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Dive into the research topics where Nam T. Tran is active.

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Featured researches published by Nam T. Tran.


Stroke | 2006

Association Between Carotid Plaque Characteristics and Subsequent Ischemic Cerebrovascular Events A Prospective Assessment With MRI—Initial Results

Norihide Takaya; Chun Yuan; Baocheng Chu; Tobias Saam; Hunter R. Underhill; Jianming Cai; Nam T. Tran; Nayak L. Polissar; Carol Isaac; Marina S. Ferguson; Gwenn A. Garden; Steven C. Cramer; Kenneth R. Maravilla; Beverly E. Hashimoto; Thomas S. Hatsukami

Background and Purpose— MRI is able to quantify carotid plaque size and composition with good accuracy and reproducibility and provides an opportunity to prospectively examine the relationship between plaque features and subsequent cerebrovascular events. We tested the hypothesis that the characteristics of carotid plaque, as assessed by MRI, are possible predictors of future ipsilateral cerebrovascular events. Methods— A total of 154 consecutive subjects who initially had an asymptomatic 50% to 79% carotid stenosis by ultrasound with ≥12 months of follow-up were included in this study. Multicontrast-weighted carotid MRIs were performed at baseline, and participants were followed clinically every 3 months to identify symptoms of cerebrovascular events. Results— Over a mean follow-up period of 38.2 months, 12 carotid cerebrovascular events occurred ipsilateral to the index carotid artery. Cox regression analysis demonstrated a significant association between baseline MRI identification of the following plaque characteristics and subsequent symptoms during follow-up: presence of a thin or ruptured fibrous cap (hazard ratio, 17.0; P≤0.001), intraplaque hemorrhage (hazard ratio, 5.2; P=0.005), larger mean intraplaque hemorrhage area (hazard ratio for 10 mm2 increase, 2.6; P=0.006), larger maximum %lipid-rich/necrotic core (hazard ratio for 10% increase, 1.6; P=0.004), and larger maximum wall thickness (hazard ratio for a 1-mm increase, 1.6; P=0.008). Conclusions— Among patients who initially had an asymptomatic 50% to 79% carotid stenosis, arteries with thinned or ruptured fibrous caps, intraplaque hemorrhage, larger maximum %lipid-rich/necrotic cores, and larger maximum wall thickness by MRI were associated with the occurrence of subsequent cerebrovascular events. Findings from this prospective study provide a basis for larger multicenter studies to assess the risk of plaque features for subsequent ischemic events.


Circulation Research | 1993

Proliferation in primary and restenotic coronary atherectomy tissue. Implications for antiproliferative therapy.

Edward R. O'Brien; Charles E. Alpers; Douglas K. Stewart; Marina S. Ferguson; Nam T. Tran; David Gordon; Earl P. Benditt; Tomoaki Hinohara; John B. Simpson; Stephen M. Schwartz

On the basis of animal models of arterial injury, smooth muscle cell proliferation has been posited as a dominant event in restenosis. Unfortunately, little is known about this proliferation in the human restenotic lesion. The purpose of this study was to determine the extent and time course of proliferation in primary and restenotic coronary atherectomy-derived tissue. Primary (n = 118) and restenotic (n = 100) coronary atherectomy specimens were obtained from 211 nonconsecutive patients. Immunocytochemistry for the proliferating cell nuclear antigen (PCNA) was used to gauge proliferation in the atherectomy specimens. The identity of PCNA-positive cells was then determined using immunohistochemical cell-specific markers. Eighty-two percent of primary specimens and 74% of restenotic specimens had no evidence of PCNA labeling. The majority of the remaining specimens had only a modest number of PCNA-positive cells per slide (typically < 50 cells per slide). In the restenotic specimens, PCNA labeling was detected over a wide time interval after the initial procedure (eg, 1 to 390 days), with no obvious proliferative peak. Cell-specific immunohistochemical markers identified primary and restenotic PCNA-positive cells as smooth muscle cells, macrophages, and endothelial cells. In conclusion, the findings were as follows: (1) Proliferation in primary and restenotic coronary atherectomy specimens, as indicated by PCNA labeling, occurs infrequently and at low levels. (2) The response to injury in existing animal models of angioplasty may follow a very different course of events from the clinical reality in human atherosclerotic coronary arteries and may help explain why current approaches to restenosis therapy have been ineffective.


Journal of Vascular Surgery | 2010

Management of ruptured abdominal aortic aneurysm in the endovascular era.

