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Ann Thorac Surg 2005;80:564-569
© 2005 The Society of Thoracic Surgeons

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Original article: Cardiovascular

Concomitant Brachiocephalic and Coronary Artery Disease: Outcome and Decision Analysis

^a Department of Cardiovascular Surgery, Texas Heart Institute at St. Luke’s Episcopal Hospital, Houston, Texas
^b Department of Cardiology, Texas Heart Institute at St. Luke’s Episcopal Hospital, Houston, Texas, USA

Accepted for publication February 17, 2005.

^_* Address reprint requests to Dr Cooley, Department of Cardiovascular Surgery, Texas Heart Institute, P.O. Box 20345, MC 1-194, Houston, TX 77225-0345 (Email: dcooley{at}heart.thi.tmc.edu).

Presented at the Poster Session of the Fifty-first Annual Meeting of the Southern Thoracic Surgical Association, Cancun, Mexico, Nov 2–4, 2004.

	Abstract

Top Abstract Introduction Patients and Methods Results Comment Acknowledgments References

 
BACKGROUND: In patients with coronary artery disease, concomitant brachiocephalic disease may affect outcome and influence decision making regarding operative staging, technique, and choice of conduit.

METHODS: Eighty consecutive patients (mean age, 59.3 years; 60.0% male) with concomitant brachiocephalic and coronary artery disease were identified either before (group A, n = 48) or after (group B, n = 32) coronary artery bypass grafting. Patients who had symptomatic brachiocephalic and coronary artery disease before surgery underwent concomitant brachiocephalic reconstruction and coronary artery bypass grafting using either all-vein coronary conduits (n = 41) or vein-and-internal mammary artery conduits (n = 7). Patients who had coronary-subclavian steal syndrome after coronary artery bypass (group B, n = 32) underwent either surgical (n = 5) or endovascular (n = 27) brachiocephalic reconstruction only.

RESULTS: All patients were asymptomatic after intervention. Operative mortality was 4.2% for group A and 3.1% for group B. The perioperative stroke rate was 2.1% for group A and 0% for group B. Actuarial 10-year freedom from specific events for group A was as follows: death 59.9 ± 12.8%, brachiocephalic restenosis 100%, coronary-subclavian steal syndrome 100%, myocardial infarction 83.5 ± 10.5%, stroke 82.1 ± 9.9%, redo coronary artery bypass grafting 95.8 ± 4.1%, other vascular operation 82.2 ± 8.9%, and adverse cardiac outcome (death, redo coronary artery bypass grafting, or myocardial infarction) 52.9% ± 13.2% (for patients with all-vein conduits) or 100% (for patients with vein-and-internal mammary artery conduits). At midterm follow-up (mean, 2.92 years), both the surgical and the endovascular treatment subgroups of group B had 100% brachiocephalic patency.

CONCLUSIONS: Long-term results in a limited population support continued evaluation of concomitant brachiocephalic reconstruction and coronary artery bypass grafting with use of the internal mammary artery conduit in an attempt to improve late survival in patients with concomitant disease. The excellent midterm brachiocephalic patency after either surgical or endovascular treatment of patients with coronary-subclavian steal syndrome supports continued evaluation of both methods.

	Introduction

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The presence of concomitant brachiocephalic disease (BCD) and coronary artery disease (CAD) may affect outcome and influence decision-making regarding operative staging, approach, technique, and choice of conduit. Several issues related to the management of patients with concomitant BCD and CAD remain unsettled. In patients with CAD in whom BCD is recognized before coronary artery bypass grafting (CABG) is performed, these issues include the safety of concomitant brachiocephalic (BC) reconstruction and CABG, the durability of BC reconstruction, and the influence of approach, technique, and conduit choice on operative and long-term outcome. Furthermore, there is a lack of consensus regarding the optimal management of coronary-subclavian steal syndrome (CSS) in patients in whom concomitant BCD is recognized after CABG. For these reasons, we examined the outcomes of different treatment approaches in both types of patients.

	Patients and Methods

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We reviewed the hospital records and postoperative clinical charts of 80 consecutive patients (mean age, 59.3 years; 60.0% male) with concomitant BCD and CAD who were treated at our institution between January, 1972 and June, 2004. Supplemental information was obtained from each patient’s private cardiologist and family as needed.

Preoperative risk factors were assessed in all patients (Table 1). These included hypertension, diabetes, tobacco use, known CAD, previous myocardial infarction (MI), hyperlipidemia, chronic obstructive pulmonary disorder, and known peripheral vascular disease involving the cerebrovascular (carotid), abdominal aortic, or lower extremity vascular distribution.

View larger version (50K): [in this window] [in a new window]   Fig 1. Brachiocephalic disease symptoms for group A and group B*. (TIAs = transient ischemic attacks; CHF = congestive heart failure; MI = myocardial infarction.)

