Myocardial protection: a forgotten modality.

The goals of a cardiac surgical procedure are both technical excellence and complete protection of cardiac function. Cardioplegia is used almost universally to protect the heart and provide a quiet bloodless field for surgical accuracy. Yet, despite the importance of myocardial protection in cardiac surgery, manuscripts or dedicated sessions at major meetings on this subject have become relatively rare, as though contemporary techniques now make them unnecessary. Nevertheless, septal dysfunction and haemodynamic support (inotropes, intra-aortic balloon pump, assist devices) are common in postoperative patients, indicating that myocardial damage following cardiac surgery is still prevalent with current cardioplegic techniques and solutions. This article first describes why cardiac enzymes and septal function are the ideal markers for determining the adequacy of myocardial protection. It also describes the underappreciated consequences of postoperative cardiac enzyme release or septal dysfunction (which currently occurs in 40-80% of patients) from inadequate protection, and how they directly correlate with early and especially late mortality. Finally, it reviews the various myocardial protection techniques available to provide a detailed understanding of the cardioplegic methods that can be utilized to protect the heart. This will allow surgeons to critically assess their current method of protection and, if needed, make necessary changes to provide their patients with optimal protection.

Studies of isolated global brain ischaemia: I. Overview of irreversible brain injury and evolution of a new concept - redefining the time of brain death.

Despite advanced cardiac life support (ACLS), the mortality from sudden death after cardiac arrest is 85-95%, and becomes nearly 100% if ischaemia is prolonged, as occurs following unwitnessed arrest. Moreover, 33-50% of survivors following ACLS after witnessed arrest develop significant neurological dysfunction, and this rises to nearly 100% in the rare survivors of unwitnessed arrest. Although, whole body (cardiac) survival improves to 30% following recent use of emergency cardiopulmonary bypass, sustained neurological dysfunction remains a devastating and unresolved problem. Our studies suggest that both brain and whole body damage reflect an ischaemic/reperfusion injury that follows the present reperfusion methods that use normal blood, which we term 'uncontrolled reperfusion'. In contrast, we have previously introduced the term 'controlled reperfusion', which denotes controlling both the conditions (pressure, flow and temperature) as well as the composition (solution) of the reperfusate. Following prolonged ischaemia of the heart, lung and lower extremity, controlled reperfusion resulted in tissue recovery after ischaemic intervals previously thought to produce irreversible cellular injury. These observations underlie the current hypothesis that controlled reperfusion will become an effective treatment of the otherwise lethal injury of prolonged brain ischaemia, such as with unwitnessed arrest, and we tested this after 30 min of normothermic global brain ischaemia. This review, and the subsequent three studies will describe the evolution of the concept that controlled reperfusion will restore neurological function to the brain following prolonged (30 min) ischaemia. To provide a familiarity and rationale for these studies, this overview reviews the background and current treatment of sudden death, the concepts of controlled reperfusion, recent studies in the brain during whole body ischaemia, and then summarizes the three papers in this series on a new brain ischaemia model that endorses our hypothesis that controlled reperfusion allows complete neurological recovery following 30 min of normothermic global brain ischaemia. These findings may introduce innovative management approaches for sudden death, and perhaps stroke, because the brain is completely salvageable following ischaemic times thought previously to produce infarction.

Studies of isolated global brain ischaemia: II. Controlled reperfusion provides complete neurologic recovery following 30 min of warm ischaemia - the importance of perfusion pressure.

