Anders Winnerkvist

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.

Staged repair of extensive aortic aneurysms

BACKGROUND We adopted a two-stage approach (elephant trunk procedure) in the repair of extensive aortic aneurysms in 1991, performing 241 procedures in 155 patients. METHODS Reversed elephant trunk (graft replacement of the descending thoracic aorta followed by ascending/arch replacement) was performed in 18 patients. All other patients underwent conventional staged repair. The first stage was performed in 137 patients, with 86 patients returning for the second stage. RESULTS First stage 30-day mortality was 9.5% (13 of 137). There was no second stage immediate neurologic deficit. Second stage mortality was 7.0% (6 of 86). During the interval of 31 days to 6 weeks after stage one, mortality was 10 of 124 (8%). Seven of the 10 interval deaths (70%) were due to rupture of the untreated aortic segment. The mortality rate was 32.1% (18 of 56) in the group of patients who did not return for the second stage repair. CONCLUSIONS Extensive aortic aneurysms can be repaired with acceptable morbidity and mortality using the elephant trunk technique. After stage one, prompt treatment of the remaining aneurysm is crucial to success.

Effect of Extended Cross-Clamp Time During Thoracoabdominal Aortic Aneurysm Repair

BACKGROUND In previous studies of the neurologic outcome of patients undergoing thoracoabdominal aortic aneurysm repair with the simple cross-clamp technique, cross-clamp time of greater than 30 minutes was identified as an important risk factor. We retrospectively examined the effect of clamp time of 30 minutes or greater on outcome for patients undergoing repair with the addition of surgical adjuncts. METHODS Between February 1991 and June 1996 we operated on 370 patients for thoracoabdominal or descending thoracic aortic aneurysm. Two hundred seventy-one of these patients with cross-clamp times of 30 minutes or greater were included in this study. One hundred twelve patients underwent simple cross-clamp repair, whereas 159 were operated on with the surgical adjuncts of distal aortic perfusion and cerebrospinal fluid drainage. RESULTS By multivariate analysis, acute dissection, surgical adjuncts, and aneurysm extent proved most significant in overall patient outcome. The overall rate of early neurologic deficits was 23 of 271 (8.5%). For highest risk patients with type II thoracoabdominal aortic aneurysms, the rate of neurologic deficits was 11 of 29 (38%) for cross-clamp versus 6 of 82 (7.3%) for adjunct operation patients (odds ratio = 0.13; p < 0.001). CONCLUSIONS The adjuncts of cerebrospinal fluid drainage and distal aortic perfusion decreased the risk of extended cross-clamp time during thoracoabdominal aortic aneurysm repair, particularly for highest risk type II.

Biochemical markers of cerebrospinal ischemia after repair of aneurysms of the descending and thoracoabdominal aorta.

OBJECTIVE To investigate the clinical potential of several markers of spinal cord ischemia in cerebrospinal fluid (CSF) and serum during aneurysm repair of the descending thoracic or thoracoabdominal aorta. DESIGN Observational study of consecutive patients. Nonblinded, nonrandomized. SETTING University hospital thoracic surgical unit. PARTICIPANTS Eleven consecutive elective patients. INTERVENTIONS Distal extracorporeal circulation and maintenance of CSF pressure <10 mmHg until intrathecal catheter removal. MEASUREMENTS AND MAIN RESULTS CSF and serum levels of S100B (and its isoforms S100A1B and S100BB), neuronal-specific enolase (NSE), and the CSF levels of glial fibrillary acidic protein (GFAp) and lactate were determined. Two patients had postoperative neurologic deficit. One with a stroke showed a 540-fold increased GFAp, a 6-fold NSE, and S100B increase in CSF. One with paraplegia had a 270-fold increase in GFAp, a 2-fold increase in NSE, and 5-fold increased S100B in CSF. One patient without deficit increased GFAp 10-fold, NSE 4-fold, and S100B 23-fold in CSF. CSF lactate increased >50% in 6 of 9 patients without neurologic deficit. Serum S100B increased within 1 hour of surgery in all patients without any concomitant increase in CSF. S100A1B was about 70% of total S100B in both serum and CSF in patients with or without neurologic defects. S100B in CSF increased 3-fold in 3 of 9 asymptomatic patients. CONCLUSIONS In patients with neurologic deficit, GFAp in CSF showed the most pronounced increase. Biochemical markers in CSF may increase without neurologic symptoms. There is a significant increase in serum S100B from surgical trauma alone without any increase in CSF.