Myocardial perfusion was assessed and the presence of ischemia was documented in patients with stable angina by exercise electrocardiography, thallium stress testing, or dipyridamole infusion imaging. Symptoms of ischemia in the upper extremities and hemodynamic changes were reproduced in patients with a stable cardiac status using the method described by Grosveld and colleagues [2]. Ultrasonic duplex scanning with hemodynamic measurements before and after exercise differentiated hemodynamically significant and nonsignificant lesions.

All patients underwent full invasive radiologic evaluation, including cineangiography of the coronary vessels and arch aortography with runoff views of the carotid, subclavian, and vertebral circulations. Vessel stenosis was determined angiographically by the following formula: (1 – [diameter at point of greatest stenosis/diameter at point of greatest patency]) x 100%. Significant stenosis in the BC vascular distribution was defined as an 80% or greater narrowing of the vessel lumen.

Operative and endovascular interventions were classified as elective, urgent, or emergent. Urgent interventions were defined as procedures performed in patients whose accelerated symptoms required immediate hospital admission for evaluation and who were judged too unstable to discharge before intervention. Emergent interventions were defined as procedures performed in patients with accelerated symptoms so unstable as to require immediate intervention.

All patients in group A underwent concomitant CABG (mean, 2.7 grafts per patient) and reconstruction of at least 1 BC vessel (mean, 2.0 vessels/patient). All significant and symptomatic BCD was treated in each patient. In patients with multivessel BCD (n = 37), BC vessels were reconstructed using operative bypass and a transthoracic approach. Patients with single-vessel BCD (n = 11) underwent BC reconstruction using operative bypass and an extrathoracic (cervical) approach. The details of our surgical techniques and our rationale for choosing specific approaches based on the complexity of the BCD have been described previously [3–5]. After CSS was diagnosed after recent or previously completed CABG, patients in group B underwent BC reconstruction only. In this group, BC reconstruction of the SCA was performed with either surgical (bypass, n = 5) or endovascular (percutaneous transluminal angioplasty [PTA] and stenting, n = 27) intervention.

All operative procedures were conducted under general anesthesia with high-dose administration of barbiturates during clamp occlusion of the aorta. Intraoperative electroencephalography was used to control the depth of anesthesia and to guide barbiturate administration. The position of the head was monitored closely to prevent compromise of the collateral blood supply to the brain. Intraoperative blood pressure and cardiac rhythm were maintained continuously and monitored closely, especially during periods of arterial clamping.

During concomitant procedures (CABG and BC reconstruction), CABG was performed first, using cardiopulmonary bypass with hypothermic, hyperkalemic cardiac arrest in each case. After coronary grafts were placed and normal sinus rhythm was reinstated, BC reconstruction was initiated. Patients in group A received either all-vein coronary conduits (n = 41) or vein-and-IMA coronary conduits (n = 7) during CABG.

Perioperative MI was defined as the presence of new Q waves, elevation of the myocardial fraction of creatine kinase or troponin in association with persistent ST-segment changes, or new conduction abnormalities. Perioperative stroke was defined as a new neurologic, focal change on physical examination with radiologic (computed tomographic scan) confirmation of infarction.

Long-term follow-up of the 77 survivors totaled 327.1 patient-years (mean, 5.14 years/patient, group A; mean, 2.92 years/patient, group B). To describe the long-term results, actuarial curves were obtained using Kaplan-Meier statistical analysis. Late actuarial freedom from specific events was calculated and statistical analysis was performed using SAS software (Statistical Analysis Systems Institute, Cary, NC).

	Results

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All patients in both groups were asymptomatic after surgery. Mortality was 4.2% (2/48) for group A and 3.1% (1/32) for group B. The postoperative stroke rate was 2.1% (1/48) for group A and 0 (0/32) for group B. Of the 2 deaths in group A, 1 resulted from a respiratory arrest that occurred 13 days after surgery, and the other was caused by stroke. The single death in group B resulted from preexisting multisystem organ failure in a patient in whom the procedure was performed at the request of the primary medical team as a heroic attempt to stem the consequences of CHF. Actuarial 10-year freedom from specific events for group A was as follows: death 59.9 ± 12.8%, BC restenosis 100%, CSS 100%, MI 83.5 ± 10.5%, stroke 82.1 ± 9.9%, redo coronary revascularization (CABG) 95.8 ± 4.1%, other vascular operation 82.2 ± 8.9%, and adverse cardiac outcome (death, redo CABG, or MI) 52.9% ± 13.2% (all-vein conduit subgroup) or 100% (vein-and-IMA conduit subgroup). In group B, BC patency was 100% for both reconstruction methods at midterm follow-up (mean, 2.9 y).