OBJECTIVES: Neurologic injury after sudden death is likely due to a reperfusion injury following prolonged brain ischaemia, and remains problematic, especially if the cardiac arrest is unwitnessed. This study applies a newly developed isolated model of global brain ischaemia (simulating unwitnessed sudden death) for 30 min to determine if controlled reperfusion permits neurologic recovery. METHODS: Among the 17 pigs undergoing 30 min of normothermic global brain ischaemia, 6 received uncontrolled reperfusion with regular blood (n = 6), and 11 were reperfused for 20 min with a warm controlled blood reperfusate containing hypocalcaemia, hyper-magnesemia, alkalosis, hyperosmolarty and other constituents that were passed through a white blood cell filter and delivered at flow rates of 350 cc/min (n = 3), 550 cc/min (n = 2) or 750 cc/min (n = 6). Neurologic deficit score (NDS) evaluated brain function (score 0 = normal, 500 = brain death) 24 h post-reperfusion and 2,3,5-triphenyltetrazolium chloride (TTC) staining determined brain infarction. RESULTS: Regular blood (uncontrolled) reperfusion caused negligible brain O(2) uptake by IN Vivo Optical Spectroscopy (INVOS) (<10-15% O(2) extraction), oxidant damage demonstrated by raised conjugated diene (CD) levels (1.78 ± 0.13 A233 mn), multiple seizures, 1 early death from brain herniation, high NDS (249 ± 39) in survivors, brain oedema (84.4 ± 0.6%) and extensive cerebral infarctions. Conversely, controlled reperfusion restored surface brain oxygen saturation by INVOS to normal (55-70%), but the extent of neurologic recovery was determined by the brain reperfusion pressure. Low pressure reperfusion (independent of flow) produced the same adverse functional, metabolic and anatomic changes that followed uncontrolled reperfusion in seven pigs (three at 350 cc/min, two at 550 and two at 750 cc/min). Conversely, higher reperfusion pressure in four pigs (all at 750 cc/min) resulted in NDS of 0-70* indicating complete (n = 2) or near complete (n = 2) neurological recovery, negligible CDs production (1.29 ± 0.06 A233mn)*, minimal brain oedema (80.6 ± 0.2%)* and no infarction by TTC stain. CONCLUSIONS: Brain injury can be avoided after 30 min of normothermic cerebral ischaemia if controlled reperfusion pressure is >50 mmHg, but the lower pressure (<50 mmHg) controlled reperfusion that is useful in other organs cannot be transferred to the brain. Moreover, INVOS is a poor guide to the adequacy of cerebral perfusion and the capacity of controlled brain reperfusion to restore neurological recovery. *P < 0.001 versus uncontrolled or low pressure controlled reperfusion.

Studies of isolated global brain ischaemia: III. Influence of pulsatile flow during cerebral perfusion and its link to consistent full neurological recovery with controlled reperfusion following 30 min of global brain ischaemia.

OBJECTIVE: Brain damage is universal in the rare survivor of unwitnessed cardiac arrest. Non-pulsatile-controlled cerebral reperfusion offsets this damage, but may simultaneously cause brain oedema when delivered at the required the high mean perfusion pressure. This study analyses pulsatile perfusion first in control pigs and then using controlled reperfusion after prolonged normothermic brain ischaemia (simulating unwitnessed arrest) to determine if it might provide a better method of delivery for brain reperfusion. METHODS: Initial baseline studies during isolated brain perfusion in 12 pigs (six non-pulsatile and six pulsatile) examined high (750 cc/min) then low (450 cc/min) fixed flow before and after transient (30 s) ischaemia, while measuring brain vascular resistance and oxygen metabolism. Twelve subsequent pigs underwent 30 min of normothermic global brain ischaemia followed by either uncontrolled reperfusion with regular blood (n = 6) or pulsatile-controlled reperfusion (n = 6) before unclamping brain inflow vessels. Functional neurological deficit score (NDS; score: 0, normal; 500, brain death) was evaluated 24 h post-reperfusion. RESULTS: High baseline flow rates with pulsatile and non-pulsatile perfusion before and after transient ischaemia maintained normal arterial pressures (90-100 mmHg), surface oxygen levels IN Vivo Optical Spectroscopy (INVOS) and oxygen uptake. In contrast, oxygen uptake fell after 30 s ischaemia at 450 cc/min non-pulsatile flow, but improved following pulsatile perfusion, despite its delivery at lower mean cerebral pressure. Uncontrolled (normal blood) reperfusion after 30 min of prolonged ischaemia, caused negligible INVOS O(2) uptake (<10-15%), raised conjugated dienes (CD; 1.75 ± 0.15 A(233 mn)), one early death, multiple seizures, high NDS (243 ± 16) and extensive cerebral infarcts (2,3,5-triphenyl tetrazolium chloride stain) and oedema (84.1 ± 0.6%). Conversely, pulsatile-controlled reperfusion pigs exhibited normal O(2) uptake, low CD levels (1.31 ± 0.07 A(233 mn); P < 0.01 versus uncontrolled reperfusion), no seizures and a low NDS (32 ± 14; P < 0.001 versus uncontrolled reperfusion); three showed complete recovery (NDS = 0) and all could sit and eat. Post-mortem brain oedema was minimal (81.1 ± 0.5; P < 0.001 versus uncontrolled reperfusion) and no infarctions occurred. CONCLUSIONS: Pulsatile perfusion lowers cerebral vascular resistance and improves global O(2) uptake to potentially offset post-ischaemic oedema following high-pressure reperfusion. The irreversible functional and anatomic damage that followed uncontrolled reperfusion after a 30-min warm global brain ischaemia interval was reversed by pulsatile-controlled reperfusion, as its delivery resulted in consistent near complete neurological recovery and absent brain infarction.