Release of tissue plasminogen activator during reperfusion after different times of ischaemia in isolated, perfused rat hearts

Tissue plasminogen activator (t-PA) is a potential marker of endothelial cell activation or injury. The relationship between duration of ischaemia and release of t-PA during reperfusion was investigated in isolated rat hearts exposed to either 5, 10, 20, 30, 40, or 60 min of global, normothermic ischaemia followed by 30 min of reperfusion (n = 8 in each group). t-PA activity was measured (chromogenic peptide substrate assay) in the effluent before ischaemia, and after 2.5, 5, 7.5, 10, 20, and 30 min of reperfusion. Release of lactate dehydrogenase (LD), a marker of myocyte injury, was measured before ischaemia and after 5 min reperfusion. Left ventricular pressures were measured by a balloon in the left ventricle. Ischaemia for 20 min or less had only minor effects on cardiac function. Thirty min or more of ischaemia induced ventricular fibrillation during reperfusion in most hearts. After ischaemia t-PA outflow increased, but without any significant difference between groups. Peak release occurred after either 2.5 or 5 min of reperfusion. After 10 min reperfusion the release was not different from the basal value. In contrast, postischaemic release of LD correlated to the length of ischaemia. To conclude, t-PA release from the ischaemic-reperfused rat heart is independent of the length of ischaemia. Thus the potential of t-PA to quantify endothelial injury appears to be limited.

Actual versus actuarial analysis for cardiac valve complications: the problem of competing risks.

Methods for analyzing rates of events such as heart valve failure following surgery are important for comparing different techniques and devices; however, in patients undergoing major surgery, other risks such as mortality compete with the risk of heart valve failure to determine each patients final outcome. When multiple, mutually exclusive endpoints are possible, a situation known to statisticians as a competing risks problem arises. No single statistical technique that is currently available provides an entirely satisfactory solution to this problem. We argue that in order for valve failure incidences to be useful clinically, the overall patient outcome milieu from which these failures arise must be considered. In this article, we review recent work in the area of competing-risks analysis as it pertains to heart valve surgery outcome.

OXIDATIVE STRESS AND:RELEASE OF TISSUE PLASMINOGEN ACTIVATOR IN ISOLATED RAT HEARTS

UNLABELLED To evaluate the potential of tissue plasminogen activator (t-PA) as a marker of endothelial activation or injury, the dose-response relationship between reactive oxygen intermediates and t-PA release was investigated in isolated rat hearts. After stabilization the hearts were perfused for 10 minutes with different concentrations of hydrogen peroxide (H2O2) (0 (control perfusion), 20, 40, 80, 120, 160, or 200 microM) (n = 8 hearts/group), followed by 30 minutes recovery. Higher concentrations than 80 microM induced cardiac dysfunction and a dose-dependent release of lactate dehydrogenase, indicating myocyte injury. H2O2-concentrations of 80 microM and more caused a significant, but temporary t-PA release. Peak t-PA release occurred more rapidly with higher concentrations, but otherwise there was no difference dependent on the H2O2-dose. The effects of H2O2 (120 or 200 microM) on t-PA release were also compared to the effects of bradykinin. Both were given for 10 minutes as above, and the procedure was repeated after 10 minutes recovery. Bradykinin (50 or 500 nM) released t-PA with the same magnitude, but with peak values occurring earlier than t-PA release induced by H2O2. Bradykinin, but not H2O2, induced t-PA release during the second exposure, suggesting different mechanisms of release. IN CONCLUSION Perfusion with H2O2 leads to a dose-dependent myocardial injury in isolated rat hearts. H2O2 also causes an acute t-PA release without dose-dependency, suggesting an all or nothing response of the endothelium. t-PA may be used as an indicator of, but cannot quantify endothelial activation or injury.

Spinal Cord Protection during Aortic Cross Clamping: Retrograde Venous Spinal Cord Perfusion, Distal Aortic Perfusion, and Cerebrospinal Fluid Drainage

Objective - We investigated retrograde venous spinal cord perfusion (RVP), with the established adjuncts cerebrospinal fluid drainage (CSFD), and distal aortic perfusion (DAP) in the canine model. We then examined the clinical feasibility of RVP, DAP, and CSFD. Design - Canine study : Twenty dogs were randomized to four treatment groups. All animals underwent 60 min of complete aortic cross-clamp. Group 1 was the control and received only aortic cross-clamp; group 2 DAP and CSFD; group 3 DAP, CSFD, and RVP; and group 4 CSFD plus RVP. Human study : Five patients underwent aortic graft replacement of the descending or thoracoabdominal aorta, while receiving CSFD, DAP, and RVP. Results - Canine study : All animals in groups 1 and 4 awoke paralyzed. One animal each in groups 2 and 3 were paraparetic, with the remaining dogs neurologically intact. Groups 2 and 3 differed from groups 1 and 4 at p < 0.0001. Human study : No mortality or permanent complications were observed in this group. Conclusion - While RVP did not reduce neurologic injury, neither did it increase morbidity. In humans the method is technically feasible and free from major problems. Further animal studies and randomized trials are underway at our center.