[The staged approach--an overview on a strategy to reduce spinal cord injury in thoracoabdominal aortic aneurysm repair]. / Das zweizeitige Vorgehen zur Reduktion der spinalen Ischämie bei der Ausschaltung thorakoabdomineller Aortenaneurysmen - eine Übersicht.

The spinal cord is particularly susceptible to ischaemic injury following repair of extensive descending thoracic and thoracoabdominal aortic aneurysms (TAAA). For the past decade, the Mount Sinai group in New York has intensively studied the anatomy of the extensive vascular network surrounding the spinal cord, as well as its dynamic morphology in response to decreased blood pressure and flow. Along with clinical data, experimental findings gave rise to the Collateral Network Concept, by which spinal cord injury in open TAAA repair can be significantly reduced. With the more recent widespread use of endovascular repair, strategies to prevent ischaemic spinal cord damage after extensive segmental artery sacrifice/occlusion are still evolving. The hypothesis that dividing extensive aneurysm repair into two steps may mitigate the impact of diminished blood flow to the collateral network has led to a recently conducted series of staged repair experiments. By exploiting the resources of the collateral network, spinal cord injury could be minimised in staged open, as well as in staged hybrid repair and seems equally adoptable for endovascular procedures. The contribution presented herein provides an overview of clinical and experimental studies on the staged approach. Furthermore, it briefly assesses the anatomic rationale for the collateral network concept.

Mathematical model for describing cerebral oxygen desaturation in patients undergoing deep hypothermic circulatory arrest.

BACKGROUND: Surgical treatment for aortic arch disease requiring periods of circulatory arrest is associated with a spectrum of neurological sequelae. Cerebral oximetry can non-invasively monitor patients for cerebral ischaemia even during periods of circulatory arrest. We hypothesized that cerebral desaturation during circulatory arrest could be described by a mathematical relationship that is time-dependent. METHODS: Cerebral desaturation curves obtained from 36 patients undergoing aortic surgery with deep hypothermic circulatory arrest (DHCA) were used to create a non-linear mixed model. The model assumes that the rate of oxygen decline is greatest at the beginning before steadily transitioning to a constant. Leave-one-out cross-validation and jackknife methods were used to evaluate the validity of the predictive model. RESULTS: The average rate of cerebral desaturation during DHCA can be described as: Sct(o(2))[t]=81.4-(11.53+0.37 x t) (1-0.88 x exp (-0.17 x t)). Higher starting Sct(o(2)) values and taller patient height were also associated with a greater decline rate of Sct(o(2)). Additionally, a predictive model was derived after the functional form of a x log (b+c x delta), where delta is the degree of Sct(o(2)) decline after 15 min of DHCA. The model enables the estimation of a maximal acceptable arrest time before reaching an ischaemic threshold. Validation tests showed that, for the majority, the prediction error is no more than +/-3 min. CONCLUSIONS: We were able to create two mathematical models, which can accurately describe the rate of cerebral desaturation during circulatory arrest at 12-15 degrees C as a function of time and predict the length of arrest time until a threshold value is reached.

Changes in regional cerebral blood flow under hypothermic selective cerebral perfusion.

OBJECTIVE: Currently the most frequently used perfusion technique during aortic arch surgery to prevent cerebral damage is hypothermic selective cerebral perfusion (SCP). Changes in cerebral blood flow (CBF) are known to occur during these procedures. We investigated regional changes of CBF under conditions of SCP in a porcine model. METHODS: In this blinded study, twenty-three juvenile pigs (20 - 22 kg) were randomized after cooling to 20 degrees C on CPB. Group I (n = 12) underwent SCP for 90 minutes, while group II (n = 11) underwent total body perfusion. Fluorescent microspheres were injected at seven time-points to calculate total and regional CBF. Hemodynamics, intracranial pressure (ICP), cerebrovascular resistance (CVR) and oxygen consumption were assessed. Tissue samples from the neocortex, cerebellum, hippocampus and brain stem were taken for a microsphere count. RESULTS: CBF decreased significantly (p = 0.0001) during cooling, but remained at significantly higher levels with SCP than with CPB throughout perfusion (p < 0.0001) and recovery (p < 0.0001). These findings were similar among all regions of the brain, certainly at different levels. Neocortex CBF decreased 50%, whereas brain stem and hippocampus CBF decreased by only 25 % during total body perfusion. All four regions showed 10 - 20% less CBF in the post-CPB period. CBF during SCP did not fall by more than 20% in any analysed region. The hippocampus turned out to have the lowest CBF, while the neocortex showed the highest CBF. CONCLUSION: SCP improves CBF in all regions of the brain. Our study characterizes the brain specific hierarchy of blood flow during SCP and total body perfusion. These dynamics are highly relevant for clinical strategies of perfusion.