Studies of isolated global brain ischaemia: I. A new large animal model of global brain ischaemia and its baseline perfusion studies.

OBJECTIVES: Neurological injury after global brain ischaemia (i.e. sudden death) remains problematic, despite improving cardiac survival. Unfortunately, sudden death models introduce unwanted variables for studying the brain because of multiple organ injury. To circumvent this, a new minimally invasive large animal model of isolated global brain ischaemia, together with baseline perfusion studies is described. METHODS: The model employs neck and small (3-4 inches) supra-sternal incisions to block inflow from carotid and vertebral arteries for 30 min of normothermic ischaemia. Neurological changes after 24 h in six pigs was compared with six Sham pigs assessing neurological deficit score (NDS, 0 = normal, 500 = brain death), brain oedema and cerebral infarction by 2,3,5-triphenyltetrazolium chloride (TTC) stain. Six other pigs had baseline perfusion characteristics in this new model evaluated at carotid flows of 750, 550 and 450 cc/min, with cerebral perfusion pressure, cerebral oximeter saturation [IN Vivo Optical Spectroscopy (INVOS)] and transcranial O(2) uptake measurements. RESULTS: The model never altered cardiac or pulmonary function, and six Sham pigs had normal (NDS = 0) neurological recovery without brain injury. Conversely, 24 h analysis showed that 30 min of global normothermic brain ischaemia caused multiple post-reperfusion seizures (P < 0.001 versus Sham), raised NDS (231 ± 16; P < 0.001 versus Sham) in four of six survivors and caused marked post-brain oedema (P < 0.001 versus Sham) and extensive cerebral infarctions (TTC stain; P < 0.001 versus Sham). Baseline perfusion showed 750 cc/min flow rate produced normal INVOS levels and O(2) consumption at mean 90-100 mmHg carotid pressure. Carotid pressure and INVOS fell at mid- and low-flow rates. Although INVOS did not change, 450 cc/min flow lowered global O(2) consumption, which further decreased after transient ischaemia (30 s) and 5 min of reperfusion. CONCLUSIONS: This new isolated global brain model consistently caused anatomic, biochemical and functional neurological damage in pigs after 30 min of ischaemia. Flows of 750 cc/min maintained normal mean systemic arterial (90-100 mmHg) pressure, INVOS levels and O(2) consumption. Cerebral pressure and INVOS fell in mid- and low-flow studies. A disparity existed between INVOS oxygen saturation and global O(2) consumption at lower flow rates of 450 cc/min following transient ischaemia, indicating that surface oxygen saturation measurement does not reflect global brain O(2) consumption.

Resuscitation after prolonged cardiac arrest: effects of cardiopulmonary bypass and sodium-hydrogen exchange inhibition on myocardial and neurological recovery.

OBJECTIVE: To determine if cardiopulmonary bypass (CPB), together with inhibition of the sodium-hydrogen exchanger (NHE), limits myocardial and neurological injury and improves recovery after prolonged (unwitnessed) cardiac arrest (CA), as NHE inhibition improved recovery after deep hypothermic circulatory arrest. METHODS: Twenty-seven pigs (31-39 kg) underwent 15 min of prolonged (no-flow) CA followed by 10 min of cardiopulmonary resuscitation-advanced life support (CPR-ALS). Subjects with restoration of spontaneous circulation (ROSC) during CPR-ALS received either no drug (n=6) or an inhibitor of the NHE (HOE-642; n=5). In the 16 unsuccessfully resuscitated animals, peripheral normothermic CPB was instituted, and either no drug (n=9) or similar HOE-642 (n=7) therapy started. Hemodynamic data, a species-specific neurological deficit score (0=normal to 500=brain death), and mortality were recorded at 24h, and biochemical variables of organ injury measured. RESULTS: CPR-ALS restored ROSC in 41% (11/27) of animals, but was unsuccessful in 59% (16/27) that required CPB. Without CPB, HOE-642 increased cardiac index and decreased vascular resistance; with CPB, HOE-642 caused higher pump flows (3.4±0.6 l min(-1)m(-2) vs 2.5±0.7 l min(-1)m(-2); p<0.001) and higher post-arrest cardiac index; but animals required more vasopressors (p=0.019) from drug-induced vasodilation. No differences between biochemical markers of oxidative and organ injury and overall 24-h mortality (20%) were found between groups. Neurological score was improved at 24h compared with 4h only after HOE-642 treatment with (150±34 vs 220±43; p=0.003) or without CPB (162±39 vs 238±48; p≤0.001), but failed to reach statistical difference with respect to the untreated group. CONCLUSIONS: CPB is an effective resuscitative tool to treat prolonged CA but there is limited improvement of neurological function. NHE inhibition augments cardiac and neurological function, but its effect was less pronounced than in other studies.