Benjamin W. Starnes; Elina Quiroga; Carolyn M. Hutter; Nam T. Tran; Thomas S. Hatsukami; Mark H. Meissner; Gale Tang; Ted R. Kohler

OBJECTIVES Our institution treats about 30 patients per year with ruptured abdominal aortic aneurysms (rAAA). Between 2002 and 2007, our 30-day mortality averaged 58%. In July 2007, we implemented an algorithm to promote endovascular aneurysm repair (EVAR) when feasible. This report describes the outcome with this approach. METHODS Data on patients presenting with rAAA between July 1, 2002, and June 30, 2007, were reviewed and used for comparison to prospectively collected data. Data on patients presenting between July 1, 2007, and April 30, 2009, were collected on all patients after implementation of a structured protocol. The primary outcome measure was 30-day mortality. Data were analyzed using logistic regression. Kaplan-Meier survival curves and a log-rank test were performed to compare survival times for three groups (pre-protocol, post-protocol with open surgery, and post-protocol with EVAR). RESULTS During the study period, 187 patients with rAAA presented to our institution. Before implementation of the algorithm, 131 patients with rAAA presented and 128 were treated. The 30-day mortality rate was 57.8%. After implementation of the protocol, 56 patients with rAAA were managed. Twenty-seven patients (48%) underwent successful EVAR, and 24 patients (43%) underwent open repair. Five patients (9%) underwent comfort care only. In the post-protocol period, 5 patients in the EVAR group (18.5%) and 13 patients in the open group (54.2%) died during the follow-up period for an overall 30-day mortality rate of 35.3% (P = .008 vs 57.8% pre-protocol). After implementation of a structured protocol for managing rAAA, there was a relative risk reduction in 30-day mortality of 35% compared to the time before implementation of the protocol (95% confidence interval [CI], 14%-51%) corresponding to an absolute risk reduction of 22.5% (95% CI, 6.8%-38.2%) and an odds ratio of 0.40 (95% CI, 0.20-0.78; P = .007). After adjusting for key factors predicting mortality, the odds ratio is 0.25 (95% CI, 0.10-0.57; P = .001). CONCLUSION Use of an algorithm favoring endovascular repair resulted in a highly significant reduction in rAAA mortality in our urban hospital. Thirty-day mortality for open repair was no different between pre- and post-protocol eras. With modern techniques of resuscitation and surgical management, a majority of patients presenting with rAAA can survive.


Spine | 1995

Mechanism of the burst fracture in the thoracolumbar spine. The effect of loading rate.

Nam T. Tran; Nathan A. Watson; Allan F. Tencer; Randal P. Ching; Paul A. Anderson

Study Design Calf lumbar spine motion segments were randomly assigned to two groups. After insertion of a transducer capable of measururing transient occlusion of the spinal canal during impact, a low rate axial impact was applied in one group and a high rate load in the other.Post -injury computed tomography to determine the effect of rate of load application on occlusion of the spinal canal. Objectives This study was designed to determine if for the same direction of impact and total energy delivered, occlusion of the spinal canal postvertebral fracture was related to the rate at which the impact was delivered (time from zero to peak load). Summary of Background Data Several reports based on clinical observation have hypothesized that axial burstfractures, which displace bone fragments into the canal. occur because of internal pressurization and explosion of the vertebral body.The extent of bursting of the body, which could be related to the rate at which the load is applied. Method Using calf lumbar spines, a transducer was placed within the spinal canal, after removal of the cord, to measure canal occlusion during impact. One group received axial compressive impacts at a mean loading rate of 400 msec (zero to peak load) using a materials-tesing machine. The energy of failure was determined and used to select a drop weight and distance for the high loading rate tests, which would yield equivalent impact energy. The second group received impacts at a loading rate of 20 msec.The pos-injury radiographs and canal occlusion measurements were compared. Results The same mean energy of impact was used in the fractures for both groups. Post-injury radiographs of the low loading rate group showed compressive fractures with a mean canal occlusion of 6.84%, whereas the high loading rate group had burst fractures with mean canal encroachment of 47.6% (P=0.0007> Conclusions For the same energy and direction of impact, a high impact loading rate produces fractures with significant canal encroachment, whereas minimal encoachment is seen for fractures produced at a low loading rate.


