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Anthony L Estrera

Publications and source records attributed to Anthony L Estrera.

At least 19 recordsLinked to original sources
PubMed2006

Inflammatory aneurysm of the ascending aorta.

Inflammatory aneurysms of the aorta are usually seen in the infrarenal abdominal aorta and very rarely in the ascending aorta. We present the case of a 76-year-old male with inflammatory aneurysm of the ascending aorta.

Aged↗
PubMed2006

Outcomes of medical management of acute type B aortic dissection.

BACKGROUND: Currently, the optimal treatment of acute type B aortic dissection remains controversial. The purpose of this study was to report early clinical outcomes of medical management for acute type B aortic dissection. METHODS AND RESULTS: Between January 2001 and March 2005, 129 consecutive patients with the confirmed diagnosis of acute type B aortic dissection were studied. Mean age was 61 years (range, 29 to 94), with 33.3% (43/129) female. Acute type B aortic dissection protocol was instituted with the intent to manage all patients medically. Indications for surgical intervention included rupture, aortic expansion, malperfusion, and intractable pain. All patients were followed-up after discharge. Hospital mortality was 10.1% (13/129), 19% (4/21) when vascular intervention was required, and 8.3% (9/108) when medical management was maintained. Early intervention was required in 21 cases (16.2%), 19 (14.7%) open vascular/aortic cases and 2 cases (1.6%) of percutaneous aortic interventions. Morbidity included rupture (4.7%), stroke (4.7%), paraplegia (8.5%), bowel ischemia (7%), acute renal failure (21%), dialysis requirement (13%), and peripheral ischemia (4.7%). Late vascular-related procedures were performed in 5.2% (6/116) of cases. Univariate risk factors for early mortality were rupture (P<0.0001), need for laparotomy (P<0.008), acute renal failure (P<0.0001), need for dialysis (P<0.0001), and lower extremity ischemia (P<0.0004). The only independent risk factors for hospital mortality by multiple logistic regression was rupture (P<0.0009), and independent risk factors for midterm death were history of chronic obstructive pulmonary disease (P<0.002) and low glomerular filtration rate (<57 mL/min; P<0.0001). CONCLUSIONS: Medical management for acute type B aortic dissection is associated acceptable outcomes. Outcomes of other management strategies, eg, endovascular stenting, for acute type B aortic dissection need to be compared with these results.

Acute Disease↗
PubMed2006

Characterization of the inflammatory and apoptotic cells in the aortas of patients with ascending thoracic aortic aneurysms and dissections.

OBJECTIVE: The histopathologic abnormality underlying ascending aortic aneurysm and dissection is medial degeneration, a lesion that is described as the noninflammatory loss of smooth muscle cells and elastic fibers. This study sought to determine whether inflammatory cells are present in medial degeneration and assess any possible contribution of these cells to apoptosis of smooth muscle cells. METHODS: Aortic specimens were obtained from patients undergoing prophylactic surgical repair of an ascending aortic aneurysm (n = 9) and type A dissection (n = 7), along with control patients dying of causes unrelated to aortic disease (n = 5). Immunohistochemical staining was performed to evaluate the presence of lymphocytes and macrophages, and markers of apoptosis were assessed in the aortas of patients with ascending aortic aneurysm and dissection. RESULTS: Immunohistochemical study indicated significantly more CD3+ cells in the aortas of patients with aneurysms or dissections than in control aortas (P = .020 and P = .0022, respectively). In addition, aortas of patients with aneurysms or dissections had more CD68+ cells (P = .01 and P = .005, respectively). CD3+ cells were localized in the media and surrounding the vasa vasorum in the adventitia. Cells yielding a positive result on in situ terminal transferase-mediated deoxyuridine triphosphate nick end-labeling were found in increased numbers in the aortas of patients with aneurysms or dissections relative to control aortas (P = .005 and P = .002, respectively). Furthermore, Fas and FasL were increased in the aortic samples from patients with aneurysms and dissections relative to control aortas. CONCLUSION: The coexistence of inflammatory cells with markers of apoptotic vascular cell death in the media of ascending aortas with aneurysms and type A dissections raises the possibility that activated T cells and macrophages may contribute to the elimination of smooth muscle cells and degradation of the matrix associated with thoracic aortic aneurysms and dissections.

