tehran, Iran): I was wondering whether these excellent results that you are showing were also due to some sort of anticoagulation, anti-platelet therapy after the operation? I mean, do you use any special methods for that?
Dr Barra: Yes, we have a protocol for anticoagulation, 8 days of heparin and 1 month of percutaneous heparin.
Dr C. Yankah (Berlin, Germany): Doing the endarterectomy means you are creating a new pathology of the arterial wall which might cause accelerated neointimalisation, and my question is, do you have histology with regard to the pathology of this arterial wall with the arteriosclerosis which might probably be secondary to any other problem regarding this coronary stenosis?
And also a second question is, did you also perform endarterectomy of the septal arteries which occasionally might be necessary in order to achieve better circulation in the septal artery, however this manipulation might be complicated by local thrombosis and infarction?
Dr Barra: The aim of this technique is to avoid endarterectomy. We have done endarterectomy only in 16% of the cases, when we found very calcified plaque. It has been proved experimentally that rapid re-endothelialisation of the endarterectomised wall prevents intimal proliferation. When we are obliged to do endarterectomy, we exclude the endarterectomised wall; the major part of the endarterectomised wall is excluded from the lumen of the new reconstructed vessel. So it remains in contact with the blood in only 25% of the surface of the endarterectomised LAD. The rest of the new reconstructed vessel is internal thoracic artery wall. So the re-endothelialisation is rapid and this prevents major intimal hyperplasia. At the level of the septal artery, it is possible to endarterectomise the origin of one septal artery, but as it is a small endarterectomy, this in fact involved only one or two septal arteries, not more.
Dr A. Moritz (Frankfurt, Germany): Do you have any indication that it is really necessary to exclude those plaques? From vascular surgery we know that it is not a problem to simply extend the anastomosis over a plaqued area; it doesn't influence patency. So if you simply make a long anastomosis without the cumbersome sewing to the edges of the plaque, do you have any indication that this is decreasing your patency?
Dr Barra: Yes. Valentine Fuster has proved that plaques of about 40% of stenosis are very dangerous in the long run, because these kind of plaques are fragile and there is a high possibility of thrombosis, rupture or interplaque haemorrhage, and we think it is good to exclude these kinds of plaques from the lumen.
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