Cerebral Malperfusion Research Articles

Management of cerebral malperfusion in surgical repair of acute type A aortic dissection.

Cerebral malperfusion for patients with acute type A aortic dissection (AAAD) remains an unsolved problem. The present study aimed to evaluate our management of cerebral perfusion and identify predictors of perioperative cerebral malperfusion in patients undergoing surgical repair of AAAD. Between January 2004 and December 2015, 137 consecutive patients with AAAD underwent aortic replacement at Tsuchiya General Hospital. The status of the dissected supra-aortic branch vessels (SABVs) was classified as patent or thrombosis by preoperative computed tomographic angiography. Intraoperative cerebral perfusion was monitored by transcutaneous carotid echo and regional oxygen saturation. In cases with neurological symptoms or cerebral malperfusion, quick cerebral perfusion was immediately started using a quick cutdown technique. We assessed clinical outcomes, including mortality and complications, and analysed predictors of early mortality and cerebral malperfusion. The early mortality rate was 8.0%. Postoperative cerebral injury was observed in 4 patients (2.9%). Nineteen patients had perioperative cerebral malperfusion. There were no postoperative cerebral injuries in the patients in whom intraoperative cerebral malperfusion was corrected. Multivariable analysis revealed that preoperative shock (odds ratio [OR] 22.60, P < 0.0001) and extension of dissection to the abdominal aorta (OR 9.31, P = 0.0064) were significant risk factors for early mortality. Preoperative neurological symptoms (OR 12.40, P = 0.0006) and partial or complete thrombosis of the SABV (OR 64.10, P < 0.0001) were identified as independent predictors of perioperative cerebral malperfusion. Perioperative cerebral perfusion should be carefully managed, especially in the patients with preoperative neurological symptoms or partial or complete thrombosis of the SABV.

Cerebral malperfusion in acute aortic dissection.

Cerebral malperfusion in association with acute type A aortic dissection is uncommon but can have a considerable effect on the outcome of treatment. Successful treatment requires the individual and effective removal of each of the factors associated with malperfusion. In addition to the conventional surgical procedures, endovascular treatment has become an option for restoring perfusion. However, artificial perfusion and/or surgical procedures can lead to new malperfusion, which is not necessarily apparent to surgeons and which is difficult to predict. Thus, a number of modalities need to be applied to monitoring the current status of perfusion to enable timely treatment. Since each of the diagnostic modalities has its merits and demerits, one should use them effectively while being mindful of the pitfalls. In addition, a delay in the diagnosis in the pre-hospital stage is an important determinant of the surgical outcomes of aortic dissection. Portable echocardiography, which has been recently developed, may be useful for improving this situation. However, an early diagnosis largely depends on the physician's awareness and basic echocardiography skills. Surgeons should make general physicians aware of this message.

Type A Acute Aortic Dissection Complicated With Cerebral Malperfusion

Type A Acute Aortic Dissection Complicated With Cerebral Malperfusion

Differential outcomes of type A dissection with malperfusion according to affected organ system.

The management of malperfusion in patients with acute Stanford type A aortic dissection is controversial. We sought to determine the rate of resolution of malperfusion following primary repair of the dissection and to identify anatomic sites of malperfusion that may require additional management. We reviewed the hospital records of patients who presented to our institution with acute type A aortic dissection. Patient demographics, operative details and post-operative course were retrospectively extracted from our institutional electronic database. Depending upon the anatomic site, malperfusion was identified by a combination of radiographic and clinical definitions. Data were analyzed using standard univariable and multivariable methods. Between 1997-2013, 101 patients underwent repair of an acute type A dissection. Thirty-day mortality was 14.9% (15/101); there were five intraoperative deaths. There was no difference in 30-day mortality between patients with or without malperfusion (15.4% vs. 14.7%, P=0.93). Twenty-five patients (24.7%), who survived surgery, presented with 31 sites of malperfusion. Anatomic sites included extremities [14], renal [10], cerebral [5] and intestinal [2]. Of these 31 sites, malperfusion resolved in 18 (58.1%) with primary aortic repair. Renal malperfusion resolved radiographically in 80.0%, with no difference in the incidence of insufficiency (44.0% vs. 35.2%; P=0.44) or dialysis (20.0% vs. 15.5%; P=0.61) between malperfusion and non-malperfusion patients. Extremity malperfusion resolved postoperatively in six out of 14 patients. Of the remaining eight, concomitant revascularization was performed in four, one had an amputation and three required postoperative interventions. Advanced patient age (OR: 1.06, 95% CI: 1.01-1.12, P=0.02) was an independent predictor of 30-day mortality, while preoperative malperfusion was not (OR: 0.77, 95% CI: 0.18-3.31, P=0.73). Malperfusion complicating acute type A dissection can be managed in many patients by aortic replacement alone with low overall mortality. Most cases of renal and cerebral malperfusion resolved following aortic surgery. Revascularization was frequently necessary in patients with extremity malperfusion. Patients presenting with intestinal ischemia had very poor outcomes. A patient-specific approach is recommended in such complex patients.