Aortic Dissection↗
PubMed2006

Acute type A aortic dissection complicated by stroke: can immediate repair be performed safely?

OBJECTIVE: Emergency surgical intervention for acute type A aortic dissection complicated by stroke remains controversial. The urgency of immediate repair in this setting is tempered by the concern that cerebral reperfusion may worsen neurologic outcome. The purpose of this study was to report and analyze our results with acute type A aortic dissection complicated by stroke. METHODS: Between September 1999 and March 2005, 151 consecutive patients presented with acute type A aortic dissection. Of this group, 16 (10.6%) patients had sustained a preoperative stroke. Mean age was 56 years (range 43-73 years), with 6 (38%) women. Right hemispheric, left hemispheric, and bilateral strokes occurred in 81%, 13%, and 6%, respectively. Computed tomographic scan or transesophageal echocardiography diagnosed aortic dissection; clinical examination, computed tomographic scan, or transcranial Doppler ultrasound diagnosed stroke. Aortic repair was performed with cardiopulmonary bypass, profound hypothermic circulatory arrest, and retrograde cerebral perfusion. One patient with complete neurologic devastation (coma) was not operated on. RESULTS: Overall hospital mortality was 18.8% (3/16). Mortality in 2 patients who did not undergo surgery (1 patient who was neurologically devastated, and 1 patient whose aorta ruptured while awaiting surgery) was 100% (2/2). Operative mortality was 7% (1/14). Among patients undergoing surgery, neurologic status completely recovered in 2 (14%) patients, improved in 6 (43%) patients, remained the same in 6 (43%) patients, and worsened in none. Median time from onset of stroke to surgery was 9 hours (range 1-240 hours). Eighty percent of patients who underwent surgical repair within 10 hours had improvement in neurologic status, where as none operated on beyond 10 hours improved (P < .02). CONCLUSIONS: In our experience, surgical repair of acute type A aortic dissection can be performed in the setting of preoperative stroke with acceptable mortality. Moreover, no worsening of neurologic condition was observed after surgical repair. Immediate surgical repair is warranted even if acute type A aortic dissection is complicated by stroke.

Acute Disease↗
PubMed2006

Gastrointestinal complications after descending thoracic and thoracoabdominal aortic repairs: a 14-year experience.

OBJECTIVE: There is a paucity of data regarding gastrointestinal (GI) complications after descending thoracic and thoracoabdominal aortic (DTA/TAA) surgical repairs. We examined our 14-year experience with these repairs to determine the incidence, outcomes, and risk factors for postoperative GI complications. METHODS: Between February 1991 and February 2005, we repaired 1,159 DTA/TAA. Data were prospectively collected. The mean patient age was 68 years and 36% were women. Complications were classified as biliary disease, hepatic dysfunction, pancreatitis, GI bleeding, peptic ulcer disease, bowel ischemia, and ileus. Risk factors for the occurrence of GI complications were ascertained by univariate and multivariable analysis. RESULTS: Of the 1,159 patients, 81 had 109 GI complications, for a 7% incidence. The mortality associated with GI complications was 39.5% compared with 13.5% (P < .0001) in patients without GI complications. The incidences of complications were bowel ischemia, 2.5% with 62% mortality; biliary disease, 0.3% with 75% mortality; hepatic dysfunction, 1.6% with 38% mortality; acute pancreatitis, 0.3% with 20% mortality; GI bleeding, 1.5% with 29% mortality; peptic ulcer disease, 0.9% with 30% mortality; and ileus, 2.2% with 26% mortality. Postoperative biliary disease (odds ratio [OR], 16.58; P = .001), hepatic dysfunction (OR, 3.58; P = .006), and bowel ischemia (OR, 10.03; P = .0001) were significantly associated with an increased postoperative mortality. Risk factors for the occurrence of GI complications were visceral involvement of the aortic repair (TAA extent II, III, and IV) (OR, 2.08; P = .002) and low preoperative glomerular filtration rate (OR, .98; P = .0002). CONCLUSION: Biliary disease, hepatic dysfunction, and bowel ischemia after DTA/TAA surgical repairs were associated with an increased mortality. Visceral involvement and preoperative renal insufficiency were risk factors for the occurrence of GI complications.

