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Dive into the research topics where Jennifer D. Walker is active.

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Featured researches published by Jennifer D. Walker.


Anesthesia & Analgesia | 2012

Guidelines for Performing Ultrasound Guided Vascular Cannulation: Recommendations of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists

Christopher A. Troianos; Gregg S. Hartman; Kathryn E. Glas; Nikolaos J. Skubas; Robert T. Eberhardt; Jennifer D. Walker; Scott Reeves

TABLE OF CONTENTS PAGEIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . .46Methodology and Evidence Review . . . . . . .46Ultrasound-Guided Vascular Cannulation . . . . . . . . . . . . . . . . . . . . . . . . . . . .47Ultrasound Principles for Needle-Guided Catheter Placement . . . .


Journal of Cardiovascular Pharmacology | 1998

Chronic dual inhibition of angiotensin-converting enzyme and neutral endopeptidase during the development of left ventricular dysfunction in dogs.

Thomas Cv; McDaniel Gm; Holzgrefe Hh; Rupak Mukherjee; Hird Rb; Jennifer D. Walker; Hebbar L; Powell; Francis G. Spinale

Angiotensin-converting enzyme (ACE) inhibition as well as neutral endopeptidase (NEP) inhibition was demonstrated to influence hemodynamics in various cardiac disease states. However, specific effects of chronic combined ACE and NEP inhibition on left ventricular (LV) and myocyte geometry and function remain unclear. In this study, a dual-acting metalloprotease inhibitor (DMPI), which possesses both ACE and NEP inhibitory activity, was used in a rapid-pacing model of LV dysfunction. LV and myocyte geometry and function were examined in control dogs (n = 6), in dogs with pacing-induced LV dysfunction (216 +/- 2 beats/min, 28 days, n = 7), and in dogs with DMPI treatment during rapid pacing (10 mg/kg p.o., b.i.d., n = 6). With chronic rapid pacing, LV end-diastolic volume increased (84 +/- 4 vs. 49 +/- 3 ml), and LV ejection fraction decreased (38 +/- 3% vs. 68 +/- 3%) compared with control (p < 0.05). DMPI concomitantly administered during long-term rapid pacing did not change LV ejection fraction (35 +/- 3%), but LV end-diastolic volume was reduced (70 +/- 5 vs. 84 +/- 4 ml; p < 0.05) when compared with rapid pacing only. With long-term rapid pacing, myocyte cross-sectional area was decreased (278 +/- 5 vs. 325 +/- 5 microm2), and resting length increased (178 +/- 2 vs. 152 +/- 1 microm) when compared with control (p < 0.05). With DMPI concomitantly administered during rapid pacing, myocyte cross-sectional area (251 +/- 5 microm2) and resting length (159 +/- 4 microm) were reduced when compared with rapid pacing only (p < 0.05). Myocyte velocity of shortening decreased from control values with long-term rapid pacing (39.3 +/- 3.9 vs. 73.2 +/- 5.9 microm/s; p < 0.05) but improved with DMPI treatment during rapid pacing when compared with rapid pacing only (58.9 +/- 6.7 microm/s; p < 0.05). Myocyte velocity of shortening with beta-adrenergic-receptor stimulation (25 nM isoproterenol) was reduced from controls with rapid pacing (125 +/- 12 vs. 214 +/- 30 microm/s; p < 0.05) but was improved with DMPI treatment during rapid pacing when compared with rapid pacing only (178 +/- 12 microm/s; p < 0.05). In a model of rapid pacing-induced LV failure, concomitant DMPI treatment significantly reduced the degree of LV dilation with no apparent effect on LV pump function. At the level of the LV myocyte, long-term DMPI treatment with rapid pacing improved myocyte performance and beta-adrenergic response. Thus the improvement in isolated myocyte contractile function was not translated into improved global LV-pump performance. The mechanisms by which improved myocyte contractility was not translated into a beneficial effect on LV-pump function with DMPI treatment during rapid pacing remain speculative, but likely include significant changes in LV remodeling and loading conditions.


The Annals of Thoracic Surgery | 2017

Experience With the Cardiac Surgery Simulation Curriculum: Results of the Resident and Faculty Survey

Nahush A. Mokadam; James I. Fann; George L. Hicks; Jonathan C. Nesbitt; Harold M. Burkhart; John V. Conte; Daniel Coore; Paul S. Ramphal; K. Robert Shen; Jennifer D. Walker; Richard H. Feins