Involvement of apoptosis in neurological injury after hypothermic circulatory arrest: a new target for therapeutic intervention?

BACKGROUND: This study was undertaken to evaluate the role of apoptosis in neurological injury after hypothermic circulatory arrest (HCA). METHODS: Twenty-one pigs (27 to 31 kg) underwent 90 minutes of HCA at 20 degrees C and were electively sacrificed at 6, 24, 48, and 72 hours, and at 7, 10, and 12 days after HCA, and compared with unoperated controls. In addition, 3 animals that had HCA at 10 degrees C, and 3 treated with cyclosporine A (CsA) in conjunction with HCA at 20 degrees C, were examined 72 hours after HCA. After selective perfusion and cryopreservation, all brains were examined to visualize apoptotic DNA fragmentation and chromatin condensation on the same cryosection of the hippocampus: fluorescent in situ end labeling (ISEL) was combined with staining with a nucleic acid-binding cyanine dye (YOYO). RESULTS: In addition to apoptosis, which was seen at a significantly higher level (p = 0.05) after HCA than in controls, two other characteristic degenerative morphological cell types (not seen in controls) were characterized after HCA. Cell death began 6 hours after HCA and reached its peak at 72 hours, but continued for at least 7 days. Compared with the standard protocol at 20 degrees C, HCA at 10 degrees C and CsA treatment both significantly reduced overall cell death after HCA, but not apoptosis. CONCLUSIONS: The data establish that significant neuronal apoptosis occurs as a consequence of HCA, but at 20 degrees C, other pathways of cell death, probably including necrosis, predominate. Although preliminary results suggest that the neuroprotective effects of lower temperature and of CsA are not a consequence of blockade of apoptotic pathways, inhibition of apoptosis nevertheless seems promising as a strategy to protect the brain from the subtle neurological injury that is associated with prolonged HCA at clinically relevant temperatures.

Retrograde cerebral perfusion as a method of neuroprotection during thoracic aortic surgery.

Retrograde cerebral perfusion is commonly used as an adjunct to hypothermic circulatory arrest to enhance cerebral protection during thoracic aortic surgery. This review summarizes a large number of studies that demonstrate a spectrum of beneficial, neutral, and detrimental effects of retrograde cerebral perfusion in humans and experimental animal models. It remains unclear whether retrograde cerebral perfusion provides effective cerebral perfusion, metabolic support, washout of embolic material, and improved neurological and neuropsychological outcome.

Retrograde cerebral perfusion provides negligible flow through brain capillaries in the pig.