Type A Acute Aortic Dissection Complicated With Cerebral Malperfusion

Type A Acute Aortic Dissection Complicated With Cerebral Malperfusion

Aggressive Aortic Arch and Carotid Replacement Strategy for Type A Aortic Dissection Improves Neurologic Outcomes

International registries for acute type A aortic dissection (TAAD) demonstrate stagnant operative mortality rates in excess of 20% and stroke rates of 9% to 25%, with little global emphasis on stroke reduction or carotid involvement. Cerebral malperfusion with TAAD has been linked to poorer outcome. We hypothesize that concomitant carotid dissection or complex dissection flaps in the arch play a major role in stroke development and that aggressive reconstruction of the arch and carotid arteries can improve neurologic outcomes in TAAD. A standardized protocol focused on expedient care, neurocerebral protection, and common carotid and total arch reconstruction was developed for 264consecutive TAADs. Arch and complete carotid replacement was based on arch dissection anatomy, carotid involvement, or an intraarch tear. Neurocerebral monitoring with continuous electroencephalogram/somatosensory evoked potentials was used in all cases. The postoperative stroke and hospital mortality rates were 3.4% and 9.1%, and stroke rates by extent of arch replacement were 4%, 3%, and 0% for hemiarch, total arch, and total arch with complete carotid replacement, respectively. An intraoperative change in the electroencephalogram/somatosensory evoked potentials was strongly predictive of stroke and had a negative predictive value of 98.2%. An algorithmic approach to TAAD including (1) rapid transport-to-incision-to-cardiopulmonary bypass established centrally, (2) neurocerebral monitoring, (3) liberal use of total arch replacement for clearly defined indications (and hemiarch for all others), and (4) common carotid arterial replacement for concomitant carotid dissections significantly improves outcomes.

Preoperative characteristics and surgical outcomes of acute intramural hematoma involving the ascending aorta: A propensity score–matched analysis

ObjectiveWe aimed to evaluate the preoperative characteristics and surgical outcomes of acute type A intramural hematoma. MethodsBetween January 2000 and June 2011, 460 consecutive patients underwent emergency open surgery for type A acute aortic syndrome at Sakakibara Heart Institute. Among these patients, 121 had intramural hematoma and 339 had typical aortic dissection. We compared the clinical characteristics and surgical outcomes using propensity score matching. ResultsIn all patients, the intramural hematoma group had an older age (69.2 ± 10.4 years vs 63.4 ± 13.5 years; P < .001), included a higher ratio of female patients (56.2% vs 44.0%, P = .020), and more frequently had hypertension (94.2% vs 83.5%, P = .005), hyperlipidemia (25.6% vs 12.7%, P < .001), and cardiac tamponade (33.1% vs 18.3%, P < .001) than patients with aortic dissection. Cerebral malperfusion (0.8% vs 5.3%, P = .033), myocardial malperfusion (0.8% vs 8.2%, P = .002), lower limb malperfusion (1.7% vs 7.9%, P = .015), Marfan syndrome (0% vs 3.5%, P = .042), and aortic valve insufficiency (2.5% vs 15.0%, P < .001) were less frequently observed in the intramural hematoma group than in the aortic dissection group. After propensity score matching, 116 matched pairs were created. In the matched analysis, operative mortality was 0.9% in the intramural hematoma group (1/116) and 3.4% in the aortic dissection group (4/116, P = .179). The intramural hematoma group demonstrated higher actuarial 1- and 5-year survivals than the aortic dissection group (99.1 % vs 93.6% and 97.3% vs 85.9%, respectively, P = .006). In the multivariate analysis, intramural hematoma was shown to be associated with lower midterm mortality (hazard ratio, 0.316; 95% confidence interval, 0.102-0.974; P = .045). ConclusionsPatients with intramural hematoma have different preoperative clinical characteristics compared with patients with aortic dissection. Emergency open surgery for type A intramural hematoma demonstrated low operative mortality and excellent 5-year survival.

