Hypothermic Circulatory Arrest
Historical and Theoretical Considerations
Some of the earliest cardiac procedures were performed using HCA and in the 1960s, isolated case reports described the use of HCA in repair of AA aneurysms.37 Successful experience using HCA for correction of complex congenital heart lesions in infants, as advocated by Barratt-Boyes and associates,38 prompted renewed interest in its use in adults with aneurysms of the AA. The first series of such cases was reported by Griepp and associates,39 which promoted wide acceptance of the efficacy of HCA in protecting the brain in adult AA surgery. With experience, limitations of HCA were described, especially concerning the adequacy of cerebral protection during extended periods of HCA. More recently, strategies using HCA and SCP have been described, combining benefits of both techniques.
Enthusiasm for the use of hypothermia to protect the brain during circulatory arrest began with a series of investigations in adult dogs that documented profound inhibition of cerebral metabolism with lowering of brain temperature.40 Based on hypothermic versus normothermic metabolic rates, Michenfelder and Milde postulated that complete cerebral circulatory arrest for 30 minutes at 18°C would not result in permanent neurologic injury and subsequent experiments indicated that HCA for as long as 60 minutes should be safe.41 However, investigations in puppies42 and piglets43 showed that hypothermia suppresses cerebral metabolism less than that Michenfelder predicted. In puppies, cerebral metabolic rate at 18°C is reduced to only 40% of control levels, and HCA for 60 minutes at 18°C results in detectable early behavioral dysfunction and quantitative EEG changes.42,44 More prolonged HCA at 20°C in young piglets produces unequivocal behavioral sequelae and histologic evidence of cerebral damage.45
Experimental evidence indicates that the period of recovery following HCA is also critical. HCA, even for short intervals, engenders severe cerebral vasoconstriction that may last for hours. During this period, cerebral metabolism is maintained by increased oxygen extraction and thus is particularly vulnerable to hypoxic insult.44,46,47 High intracranial pressure also correlates with delayed neurologic recovery and subsequent cerebral histopathologic abnormalities. Oxygen saturation data also imply that cold reperfusion enhances cerebral blood flow for several hours postoperatively.
There are two basic mechanisms that lead to ischemic cerebral injury during operations on the thoracic aorta. Stroke, the first type of injury, has received the most attention, mainly because of its devastating consequences.48 These ischemic infarcts, detectable by conventional imaging techniques, result from embolic events, and are thought to be independent of the method of brain protection.49 The second type of injury results from focal or global ischemia, because of interrupted or inadequate flow, giving rise to the clinical syndrome temporary neurologic dysfunction (TND),49 which is characterized by varying degrees of obtundation, confusion, agitation, or transient parkinsonism. It is now generally accepted that TND is a direct consequence of inadequate cerebral protection and therefore related to the method of protection used.50,51
The incidence of TND in 200 adults who underwent HCA during thoracic aortic surgery was 19%, correlating significantly with age and duration of HCA. In this study, HCA averaged 47 minutes in patients with TND, and 33 minutes in those without TND. HCA duration did not correlate with mortality or permanent neurologic injury, which was usually focal, and was significantly more frequent in older patients and those with obvious atheromatous debris in the arch or descending aorta.49,50,52
Sensitive neuropsychologic testing showed that HCA exceeding 25 minutes and advanced age predicted poor performance in examinations of memory and fine motor function.53 Patients with impaired neurocognitive function several weeks postoperatively were significantly more likely to have manifested TND immediately postoperatively. Based on these findings, HCA exceeding 25 minutes must be considered a risk factor for long-term, albeit perhaps subtle, deficits in cognitive function. Impairment of memory may be related to injury of the hippocampus, which is particularly sensitive to ischemic injury because of its high metabolic rate.54
