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Background Complete embolization of a prosthetic heart valve is extremely rare and dangerous. This case reports a total embolization of a mechanical aortic valve and contributes to the literature regarding the diagnostic challenges related to infective endocarditis and follow-up after valvular surgery. Case summary A 28-year-old male 11.5 years status-post a mechanical aortic valve replacement presented with acute onset of chest pain and dyspnoea while jogging. The patient lost consciousness and went into cardiopulmonary arrest with acute pulmonary oedema and circulatory shock. An echocardiogram revealed an empty aortic annulus, and a chest radiograph showed an embolized valve in the aortic arch. The patient underwent emergent removal of the embolized valve and replacement with a new mechanical aortic valve. The patient survived with minimal sequelae. At a 3-month follow-up, he had resumed work, and the only sequelae were mild left ventricular dysfunction and minor vision loss. Although he experienced no warning signs or symptoms, the most likely aetiology for embolization of the valvular prosthesis was infective endocarditis, which was revealed by re-evaluation of an echocardiogram recorded 1 month before the presentation which demonstrated a subtle motion abnormality of the valve. Conclusions We present a case of a late complete embolization of a mechanical aortic valve most likely caused by asymptomatic infective endocarditis. The case illustrates the challenges in follow-up after valvular surgery and highlights the ultimate benefit of a well-functioning pre-hospital to hospital chain.

Background Less-than-optimal long-term patency of the saphenous vein is one of the main obstacles for the success of coronary artery bypass grafting (CABG). Results from the IMPROVE-CABG trial has shown that harvesting the saphenous vein with a pedicle of perivascular tissue less than 5 mm while using manual distention provides comparable occlusion rates but significantly less intimal hyperplasia at early follow-up. The impact of pedicled veins on duration of operations, leg wound infections, and postoperative bleeding is unknown. Methods One hundred patients undergoing first-time elective CABG were randomly assigned to conventional or pedicled vein harvesting. Perioperative and postoperative data were collected prospectively during the hospital stay and at follow-up. Results Duration of extracorporeal circulation was significantly longer in the pedicled vein group (mean: 76 min versus 65 min, p = 0.006); however, no significant difference was found in the cross-clamp time. No significant difference was found in intraoperative vein graft flow, postoperative bleeding, or leg wound infections (4% in each group). No reoperations were due to vein graft bleeding. Conclusions Harvesting a pedicled vein provides comparable postoperative bleeding and leg wound infection rates in selected patients. The technique is associated with a slightly longer duration of extracorporeal circulation than harvesting conventional veins. Promising early results using the pedicled vein technique may contribute to a change in standard vein harvesting technique for CABG in selected patients.

Objective: Multilevel somatosensory evoked potentials (SSEP) and the release of biochemical markers in cerebrospinal fluid (CSF) were investigated to identify patients with spinal cord ischemia during thoracoabdominal aortic repair and/or a vulnerable spinal cord during the postoperative period. Methods: Thirty-nine consecutive patients undergoing elective aneurysm repair using distal aortic perfusion and cerebrospinal fluid drainage were studied. Continuous SSEP were monitored using nerve stimulation of the right and left posterior tibial nerves with signal recording at the level of both common peroneal nerves, the cervical cord and at the cortical level. CSF concentrations of the markers glial fibrillary acidic protein (GFAp), the light subunit of neurofilament triplet protein (NFL), and S100B were determined at different time points from before surgery until 3 days postoperatively. Results: SSEP indicated spinal cord ischemia in two patients leading to additional intercostal artery reattachments. In one of them the signal loss was permanent and the patient woke up with paraplegia. In the other the signal returned but the patient later developed delayed paraplegia. Three patients without SSEP indications of spinal cord ischemia during surgery later developed delayed paraplegia. The patients with spinal cord symptoms had significant increases, during the postoperative period of CSF biomarkers GFAp (571-fold), NFL (14-fold) and S100B (18-fold) compared to asymptomatic patients. GFAp increased before or in parallel to onset of symptoms in the patients with delayed paraplegia. Conclusions: Peroperative multilevel SSEPhas a high specificity in detecting spinal cord ischemia but does not identify all patients with a postoperative vulnerable spinal cord. Biochemical markers in CSF increase too late for intraoperative monitoring but GFAp is promising for identifying patients at risk for postoperative delayed paraplegia. # 2007 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.

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 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.