The Impact of Pre-Operative Malperfusion on Outcome in Acute Type A Aortic Dissection: Results From the GERAADA Registry

BackgroundMalperfusion adversely affects outcomes in patients with acute type A aortic dissection, but reliable quantitative data are lacking. ObjectivesThe aim of this study was to analyze the impact of various forms of malperfusion on early outcome. MethodsA total of 2,137 consecutive patients enrolled in GERAADA (German Registry for Acute Aortic Dissection Type A) who underwent surgery between 2006 and 2010, of whom 717 (33.6%) had any kind of pre-operative malperfusion, were retrospectively analyzed. ResultsAll-cause 30-day mortality was 16.9% and varied substantially according to the number of organ systems affected by malperfusion (none, 12.6%; 1 system, 21.3%; 2 systems, 30.9%; 3 systems, 43.4%; p < 0.001). Pre-operative cerebral malperfusion, comatose state, peripheral malperfusion, visceral malperfusion, involvement of supra-aortic branches, coronary malperfusion, and renal malperfusion were all independent predictors of developing any post-operative malperfusion syndrome. When survival was considered, age, peripheral malperfusion, involvement of supra-aortic branches, coronary malperfusion, spinal malperfusion, a primary entry in the descending aorta, and pre-operative comatose state were independent predictors, again with increasing significance. ConclusionsMalperfusion remains a severe clinical condition with strong potential for adverse outcomes in patients undergoing surgery for acute type A aortic dissection. The GERAADA registry suggests that the impact of the number of organs involved and the type of malperfusion on outcome differs substantially. Introducing an appropriate classification system, such as “complicated” and uncomplicated” acute type A aortic dissection, might help predict individual risk as well as select a surgical strategy that may quickly resolve malperfusion.

Circumferential Intimal Intussusception in a Case of Stanford Type-A Dissection.

Intimointimal intussusception is a rare but serious complication of aortic dissection (1). Under hemodynamic forces, this cylindrical flap of tissue can intussuscept within the false lumen causing distal obstruction (1). A 58 year-old male patient was referred to us with chest pain that had started 3 days previously. On physical examination he had no neurological problems. Upper extremity pulses were filiform but lower extremity pulses were palpable. Echocardiography (Vivid S5, General Electric, America) showed minimal aortic regurgitation with 65% ejection fraction and minimal pericardial effusion. The patient had no malperfusion findings. A contrast-enhanced computed tomography (CT) (Toshiba Asteion 4, Japan) scan of the patient’s chest and abdomen showed no flaps in the ascending aorta (Figure 1a, Figure 1b), but a dissection flap appeared below the innominate artery (Figure 1a, Figure 1b, Figure 2a and Figure 2b). A nested double lumen was seen in both arcus and descenden aorta (Figure 1a, Figure 1b, Figure 2a and Figure 2b). We made a diagnosis of Stanford type-A acute dissection. FIG. 1. a, b. Preoperative horizontal section of CT Angiography (a). Preoperative horizontal section of CT Angiography (b). FIG. 2. a, b. Preoperative vertical section of CT Angiography. In Figure 2a and Figure 2b, dissection of the membrane started below the innominate artery and innominate artery occlusion can be seen. Figure 2 shows arcus aorta with subclavien artery and descenden aorta. ... Patient and relatives’ informed consent was obtained for surgery and scientific purposes. Emergency surgery was performed. After median sternotomy, hematoma was seen on the aorta (Figure 3). Antegrade cerebral perfusion was used and complete circumferential intussusception into the descending aorta was seen with the open aortic arch technique. The aortic valve had no problems and we replaced the ascending aorta successfully. The patient’s postoperative course was uneventful, and he was discharged in good condition 7 days after the operation. FIG. 3. Hematoma was seen over the aorta and right ventriculum. A 6 mm chimney graft was applied. In all cases with antegrade invagination, circumferential dissection occurred exclusively above the coronary ostia, which coincides with wall stress distributions in the ascending aorta (2). Antegrade intussusception may occlude the arch vessels partly or completely, causing neurologic symptoms. As many as 30% of aortic dissection cases are complicated by malperfusion of a critical organ (3). Alongside other complications, cerebral malperfusion is the most devastating (4). To react appropriately, early detection is mandatory. Interestingly, in our case, the patient had extremity pulses that were usually palpable but there was no sign of malperfusion. An enhanced CT scan is the primary diagnostic procedure for almost all aortic dissection. However, the diagnosis of aortic dissection with intimal intussusception is difficult because of the lack of a flap in the ascending aorta and the unusual form of invaginated flaps. Transesophageal echocardiography and magnetic resonance imaging are also sensitive diagnostic procedures for aortic dissection, but require much more time for making an accurate diagnosis. Appropriate and prompt diagnosis will permit timely and lifesaving surgical interventions for the patient.