Past projections of the theoretical safe duration of HCA, based on rates of oxygen consumption at various brain temperatures, are now considered to have been misleading. The relationship between temperature and the cerebral metabolic rate for oxygen (CMRO<sub>2</sub>) can be expressed as the temperature coefficient Q<sub>10</sub>, which reflects the rate of reduction in the metabolism for a 10°C interval.55 The reduction of CMRO<sub>2</sub> with temperature is substantially more modest than that reported originally. In one experimental study, 39% of baseline CMRO<sub>2</sub> was still present at 18°C, a temperature previously thought to be safe for prolonged periods of clinical HCA; quantitative electroencephalography (EEG) showed significant slow-wave activity at 18°C, whereas EEG silence was present at 13 and 8°C.41
McCullough and associates55 recalculated Q<sub>10</sub> for the adult human brain based on direct measurements of CMRO<sub>2</sub> during HCA. These data predict that the safe period of arrest is about 30 minutes at 15°C and 40 minutes at 10°C, after which cerebral cellular anoxia occurs. These experimental findings correlate with ample clinical pediatric experience indicating that arrest times greater than 40 minutes portend poor neurodevelopmental outcomes.56 These observations support the use of truly profound hypothermia for circulatory arrest to achieve maximum cerebral metabolic suppression, particularly if arrest time will exceed 30 minutes. Intracranial temperatures should be protected from rising during HCA by packing the head in ice.43,44,46,47,57,58
High-dose methylprednisolone, given 2 and 8 hours before CPB, reduces the change in cerebrovascular resistance and improves cerebral blood flow, cerebral arteriovenous oxygen difference, and oxygen metabolism following deep HCA, and may serve as a neuroprotective agent.59 Additionally, in 4-week-old piglets, pretreatment with corticosteroids 4 hours before CPB—compared with steroids in the CPB prime—reduced total body edema and cerebral vascular leakage, with improved immunohistochemical indices of neuroprotection.60 The beneficial effect of corticosteroid pretreatment derives from alterations in de novo protein synthesis at the mRNA level61 and inhibition of adhesion molecule expression in the endothelial cells, which impacts the trafficking of leukocytes into the injured areas.62 Other benefits of methylprednisolone given 8 hours before CPB and HCA are improved pulmonary compliance and alveolar-arterial gradient, and decreased pulmonary vascular resistance.63 Consistently, benefits are more apparent when steroids are given several hours before the institution of CPB.
Because brain temperature primarily determines the safety of HCA, it must be measured accurately. Clinically available sites for measurement include: tympanic membrane, jugular venous bulb, nasopharyngeal, esophageal, bladder, and rectal. In our practice, we routinely monitor two different measurement sites to guide various phases of cooling and rewarming.
Throughout the duration of cardiopulmonary bypass, we follow arterial perfusate temperature, which best reflects the temperature that the brain is exposed to.
During cooling, esophageal or tympanic membrane temperature is used to reflect intracranial temperature and is monitored to guide the initiation of arrest. Based on clinical and laboratory studies,45,46,58 we cool for a minimum of 30 to 40 minutes, to an esophageal temperature of 15 to 18°C, with the perfusate lowered to 10°C. The head is packed in ice to prevent rewarming during HCA. Because continuing oxygen extraction reflects ongoing cerebral metabolic activity, we also monitor jugular venous saturation, using a target O<sub>2</sub> saturation of greater than 95% to indicate adequate cerebral cooling and metabolic suppression.
During rewarming, we primarily monitor the perfusate and bladder temperatures. The perfusate is kept at a gradient of no more than 10°C above the esophageal or tympanic membrane temperature, which reduces the likelihood that oxygen demand will exceed oxygen supply during the interval of inappropriate cerebral vasoconstriction after HCA.44,46,47,64 Avoiding high perfusate temperatures is also essential21 and we never allow it to exceed 37°C. The bladder temperature, which is raised to around 32–34°C, reflects total body or “core” temperature and lags considerably behind changes in the other temperature measurements during cooling and rewarming. Using the bladder temperature to guide rewarming helps to ensure uniform rewarming and prevent dangerous rebound hypothermia after CPB.
Following CPB, achieving hemostasis and maintaining normal hemodynamics are also important, since the vulnerable period of cerebral recovery, during which increased oxygen extraction is relied on to support adequate cerebral metabolism, may extend up to 8 hours postoperatively.