Adolescent↗
PubMed2006

Chylothorax complicating repairs of the descending and thoracoabdominal aorta.

BACKGROUND: Chylothorax occurring during thoracic aortic surgery is an infrequent but serious complication. The purpose of this study was to analyze our experience with this complication and the resulting outcomes. METHODS: From January 1991 to July 2005, we performed 1,233 descending thoracic and thoracoabdominal aortic surgical procedures. A retrospective review was performed to analyze and identify preoperative and operative risk factors as well as management outcomes of postoperative chylothorax (PCT). RESULTS: PCT developed in five patients (0.4%). All five cases occurred with descending thoracic aortic aneurysm repair, and 80% (four of five patients) were undergoing aortic reoperation. All patients were managed successfully with no mortality. Risk factors for the development of chylothorax were descending thoracic aortic repair (p = 0.006) and thoracic aortic reoperations (p = 0.0003). Nonoperative management was successful in 60% (three of five patients). Two patients required left thoracotomy with direct ligation. Mean hospital length of stay was 35 days (range, 15 to 60 days). Mean follow-up was 33 months (range, 3 to 69 months) with no recurrence of chylothorax or additional morbidity or mortality. CONCLUSIONS: Chylothorax is more likely to occur with reoperations and repairs involving the descending thoracic aorta. Although PCT is associated with longer hospital length of stay, it is not associated with increased infectious complications. Early identification and prompt treatment may decrease both early and late morbidity and mortality.

Aged↗
PubMed2005

Mutations in transforming growth factor-beta receptor type II cause familial thoracic aortic aneurysms and dissections.

BACKGROUND: A genetic predisposition for progressive enlargement of thoracic aortic aneurysms leading to type A dissection (TAAD) is inherited in an autosomal-dominant manner in up to 19% of patients, and a number of chromosomal loci have been identified for the condition. Having mapped a TAAD locus to 3p24-25, we sequenced the gene for transforming growth factor-beta receptor type II (TGFBR2) to determine whether mutations in this gene resulted in familial TAAD. METHODS AND RESULTS: We sequenced all 8 coding exons of TGFBR2 by using genomic DNA from 80 unrelated familial TAAD cases. We found TGFBR2 mutations in 4 unrelated families with familial TAAD who did not have Marfan syndrome. Affected family members also had descending aortic disease and aneurysms of other arteries. Strikingly, all 4 mutations affected an arginine residue at position 460 in the intracellular domain, suggesting a mutation "hot spot" for familial TAAD. Despite identical mutations in the families, assessment of linked polymorphisms suggested that these families were not distantly related. Structural analysis of the TGFBR2 serine/threonine kinase domain revealed that R460 is strategically located within a highly conserved region of this domain and that the amino acid substitutions resulting from these mutations will interfere with the receptor's ability to transduce signals. CONCLUSIONS: Germline TGFBR2 mutations are responsible for the inherited predisposition to familial TAAD in 5% of these cases. Our results have broad implications for understanding the role of TGF-beta signaling in the pathophysiology of TAAD.

Adult↗
PubMed2005

Correlations of cerebrospinal fluid pressure with hemodynamic parameters during thoracoabdominal aortic aneurysm repair.

Central venous pressure (CVP) has long been thought to correlate with cerebrospinal fluid (CSF) pressure during thoracoabdominal aortic aneurysm repair. We examined hemodynamic factors during thoracoabdominal aortic aneurysm surgery to determine their relationship with CSF pressure and aortic cross-clamping. Hemodynamic parameters and CSF pressure were measured in 124 patients at six different stages during repair of descending thoracic or thoracoabdominal aortic aneurysms: skin incision, left lung collapse, pump on, aortic clamp on, aortic clamp off, and pump off. Stepwise multiple regression analysis was used for statistical analysis. CVP was a weak predictor for CSF pressure at the beginning of surgery and when the pump was initiated. At the onset of left lung collapse, cardiac output correlated with CSF pressure. There were no predictors during aortic cross-clamping. Model r2 values were low, ranging 0.03-0.15. We found no hemodynamic predictors of CSF pressure throughout the period of aortic cross-clamping during descending thoracic or thoracoabdominal aortic aneurysm surgery. Model r2 values were low, indicating generally poor prediction of CSF pressure.