Extra-anatomic revascularization for preoperative cerebral malperfusion due to distal carotid artery occlusion in acute type A aortic dissection.

Management of patients with acute aortic dissection type A (AADA) and cerebral malperfusion secondary to occlusion or stenosis of the left common carotid artery (LCCA) or right common carotid artery (RCCA) is a significant challenge. The aim of this study is to present our institutional strategy and postoperative results for this high-risk patient cohort. Between November 2005 and July 2013, 23 of 354 consecutively operated AADA patients [median age: 66.3; interquartile range (IQR): 55.2-69.9] suffered from cerebral malperfusion due to bilateral (n = 1) or unilateral occlusion of the LCCA/RCCA (n = 22). AADA repair comprised hemi- (n = 14) or total (n = 9) arch replacement in combination with aortic valve repair (n = 7) or replacement (n = 11), root replacement (n = 15) and coronary bypass (n = 3). Extra-anatomic aorto-carotid bypass was performed in all patients. Aorto-carotid bypass was performed at the beginning of the procedure to allow for unilateral selective cerebral perfusion (n = 17; 73.9%) or during the procedure if persisting malperfusion was suspected by near-infrared spectroscopy (n = 6; 26.1%). The median follow-up was 15.2 months (IQR: 4.8-34.1) and 100% complete. Median hospital stay and ICU stay were 16.0 (IQR: 12.5-26.0) and 13.7 (IQR: 2.0-16.5) days, respectively. Rethoracotomy for haemorrhage or cardiac tamponade was performed in 6 (26.1%) patients. Other postoperative complications comprised low cardiac output with extracorporeal membrane oxygenation (n = 2; 8.7%), sepsis (n = 4; 17.4%), respiratory insufficiency (n = 10; 43.5%), renal failure with temporary dialysis (n = 7; 30.4%) and visceral malperfusion (n = 2; 8.7%) requiring stent grafting (n = 1) or laparotomy with intestinal resection (n = 1). New stroke with or without permanent sensory or motor deficit was diagnosed in 8 (34.8%) patients. Temporary neurological deficits were seen in 9 (39.1%) individuals. Hospital and 1-year mortality rates were 13.0 and 30.4%, respectively. Overall survival after 36 months of the 23 patients (Group I = Extra-anatomic bypass) versus the remaining 331 AADA patients without distal RCCA/LCCA occlusion (Group II = no extra-anatomic bypass) was 69.6% (n = 16) in Group I vs 72.5% (n = 240) in Group II (P = 0.90). Extra-anatomic bypass for LCCA or RCCA occlusion allows for early selective cerebral perfusion during AADA repair, and may reduce the risk of neurological complications in patients with preoperative cerebral malperfusion.

Stanford A型大動脈解離に対して弓部大動脈全置換術を施行したのち, 合併した両側総頚動脈解離に対して頚動脈ステント留置術を施行したMarfan症候群の1例

Marfan症候群に伴う急性大動脈解離に合併した両側頚動脈解離に対し, ステント留置術が有効であった1例を経験した. Stanford A型大動脈解離に対し弓部大動脈全置換術を施行されたのち脳梗塞を合併, 3D-CTAで両側総頚動脈の解離と診断された. 小切開下に直接頚動脈を穿刺し逆行性にアプローチしステント留置術を施行した. アクセスルート, 人工血管との吻合部のデバイス通過, 真腔の確保が重要となるが, アプローチの工夫でステント留置術が安全に施行でき有用であった.