Historical and Theoretical Considerations
DeBakey reported the earliest attempts to repair AA aneurysms,65 in which a complicated technique of normothermic SCP was used, involving several pumps and bilateral cannulation of the subclavian and carotid arteries. Difficulty controlling pressure and flow to uniformly perfuse these separate vascular beds, as well as high operative mortality, led to early abandonment of this technique. However, SCP was revisited in the late 1980s, as mounting evidence indicated that HCA was not safe for the long durations required for repairing complex and extensive aneurysms. It was recognized that combining SCP with hypothermia permitted lower flow rates, while affording better cerebral protection than HCA alone or HCA plus RCP.66,67
Bachet and associates described perfusing the innominate and left carotid arteries with 6 to 12°C blood (flow 250 to 350 cc/min), which he termed “cold cerebroplegia.” Mortality for 54 AA cases was 3%, with only one severe neurologic injury and two transient focal lesions.68 Matsuda and associates69 used SCP at 16 to 20°C in 34 AA cases, with 9% mortality, 3% stroke, and 5% TND. His technique required a two-pump system and cannulation of the brachiocephalic and left carotid arteries; bilateral temporal artery and continuous internal jugular venous saturation were monitored and, importantly, the results demonstrated that hypothermic CPB did not carry a higher risk of coagulopathy.
Kazui first described his approach to SCP in 1986.70 Between 1990 and 1999, 220 patients underwent total arch replacement with SCP and open distal anastomosis, with 12.7% in-hospital mortality and 3.3% permanent neurologic dysfunction. Multivariate analysis showed in-hospital mortality was determined by renal failure, long CPB time, and shock; permanent neurologic deficit was associated with old cerebrovascular accident and long CPB duration.71 Perfusing two arteries with flows of 10 cc/kg/min at 22°C—considered 50% of physiologic levels, based on experimental studies—SCP duration had no significant impact on outcome.72
In a multicenter study, Di Eusanio definitively demonstrated the efficacy of SCP in reducing temporary and permanent neurologic dysfunction. In 588 patients undergoing both partial and full AA replacement, the risks of permanent and temporary neurologic injury were 3.8 and 5.6%, respectively; overall mortality was 8.7%.73
Clot or atheroma in the aorta, which often develops at the origin of the brachiocephalic vessels, predisposes to stroke during AA surgery. Therefore, complete arch resection should reduce the rate of neurologic injury. Accordingly, in 50 recent AA resections,74 Kazui and associates reported 2% mortality; permanent neurologic injury occurred in 4%, and TND in 4% (adverse outcome 6%), with a history of cerebrovascular disease a risk factor for permanent neurologic dysfunction.
The Kazui technique (Fig. 52-2A–H) begins with systemic cooling to 22°C, followed by circulatory arrest and SCP (22°C) delivered via malleable cannulas (Fuji System, Tokyo) inserted into the innominate and left common carotid arteries (Fig. 52-2B). Newly designed malleable cannulas allow superior visibility and simultaneous pressure monitoring (personal communication). With the left subclavian artery clamped, a four-branch graft is anastomosed to the descending aorta (Fig. 52-2C) and lower- body perfusion is begun via a side branch (Fig. 52-2D). Next, the left subclavian is anastomosed and perfused (Fig. 52-2E) followed by construction of the proximal anastomosis (Fig. 52-2F). Finally, full perfusion is restored by anastomosing the innominate and left common carotid arteries to the remaining side branches (Fig. 52-2G,H). Importantly, this technique includes transsection of the brachiocephalic vessels distal to their origins, precluding embolization of debris, and completely excluding the arch, which often contains friable atheromatous lesions.
(A–F) Dr. Kazui's technique for total arch replacement with a four-branch graft.
Extensive aneurysmal disease, involving the ascending, arch, and descending aorta, can be resected in a single stage or may be approached by performing a two-stage procedure, wherein an elephant trunk graft, placed in the descending aorta during arch replacement, is used to simplify a subsequent procedure, performed via a left thoracotomy. In both approaches, SCP affords cerebral protection while permitting unhurried reconstruction of aortic continuity.