Resuscitation after prolonged cardiac arrest: role of cardiopulmonary bypass and systemic hyperkalemia.

BACKGROUND: The purpose of this study was to determine (1) the role of emergency cardiopulmonary bypass (CPB) after prolonged cardiac arrest and failed cardiopulmonary resuscitation, and (2) the use of systemic hyperkalemia during CPB to convert intractable ventricular fibrillation (VF). METHODS: Thirty-one pigs (34 +/- 2 kg) underwent 15 minutes of cardiac arrest after induced VF, followed by 10 minutes of cardiopulmonary resuscitation-advanced life support. Peripheral CPB was used if cardiopulmonary resuscitation failed to restore stable circulation. Damage was assessed by evaluating hemodynamics, biochemical variables (creatine kinase-MB, neuron-specific enolase), neurologic deficit score, and brain magnetic resonance imaging. RESULTS: Cardiopulmonary resuscitation alone was successful in only 19% (6 of 31 pigs). Cardiopulmonary bypass was initiated in 81% of animals (25 of 31 pigs) either for hypotension (5 of 25 pigs) or intractable VF (20 of 25 pigs). Defibrillation was successful in 7 of 20 animals during the first 10 minutes after initiating CPB. Ventricular fibrillation persisted more than 10 minutes in 13 of 20 pigs, and animals were treated either with repeated defibrillation (6 of 13 pigs) or with a potassium bolus (7 of 13 pigs) to induce transient cardiac arrest. Overall survival at 24 hours was 84% with cardiopulmonary resuscitation (100% of pigs with hypotension; 71% in CPB-VF < 10 minutes). Despite CPB, fatal myocardial failure occurred after VF duration of more than 10 minutes in all pigs treated with electrical defibrillation, whereas hyperkalemia allowed 100% cardioversion and 86% survival. Biochemical variables remained elevated in all groups. Similarly, severe brain injury was present in all animals as confirmed by neurologic deficit score (197 +/- 10) and magnetic resonance imaging. CONCLUSIONS: Emergency CPB after prolonged cardiac arrest improves survival and allows systemic hyperkalemia to convert intractable VF, but fails to reduce neurologic damage.

WITHDRAWN: Influences of Perfusion Pressure and Pulsatile Flow on Cerebral Flow Reserve and Oxygenation in the Isolated Perfused Swine Brain under Normothermia.

This article has been removed at the request of the Editor-in-Chief. Please see Elsevier Policy on Article Withdrawal: (http://www.elsevier.com/locate/withdrawalpolicy).

Sudden cardiac death: directing the scope of resuscitation towards the heart and brain.