OBJECTIVES: Although retrograde cerebral perfusion is being used clinically during aortic arch surgery, whether retrograde flow perfuses the brain effectively is still uncertain. METHODS: Fourteen pigs were cooled to 20 degrees C with cardiopulmonary bypass and perfused retrogradely via the superior vena cava for 30 minutes: 7 underwent standard retrograde cerebral perfusion and 7 underwent retrograde perfusion with occlusion of the inferior vena cava. Antegrade and retrograde cerebral blood flow were calculated by quantitating fluorescent microspheres trapped in brain tissue after the animals were put to death; microspheres returning to the aortic arch, the inferior vena cava, and the descending aorta were also analyzed during retrograde cerebral perfusion. RESULTS: Antegrade cerebral blood flow was 16 +/- 7.7 mL. min(-1). 100 g(-1) before retrograde cerebral perfusion and 22 +/- 6.3 mL. min(-1). 100 g(-1) before perfusion with caval occlusion (P =.14). During retrograde perfusion, calculations based on the number of microspheres trapped in the brain showed negligible flows (0.02 +/- 0.02 mL. min(-1). 100 g(-1) with retrograde cerebral perfusion and 0.04 +/- 0.02 mL. min(-1). 100 g(-1) with perfusion with caval occlusion; P =.09): only 0.01% and 0.02% of superior vena caval inflow, respectively. Less than 13% of retrograde superior vena caval inflow blood returned to the aortic arch with either technique. During retrograde cerebral perfusion, more than 90% of superior vena caval input was shunted to the inferior vena cava and was then recirculated, as indicated by rapid development of an equilibrium in microspheres between the superior and inferior venae cavae. With retrograde perfusion and inferior vena caval occlusion, less than 12% of inflow returned to the descending aorta and only 0.01% of microspheres. CONCLUSIONS: The paucity of microspheres trapped within the brain indicates that retrograde cerebral perfusion, either alone or combined with inferior vena caval occlusion, does not provide sufficient cerebral capillary perfusion to confer any metabolic benefit. The slightly improved outcome previously reported with retrograde cerebral perfusion during prolonged circulatory arrest in this model may be a consequence of enhanced cooling resulting from perfusion of nonbrain capillaries and from venoarterial and venovenous shunting.

Neurologic outcome after ascending aorta-aortic arch operations: effect of brain protection technique in high-risk patients.

OBJECTIVE: We sought to assess the optimal strategy for avoiding neurologic injury after aortic operations requiring hypothermic circulatory arrest. METHODS: All 717 patients who survived ascending aorta-aortic arch operations through a median sternotomy since 1986 were examined for factors influencing stroke. Temporary neurologic dysfunction was assessed in all patients who survived the operation without stroke since 1993. Multivariate analyses were carried out to determine independent risk factors for neurologic injury. RESULTS: Independent risk factors for stroke were as follows: age greater than 60 years (P <.001; odds ratio, 4.5); emergency operation (P =.02; odds ratio, 2.2); new preoperative neurologic symptoms (P =.05; odds ratio, 2.9); presence of clot or atheroma (P <.001; odds ratio, 4.4); mitral valve replacement or other concomitant procedures (P =.055; odds ratio, = 3.7); and total cerebral protection time, defined as the sum of hypothermic circulatory arrest and any retrograde or antegrade cerebral perfusion (P =.001; odds ratio, 1.02/min). In 453 patients surviving operations without stroke after 1993, independent risk factors for temporary neurologic dysfunction included age (P <.001; odds ratio, 1.06/y), dissection (P =.001; odds ratio, 2.2), need for coronary artery bypass grafting (P =.006; odds ratio, 2.1) or other procedures (P =.023; odds ratio, 3.4), and total cerebral protection time (P <.001; odds ratio, 1.02/min). When all patients with total cerebral protection times between 40 and 80 minutes were examined, the method of cerebral protection did not influence the occurrence of stroke, but antegrade cerebral perfusion resulted in a significant reduction in incidence on temporary neurologic dysfunction (P =.05; odds ratio, 0.3). CONCLUSIONS: The occurrence of stroke is principally determined by patient- and disease-related factors, but use of antegrade cerebral perfusion can significantly reduce the occurrence of temporary neurologic dysfunction.

Favorable outcome after composite valve-graft replacement in patients older than 65 years.