Rokkas and Kouchoukos75 described a single-stage reconstruction, the “arch first” technique, performed via bilateral anterior thoracotomies. This technique employs an interval of HCA followed by SCP while aortic continuity is restored. In 46 “arch first” procedures, the hospital mortality was 6.5%, with no permanent neurologic event and 13% TND.76 In 12 cases, HCA was minimized by administering unilateral SCP via the right axillary artery, averaging only 8.8 minutes.77
Unilateral administration of SCP has also been reported. For example, Kucuker and associates78 reported on 181 patients who underwent ascending and hemiarch replacement (90 patients) or total arch replacement (91 patients) with SCP delivered via the right brachial artery; hospital mortality was 6.6%, with 2.2% permanent strokes. The patients were cooled to 26°C and with the innominate, left common carotid, and occasionally the left subclavian artery clamped, arch replacement was performed with flow decreased to 8 to 10 cc/kg/min. The mean SCP duration was 36 ± 27 minutes (range 17 to 80 minutes). Contralateral cerebral flow was monitored by transcranial Doppler of the left middle cerebral artery. In the rare case of inadequate left hemispheric perfusion, an additional catheter was placed into the left common carotid artery. In this study, no mention was made of TND, but in a separate cohort of patients, neurocognitive testing revealed no postoperative deficits.79
Although contralateral perfusion was not problematic in these studies, a certain level of caution is prudent based on anatomic studies. Merkkola and colleagues found insufficient collateral circulation (<0.5 mm) through the circle of Willis in 14% of autopsy specimens.80
Recent clinical series have confirmed the relative safety of SCP. Khaladj and associates81 reported 501 consecutive cases (181 emergent), using moderate systemic hypothermia (25°C) and 14°C SCP administered via the innominate and left carotid arteries, maintaining perfusion pressure between 40 and 60 mm Hg and flows of 400 to 650 cc/min. The overall mortality was 11.6%, with 9.6% strokes and 13.4% TND. Permanent stroke risk increased with renal insufficiency and prolonged operative times, and TND risk increased with increased circulatory arrest time, emergency status, and concomitant coronary artery disease.
A small, randomized study by Kamiya and associates9 addressed a widespread concern that cannulation of the brachiocephalic arteries for SCP may cause cerebral embolization. High-intensity transient signals (HITS), indicative of microembolization—from sources such as gaseous microemboli, atherosclerotic debris, lipid microemboli, and blood-platelet aggregates—were quantified by transcranial Doppler monitoring in patients undergoing circulatory arrest with and without SCP. Only 0.6% of HITS were recorded during SCP, with most occurring during the interval between aortic cross-clamp removal and the termination of CPB. Thus, in this small subset of patients, SCP did not increase the risk of cerebral microembolization.
Using antegrade SCP for cerebral protection, many surgeons are performing arch surgery with moderate hypothermia (20 to 28°C). However, caution needs to be exercised at these temperatures, because end organs are more vulnerable to ischemia. To limit lower-body ischemia, thoracoabdominal perfusion during antegrade SCP has been recommended—via the femoral artery while clamping the proximal descending aorta, or with antegrade perfusion via an endoluminal balloon cannula in the descending aorta or via a sidearm graft branch of an arch graft.
Nonetheless, with precautions to prevent end-organ ischemia, a “global warming” trend has emerged, as surgeons have investigated ways to minimize or eliminate HCA. For example, 305 patients in Osaka, Japan underwent total arch replacement with SCP, combining right axillary and left common carotid perfusion.82 Perfusate temperature was progressively increased from 20 to 28°C. The duration of SCP was 150.1 minutes, with 60.9 minutes of circulatory arrest to the lower body. Operative mortality was 2.3%, with 1.6% permanent neurologic injury. Preoperative cerebral dysfunction was a risk factor for TND, which occurred in 6.6%. The strategy for patients with prior stroke included: higher CPB perfusion pressures (>60 mm Hg), more profound hypothermia (20 to 22°C), and higher SCP flows. In 67 aortic arch repairs at 28°C, the left subclavian artery was also selectively perfused, to increase collateral spinal cord blood flow during lower-body ischemia, and SCP flows were increased to 19 cc/kg/min to maintain arterial pressure at 60 mm Hg. Despite warmer SCP, outcomes remained consistent, with 6% mortality, 6% stroke, 1.5% TND, and no paraplegia. Another series of 120 acute type A aortic dissections had SCP administered via the right subclavian artery at 30°C, with snared brachiocephalic vessels,83 flow at 1320 cc/min, a perfusion pressure of 75 mm Hg, and average cerebral perfusion time 25 ± 12 minutes: 30-day mortality was 5%, stroke rate 4.2%, and TND rate 2.5%.