BACKGROUND The Cardiac Surgery Simulation Curriculum was developed at 8 institutions from 2010 to 2013. A total of 27 residents were trained by 18 faculty members. A survey was conducted to gain insight into the initial experience. METHODS Residents and faculty were sent a 72- and 68-question survey, respectively. In addition to demographic information, participants reported their view of the overall impact of the curriculum. Focused investigation into each of the 6 modules was obtained. Participants evaluated the value of the specific simulators used. Institutional biases regarding implementation of the curriculum were evaluated. RESULTS Twenty (74%) residents and 14 (78%) faculty responded. The majority (70%) of residents completed this training in their first and second year of traditional-track programs. The modules were well regarded with no respondents having an unfavorable view. Both residents and faculty found low, moderate, and high fidelity simulators to be extremely useful, with particular emphasis on utility of high fidelity components. The vast majority of residents (85%) and faculty (100%) felt more comfortable in the resident skill set and performance in the operating room. Simulation of rare adverse events allowed for development of multidisciplinary teams to address them. At most institutions, the conduct of this curriculum took precedence over clinical obligations (64%). CONCLUSIONS The Cardiac Surgery Simulation Curriculum was implemented with robust adoption among the investigating centers. Both residents and faculty viewed the modules favorably. Using this curriculum, participants indicated an improvement in resident technical skills and were enthusiastic about training in adverse events and crisis management.


American Journal of Cardiology | 2011

Effect of gender on treatment and outcomes in severe aortic stenosis.

Maryanne Hartzell; Rajeev Malhotra; Kibar Yared; Hannah R. Rosenfield; Jennifer D. Walker; Malissa J. Wood

The aim of this study was to evaluate the effect of gender on operative rates and outcomes in men and women with severe aortic stenosis. An institutional echocardiographic database was used to identify all adult patients with severe aortic stenosis from 2004 through 2005. Only patients with class I indication for aortic valve replacement (AVR) during the period of follow-up were included in the study. Three hundred sixty-two patients were identified with severe aortic stenosis and class I indication for AVR (52% women). Overall operative rate for the cohort was 72%. In patients who underwent AVR, Kaplan-Meier survival rates were the same for men and women. Sixty-four percent of women versus 81% of men underwent AVR (p <0.001). After adjusting for multiple covariates, women had a 2.1-fold lower odds of undergoing AVR compared to men (p = 0.02). After matching for age and Society of Thoracic Surgery risk score, women underwent AVR at a 19% lower relative rate compared to men (p = 0.03); when stratified by gender, there was no difference in reasons for not undergoing AVR. In conclusion, despite similar outcomes after surgery, women with severe aortic stenosis are less likely than men to undergo AVR.


American Journal of Pathology | 2010

Protein Kinase CK1αLS Promotes Vascular Cell Proliferation and Intimal Hyperplasia

Mikhail P. Panchenko; Zakir Siddiquee; David Dombkowski; Yuriy O. Alekseyev; Marc E. Lenburg; Jennifer D. Walker; Thomas E. MacGillivray; Frederic I. Preffer; James R. Stone

Protein kinase CK1alpha regulates several fundamental cellular processes including proliferation and differentiation. Up to four forms of this kinase are expressed in vertebrates resulting from alternative splicing of exons; these exons encode either the L-insert located within the catalytic domain or the S-insert located at the C terminus of the protein. Whereas the L-insert is known to target the kinase to the nucleus, the functional significance of nuclear CK1alphaLS has been unclear. Here we demonstrate that selective L-insert-targeted short hairpin small interfering RNA-mediated knockdown of CK1alphaLS in human vascular endothelial cells and vascular smooth muscle cells impairs proliferation and abolishes hydrogen peroxide-stimulated proliferation of vascular smooth muscle cells, with the cells accumulating in G(0)/G(1). In addition, selective knockdown of CK1alphaLS in cultured human arteries inhibits vascular activation, preventing smooth muscle cell proliferation, intimal hyperplasia, and proteoglycan deposition. Knockdown of CK1alphaLS results in the harmonious down-regulation of its target substrate heterogeneous nuclear ribonucleoprotein C and results in the altered expression or alternative splicing of key genes involved in cellular activation including CXCR4, MMP3, CSF2, and SMURF1. Our results indicate that the nuclear form of CK1alpha in humans, CK1alphaLS, plays a critical role in vascular cell proliferation, cellular activation, and hydrogen peroxide-mediated mitogenic signal transduction.


Circulation | 2007

Images in cardiovascular medicine. Left atrial-esophageal fistula after pulmonary vein isolation: a cautionary tale.

