Mohamed A.S.,The Methodist key Heart and Vascular Center |
Peden E.K.,The Methodist key Heart and Vascular Center
Journal of Vascular Access | Year: 2017
Introduction: In this article, we will review the clinical symptoms of dialysis access steal syndrome (DASS), evaluation, treatment options, and our approach and treatment algorithm. Methods: We reviewed the literature discussing different aspects of DASS including its epidemiology, pathogen-esis, clinical presentation, evaluation and management options. Results: DASS is the most dreaded complication of access surgery. Although the incidence is low, all providers caring for dialysis patients should be aware of this problem. Symptoms can range from mild to limb threatening. Although various tests are available, the diagnosis of DASS remains a clinical one and requires thoughtful management to have the best outcomes. Conclusions: Multiple treatment options exist for steal. We present diagnostic evaluation and management algorithm. © 2017 Wichtig Publishing.
Leja M.J.,The Methodist key Heart and Vascular Center |
Perryman L.,United Methodist University |
Perryman L.,The Methodist key Heart and Vascular Center |
Reardon M.J.,United Methodist University |
Reardon M.J.,The Methodist key Heart and Vascular Center
Texas Heart Institute Journal | Year: 2011
Cardiac fibroma is a rare, benign tumor that occurs chiefly in children and rarely in adults. Most fibromas occur in the ventricles and may reach a very large size that complicates surgical removal. Herein, we report the case of a 38-year-old woman who presented with shortness of breath, fatigue, and lightheadedness and was found to have a 6 × 8-cm fibroma of the left ventricle. Surgical resection was successful, but 7 days later she developed sudden-onset severe mitral regurgitation due to partial disruption of the posterolateral papillary muscle. Mitral valve replacement with a 27-mm mechanical valve was performed. Five years later, the patient remained well, without evident tumor recurrence or cardiac dysfunction. Mitral valve dysfunction with regurgitation has been reported to occur before, immediately after, and late after the resection of left ventricular fibromas. To our knowledge, this is the 1st report of subacute papillary muscle rupture after the resection of a left ventricular fibroma. This case highlights the need to evaluate mitral valve function by carefully inspecting the resection margins after surgery and interpreting the echocardiographic results during the acute, subacute, and late time frames. © 2011 by the Texas Heart ® Institute, Houston.
White L.E.,Methodist Hospital Research Institute |
Santora R.J.,Methodist Hospital Research Institute |
Cui Y.,Methodist Hospital Research Institute |
Moore F.A.,Methodist Hospital Research Institute |
And 4 more authors.
American Journal of Physiology - Lung Cellular and Molecular Physiology | Year: 2012
Despite advancements in renal replacement therapy, the mortality rate for acute kidney injury (AKI) remains unacceptably high, likely due to remote organ injury. Kidney ischemia-reperfusion injury (IRI) activates cellular and soluble mediators that incite a distinct pulmonary proinflammatory and proapoptotic response. Tumor necrosis factor receptor 1 (TNFR1) has been identified as a prominent death receptor activated in the lungs during ischemic AKI. We hypothesized that circulating TNF-α released from the postischemic kidney induces TNFR1-mediated pulmonary apoptosis, and we aimed to elucidate molecular pathways to programmed cell death. Using an established murine model of kidney IRI, we characterized the time course for increased circulatory and pulmonary TNF-α levels and measured concurrent upregulation of pulmonary TNFR1 expression. We then identified TNFR1-dependent pulmonary apoptosis after ischemic AKI using TNFR1 -/- mice. Subsequent TNF-α signaling disruption with Etanercept implicated circulatory TNF-α as a key soluble mediator of pulmonary apoptosis and lung microvascular barrier dysfunction during ischemic AKI. We further elucidated pathways of TNFR1-mediated apoptosis with NF-κB (Complex I) and caspase-8 (Complex II) expression and discovered that TNFR1 proapoptotic signaling induces NF-κB activation. Additionally, inhibition of NF-κB (Complex I) resulted in a proapoptotic phenotype, lung barrier leak, and altered cellular flice inhibitory protein signaling independent of caspase-8 (Complex II) activation. Ischemic AKI activates soluble TNF-α and induces TNFR1-dependent pulmonary apoptosis through augmentation of the prosurvival and proapoptotic TNFR1 signaling pathway. Kidney-lung crosstalk after ischemic AKI represents a complex pathological process, yet focusing on specific biological pathways may yield potential future therapeutic targets. © 2012 the American Physiological Society.
Quaini A.,University of Houston |
Canic S.,University of Houston |
Glowinski R.,University of Houston |
Igo S.,The Methodist key Heart and Vascular Center |
And 3 more authors.