BACKGROUND: Concomitant surgical replacement of the aortic valve and ascending aorta is an ideal treatment for aortic root aneurysms, but there may be hesitation in its use in older patients, despite their known increased risk of rupture. This study was conducted to examine our results in 84 patients older than 65 years undergoing elective aortic root resection with composite valve-graft replacement. METHODS: Eighty-four patients older than 65 years were operated on between June 1987 and August 1998. Median age was 74 years (range, 66 to 89 years), and 57 patients were men. Seventeen patients were undergoing reoperation. Aortic insufficiency was present in 70 patients. Forty-seven patients received a conduit using a bioprosthesis, whereas in 37 a mechanical valved conduit (St. Jude) was used. The ascending aorta alone was replaced in 23 patients; 50 had hemi-arch replacement, and in 11 the entire aortic arch was replaced. RESULTS: Hospital mortality was 8.3% (7 of 84). Sixteen late deaths (19%) were noted during a median follow-up of 3.2 years (range, 0 to 10 years). Only one late death was aorta-related. The incidence of thrombotic or hemorrhagic complications was 2.1/100 patient-years, with equal frequency for both mechanical and bioprosthetic valves. CONCLUSIONS: We conclude that composite valve-graft replacement in elderly patients results in a low operative mortality, yields excellent long-term survival, and averts fatal aneurysm rupture in this high-risk population.

Apoptotic cell death in the hippocampus due to prolonged hypothermic circulatory arrest: comparison of cyclosporine A and cycloheximide on neuron survival.

OBJECTIVE: To determine whether cyclosporine A (CsA) or cycloheximide (CHX) can reduce neuronal apoptosis in the hippocampus in a chronic animal model of hypothermic circulatory arrest (HCA). METHODS: Twenty-eight pigs (28-33 kg) underwent 90 min of HCA at 20 degrees C. In a blinded study, animals were randomized to placebo (n=12), 5 mg/kg CsA (n=8), or 1 mg/kg CHX (n=8). After elective sacrifice 7 days postoperatively, brains were perfusion-fixed and the left hippocampus was examined for evidence of neuronal cell death. An in situ double-labeling method was used on cryosections to unequivocally identify apoptotic nuclei by the simultaneous visualization of DNA fragmentation and apoptotic chromatin condensation. Sections were also examined by immunocytochemistry for upregulation of the pro-apoptotic proteins Bax, activated caspase 3, and glyceraldehyde-3-phosphate dehydrogenase. RESULTS: Apoptotic nuclear degradation was clearly present in the CA1, CA2 and CA3 subregions of the hippocampus after HCA. However, there was also morphological evidence for an accompanying necrotic-like cell death. There was no significant difference between the number of apoptotic nuclei observed in CSA-treated animals, mean value 4.4+/-1.63 SEM or CHX-treated animals, mean value 4.0+/-1.92 SEM, and age-matched control HCA pigs, mean value 4.85+/-1.69 SEM, (P>0.10). CONCLUSIONS: The data clearly demonstrate apoptotic cell death in pigs after HCA by simultaneously demonstrating in situ end labeling (TUNEL reaction) and apoptotic chromatin condensation using a nucleic acid-binding dye. Since CsA shows promising neuroprotective effects in behavioral studies, and since the peak of HCA-induced apoptosis occurs earlier than 7 days, further studies will be required to determine whether CsA can improve neuronal survival in the first few days after HCA. CHX was not effective in reducing apoptosis in this model.

Cyclosporine A as a potential neuroprotective agent: a study of prolonged hypothermic circulatory arrest in a chronic porcine model.