Aim of the study was to assess if endovascular treatment is a feasible alternative in patients with descending thoracic aortic disease.Seventy-three patients were admitted for stent-grafting of descending thoracic aortic disease during the period 1997-2008. The majority of the patients had aneurysm (35) or type B dissection (21), but also traumas, penetrating ulcers and other conditions were treated. Sixteen (22%) were unfit for open surgery. Thirty-four (47%) of the patients were symptomatic and 18 had rupture. The primary technical success rate was 96%.Early mortality (30 days) for the whole group was 3%. Early endoleak (30 days) was identified in 11 patients (15%) of whom 4 (5%) had a secondary procedure. In addition, two trauma patients required insertion of a new stent-graft due to stent-graft collapse. Two patients had stroke, one had paraplegia and two paraparesis. Mean follow-up was 3.1 years (range 0-12 years). Late endoleak (30 days) was identified in 5 patients (7%) treated by 6 secondary procedures. One patient (1.7%) had an explant. Two patients have had extensions of endografts due to increasing diameter of the aorta at the distal end of the stent-graft.Endovascular treatment seems to be a viable alternative in patients with descending thoracic aortic disease.

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.

Thoracoabdominal aortic graft replacement has been plagued with the risk of postoperative neurologic deficits (paraplegia and paraparesis) since its inception. Before the early 1980s, the introduction of many surgical adjuncts aimed at spinal cord protection produced confusing results due to the lack of standardization in reporting criteria. The development of a meaningful system of aneurysm classification1 revealed that aneurysm extent has a significant influence in neurologic outcome (Fig. 1). Aneurysm classification also helped us to better analyze the success or failure of adjuncts. The simple cross-clamp technique was the mainstay of descending and thoracoabdominal aortic repair well into the 1980s, and the immediate survival rates and long-term results of that era were impressive. However, during that time, the rate of neurologic deficits, especially for extent II thoracoabdominal aortic aneurysm (TAAA), was persistently high. Neurologic deficits were clearly related to the duration of clamp time, aneurysm extent, rupture, patient age, proximal aortic aneurysm, and renal failure. FIGURE 1. Normal thoracoabdominal aorta and aneurysm classification. Extent I, distal to the left subclavian artery to above the renal arteries. Extent II, distal to the left subclavian artery to below the renal arteries. Extent III, from the sixth intercostal ... In the last decade an abundance of adjuncts—regional or systemic cooling, cerebrospinal fluid (CSF) drainage delivered independently, intraoperatively or postoperatively, distal aortic perfusion, also delivered independently, medications, spinal cooling, and monitoring somatosensory-evoked potentials—have met with varying degrees of success.2-9 Among this array of adjuncts, following the results of both animal and clinical studies, we became particularly interested in the use of combined CSF drainage and distal aortic perfusion. We have successfully used perioperative CSF drainage with distal aortic perfusion for the past 10 years. We have found that moderate passive hypothermia, active visceral cooling with blood or crystalloid solution, and aggressive intercostal artery reattachment further augment the success of these adjuncts. This report describes the progress of our experience with adjuncts and the way that preoperative and postoperative factors influence their success in descending thoracic and thoracoabdominal aortic repair.

Background Retrograde cerebral perfusion (RCP) during profound hypothermic circulatory arrest has been used as an adjunct for cerebral protection for repairs of the ascending and transverse aortic arch. Transcranial Doppler ultrasound has been used to monitor cerebral blood flow during RCP with varying success. The purpose of this study was to characterize cerebral blood flow dynamics during RCP using a new mode of monitoring known as transcranial power motion-mode (M-mode) Doppler ultrasound. Methods Data on pump-flow characteristics and patient outcomes were collected prospectively for patients undergoing ascending and transverse aortic arch repair. Retrograde cerebral perfusion during profound hypothermic circulatory arrest was used for all operations. Intraoperative cerebral blood flow dynamics were monitored and recorded using transcranial power M-mode Doppler ultrasound. Results Between August 2001 and March 2002, we used transcranial power M-mode Doppler ultrasound monitoring for 40 ascending and transverse aortic arch repairs during RCP. Mean RCP time was 32.2 ± 13.8 minutes. Mean RCP pump flow and RCP peak pressure for identification of cerebral blood flow were 0.66 ± 0.11 L/min and 31.8 ± 9.7 mm Hg, respectively. Retrograde cerebral blood flow during RCP was detected in 97.5% of cases (39 of 40 patients) with a mean transcranial power M-mode Doppler ultrasound flow velocity of 15.5 ± 12.3 cm/s. In the study group, 30-day mortality was 10.0% (4 of 40 patients). The incidence of stroke was 7.6% (3 of 40 patients); the incidence of temporary neurologic deficit was 35.0% (14 of 40 patients). Conclusions Transcranial power M-mode Doppler ultrasound consistently demonstrated retrograde middle cerebral artery blood flow during RCP. Transcranial power M-mode Doppler ultrasound can provide optimal RCP with individualized settings of pump flow.