126 * EXTRA-ANATOMIC REVASCULARISATION FOR DISTAL OCCLUSION OF THE LEFT OR RIGHT COMMON CAROTID ARTERY IN ACUTE TYPE A AORTIC DISSECTION WITH CEREBRAL MALPERFUSION

Objectives: Immediate restoration of cerebral perfusion in patients with acute aortic dissection type A (AADA) is crucial but may be aggravated if distal occlusion of the left (LCCA) or right common carotid artery (RCCA) is present. Methods: Between May 2007 and July 2013, 16 out of 313 conventionally operated AADA patients (median age 60.5; range 23–80) suffered from concomitant severe cerebral malperfusion with distal occlusion of the LCCA (n = 9) or RCCA (n = 8). AADA repair comprised hemi- (n = 9) or total (n = 7) arch replacement in combination with aortic valve repair (n = 6) or replacement (n = 5), root replacement (n = 9) and CABG (n = 1). Extra-anatomic carotid-to-aortic bypass was performed prior to circulatory arrest (n = 13) to allow for unilateral selective cerebral perfusion, or during the procedure if persisting malperfusion was suspected by near-infrared spectroscopy (NIRS) or Doppler (n = 3). Results: Mean ICU stay was 17.6 ± 21.1 days. Re-thoracotomy for haemorrhage (n = 1) or cardiac tamponade (n = 3) was performed in 4 patients. Postoperative complications comprised respiratory insufficiency with prolonged ventilation (n = 7), renal failure with temporary/permanent dialysis (n = 5) and persisting visceral malperfusion (n = 2) requiring stent grafting (n = 1) or intestinal resection (n = 1). Stroke with permanent sensory or motor deficits (PND) was diagnosed in 6 (37.5%) patients. Temporary neurological deficits were seen in 10 (62.5%) individuals, including 4 patients with PND. Hospital (n = 1) and 1-year (n = 3) mortality rates were 6.3% and 25.0%. Conclusion: Extra-anatomic bypass for distal LCCA or RCCA occlusion presents a valuable bail-out technique to restore cerebral perfusion during AADA repair, potentially reducing the increased incidence of neurological complications in patients with cerebral malperfusion.

Operative techniques in patients with type A dissection complicated by cerebral malperfusion.

Early mortality and morbidity after surgical treatment for acute type A aortic dissection (AAAD) has remained high over the last decades despite technical improvements and is still in the range of 10–30% [1–6]. The most important risk factor for this still high early mortality is the preoperative status of the patients [4, 7]. Especially end-organ malperfusion contributes significantly to perioperative death and is present in approximately one-third of all patients with acute aortic dissection [3, 7–9]. Coronary, cerebral, visceral and lower extremity malperfusion syndromes are most often associated with type A dissection. A significant surgical dilemma is the treatment of AAAD patients with preoperative cerebral malperfusion [7]. Intimal tears in the proximal aorta often up to 37% [10] result in the involvement of the supra-aortic branches. Consequently, the impaired flow in the brainsupplying arteries is, besides coronary arteries, the most frequent form of malperfusion [7]. The reported incidence of neurological deficit before surgery in AAAD varies between 14% [7] and 20% [11]. The general surgical strategy in AAAD patients is directed towards (i) cannulation and perfusion of the true lumen, (ii) perfusion of all body regions intraoperatively, (iii) a certain degree of hypothermia, (iv) avoiding aortic cross-clamp during distal repair (open distal anastomosis), (v) avoiding changing arterial cannulation site and uncertain de-airing manoeuvres when resuming total body perfusion after distal aortic repair and (vi) unrestricted global perfusion postoperatively. To develop an individual surgical plan for those patients with supra-aortic malperfusion, preoperative assessment of the extent of dissection and type of malperfusion is of utmost importance. This assessment is usually done with computed tomography angiography (CTA) preoperatively, which translates to only a few minutes of delay on the way to the operating theatre and is just as important for the surgical outcome as surgical experience [6, 12]. Malperfusion can be further validated intraoperatively by using transoesophageal echocardiography (TEE), orbital Doppler and near-infrared spectroscopy (NIRS) [9]. One has to keep in mind, however, that NIRS does not provide information in the basilar artery region [9]. There is an ongoing debate about the best surgical strategy for AAAD in general and even more for the high-risk subgroup of patients with cerebral malperfusion [9]. Despite a consensus that the true lumen of the arterial system should be cannulated [13], the approaches vary considerably. This lack of evidence to enable any recommendations for the choice of surgical methods is related to the fact that randomized studies in AAAD (with wide variations of pathologies) are very unlikely to be performed. Even though a meta-analysis of 14 papers between axillary artery and femoral artery perfusion has shown that axillary arterial perfusion had a significantly lower complication rate [14], routes that are currently advocated for AAAD include subclavian (right and left) cannulation, common carotid artery (right and left) cannulation [15, 16], cannulation of the innominate artery, peripheral cannulation of a non-dissected artery (femoral), ascending aortic cannulation (Fig. 1) [17] or apex of the left ventricle (transapical). There is also no agreement about optimal protection (e.g. temperature) during circulatory arrest; however, even the best method of protection would be useless if the cerebral perfusion and other end-organ perfusion have not been restored during cardiopulmonary bypass (CPB) and aortic repair. In this ‘Great Debate’, different approaches are being described and the rationale for doing so is explained by world-known experts in this field. Special emphasis will be placed on common carotid, subclavian and innominate artery cannulation for antegrade cerebral perfusion (ACP). The rationale of retrograde cerebral perfusion (RCP) during selective cerebral perfusion is also described.