OBJECTIVE: To assess whether Cyclosporine A (CsA) or cycloheximide (CHX) can reduce ischemia-induced neurological damage by blocking apoptotic pathways, we assessed their effects on cerebral recovery in a chronic animal model of hypothermic circulatory arrest (HCA). METHODS: Twenty-eight pigs (28-33 kg) underwent 90 min of HCA at 20 degrees C. In this blinded study, animals were randomized to placebo (n=12), 5 mg/kg CsA (n=8), given intravenously before and subcutaneously for 7 days after HCA, or a single dose of 1 mg/kg CHX (n=8), given after weaning from cardiopulmonary bypass. Hemodynamics, intracranial pressure (ICP) and neurophysiological data (EEG, SSEP) were assessed for 3 h after HCA; early behavioral recovery was scored, and neurological/behavioral evaluation (9=normal) was carried out daily until elective sacrifice on postoperative day (POD) 7. Brains were selectively perfused and evaluated histopathologically for apoptosis. RESULTS: Basic hemodynamic data revealed no differences between CsA or CHX and control groups. ICP was significantly lower throughout rewarming (P=0.009) and reperfusion (P=0.05) in the CsA group. EEG recovery 3 h after HCA was observed in four of eight CsA animals but in only 1 of 12 controls (P=0.11) and one of eight CHX animals; cortical SSEP recovery also seemed faster in CsA animals, but failed to reach significance. Some early recovery scores were significantly better in the CsA group, and daily behavioral scores were consistently and significantly higher in the CsA-treated animals from POD1 through POD4. CONCLUSIONS: The data indicate that treatment with Cyclosporine A but not cycloheximide has a positive effect on cerebral recovery following HCA. Whether CsA results in inhibition of neuronal apoptosis, and/or inhibits release of cytokines and thereby reduces postischemic cerebral edema remains to be elucidated. The neuroprotective effect of CsA, if confirmed in further studies, would make its clinical application conceivable.

Retrograde cerebral perfusion during thoracic aortic surgery and late neuropsychological dysfunction.

OBJECTIVE: Retrograde cerebral perfusion (RCP) is commonly used in thoracic aortic surgery, ostensibly to provide metabolic support, maintain cerebral hypothermia and/or wash out particulate emboli. We tested the hypothesis that RCP would affect neuropsychological outcome in a clinical cohort. METHODS: Ninety-four patients undergoing elective thoracic aortic repairs requiring deep hypothermic circulatory arrest consented to participate in this study. These patients underwent preoperative neuropsychological evaluation and comprise the reference group. Fifty-six of these patients also underwent neuropsychological evaluation several weeks postoperatively, 12 of whom (21%) had RCP. The neuropsychological domains tested were attention, processing speed, memory, executive function, and fine motor function. A global assessment of impairment, negative neuropsychological outcome (NNO), was defined as a postoperative decrease in function in two or more neuropsychological domains for patients with at least three domains tested both pre- and postoperatively (n=48). The relationship of three potential predictors (RCP, cerebral ischemia time and patient age) to negative outcomes was analyzed using Wilcoxon two-sample tests, chi(2) tests, Mantel-Haenszel tests and multiple logistic regression. P<0.05 was considered significant. RESULTS: Memory dysfunction and NNO had strong associations with RCP. This effect remained significant when controlling separately for age and cerebral ischemia time. CONCLUSIONS: The effects of RCP are difficult to distinguish from those of age and prolonged cerebral ischemia time, because complex thoracic aortic repairs are associated with advanced age, prolonged cerebral ischemia and use of RCP. Despite this limitation, these preliminary data indicated that RCP had no beneficial effect (and most likely a negative effect) upon cognitive outcome.

Cerebral effects of cold reperfusion after hypothermic circulatory arrest.

OBJECTIVES: This study was undertaken to explore whether an interval of cold reperfusion can improve cerebral outcome after prolonged hypothermic circulatory arrest. METHODS: Sixteen pigs (27-30 kg) underwent 90 minutes of circulatory arrest at a brain temperature of 20 degrees C. Eight animals were rewarmed immediately after hypothermic circulatory arrest (controls), and 8 were reperfused for 20 minutes at 20 degrees C and then rewarmed (cold reperfusion). Electrophysiologic recordings, fluorescent microsphere determinations of cerebral blood flow, calculations of cerebral oxygen consumption, and direct measurements of intracranial pressure (millimeters of mercury) were obtained at baseline (37 degrees C), before hypothermic circulatory arrest, after discontinuing circulatory arrest at 37 degrees C deep brain temperature, and at 2, 4, and 6 hours thereafter. Histopathologic features and percent brain water were determined after the animals were sacrificed. RESULTS: Cerebral blood flow and oxygen consumption decreased during cooling: cerebral oxygen consumption returned to baseline levels after 4 hours, but cerebral blood flow remained depressed until 6 hours in both groups. Cold reperfusion failed to improve electrophysiologic recovery or to reduce brain weight, but median intracranial pressure increased significantly less after cold reperfusion than in controls (P =.02). Although no significant difference in the incidence of histopathologic abnormalities between groups was found, all 3 animals with an intracranial pressure of more than 15 mm Hg after immediate rewarming had histopathologic lesions, and high intracranial pressure was more prevalent among all animals with subsequent histopathologic lesions (P =.03). CONCLUSIONS: Cold reperfusion significantly inhibited the rise in intracranial pressure seen in control pigs after 90 minutes of circulatory arrest at 20 degrees C, suggesting that cold reperfusion may decrease cerebral edema and thereby improve outcome after prolonged hypothermic circulatory arrest.