Although these and similar studies have yielded good clinical outcomes, there is no consensus regarding the optimal temperature for SCP and adopting warmer perfusion techniques during circulatory arrest should be approached cautiously. Experimental studies in a porcine model by Khaladj and associates84 indicate that the optimum temperature for SCP is no higher than 20°C, which resulted in lower intracranial pressures and earlier return of EEG activity than SCP at 30°C. Particularly noteworthy was evidence that although SCP provides good cerebral protection, the margin of safety for the spinal cord is thin. Our laboratory studies suggest that SCP at 10 to 15°C after HCA provides better cerebral protection than higher temperatures and clinically we use SCP at about 15°C.85
The duration of safe lower-body ischemia at 28°C is still under investigation, with evidence that 60 minutes may be the limit. If extended periods of circulatory arrest are anticipated, a method for lower-body protection should be utilized, such as femoral artery perfusion, aortic balloon occlusion with perfusion, antegrade perfusion through a sidearm graft, or deeper hypothermia. For example, 11 patients from a series of 252 ascending and arch repairs with moderately hypothermic SCP (25 to 28°C) had lower-body ischemic times greater than 60 minutes, and 2 (18%) developed paraplegia.86 In a porcine model, Etz et al. demonstrated that during 90 minutes of SCP at 28°C there is little or no spinal cord blood flow in the segment T4 to T13, resulting in a 40% spinal cord injury rate. Moreover, following SCP the lower spinal cord also lacked a normal hyperemic response, suggesting diminished vascular reactivity and localized edema. Histologic studies showed significant ischemic damage in the lower cord, even in animals that recovered clinically, suggesting that unappreciated spinal cord injury may be occurring even at shorter durations of lower-body circulatory arrest.
In the current era, cerebral injury during AA reconstruction is most often related to embolization.112–114 Often, the arch and the origins of the brachiocephalic vessels contain friable, atheromatous debris, and the risk of embolizing this material can be minimized by using a brief period of HCA to transect the brachiocephalic vessels distal to their origins, completely excluding the diseased area. Then, during SCP, the arch repair can proceed in an unhurried fashion. Laboratory studies have shown that a short period of HCA does not compromise the superior cerebral protection provided by SCP.87
Our approach then is as follows. During a brief period of HCA, the individual brachiocephalic arteries are dissected free and sequentially anastomosed to a ready-made trifurcated graft, beginning either with the left subclavian or the innominate artery. The trifurcated graft is clamped, and SCP is instituted via the axillary artery (see Fig. 52-6D,E later in the chapter). Occasionally, when the left subclavian artery is displaced laterally and cephalad, a preoperative left subclavian to left carotid bypass is performed and a bifurcated graft is used to perfuse the left common carotid and innominate arteries (Fig. 52-3). Alternatively, a graft may be anastomosed to the left axillary artery and tunneled via the second ICS into the mediastinum. Hypothermic SCP is administered via the right axillary artery, typically requiring flows of 600 to 1000 cc/min to maintain mean pressures of 40 to 60 mm Hg, and the systemic perfusate temperature is allowed to drift upward. At the end of the arch reconstruction, the proximal end of the trifurcated graft is anastomosed to the ascending aortic graft. Using such strategies as axillary artery cannulation88,89 and grafting of individual brachiocephalic vessels during HCA,74,77,90,91 followed by SCP of the brachiocephalic grafts, lengthy periods of circulatory arrest are no longer necessary.
A preoperative left subclavian artery to left common carotid artery bypass is done when the left subclavian artery is markedly displaced laterally and cephalad.