Anatomic and flow dynamic considerations for safe right axillary artery cannulation

Neuroprotection is of paramount interest in cardiac surgery. Right axillary artery cannulation is well established in aortic surgery because it significantly improves survival and outcome, but malperfusion of the right brain after direct cannulation has been reported. Anatomically, 4 vessel segments are potentially amenable for cannulation of the subclavian and axillary arteries. Clinical studies vary widely in dissection sites and cannulation techniques. We investigated critical flow dynamics in the right brain caused by arterial inflow after direct cannulation and specified cannulation positions that provide optimal cerebral perfusion. Distances from the lateral margin of the axillary artery and the subclavian artery to the origin of the vertebral artery were measured in 14 human corpses by a flexible ruler. We calculated the hemodynamics within the vertebral artery, depending on different positions of the cannula tip, in a computer-calculated model. The mean distance from the axillary artery to the vertebral artery was 8.5 cm, and the mean distance from the subclavian artery to the vertebral artery was 6.7 cm. Computed flow calculations demonstrated reversed flow in the vertebral artery when the cannula tip was positioned too close to its orifice. To ensure safe supra-aortic flow, a cannula can be inserted securely up to 6.0 cm into the axillary artery and 4.2 cm into the subclavian artery. Direct cannulation of the right axillary artery can lead to cerebral malperfusion, caused by an obstruction of the vertebral artery's orifice by the arterial cannula or a subclavian steal phenomenon due to flow reversal. The safety of direct axillary artery cannulation can be improved by a well-considered dissecting site and insertion length of the cannula.

Intraoperative thrombectomy for occluded carotid arteries in patients with acute aortic dissection: report of two cases

The present study describes two cases in which intraoperative thrombectomy was performed for occluded or severely stenosed carotid arteries in patients with acute aortic dissection complicated by cerebral malperfusion. A Fogarty catheter was inserted into the true lumen of the occluded branch under hypothermic circulatory arrest, and thrombi within the false lumen were removed. The arch vessels were patent on subsequent computed tomographic imaging, and no neurological complications were found postoperatively. In these cases, the choice of appropriate management strategies took into consideration the brain ischemic time and the presence or absence of cerebral infarction. This technique represents a useful option for the management of this clinical scenario.

Modified Perfusion Strategy and Aortic Arch Debranching in Complicated Acute Aortic Dissection Type A: A Bridge to Definitive Endovascular Therapy

Patients with acute aortic dissection type A (AADA) with aortic arch and supra-aortic vessel involvement have a higher postoperative stroke prevalence and risk of later aortic arch aneurysm development. We report a case of AADA with involvement of supraaortic arteries, complicated by cerebral malperfusion. The ascending aorta was replaced using bilateral antegrade cerebral perfusion through side-grafts attached to both carotid arteries, which were subsequently used as aorto-bi-carotid bypass. One year later, the diameter of aortic arch increased to 5 cm. The endovascular treatment of aortic arch was easily performed since debranching was already almost complete. Immediate bilateral carotid artery inflow and subsequent aorto-bi-carotid bypass is a safe way to prevent cerebral malperfusion in the setting of complicated AADA.A potential benefit of this technique is almost complete debranching that facilitates an endovascular arch replacement.