Andre d'Avila; Leon M. Ptaszek; Paul B. Yu; Jennifer D. Walker; Cameron D. Wright; Peter A. Noseworthy; Andrea P. Myers; Marwan Refaat; Jeremy N. Ruskin

A 56-year-old man presented with a 3-day history of progressive epigastric burning, dysphagia, and tactile fever. These symptoms started approximately 4 weeks after an uncomplicated pulmonary vein isolation procedure for atrial fibrillation had been performed at an outside facility. At the time of presentation, the patient was found to be febrile, and blood cultures were positive for Streptococcus viridans growth. Appropriate antibiotic therapy was started at that time. Chest x-ray did not reveal any abnormal findings. Because endocarditis was suspected, transthoracic and transesophageal echocardiograms were performed, but no valvular abnormalities were found. Subsequently, he developed right arm and right leg weakness and a naming deficit associated with anomia, acalculia, and agraphia. He was then transferred to our hospital for further evaluation. At the time of transfer, the …A 56-year-old man presented with a 3-day history of progressive epigastric burning, dysphagia, and tactile fever. These symptoms started approximately 4 weeks after an uncomplicated pulmonary vein isolation procedure for atrial fibrillation had been performed at an outside facility. At the time of presentation, the patient was found to be febrile, and blood cultures were positive for Streptococcus viridans growth. Appropriate antibiotic therapy was started at that time. Chest x-ray did not reveal any abnormal findings. Because endocarditis was suspected, transthoracic and transesophageal echocardiograms were performed, but no valvular abnormalities were found. Subsequently, he developed right arm and right leg weakness and a naming deficit associated with anomia, acalculia, and agraphia. He was then transferred to our hospital for further evaluation. At the time of transfer, the …


Circulation | 2007

Left Atrial–Esophageal Fistula After Pulmonary Vein Isolation A Cautionary Tale

Andre d’Avila; Leon M. Ptaszek; Paul B. Yu; Jennifer D. Walker; Cameron D. Wright; Peter A. Noseworthy; Andrea P. Myers; Marwan Refaat; Jeremy N. Ruskin

A 56-year-old man presented with a 3-day history of progressive epigastric burning, dysphagia, and tactile fever. These symptoms started approximately 4 weeks after an uncomplicated pulmonary vein isolation procedure for atrial fibrillation had been performed at an outside facility. At the time of presentation, the patient was found to be febrile, and blood cultures were positive for Streptococcus viridans growth. Appropriate antibiotic therapy was started at that time. Chest x-ray did not reveal any abnormal findings. Because endocarditis was suspected, transthoracic and transesophageal echocardiograms were performed, but no valvular abnormalities were found. Subsequently, he developed right arm and right leg weakness and a naming deficit associated with anomia, acalculia, and agraphia. He was then transferred to our hospital for further evaluation. At the time of transfer, the …A 56-year-old man presented with a 3-day history of progressive epigastric burning, dysphagia, and tactile fever. These symptoms started approximately 4 weeks after an uncomplicated pulmonary vein isolation procedure for atrial fibrillation had been performed at an outside facility. At the time of presentation, the patient was found to be febrile, and blood cultures were positive for Streptococcus viridans growth. Appropriate antibiotic therapy was started at that time. Chest x-ray did not reveal any abnormal findings. Because endocarditis was suspected, transthoracic and transesophageal echocardiograms were performed, but no valvular abnormalities were found. Subsequently, he developed right arm and right leg weakness and a naming deficit associated with anomia, acalculia, and agraphia. He was then transferred to our hospital for further evaluation. At the time of transfer, the …


Journal of Cardiovascular Pharmacology | 1997

Angiotensin II subtype-1 receptor blockade during the development of left ventricular hypertrophy in dogs : Effects on ventricular and myocyte function

Francis G. Spinale; Henry H. Holzgrefe; Jennifer D. Walker; Rupak Mukherjee; Scott B. Kribbs; James R. Powell; Michael J. Antonaccio