Journal of Vascular Surgery | 2010

Blunt Abdominal Aortic Injury

Sherene Shalhub; Benjamin W. Starnes; Nam T. Tran; Thomas S. Hatsukami; Rachel S. Lundgren; Christopher W. Davis; Samantha Quade; Martin L. Gunn

BACKGROUND Blunt abdominal aortic injury (BAAI) is a rare injury with less than 200 cases in the current reported world literature, mostly in case report format. We sought to describe the experience of a high-volume trauma center and to provide a contemporary review of the literature to better understand the natural history and management of this injury. METHODS This was a retrospective review of patients with BAAI between 1996 and 2010. Data collected included demographics, mechanism of injury, associated injuries, type of intervention, subsequent imaging, and follow-up. BAAI was classified by the presence of external aortic contour abnormality noted as an intimal tear, large intimal flap, pseudoaneurysm, or free rupture. Abdominal aorta zones of injury were classified by possible surgical approaches as zone I (diaphragmatic hiatus to superior mesenteric artery [SMA]), zone II (includes SMA and renal arteries), and zone III (from the inferior aspect of the renal arteries to the aortic bifurcation). RESULTS We identified 28 individuals (68% male) with BAAI (median age, 28.5; range, 6-61 years). The median injury severity score was 45 (range, 16-75), and 39% were hypotensive at presentation. BAAI presented as intimal tear (21%), large intimal flap (39%), pseudoaneurysm (11%), and free rupture (29%). Zone III was the most common location of injury. Management depended on the location and type of injury: nonoperative (32%), open aortic repair (36%), endovascular repair (21%), and multimodality (10%). Overall mortality was 32%. Most deaths occurred during the initial operative exploration. The mortality rate of free aortic rupture was 100%. Intimal tears resolved or remained stable. Median follow-up was 15.5 months (range, 8 days-7.5 years). Vascular complications due to repair included a thrombosed access femoral artery during an endovascular repair and death of a patient who underwent a hybrid repair. CONCLUSIONS This is the largest BAAI series described in the English literature at one institution. BAAIs range from intimal tears to free rupture, with outcomes and management correlating with type and location of injury. Nonoperative management with blood pressure control using β-blockers coupled with antiplatelet therapy and close follow-up is successful in individuals with intimal tears with minimal thrombus formation because they remain stable or resolve on follow-up. Free rupture remains a devastating injury, with 100% mortality. For all other categories of aortic injury, successful repair correlates with a favorable prognosis.


Journal of Trauma-injury Infection and Critical Care | 2011

Repair of blunt thoracic outlet arterial injuries: an evolution from open to endovascular approach.

Sherene Shalhub; Benjamin W. Starnes; Thomas S. Hatsukami; Riyad Karmy-Jones; Nam T. Tran

BACKGROUND Thoracic outlet artery injuries due to blunt trauma are uncommon. Exposure of these arteries is associated with significant morbidity and mortality. An endovascular approach is a less invasive alternative approach for these technically challenging injuries. METHODS A retrospective review of patients who presented with blunt traumatic injuries to the innominate, subclavian, and axillary arteries between 1998 and 2009 was performed. Demographic data, concomitant injuries, preoperative workup, treatment, and outcomes were recorded. RESULTS During the study period, 34 patients (80% men) meeting selection criteria were admitted (11 innominate, 16 subclavian, and 7 axillary). Management was nonoperative in 6, open in 16, and endovascular in 12 patients. In the latter group, eight patients had successful stent-graft insertions. These were approached in an antegrade femoral or retrograde brachial fashion. In three cases of complete artery transaction, both methods were used. Shorter operative time (149 minutes vs. 230 minutes; p = 0.03) and less blood loss (50 mL vs. 1,225 mL; p = 0.03) were seen in the endovascular group compared with the open repair group. There was a trend for less blood transfusion, but it was not significant (0 median units vs. 4.5 median units; p = 0.3). Hospital length of stay was shorter (19 days vs. 29 days; p = 0.4). CONCLUSIONS Covered stents are a feasible alternative to open repair in the multiply injured blunt trauma patients with thoracic outlet arterial injuries. This can be used in the damage control setting as it offers shorter operative time, less blood loss, and overall less morbidity to the patient. Long-term follow-up is needed.


Seminars in Vascular Surgery | 2002

The epidemiology, pathophysiology, and natural history of chronic venous disease

Nam T. Tran; Mark H. Meissner

Chronic venous disease includes a spectrum of clinical presentations ranging from varicose veins through chronic lower extremity pain and edema to venous skin changes and ulceration. Such manifestations may result from primary venous insufficiency or be secondary to other disorders, primarily acute deep venous thrombosis. Regardless of etiology, chronic venous disease has significant socioeconomic consequences and is among the most common problems encountered in surgical practice. Ambulatory venous hypertension underlies most of the sequelae of chronic venous disease, although such hemodynamic derangements may result from either valvular incompetence or venous obstruction. Unfortunately, the factors responsible for the progression of disease from mild to severe manifestations are only beginning to be understood. However, a thorough understanding of the pathophysiology and natural history of chronic venous disease is essential in its management.


Journal of Vascular Surgery | 2011

Endovascular treatment of axillosubclavian arterial transection in patients with blunt traumatic injury

Sherene Shalhub; Benjamin W. Starnes; Nam T. Tran

Axillosubclavian arterial transection due to blunt traumatic injury poses a treatment challenge in the multiply injured patient. Endovascular repair can be technically successful if the injury is focal. We describe an endovascular technique utilizing combined brachial and femoral access to create a through-and-through brachial-femoral wire and repair the arterial injury with a covered stent.