Is aortic surgery using hypothermic circulatory arrest in octogenarians justifiable?

OBJECTIVE: This study was undertaken to analyze the risk of mortality and neurological complications after aortic surgery requiring hypothermic circulatory arrest (HCA) in octogenarians. METHODS: All patients of >80 years at the time of aortic surgery requiring HCA since 1988 were examined. Of 51 patients, 23 were male; the median age was 83. Twenty-six (51%) had proximal repair; the arch was replaced in eight (16%), and 17 (33%) had descending aorta repair. Eleven (22%) were emergencies. Multivariate analysis was carried out to determine the risk factors for in-hospital mortality and/or stroke (adverse outcome) using variables with P<0.1 after univariate analysis. RESULTS: The hospital mortality was 16%. Five patients suffered strokes (9.8%): only one survived >6 months, and three died before discharge. The overall adverse outcome was 22%, but elective operation was associated with much better results, with an adverse outcome of only 3.6% after operations via a median sternotomy. Adverse outcome was strikingly higher with more distal resections via a left thoracotomy: 47 vs. 8.8% for ascending aorta/arch resections (P=0.003). Emergency operation via a lateral thoracotomy was associated with a prohibitively high adverse outcome. Twenty-nine patients (73%) had temporary neurological dysfunction (TND). Multivariate analysis revealed emergency operation (P=0.01; odds ratio (OR), 10.6) and operations via a lateral thoracotomy (P=0.008; OR, 11) as independent preoperative predictors of adverse outcome. The overall survival was 66% at 2 years and 39% at 5 years, compared with 85 and 52% among age- and sex-matched controls. CONCLUSIONS: Aortic surgery utilizing HCA in octogenarians can be performed with an acceptable risk of mortality and stroke. From the evidence in this study, it seems that elective aneurysm repair via a median sternotomy can be undertaken for the usual indications, even in octogenarians. However, the enhanced vulnerability of the brain in the elderly is reflected by a high early mortality following stroke, and a high incidence of TND. Emergency operations increase the possibility of adverse outcome dramatically, and patients who require a lateral thoracotomy are at significantly higher risk than those operated via a median sternotomy.

Juxtaposition of the atrial appendages: a clinical series of 22 patients.

Because the outcome of a large clinical series of patients with juxtaposition of the atrial appendages (JAA) has not previously been reported, a retrospective study was performed on patients diagnosed with JAA at a tertiary medical center. Patients with JAA were identified through a computerized database search, and echocardiograms and medical records of patients with JAA were reviewed. Twenty-two patients with JAA were identified, with an overall incidence of 0.28%. All but 2 patients were diagnosed prospectively with JAA by echocardiography. The lesion-specific incidences and associated lesions were similar to those of large autopsy and surgical series. Abnormal conotruncal anatomy was more frequently seen with juxtaposition of the right atrial appendage (JRAA) vs juxtaposition of the left atrial appendage (JLAA) (14/15 vs 4/7), as was atrial outlet obstruction (6/15 vs 2/7). JLAA was more frequently associated with complex atrioventricular anatomy (3/7 vs 1/15). Patients with JAA underwent single ventricle palliation in 11/22 cases with 6 deaths; biventricular repair was performed in 8/22 cases with no deaths. Surgical outcomes for patients with JRAA and JLAA were similar, and survival was predominantly influenced by suitability for biventricular repair.