BACKGROUND: The fundamental goal of cardiopulmonary resuscitation (CPR) is recovery of the heart and the brain. This is best achieved by (1) immediate CPR for coronary and cerebral perfusion, (2) correction of the cause of cardiac arrest, and (3) controlled cardioplegic cardiac reperfusion. Failure of such an integrated therapy may cause permanent brain damage despite cardiac resuscitation. METHODS: This strategy was applied at four centers to 34 sudden cardiac death patients (a) after acute myocardial infarction (n = 20), (b) "intraoperatively" following successful discontinuation of cardiopulmonary bypass (n = 4), and (c) "postoperatively" in the surgical ICU (n = 10). In each witnessed arrest the patient failed to respond to conventional CPR with ACLS interventions, including defibrillation. The cardiac arrest interval was 72 +/- 43 min (20-150 min). Compression and drugs maintained a BP > 60 mmHg to avoid cerebral hypoperfusion. Operating room (OR) transfer was delayed until the blood pressure was monitored. In four patients femoral bypass maintained perfusion while an angiographic diagnosis was made. RESULTS: Management principles included no repeat defibrillation attempts after 10 min of unsuccessful CPR, catheter-monitored peak BP > 60 mmHg during diagnosis and transit to the operating room, left ventricular venting during cardiopulmonary bypass and 20 min global and graft substrate enriched blood cardioplegic reperfusion. Survival was 79.4% with two neurological complications (5.8%). CONCLUSIONS: Recovery without adverse neurological outcomes is possible in a large number of cardiac arrest victims following prolonged manual CPR. Therapy is directed toward maintaining a monitored peak BP above 60 mmHg, determining the nature of the cardiac cause, and correcting it with controlled reperfusion to preserve function.

Cerebral monitoring with transcranial Doppler ultrasonography improves neurologic outcome during repairs of acute type A aortic dissection.

OBJECTIVE: Neurologic complications after repair of acute type A aortic dissection remain significant. The use of power M-mode transcranial Doppler monitoring to verify cerebral blood flow during these repairs might decrease cerebral ischemia by correcting malperfusion. The purpose of this study was to analyze the use of power M-mode transcranial Doppler monitoring during repairs of acute type A dissection with regard to neurologic outcome. METHODS: We performed a prospective study of patients undergoing repairs of acute type A aortic dissection. Repairs included profound hypothermic circulatory arrest and retrograde cerebral perfusion. Patients in whom transcranial Doppler monitoring was used to monitor cerebral blood flow and modify operative technique during repair (study group) were compared with those without monitoring and modification (control group). RESULTS: Between September 2001 and October 2003, we repaired 56 cases of acute type A dissection. Power M-mode transcranial Doppler monitoring was used in 50% (28/56) of cases. Power M-mode transcranial Doppler monitoring altered operative cannulation and guided retrograde cerebral perfusion flow in 28.5% (8/28) and 78.6% (22/28) of cases, respectively. Two patients presented with preoperative stroke, one in each group. One operative death occurred in each group. In-hospital mortality and the occurrence of new stroke were not significantly different between the 2 groups. Temporary neurologic dysfunction occurred less often in the study group (14.8% [4/27] vs 51.8% [14/27], P = .008). CONCLUSIONS: Identification of cerebral malperfusion requires cerebral monitoring. By ensuring cerebral blood flow by using power M-mode transcranial Doppler monitoring and correcting cerebral malperfusion by modifying operative technique, neurologic outcome was improved during repairs of acute type A aortic dissection.

Staged repair of extensive aortic aneurysms: long-term experience with the elephant trunk technique.

OBJECTIVE: This paper reports our experience of a large series of elephant trunk patients accumulated over 12 years. SUMMARY BACKGROUND DATA: Extensive aneurysms of the ascending/arch and descending thoracic or thoracoabdominal aorta are significant surgical problems that have potential for great morbidity. We adopted a staged approach known as the elephant trunk procedure in 1991, and we have used it with some modifications since that time. METHODS: Between February 1991 and December 2003, we performed 1660 operations for ascending/arch or descending thoracic/thoracoabdominal aortic aneurysms. Of these, 321 operations were performed in 218 patients for extensive aneurysms with the elephant trunk technique. We performed 218 ascending/arch repairs and 103 descending thoracic or thoracoabdominal aortic replacements. RESULTS: In 218 ascending/arch repairs, strokes occurred in 3 of 218 (2.7%) patients, with 1 of 187 (0.5%) in the retrograde cerebral perfusion group and 2 of 31 (6.5%) in the no-retrograde cerebral perfusion group (odds ratio 0.08, P < 0.009). Thirty-day mortality for this group was 19 of 218 (8.7%). Among 199 recovering patients after stage 1 repair, 4 of 199 (2%) died during the 30-day to 6-week interval between stages. After stage 2 repair, 0 of 103 patients experienced immediate neurologic deficit, and 10 of 103 (9.7%) died within 30 days of surgery. Actuarial survival after completed stage 2 was 71% at 5 years. CONCLUSION: Despite extreme underlying disease, long-term survival is excellent in patients with extensive aneurysms when both stages of repair are completed. To prevent rupture, the second stage should be completed as soon as the patient's condition permits, preferably within 6 weeks.

