Endovascular treatment of descending thoracic aortic disease. A single center experience.

AIM: Aim of the study was to assess if endovascular treatment is a feasible alternative in patients with descending thoracic aortic disease. METHODS: 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%. RESULTS: 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. CONCLUSION: Endovascular treatment seems to be a viable alternative in patients with descending thoracic aortic disease.

A prospective study of medically treated acute type B aortic dissection.

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.

Quality of life in patients with chronic type B aortic dissection.

OBJECTIVE: To study functioning and well-being among patients with conservatively treated acute type B aortic dissection. DESIGN: Cross-sectional survey. METHODS: Patients referred with acute type B dissection between January 1990 and November 2000 were prospectively followed after conservative initial management. In October 2002, we sent the SWED-QUAL questionnaire to all patients who were alive and had not undergone surgery of the dissected aorta. Fifty-three of 55 patients responded, 39 males and 14 females. Patient scores for the 12 aspects of health-related quality of life included in the SWED-QUAL were compared to a normative Swedish population, controlled for age and gender differences. RESULTS: There were only minor differences in functioning and well-being between patients and the normative population. Patients reported similar emotional well-being, cognitive functioning, quality of sleep, overall general health and quality of social relations as their normative counterparts. However, patients' perception of their current health, prior health, perceived resistance to illness and health concern was worse than in the normative population. Female patients also reported worse physical functioning and a lower satisfaction with their physical functioning than male patients or female counterparts in the normative population. We did not find any significant association between length of follow-up and quality of life scores. CONCLUSIONS: In terms of functioning and well-being, patients with uncomplicated acute type B aortic dissection, who are initially managed conservatively, differ little from a normative Swedish population. Our study supports conservative management of this group of patients.

Progress in the management of type I thoracoabdominal and descending thoracic aortic aneurysms.

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%) (p < 0.003). The adjunct group had more preoperative renal insufficiency (p < 0.05), 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.

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 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.

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.

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.

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.