Aged↗
PubMed2005

Descending thoracic aortic aneurysm repair: 12-year experience using distal aortic perfusion and cerebrospinal fluid drainage.

BACKGROUND: The benefit of distal aortic perfusion and cerebrospinal fluid drainage over the "clamp and sew" technique during repairs of the descending thoracic aorta is still being debated. The purpose of this report is to analyze our experience with regard to neurologic deficit (paraplegia and paraparesis) and mortality using the adjuncts of distal aortic perfusion and cerebrospinal fluid drainage. METHODS: Between February 1991 and September 2004, we repaired 355 descending thoracic aortic aneurysms. Excluded from analysis were 29 patients who required profound hypothermic circulatory arrest as a result of transverse arch involvement and 26 patients with aortic rupture, leaving a group of 300 patients for which outcomes were analyzed. Mean patient age was 67 years, and 102 (34%) of the patients were women. The adjunct group of distal aortic perfusion and cerebrospinal fluid drainage used in 238 (79.3%) patients was compared with a group of 62 patients who underwent simple cross-clamp with or without the addition of a single adjunct. Multivariable data were analyzed by Cox regression. RESULTS: The incidence of neurologic deficit after all repairs was 2.3% (7 of 300 patients). The incidence of neurologic deficit (immediate and delayed) in the adjunct group was 1.3% (3 of 238 patients), and in the nonadjunct group was 6.5% (4 of 62 patients; p < 0.02). One case of delayed paraplegia occurred in each group. All neurologic deficits occurred in patients with aneurysmal involvement of the entire descending thoracic aorta (extent C; p < 0.02). Statistically significant predictors for neurologic deficit were the use of the adjunct (odds ratio [OR], 0.19; p = 0.02), previous repaired abdominal aortic aneurysm (OR, 7.0; p = 0.005), type C aneurysm (OR, 13.73; p = 0.02), and cerebrovascular disease history (OR, 4.7; p < 0.03). Thirty-day mortality was 8% (24 of 300 patients). Significant multivariate predictors of 30-day mortality were preoperative renal dysfunction (OR, 4.6; p < 0.01) and female sex (OR, 2.9; p < 0.03). CONCLUSIONS: Repairs of the descending thoracic aorta using the adjunct of distal aortic perfusion and cerebrospinal fluid drainage can be performed with a low incidence of neurologic deficit and an acceptable mortality. The use of the adjuncts should be considered during elective repairs of the descending thoracic aorta.

Adolescent↗
PubMed2005

Evolution of risk for neurologic deficit after descending and thoracoabdominal aortic repair.

BACKGROUND: Cross-clamp time has been reported to correlate with risk of neurologic deficit after thoracoabdominal aortic aneurysm repair. Introduction of cerebrospinal fluid drainage and distal aortic perfusion (adjunct) has greatly reduced the incidence of neurologic deficit. We reevaluated the effect of cross-clamp time before and after introduction of adjunct during a 13-year period. METHODS: Between 1991 and 2004, we repaired 1,106 thoracic and thoracoabdominal aortic aneurysms. Four hundred one patients were female and 705 were male (median age, 67 years). Selective use of adjunct was begun in late 1992, with its routine use by 1993. RESULTS: Aortic cross-clamp times have increased significantly (34 seconds/year; p < 0.0001) since 1991. Despite this increase in cross-clamp time, neurologic deficit rates have declined from the first to the fourth quartile (p < 0.02). This decrease in neurologic deficit is most pronounced with the extent II thoracoabdominal aortic aneurysms (21.1% to 3.3%). The use of the adjunct increased the cross-clamp time by a mean of 12 minutes (p < 0.0001), but was associated with a significant protective effect against neurologic deficit (odds ratio = 0.4; p < 0.0002). Although other previously established risk factors remained significantly associated with neurologic deficit, cross-clamp time is no longer significant. CONCLUSIONS: Adjunct significantly reduced the risk of neurologic deficit, despite increasing cross-clamp time. The use of the adjunct appears to blunt the effect of the cross-clamp time and may provide the surgeon the ability to operate without being hurried. Because cross-clamp time has been effectively eliminated as a risk factor with the use of the adjunct, using this variable to construct risk models becomes irrelevant in our experience.

Adolescent↗