Pediatric myocardial protection: a cardioplegic strategy is the "solution".

This article describes the experimental infrastructure and subsequent successful clinical application of a comprehensive cardioplegic strategy that limits intraoperative injury and improves postoperative outcomes in pediatric patients. The infant heart is at high risk of damage from poor protection as a result of preoperative hypertrophy, cyanosis, and ischemia. These factors may also make the immature (pediatric) heart more sensitive to cardioplegic arrest compared with the mature (adult) heart. The preoperative factors of cyanosis and pressure volume overload are discussed, followed by the infrastructure of the strategies of warm induction and reperfusion with substrate enhancements, multidose cardioplegia, and a "modified" integrated approach to allow ischemia only when visualization is needed in pediatric surgeries. The importance of using a blood cardioplegia solution, with reduced calcium, increased magnesium, and low perfusion pressure are also shown. A practical clinical framework based on these experimentally proven principles is then presented to allow the surgeon to apply these strategies clinically. The results of using these principles are depicted in a series of 567 patients, including 93 patients with hypoplastic left heart syndrome. Applications of these concepts should improve the safety of protection of the infant heart and reduce postoperative morbidity and mortality.

Conditioned blood reperfusion markedly enhances neurologic recovery after prolonged cerebral ischemia.

OBJECTIVES: To determine whether controlled reperfusion using conditioned leukodepleted blood can substantially limit cerebral reperfusion injury following prolonged ischemia. METHODS: Eighteen pigs (25-35 kg) underwent 90 minutes of hypothermic circulatory arrest (19 degrees C) to produce brain ischemia. At the start of rewarming, 10 pigs received uncontrolled reperfusion with unmodified (normal) blood. The other 8 pigs underwent 10 minutes of controlled reperfusion by selectively perfusing both common carotid arteries with blood passed through a CoBRA filter. This filter conditions the blood by removing white blood cells, platelets, and attenuating complement. Two other pigs underwent cooling and rewarming only (controls) without ischemia. Neurologic assessment was done using neurologic deficit scoring (0 = normal, 500 = brain death), and jugular venous samples were obtained for biochemical analysis postreperfusion. RESULTS: There were no statistical differences in hemodynamics between groups. At 6 hours postanesthesia, all animals receiving normal blood were substantially neurologically impaired. At 24 hours, they all had abnormal positioning and all but 1 were unable to sit or stand (neurologic score 124 +/- 19). In contrast, nonischemic controls and pigs receiving conditioned blood reperfusion showed only minor neurologic deficits at 6 hours, and at 24 hours all were considered normal (neurologic scores 0 and 6 +/- 5; P <.005 vs uncontrolled reperfusion). Compared with pigs receiving normal blood reperfusion, oxygen free radical formation (conjugated dienes 1.70 +/- 0.03 vs 1.60 +/- 0.02 Abs 240 nm; P <.05 vs uncontrolled reperfusion), and endothelin-1 release (2.12 +/- 0.09 vs 1.84 +/- 0.06 pg/mL; P <.05 vs uncontrolled reperfusion) were also significantly lower in animals receiving conditioned blood. CONCLUSIONS: Following prolonged cerebral ischemia, reperfusion injury is avoided by delivering conditioned blood, which is devoid of white cells, platelets, and membrane attack complex. These results suggest that this modality is clinically useful in situations where the brain is subjected to prolonged ischemia.

Experience with an alternative technique for the management of anomalous left coronary artery from the pulmonary artery.