	Comment

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The presence of concomitant BCD in patients with CAD raises several issues regarding treatment decisions and the development of a rational approach to the management of these patients. These issues relate to the safety of concomitant reconstruction, the durability of BC reconstruction, and the influence of approach, technique, and conduit choice on operative and long-term outcome.

As demonstrated in this study, concomitant operative reconstruction of the BC and coronary systems can be accomplished with acceptably low operative morbidity and mortality. This finding is in concordance with those of earlier, smaller studies [6–8]. The safety of transthoracic BC reconstruction is also supported by the results of our recent study [5] of the surgical treatment of multivessel BCD, in which 113 consecutive patients with multivessel disease had transthoracic repair. These patients had an operative mortality of 2.7% (3/113) and a stroke rate of 2.7% (3/113). In contrast, Berguer and colleagues [9] report a mortality rate of 29% in their series of 7 patients who had concomitant BC reconstruction and CABG. However, that study examined a much smaller patient population, and it involved two independent operative teams (cardiothoracic surgery and vascular surgery) that separately reconstructed the coronary and BC systems.

The durability of BC reconstruction is related to the choice of technique and approach. Our earlier studies [5] showed that operative bypass using an extrathoracic (cervical) approach provides excellent long-term patency for single-vessel BC reconstruction but inferior long-term patency (vs transthoracic bypass) for complex (multivessel) BC reconstruction. In patients with multivessel BCD, we found that long-term patency after reconstruction was adversely affected if nonaortic inflow or "long" cervical bypass grafts were used [5]. On the basis of those findings, we used either transthoracic bypass for complex (multivessel) BCD or extrathoracic (cervical) bypass for isolated single-vessel BCD with all patients in group A. The actuarial 10-year patency of 100% for BC reconstruction in this study reflects the effectiveness of this practice.

As an alternative to surgical reconstruction, less invasive endovascular methods are now being applied to and evaluated in these patients. Although long-term patency results after PTA are not yet available, the early and midterm patency rates associated with this technique are similar to those associated with operative (bypass) procedures [6, 10]. Although operative bypass remains the gold standard for the management of this problem and long-term results of PTA are not yet available, the proponents of endovascular intervention list several potential advantages of this technique over surgery. These include shorter hospital stay, less initial cost, less invasiveness, and avoidance of general anesthesia [6, 10]. However, many of these advantages are moot in the setting of concomitant treatment of BCD and CAD if median sternotomy exposure is required. The proven safety and long-term durability of the open technique at this institution, the lack of long-term results after PTA, and the possibility that the first manifestation of CSS will be a catastrophic event (MI or sudden death) has led us to use operative bypass reconstruction preferentially for BCD when treating concomitant disease identified before a planned CABG. We are currently using PTA as treatment for BCD that manifests as CSS after a recent or previous CABG. This practice is part of an ongoing study to evaluate the long-term results of PTA in this setting and requires close follow-up and serial examinations of these patients [2]. These patients have serial duplex examinations before and after exercise as part of this study [2]. In addition to long-term durability, other unknowns regarding the use of endovascular intervention include pattern(s) of failure, need for anticoagulation, and efficacy for treatment of complex (multivessel) BCD.

Although patients with primary and recurrent CSS typically experience angina [11, 12], other modes of presentation have also been reported, including "silent" ischemia, ischemic cardiomyopathy, CHF, and MI [6, 11, 13]. It is not inconceivable that more severe modes of presentation can occur as well, including sudden death. Therefore, it is extremely important to monitor all patients closely regardless of reconstruction method.

The issue of anticoagulation in patients having concomitant CABG and BC reconstruction using PTA is not settled and may affect CABG outcome. Many physicians who perform PTA use antiplatelet medications (aspirin and clopidogrel) at the time of stent placement [14]. If PTA and stent placement are performed at the time of cineangiography and CABG is to be performed subsequently, the question remains whether to give antiplatelet medication during PTA and risk bleeding at the time of CABG, or hold the antiplatelet medication and risk compromising stent patency. Additionally, mechanical compression of subclavian stents, caused by pressure exerted by the chest retractor during CABG, can cause stent deformation and stenosis.

The use of the IMA conduit has a proven long-term survival benefit when used as an isolated conduit for single-vessel CAD or in combination with vein conduits for multivessel CAD [15]. However, the presence of proximal SCA disease in a patient with concomitant CAD has been reported to contraindicate using the IMA [16]. Using all-vein coronary conduits will eliminate the potential occurrence of CSS but will also eliminate the potential survival benefit conferred by using the IMA as a conduit. The absence of the IMA conduit in the majority of patients in group A in this study may have contributed to the poor long-term survival and the occurrence of late adverse outcomes in these patients. These findings, as well as the safety of concomitant BC reconstruction and CABG and the proven long-term durability of BC reconstruction, have led us to explore the use of the IMA conduit after BC reconstruction in patients with concomitant disease. As noted in this study, early results in a limited population are promising.