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.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.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 p0.0001. Human study: No mortality or permanent complications were observed in this group.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.

We reviewed our categorization of patients at high risk for neurologic complications in the repair of descending thoracic and thoracoabdominal aortic aneurysm in which we used cerebrospinal fluid drainage and distal aortic perfusion (adjuncts). A total of 409 patients were operated on by one surgeon for descending thoracic or thoracoabdominal aortic aneurysm between 1992 and 1997. Of these patients, 232 had total descending thoracic or type I thoracoabdominal aortic aneurysm, 131 (56%) of whom were operated on with adjuncts. These patients were compared to 101 nonadjunct patients for demographic variables, intraoperative variables, blood product consumption, and neurologic status. In 131 consecutive patients with adjuncts, all but one awoke from anesthesia without neurologic deficit. In nonadjunct patients, however, neurologic deficit occurred in 6 of 101 (6%) (p0.003). The adjunct group had more preoperative renal insufficiency (p0.05), an established risk factor for neurologic deficit (odds ratio = 2.2 in published studies). All other risk factors for neurologic deficit occurred with comparable frequency in both groups. We conclude that the introduction of adjuncts has dramatically reduced the neurologic risk associated with type I thoracoabdominal or total descending thoracic aortic repair. Previously considered high risk for neurologic complications, these aneurysms can now be reclassified as low risk in surgery accompanied by adjuncts. Future investigations will focus on type II thoracoabdominal aortic aneurysm as the major source of neurologic morbidity.

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 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.

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 (H 2 O 2 ) (0 (control perfusion), 20, 40, 80, 120, 160, or 200 μM) (n=8 hearts/group), followed by 30 minutes recovery. Higher concentrations than 80 μM induced cardiac dysfunction and a dose-dependent release of lactate dehydrogenase, indicating myocyte injury. H 2 O 2 -concentrations of 80 μM 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 H 2 O 2 -dose. The effects of H 2 O 2 (120 or 200 μM) 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 H 2 O 2 . Bradykinin, but not H 2 O 2 , induced t-PA release during the second exposure, suggesting different mechanisms of release. In conclusion: Perfusion with H 2 O 2 leads to a dose-dependent myocardial injury in isolated rat hearts. H 2 O 2 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. Copyright © 1997 Elsevier Science Ltd

Objective To study prospectively aneurysm formation, need of surgery, incidence of rupture and mortality in patients with conservatively treated acute type B aortic dissection. Methods All patients referred to us with acute type B dissection between January 1990 and December 2001 were candidates for this prospective treatment and follow-up study. Patients deemed not to be in need of acute surgical repair were included after aggressive antihypertensive treatment. The follow-up protocol included close blood pressure control, clinic visits with physical examination, chest x-ray and spiral CT or MRI at 3 and 6 months and annually thereafter. Results Sixty-six patients were followed for a mean of 79 months (range 22–179). The actuarial survival rate was 82% at 5 years and 69% at 10 years. Eighty-five percent remained free from dissection-related death at 5 years and 82% at 10 years. Ten patients (15%) developed aneurysm (>6 cm) of the dissected aorta. Three of these 10 patients died from aortic rupture and 2 underwent elective surgical repair. Of the 56 patients without aneurysm, one died from rupture and one died suddenly for causes unknown. One patient was treated with endovascular stent-graft. Five patients sustained a new type A aortic dissection which in all but one were fatal. In 26 patients the initial dissection was categorized as intramural hematoma. Twelve of these patients had, in addition to the hematoma, areas with localized dissection/ulcer-like projection. The latter was found to be a predictor of aortic event (dissection-related death, rupture, new type A aortic dissection, aneurysm formation) during follow-up, as was an initial diameter of >4.0 cm at first CT-scan during the acute event. Conclusions Conservatively treated acute type B dissection has a low incidence of aneurysm formation and rupture during the chronic phase. These results must be matched or improved upon before endovascular stent-grafting or early aortic surgical repair can be regarded as the primary treatment of choice.

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 patient's 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.