Retrograde Cerebral Perfusion
The early 1990s saw widespread enthusiasm for RCP92 based on the limitations of HCA, the success of retrograde cardioplegia, and isolated encouraging reports regarding the efficacy of RCP in treating massive air embolism.93 Purported mechanisms whereby RCP accomplishes neuroprotection include: (1) flushing embolic material from the cerebral circulation94 (2) providing cerebral flow sufficient to support cerebral metabolism95 and (3) maintaining cerebral hypothermia.96 There is, however, evidence that RCP may worsen neurologic outcome by inducing cerebral edema.97
Although initial laboratory and clinical reports regarding RCP were encouraging, many of the early studies used historical controls and short durations of RCP—well within the safe limits for HCA alone. Also, studies, in several animal species, demonstrated no flow to the brain during RCP.98–100 In other experimental studies, the most effective conditions for retrograde flow—including clamping inferior vena cava and high venous perfusion pressures—resulted in fluid sequestration, significant cerebral edema, and mild cerebral histopathology, sequelae observable even after relatively short intervals of RCP.94 Studies in our laboratory, measuring cerebral blood flow by collecting AA return and quantifying microspheres trapped in the brain, demonstrated that too little capillary flow occurs during RCP to confer metabolic benefit, even with inferior vena cava occlusion or during deep hypothermia.101 Similarly, directly visualizing cerebral capillaries with intravital microscopy showed that RCP does not provide adequate cerebral capillary blood flow to prevent ischemia but may induce brain edema.97 A cadaver study provided an anatomical explanation for poor retrograde flow, as functionally competent valves, demonstrated in the proximal internal jugular vein, obstruct direct retrograde intracranial venous flow, causing unbalanced and unreliable brain perfusion.102 However, a recent animal study showed that RCP may be helpful under some conditions, as intermittent pressure augmentation during moderate hypothermic RCP efficiently dilated the cerebral vessels, allowing an adequate blood supply without brain injury, and provided neuroprotection equivalent to antegrade SCP.103
The evidence from clinical studies is harder to interpret. Some studies show that RCP duration predicts mortality92,104 but others do not.105,106 Clinical studies comparing HCA+RCP and HCA alone have also yielded mixed results; some showed mortality rates comparable to other cerebral protection methods,107 and others showed reduced mortality rates with RCP.108–110 In three studies that included patients with SCP, HCA+RCP patients had similar mortality rates.111–113
In our own clinical studies,50,114 we have been unable to demonstrate any benefit of RCP. In a recent clinical study,50 we could not show a decrease in the incidence of stroke with RCP, perhaps because of a greater prevalence of patients with clot or atheroma in the RCP group, but arguably because RCP is not effective in preventing stroke. Mortality was higher in the RCP group, and TND was higher with RCP than with SCP. Furthermore, RCP resulted in no reduction of TND compared with HCA alone, reinforcing the notion that RCP probably has no nutritive value for brain tissue. As mentioned, our laboratory data suggest that RCP, especially at high pressures, although successful in removing some emboli, may aggravate cerebral injury.94 Clinically, this effect is not easy to demonstrate but may help account for our repeated observation that neurologic recovery is delayed in patients treated with RCP. Recently, we studied neuropsychologic dysfunction after RCP and found that RCP probably had a negative impact on cognitive outcome.115 Other investigators believe that neurocognitive dysfunction depends on the duration of RCP; if RCP duration is less than 60 minutes, recovery is comparable to that after CABG, whereas prolonged RCP is associated with neurocognitive impairment.116
In general, based on laboratory studies,96 we believe that the major benefit of RCP stems from continued cerebral cooling by venoarterial and venovenous anastomoses, which is especially helpful if systemic cooling is not as thorough or prolonged as it should be. Clinically, we no longer use RCP, feeling that its benefits derive not from providing nutritive support but from aiding in cerebral cooling and helping to prevent rewarming during HCA. However, we believe that it is safer to prevent rewarming by thorough initial cooling and packing the head in ice.
Although we do not routinely use RCP for cerebral protection, many surgeons do administer RCP briefly following HCA in patients who have a high risk of embolization to help flush debris from the cerebral circulation.
RCP, which is always employed in conjunction HCA, by perfusing blood into either one or both venae cavae at a flow rate to maintain pressures of 15 to 20 mm Hg in the superior vena cava. Cardiac distention is avoided by choking both venae cavae. Given the rich network of collaterals between the superior vena cava and inferior vena cava, it probably makes no difference whether inflow is into one, the other, or both. When whole-body retrograde perfusion is carried out, the initial flow rate is usually 800 to 1000 cc/min, but once the venous capacitance vessels have been filled, flows of 100 to 500 cc/min are usually sufficient to maintain superior vena caval pressures at 15 to 20 mm Hg.