Journal of Endovascular Therapy | 2010

Hypothermia is Associated with Increased Mortality in Patients Undergoing Repair of Ruptured Abdominal Aortic Aneurysm

Elina Quiroga; Nam T. Tran; Thomas S. Hatsukami; Benjamin W. Starnes

Purpose: To evaluate the impact of hypothermia on mortality in patients presenting with ruptured abdominal aortic aneurysms (rAAA). Methods: Between July 2007 and September 2009, 73 patients with ruptured AAAs presented to our Emergency Department (ED). Thirteen patients did not receive surgical treatment; of the 60 patients (46 men; mean age 76 years, range 63–90) who did, 35 had endovascular aneurysm repair (EVAR) and 25 open repair. Body temperatures, which were recorded upon arrival to the ED and operating room, during the procedure, and just prior to leaving the operating room, were analyzed for any association with mortality or hypotension. The primary outcome measure was the 30-day mortality rate. Results: Six (17%) patients in the EVAR group and 10 (40%) patients in the open group died during the 30-day period. Temperature upon arrival to OR, lowest temperature recorded during the procedure, and temperature at the end of the procedure were higher among survivors (p<0.005), independent of the repair technique implemented. Patients in the EVAR group left the OR with a mean temperature of 35.5°C versus 35.0°C for patients in the open group (p=0.12). Conclusion: Hypothermia is associated with increased mortality after repair of rAAA. Efforts to correct hypothermia are more frequently successful in patients undergoing EVAR. Increased communication with anesthesia providers, as well as aggressive measures to correct hypothermia, including active intravascular rewarming methods, should be considered to improve mortality in this gravely ill patient population.


Journal of Vascular Surgery | 2014

Outcomes after stent graft therapy for dissection-related aneurysmal degeneration in the descending thoracic aorta

Derek P. Nathan; Sherene Shalhub; Gale L. Tang; Matthew P. Sweet; Edward D. Verrier; Nam T. Tran; Gabriel S. Aldea; Benjamin W. Starnes

OBJECTIVE Stent graft therapy has emerged as an alternative to open surgery in the management of chronic dissection-related aneurysmal degeneration (DRAD) in the descending thoracic aorta (DTA). The incidence of perioperative complications, need for secondary aortic intervention (SAI), and rate of aneurysmal false-lumen thrombosis have not been thoroughly described. METHODS Perioperative and midterm outcomes in patients who underwent stent graft therapy for chronic DRAD DTA at a single institution between January 2006 and September 2013 were retrospectively analyzed. Preoperative anatomic factors, including the number of visceral and renal side branches off the false lumen, and false lumen volume, were analyzed for their ability to predict treatment failure. Treatment failure was defined as death, need for a SAI, and failure to achieve thrombosis of the DRAD DTA. Treatment success was defined as thrombosis of the false lumen in the area of the DRAD DTA with stability or a decrease in the maximum diameter of the DRAD DTA. RESULTS During the study period, 47 patients underwent stent graft therapy for chronic DRAD DTA. Patients were a mean age of 58.3 ± 11.7 years, 74.5% (n = 35) were male, and 14.9% (n = 7) had a history of connective tissue disease. The left subclavian artery was covered in 48.9% (n = 23), and revascularization was performed in 87.0% (n = 20). Spinal drains were used in 74.5% (n = 35). Spinal cord ischemia developed in 6.4% (n = 3), which resolved in two and improved in one. No retrograde aortic dissections occurred. The 30-day mortality was 4.3% (n = 2); one death was in a patient with rupture. Mean clinical follow-up was 35.1 ± 20.9 months. The 5-year Kaplan-Meier survival was 89% ± 5%. Treatment failure occurred in 18 patients (38.3%): 9 required SAIs, 6 did not have thrombosis of the false lumen in the area of the DRAD DTA, and 4 died, with 1 patient dying during a SAI. No preoperative anatomic factor predicted treatment failure. The 5-year freedom from treatment failure was 54% ± 9%. Including the nine patients who underwent SAI, treatment success was achieved in 85.2% of patients. CONCLUSIONS In this single-center experience of stent graft therapy for chronic DRAD DTA, treatment success was achieved in 85% of patients after a SAI rate of 20%. No preoperative anatomic factor predicted treatment failure, which occurred in almost 40% of the patients. Identifying predictors of treatment failure may improve future outcomes.

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Elina Quiroga

University of Washington

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Niten Singh

University of Washington

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Shahram Aarabi

University of Washington

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