Inhibition of the angiotensin-converting enzyme (ACE) in developing left ventricular (LV) hypertrophy has been demonstrated to have inhibitory effects on myocardial growth. An important mechanism of action of ACE inhibition is modulation of myocardial AT1 Ang II-receptor activity. However, whether and to what extent AT1 Ang II-receptor blockade may influence LV and myocyte function during the hypertrophic process remains unclear. Accordingly, our project examined the relation between changes in LV and myocyte function during the LV hypertrophic process that occurs after recovery from long-term rapid pacing. Dogs were randomly assigned to the following treatment groups: (a) Pace and Recovery, long-term rapid pacing (4 weeks; 216 +/- 2 beats/min) followed by a 4-week recovery period (n = 6); (b) Recovery/AT1 Block, concomitant AT1 Ang II-receptor blockade [irbesartan (SR 47436; BMS-186295) 30 mg/kg b.i.d.] administered during the 4-week recovery period (n = 5); and (c) Control, sham controls (n = 6). There was no difference in mean arterial pressure in any of the three groups. With pacing and recovery, LV end-diastolic volume and mass were increased by >50% from control values. The significant LV remodeling that occurred with recovery from long-term rapid pacing was associated with a decline in LV ejection fraction (59 +/- 3% vs. 68 +/- 4%) and myocyte velocity of shortening (43 +/- 3 microm/s vs. 63 +/- 3 microm/s) when compared with controls (p < 0.05). With recovery from long-term rapid pacing, LV myocyte length (176 +/- 6 microm vs. 150 +/- 1 microm) and cross-sectional area were increased (292 +/- 7 microm2 vs. 227 +/- 6 microm2) compared with controls (p < 0.05). With AT1 Ang II block during recovery from rapid pacing, LV end-diastolic volume was similar to untreated recovery values, but LV mass was normalized. LV ejection fraction was not different from control values with AT1 Ang II-receptor block. Steady-state myocyte velocity of shortening with AT1 Ang II block was similar to control values (55 +/- 5 microm/s), but percentage shortening remained reduced from control (3.55 +/- 0.37% vs. 4.71 +/- 0.12%, respectively, p < 0.05) and was similar to untreated recovery (3.59 +/- 0.23%). With AT1 Ang II block, myocyte length was similar to untreated recovery values, but cross-sectional area was reduced (260 +/- 5 microm2, p < 0.05). Thus AT1 Ang II-receptor blockade instituted in this model of developing LV hypertrophy, significantly reduced LV mass but did not reduce the degree of LV dilation. The cellular basis for these effects of AT1 Ang II-receptor blockade included persistent abnormalities in LV myocyte geometry. AT1 Ang II-receptor blockade improved certain indices of myocyte contractile function from untreated hypertrophy values. These findings suggest that in this pacing-recovery model, the development of LV hypertrophy and myocyte contractile dysfunction may be caused, at least in part, by AT1 Ang II-receptor activation.


PLOS ONE | 2011

Pattern Specification and Immune Response Transcriptional Signatures of Pericardial and Subcutaneous Adipose Tissue

Frank H. Lau; Rahul C. Deo; Gregory Mowrer; Joshua Caplin; Tim Ahfeldt; Adam Kaplan; Leon M. Ptaszek; Jennifer D. Walker; Bruce R. Rosengard; Chad A. Cowan

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality in the United States. Recent studies suggest that pericardial adipose tissue (PCAT) secretes inflammatory factors that contribute to the development of CVD. To better characterize the role of PCAT in the pathogenesis of disease, we performed a large-scale unbiased analysis of the transcriptional differences between PCAT and subcutaneous adipose tissue, analysing 53 microarrays across 19 individuals. As it was unknown whether PCAT-secreted factors are produced by adipocytes or cells in the supporting stromal fraction, we also sought to identify differentially expressed genes in isolated pericardial adipocytes vs. isolated subcutaneous adipocytes. Using microarray analysis, we found that: 1) pericardial adipose tissue and isolated pericardial adipocytes both overexpress atherosclerosis-promoting chemokines and 2) pericardial and subcutaneous fat depots, as well as isolated pericardial adipocytes and subcutaneous adipocytes, express specific patterns of homeobox genes. In contrast, a core set of lipid processing genes showed no significant overlap with differentially expressed transcripts. These depot-specific homeobox signatures and transcriptional profiles strongly suggest different functional roles for the pericardial and subcutaneous adipose depots. Further characterization of these inter-depot differences should be a research priority.


Journal of Cardiothoracic and Vascular Anesthesia | 2016

Analysis of 43 Intraoperative Cardiac Surgery Case Cancellations.

Michael G. Fitzsimons; Joshua D. Dilley; Chris Moser; Jennifer D. Walker

OBJECTIVE Late cancellation of surgery cases imposes significant emotional distress on the patient and their family and results in wasted resources, including loss of operating room and personnel time. This study was designed to determine the causes of cancellation, preventability, total operating room time, and postoperative destination. DESIGN This study was a retrospective review of the 43 cardiac surgical cases that were cancelled while the patient was in the operating room (OR) but prior to surgical incision. SETTING The cases were performed at the Massachusetts General Hospital, a teaching hospital of Harvard Medical School. PARTICIPANTS Forty-three out of 5,110 scheduled cardiac cases were identified that were cancelled after the patient had entered the operating room between January 1, 2010 and December 31, 2013. INTERVENTIONS No interventions were made. This was a retrospective study. MEASUREMENTS AND MAIN RESULTS The most common causes of cancellation included a change in the patients health status (44%), problems associated with central catheter placement (18.6%), and unsatisfactory donor organs for planned transplantation (12%). The majority were inpatients (65%) prior to the procedure. The cumulative OR time for all cancelled cases was 5,374 minutes (89 hours and 34 minutes). CONCLUSIONS The reason for cancellation, preventability, total operating room time, and postoperative destination were determined. The information can be utilized to decrease the number of future cancellations.

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Francis G. Spinale

University of South Carolina

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Rupak Mukherjee

Medical University of South Carolina

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Fred A. Crawford

Medical University of South Carolina

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