Hybrid Aortic Arch Repair
Endograft technology has permitted combining traditional open procedures with endovascular grafting, so-called hybrid procedures. Initially, stent grafts were deployed in the descending aorta for aneurysms involving the distal arch, or in lieu of an open stage II elephant trunk procedure. As experience accumulated, two problems attending aortic arch endografting became evident. First, there is often insufficient undilated aorta distal to the brachiocephalic vessels to seat the proximal portion of a stent graft. Second, the arch is often severely diseased and endograft procedures, which entail negotiating the arch with stiff wires and large-bore catheters, carry a risk of embolic stroke. In fact, experience showed that the more proximally an endograft was deployed, the higher was the risk of embolic stroke.117
The technique of covering the origin of one or more brachiocephalic vessels with an endograft, generally in concert with bypassing or transposing them, addressed both problems by extending the proximal landing zone and minimizing the risk of atheroembolization. These debranching procedures118 involve transposing some or all of the brachiocephalic arteries to the ascending aorta. Initially performed on hypothermic CPB, debranching operations are now commonly done off pump, and permit endografting that partially or even completely excludes the aortic arch. The endograft may be introduced retrograde, via the common femoral artery, or antegrade, generally via a sidearm graft, variously configured to allow proximal access. Antegrade deployment offers the advantage of avoiding diseased and/or stenotic aortoiliac vessels. Debranching procedures presented many anatomical variations for endografting. The classification of landing zones described by Mitchell and associates (Fig. 52-4) allowed meaningful comparisons of different hybrid arch series.119 For comparisons of traditional total aortic arch repairs with current endograft-and-debranching procedures, only patients with zone 0 deployment constitute an equivalent match.
Thoracic endovascular landing zone designation.
The Left Subclavian Artery
If the left subclavian artery is not accessible in the mediastinum, options for covering the subclavian origin with an endograft include: no revascularization; preemptive transposition or bypass of the left subclavian artery using the left common carotid artery; and left axillary artery bypass, wherein an axillary graft is tunneled into the chest and anastomosed centrally, often with subsequent coil embolization of the proximal left subclavian artery to prevent a type II endoleak.
Several branched graft techniques have been described for debranching. Canaud reported six cases with proximal endograft placement in zone 0, wherein debranching was achieved with a single 10-mm graft; end-to-side anastomoses were constructed to the brachiocephalic trunk and left common carotid artery and an end-to-end anastomosis was made to the left subclavian artery.120 Early postoperative complications included transient paraplegia, transient cerebral ischemia, cardiac tamponade, and a retrograde type A aortic dissection, successfully treated; there was no mortality at 30 days. With retrograde deployment in five patients, Chan placed endografts that occluded all the supra-aortic branches, revascularizing the innominate and left common carotid arteries using a bifurcated graft (14 × 7 × 7 mm)121 the left subclavian artery was revascularized only in cases of left vertebral dominance, left arm dialysis dependence, or a patent left internal mammary graft. Technical success was 100%, no neurologic complications, but two patients required reoperation for tamponade. Szeto and associates reported eight hybrid arch repairs performed via median sternotomy, with retrograde endograft deployment.122 Debranching was achieved using a patch giving off three branches, fashioned from a commercially available four-branched arch graft; the patch was anastomosed to the proximal ascending aorta using CPB, moderate hypothermia, and aortic cross-clamping. Two patients suffered TND and required long-term tracheostomy, and one died of myocardial infarction. Finally, Hughes published a series of 28 arch aneurysms, wherein 12 patients underwent total arch debranching using a custom-designed graft (Vascutek USA, Ann Arbor, MI), with limbs to allow transposition of the left common carotid and innominate arteries and antegrade stent-graft deployment.123 The left subclavian origin was covered in all patients, and two underwent left subclavian to common carotid bypass during the same procedure. Outcomes were excellent, with no deaths or strokes and one case of delayed paraparesis.
Although debranching has permitted stent grafting into zone 0, the stability of the proximal landing zone remains a focus of concern with current stent-graft technology. In the Hughes study,123 two type I endoleaks occurred, despite seating the proximal graft directly into a Dacron graft. To minimize this complication, the authors recommend oversizing the endograft by 20% and creating a 4-cm zone of coaptation when stenting into prosthetic grafts. Antona described a novel technique for ensuring stable proximal fixation, involving banding the aorta with a separate vascular graft to create a nonexpandable, cylindrical landing zone.124 The graft is opened longitudinally and wrapped around the aorta to create a 3- to 4-cm zone with an outer diameter of 32 mm. A radiopaque wire is used to mark its proximal and distal extent, facilitating subsequent retrograde endografting. In light of these experiences, most agree that future endograft systems must provide increased flexibility to follow the curvature of the aortic arch, yet achieve strong fixation to prevent endoleaks and secondary migration.