Editorial Comment: Aortic branch vessel compromise vs clinically overt malperfusion in acute type A aortic dissection

branches. The complexity is a clear limitation of the proposed classification system. The authors state in their article that ‘malperfusion syndromes associated with acute aortic dissection represent only a small proportion of identified aortic branch compromises’. However, this statement questions the clinical implications of the presented classification system. Despite a significant number of high-risk perfusion patterns in a total of 61 aortic branches before the surgery, clinically overt malperfusion syndromes were present in only 16 (26%) patients (9 patients with cerebral malperfusion and 7 with lower limb ischaemia) preoperatively. A total of 92% of these high-risk perfusion patterns were resolved sufficiently by means of the central aortic repair, without any clinical evidence of postoperative end-organ ischaemia. High-risk perfusion patterns persisted in only five (8%) aortic branches (i.e. four cervical branches and one abdominal branch) postoperatively. However, only a single patient suffered a new-onset cerebral malperfusion event postoperatively. Therefore, the clinical relevance of asymptomatic high-risk perfusion patterns in the aortic branches, as defined by means of CT imaging, may not be definitely answered by the present study. Moreover, the persistence of asymptomatic high-risk perfusion patterns after the surgery precludes any clinical implications in this specific cohort of aortic dissection patients. Given the large proportion of aortic dissection patients with highrisk perfusion patterns and no deleterious end-organ malperfusion, the role of percutaneous endovascular interventions remain unclear. However, as fairly recognized by the authors, the study cohort is very small, with only a few cases of clinically overt end-organ malperfusion. Despite the above-mentioned limitations, this study provides a very detailed picture of the involvement of the aortic branches in the acute type A aortic dissection before and after surgery, which is followed by meaningful and sharable comments and conclusions. The authors were able to convincingly demonstrate the key role of central aortic repair in resolving the high-risk perfusion patterns in the aortic branches as well as the clinically overt malperfusion. Another important message derived from this article is that the II-b-2 perfusion patterns are not always static lesions and may be resolved by the central aortic repair, particularly in the cervical aortic branches. Incomplete decompression of the false lumen after central aortic repair may be encountered

右共同偏視，左片麻痺で発症した Stanford A 型急性大動脈解離の1例

右共同偏視，左片麻痺で発症した Stanford A 型急性大動脈解離の1例

Near-infrared spectroscopy for neuromonitoring of unilateral cerebral perfusion

There is neither consensus regarding which methods of neuromonitoring are adequate and reliable for assessing cerebral cross-perfusion during unilateral cerebral perfusion (UCP) nor are any threshold values defined. The aim of the study was to evaluate the usefulness of near-infrared spectroscopy (NIRS) for the neuromonitoring of right-sided UCP, which is increasingly used for cerebral protection as a consequence of the recent rise in supra-aortic cannulation methods. For the purpose of the study, 122 patients (mean age 67 ± 12 years) who underwent open aortic arch surgery between August 2007 and July 2011 using right-sided UCP with a duration time exceeding 20 min were evaluated. The neuromonitoring consisted of NIRS and pressure measurement in both radial arteries in all patients. Forty-four (36%) patients suffered acute aortic dissection (3 having cerebral malperfusion), and 89 (73%) underwent total or subtotal arch replacement. Logistic regression analysis was used to model neurological adverse outcome (permanent and temporary neurological dysfunctions) as a function of cerebral oxygen saturation and other covariates. During UCP (mean duration 38 ± 18 min) performed at a constant blood temperature of 28°C, the mean brain oxygen saturation dropped on the non-direct perfused side from 66 to 61% on average, corresponding to 92% of the baseline. In only 1 patient, an insufficient cross-over perfusion was presumed due to an intense drop of the saturation to 15% and was treated by employment of bilateral perfusion. In all remaining patients, the drop was not below 40% and/or 70% of the baseline. In the adjusted analysis, acute aortic dissection could be found as an independent predictor of an adverse neurological outcome (5 permanent, all in acute dissections, and 9 temporary dysfunctions), while there was no association between the occurrence of adverse neurological outcome and the values of regional cerebral oxygen saturation during UCP. NIRS seems to be a reliable instrument to recognize a relevant disruption of cerebral cross-perfusion during UCP. A drop of brain oxygen saturation to 40% and/or 70% of the baseline can be considered a threshold value for sufficient cerebral cross-perfusion, at least under the flow and temperature management presented.

Perfusion and repair technique in acute aortic dissection with cerebral malperfusion and damage of the innominate artery

Perfusion and repair technique in acute aortic dissection with cerebral malperfusion and damage of the innominate artery