BACKGROUND: Several operative approaches are utilized for the management of anomalous origin of the left coronary artery from the pulmonary artery, each with some limitation. The long-term results of a technique that facilitates direct and tension-free implantation of the anomalous artery to the aorta in all patients are described. METHODS: From January 1, 1992 through August 30, 2000, 10 consecutive patients with anomalous left coronary artery underwent operation using this technique. It consists of isolating an anterior and posterior transverse segment of pulmonary artery in continuity with the origin of the anomalous coronary artery. The two segments are folded with the orifice of the coronary as its fulcrum, and the edges sutured together to form an extension tube of pulmonary artery tissue. This lengthens the coronary artery and allows direct aortic implantation (posterior to the pulmonary artery) without tension. The pulmonary artery is reconstructed with autologous pericardium. RESULTS: Patient age ranged from 3 weeks to 3 years old (median 8 weeks), with 80% of patients less than 11 weeks old. Median weight was 4.6 kg (3.7 to 23 kg). The left ventricle was dilated with an end-diastolic diameter z-value of +1 to +3, and the shortening fraction was markedly reduced to 16% +/- 6% (7% to 28%), with 8 of 10 patients having a shortening fraction less than 20%. Mitral regurgitation was severe in 5 patients, moderate in 2 patients, and all patients were in congestive heart failure. After repair there were no hospital deaths. Inotropic support was needed in all patients, but none required mechanical assistance. At a follow-up of 4.3 +/- 2.5 years (0.5 to 8.5 years), 9 patients are asymptomatic and 1 patient has intermittent chest pain. All patients (10/10) have echocardiographic documented patency of the reimplanted coronary artery, as well as marked improvement in the left ventricular shortening fraction (37% +/- 5%; p > 0.05 versus preoperative) and decrease in the end-diastolic diameter z-value (-1 to +1; p > 0.05 versus preoperative). Mitral regurgitation was absent in 4 patients, mild in 4 patients, and moderate in 2 patients. severe in 1 patient. Four patients have evidence of mild supravalvar pulmonary stenosis (15 to 32 mm Hg), 1992. CONCLUSIONS: This technique allows a tension-free direct aortic connection in all cases, has a low rate of coronary artery occlusion, and avoids significant pulmonary artery distortion or stenosis, making it an excellent alternative for the surgical management of anomalous origin of the coronary artery.

Distal aortic perfusion and cerebrospinal fluid drainage for thoracoabdominal and descending thoracic aortic repair: ten years of organ protection.

OBJECTIVE: To report the long-term results of our experience using cerebrospinal fluid drainage and distal aortic perfusion in descending thoracic and thoracoabdominal aortic repair. SUMMARY BACKGROUND DATA: Repair of thoracoabdominal and thoracic aortic aneurysm by the traditional clamp-and-go technique results in a massive ischemic insult to several major organ systems. Ten years ago, we began to use distal aortic perfusion and cerebrospinal fluid drainage (adjunct) to reduce end-organ ischemia. METHODS: Between January 1991 and February 2003, we performed 1004 thoracoabdominal or descending thoracic repairs. Adjunct was used in 741 (74%) of 1004. Multivariable data were analyzed by Cox regression. Number needed to treat was calculated as the reciprocal of the risk difference. RESULTS: Immediate neurologic deficit was 18 (2.4%) of 741 with adjunct and 18 (6.8%) of 263 without (P < 0.0009). In high-risk extent II aneurysms, the numbers were 11 (6.6%) of 167 with adjunct, and 11 (29%) of 38 without. Long-term survival was improved with adjunct (P < 0.002). The long-term survival results persisted after adjustment for age, extent II aneurysm, and preoperative renal function. CONCLUSION: Use of adjunct over a long period of time has produced favorable results; approximately 1 neurologic deficit saved for every 20 uses of adjunct overall. In extent II aneurysms, where the effect is greatest, this increases to 1 saved per 5 uses. Adjunct is also associated with long-term survival, which is consistent with mitigation of ischemic end-organ injury. These long-term results indicate that cerebrospinal fluid drainage and distal aortic perfusion are safe and effective adjunct for reducing morbidity and mortality following thoracic and thoracoabdominal aortic repair.

The clinical significance of the reoxygenation injury in pediatric heart surgery.

Significant advances have been made in the technical performance of operations for infants and neonates with congenital heart disease. However, postoperative organ dysfunction is a frequent problem, particularly in hypoxic (cyanotic) infants. We review both our experimental and subsequent clinical experience with the injury caused by abrupt reoxygenation of the hypoxic patient and examine the modalities of gradual reoxygenation and leukodepletion in limiting this injury, thereby improving operative outcomes for cyanotic lesions. As a result of our experimental and clinical experience we conclude that: (1). reoxygenation injury is a real source of postoperative cardiac and pulmonary dysfunction; (2). white blood cells play an integral role in the production of oxygen-free radicals that are responsible for the damage; and (3). this injury can be modified and possibly ameliorated by changes in the intraoperative management of cardiopulmonary bypass.