The incidence of significant BCD in candidates for elective CABG is reported to be 0.5% to 2.0% [17]. Failure to recognize subclavian disease before placement of an ipsilateral IMA conduit, or the progression of BCD after placement of an ipsilateral IMA conduit may produce CSS [12]. Although early studies reported that the incidence of CSS was low [12, 18], recent reports, including this one, list larger numbers of patients and suggest that, in a busy cardiothoracic program, approximately 2 to 4 cases may be found per year [6, 8, 10, 13, 19, 20]. At this institution, the proximal SCA is routinely studied during elective cineangiography of the coronary arteries. If proximal SCA disease is found, arch aortography and 4-vessel cerebral angiography is performed. This has resulted in the discovery of several patients with concomitant BCD and CAD in whom the BC symptoms were either vague or not appreciated. Although this screening practice has allowed us to document increasing numbers of patients with concomitant disease, referral patterns and this institution’s known interest in BC reconstruction have produced the majority of our patients treated for CSS. These cases were referred to us for treatment after having undergone CABG elsewhere.

At this institution, despite aggressive screening for BCD in all patients being evaluated for elective CABG and the active referral pattern from outside hospitals, we have not found the high prevalence of BCD described by Brown [17]. The current frequency of BCD in patients being evaluated or treated for CAD at this institution is 0.2%. This finding is positively biased by the high number of outside referral patients, who make up more than 50% of our patients with concomitant disease, and negatively biased by the fact that only the SCA is initially screened. In general, we believe that the incidence of BCD is closer to 0.1% in most institutions that treat patients with concomitant BCD and CAD.

Significant BCD is most easily recognized when it causes an upper-extremity blood pressure differential [21]. However, this sign is not always present because 32% of patients with BCD have significant multivessel disease and 24% have multisystem disease of such severity that concomitant reconstruction is required [5]. More helpful are ultrasonic duplex scanning before and after exercise, which is especially useful for postoperative follow-up, and direct angiography, which can be performed during evaluation of the coronary arteries [2].

Successful correction of CSS with relief of symptoms has been accomplished with carotid-subclavian bypass [11], PTA [6], and atherectomy of the subclavian artery [22]. Although recurrent subclavian stenosis has been documented after each type of intervention [2, 6], bypass remains the standard to which all other procedures are compared. Multiple studies have associated operative bypass with a 10-year actuarial patency of over 90% and acceptably low morbidity and mortality [3, 5, 20, 23, 24].

The use of endovascular intervention for both recurrent and primary CSS is currently being studied at several institutions. Although acceptable early patency has been documented after PTA for CSS, midterm patency has been reported to be lower than that after operative bypass, but not to a statistically significant degree [10]. The long-term results of ongoing studies, when they become available, will provide further direction regarding the optimal management of primary and recurrent CSS. However, on the basis of current knowledge, either endovascular or surgical intervention is appropriate. Choice of intervention should be based on individual patients’ needs and risk. Close follow-up is mandatory, regardless of choice of intervention.

In summary, patients with concomitant BCD and CAD have poor long-term survival and excellent long-term BC graft patency after concomitant CABG and BC reconstruction. The absence of the IMA conduit may be a contributing factor in the poor long-term survival of this small group of patients with severe vascular disease involving multiple systems. In a limited number of patients, we have used the IMA as a coronary conduit after BC reconstruction in an attempt to improve the long-term survival of these patients; study of this subset of patients is ongoing. Lifestyle and cardiovascular risk modifications are also being introduced to these patients.

Failure to recognize significant subclavian disease before placing an ipsilateral IMA conduit or progression of subclavian disease after CABG may result in CSS. Our midterm follow-up data demonstrate that both operative and endovascular intervention manage this problem adequately. Long-term follow-up of these patients is ongoing as well.

	Acknowledgments

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Stephen N. Palmer, PhD, ELS, provided editorial support for this manuscript. Melissa Mayo, Senior Graphic Design Specialist, created graphs and formatted images, and William M. Andrews, MA, CMI, created artwork. Vei-Vei Lee, MS, performed statistical analyses. Marjorie Jackson provided technical support.

	References

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Thomas J. Takach George J. Reul J. Michael Duncan James J. Livesay Igor D. Gregoric O. Howard Frazier Denton A. Cooley Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Takach, T. J. Articles by Cooley, D. A. Search for Related Content PubMed PubMed Citation Articles by Takach, T. J. Articles by Cooley, D. A.