Results of immediate surgical treatment of all acute type A dissections.

BACKGROUND: Surgery for acute type A aortic dissection is associated with a high mortality rate and incidence of postoperative complications. This study was designed to explore perioperative risk factors for death in patients with acute type A aortic dissection. METHODS AND RESULTS: One hundred twenty-four consecutive patients with acute type A aortic dissection between 1984 and 1998 were reviewed. All underwent operation with resection of the intimal tear and open distal anastomosis: 107 patients had surgery within 24 hours and 17 patients had surgery within 72 hours of symptom onset. Median age was 62 years (23 to 89); 89 were men. Forty-three patients had ascending aortic replacement only, 72 had hemiarch repair, in 2 the entire arch was replaced, and in 7 replacement included the proximal descending aorta. The aortic valve was replaced in 54 patients, resuspended in 52, and untouched in 18. Hospital mortality rate was 15.3% (19 of 124): of these, 3 patients died during surgery, 4 had fatal rupture of the distal aorta before discharge, and 2 died of malperfusion-related complications. Multivariate analysis revealed age >60, hemodynamic compromise, and absence of hypertension as preoperative indicators of hospital death (P:<0.05); the presence of new neurological symptoms was a significant preoperative risk factor in univariate analysis. Ominous intraoperative factors included contained hematoma and a comparatively low esophageal temperature but not cerebral ischemic time (mean 32 minutes). The site of the intimal tear did not influence outcome, but mortality rate was higher with more extensive resection: 43% with resection including the descending aorta died versus 14% with only ascending aorta or hemiarch replacement. Overall 5- and 10-year survival was 71% and 54%, respectively; among discharged patients (median follow-up 41 months) survival was 84% and 64% versus expected US survival of 92% and 79%. CONCLUSIONS: Immediate surgical treatment of all acute type A dissections with resection of the intimal tear and use of hypothermic circulatory arrest for distal anastomosis results in acceptable early mortality rates and excellent long-term survival.

Predictors of adverse outcome and transient neurological dysfunction after ascending aorta/hemiarch replacement.

BACKGROUND: This study was undertaken to determine predictors of adverse outcome and transient neurological dysfunction after replacement of the ascending aorta with an open distal anastomosis. METHODS: All 443 patients (300 male, median age 63) undergoing replacement of the ascending aorta with an open distal anastomosis between 1986 and 1998 were included in the analysis. The ascending aorta alone was replaced in 190 (42.9%); 253 (57.1%) also had proximal arch replacement. Median hypothermic circulatory arrest (HCA) time was 25 minutes (range 12 to 68). Either death or permanent neurological dysfunction were considered adverse outcome (AO). RESULTS: Adverse outcome occurred in 11.5% (51 of 443) of patients overall: in 7.4% of elective (20 of 269) or urgent (4 of 54) operations, but in 17% (19 of 113) of emergencies. Multivariate analysis of the group as a whole revealed that significant (p < 0.05) independent preoperative predictors of AO were age greater than 60 [odds ratio (OR) 2.2], hemodynamic instability (OR 2.7), and dissection (OR 1.9). For the 435 operative survivors, procedural variables predictive of AO were contained rupture (OR 2.8) and HCA time (OR 1.03/min). When only the 271 elective patients were analyzed separately, the need for a concomitant procedure (p = 0.009, OR 3.6) and HCA time (p = 0.002, OR 1.06/min) were the only predictors of AO in multivariate analysis. Transient neurological dysfunction (TND) occurred in 86 of 392 patients (22%). Significant predictors of TND for all patients without AO were age (OR 1.06/y), HCA time (OR 1.04/min), coronary artery disease (OR 2.2), hemodynamic instability (OR 3.4), and acute operation (OR 2.2). Survival of discharged patients was 93% at 1 year and 83% at 5 years. CONCLUSIONS: Early elective operation and shorter HCA time during ascending aorta/hemiarch surgery will reduce both AO and TND.