Journal of Biomechanics | Year: 2012
This work presents a validation of a fluid-structure interaction computational model simulating the flow conditions in an in vitro mock heart chamber modeling mitral valve regurgitation during the ejection phase during which the trans-valvular pressure drop and valve displacement are not as large. The mock heart chamber was developed to study the use of 2D and 3D color Doppler techniques in imaging the clinically relevant complex intra-cardiac flow events associated with mitral regurgitation. Computational models are expected to play an important role in supporting, refining, and reinforcing the emerging 3D echocardiographic applications. We have developed a 3D computational fluid-structure interaction algorithm based on a semi-implicit, monolithic method, combined with an arbitrary Lagrangian-Eulerian approach to capture the fluid domain motion. The mock regurgitant mitral valve corresponding to an elastic plate with a geometric orifice, was modeled using 3D elasticity, while the blood flow was modeled using the 3D Navier-Stokes equations for an incompressible, viscous fluid. The two are coupled via the kinematic and dynamic conditions describing the two-way coupling. The pressure, the flow rate, and orifice plate displacement were measured and compared with numerical simulation results. In-line flow meter was used to measure the flow, pressure transducers were used to measure the pressure, and a Doppler method developed by one of the authors was used to measure the axial displacement of the orifice plate. The maximum recorded difference between experiment and numerical simulation for the flow rate was 4%, the pressure 3.6%, and for the orifice displacement 15%, showing excellent agreement between the two. © 2011 Elsevier Ltd.
PubMed | The Methodist key Heart and Vascular Center, University of Houston and Vascular Imaging
Type: Comparative Study | Journal: European heart journal cardiovascular Imaging | Year: 2016
The mitral annulus (MA) saddle shape is complex but vital for a normal functioning mitral apparatus. Although conventional parameters of MA geometry such as area and height are helpful, they fall short of describing its complex regional geometry.In this prospective study, novel parameters of MA curvature and torsion were derived from three-dimensional (3D) transoesophageal echocardiography. These quantitative indices were computed in 15 patients with normal valves (age 53 8 years) and in 15 patients with organic significant mitral regurgitation (MR, age 66 11 years), before and after mitral valve repair (MVR). The MA was traced and modelled in mid- and end-systole. Curvature and torsion were computed at 500 points across the MA to derive regional and global indices. Overall, patients with organic MR presented the smallest global curvature and torsion; this decrease in curvature and torsion reflects a loss of tonicity of the MA tissue. These changes were largely corrected with MVR surgery, to higher values, compared with normals. The regional analysis revealed similar trends. The maximal MA curvature was found to be at the MA anterior horn, whereas the MA posterior horn had the lowest curvature values.Novel MA parameters of curvature and torsion can be computed from 3D echocardiography and provide quantitative characteristics of dynamic regional MA geometry. In patients with organic MR, the reduced regional and global curvatures improve following surgical MVR. These quantitative parameters may help further refine the quantitative description of MA geometry in various mitral valve pathologies and after MVR.
PubMed | The Methodist key Heart and Vascular Center and St Francis Heart And Vascular Center
Type: Journal Article | Journal: Journal of vascular surgery. Venous and lymphatic disorders | Year: 2016
The standard initial noninvasive imaging modality for diagnosing May-Thurner syndrome is duplex ultrasound, but this modality provides only indirect measures and is frequently limited, necessitating further imaging to make the diagnosis. Other noninvasive imaging modalities (computed tomographic venography, time of flight, magnetic resonance venography) allow for direct visualization but lack hemodynamic and anatomic information about what is occurring throughout the cardiac cycle. Intravascular ultrasound is the invasive tool ofchoice in the setting of iliac vein compression syndrome, butquality, noninvasive imaging modalities have yet to be described. Contrast-enhanced, dynamic magnetic resonance venography allows for detailed imaging of the pelvis as well asdynamic vascular imaging, improving preoperative planning.
Kuster D.W.D.,Loyola University Chicago |
Cardenas-Ospina A.,Memorial University of Newfoundland |
Miller L.,Memorial University of Newfoundland |
Liebetrau C.,Kerckhoff Heart and Thorax Center |
And 10 more authors.
American Journal of Physiology - Heart and Circulatory Physiology | Year: 2014
Diagnosis of myocardial infarction (MI) is based on ST-segment elevation on electrocardiographic evaluation and/or elevated plasma cardiac troponin (cTn) levels. However, troponins lack the sensitivity required to detect the onset of MI at its earliest stages. Therefore, to confirm its viability as an ultra-early biomarker of MI, this study investigates the release kinetics of cardiac myosin binding protein-C (cMyBP-C) in a porcine model of MI and in two human cohorts. Release kinetics of cMyBP-C were determined in a porcine model of MI (n = 6, pigs, either sex) by measuring plasma cMyBP-C level serially from 30 min to 14 days after coronary occlusion, with use of a custom-made immunoassay. cMyBP-C plasma levels were increased from baseline (76 ± 68 ng/l) at 3 h (767 ± 211 ng/l) and peaked at 6 h (2,418 ± 780 ng/l) after coronary ligation. Plasma cTnI, cTnT, and myosin light chain-3 levels were all increased 6 h after ligation. In a cohort of patients (n = 12) with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy, cMyBP-C was significantly increased from baseline (49 ± 23 ng/l) in a time-dependent manner, peaking at 4 h (560 ± 273 ng/l). In a cohort of patients with non-ST segment elevation MI (n = 176) from the SYNERGY trial, cMyBP-C serum levels were significantly higher (7,615 ± 4,514 ng/l) than those in a control cohort (416 ± 104 ng/l; n = 153). cMyBP-C is released in the blood rapidly after cardiac damage and therefore has the potential to positively mark the onset of MI. © 2014 the American Physiological Society.
Little S.H.,The Methodist key Heart and Vascular Center
Current Cardiovascular Imaging Reports | Year: 2011
Current three-dimensional (3D) echocardiographic technology, including live 3D transesophageal echocardiography and single-beat 3D color Doppler imaging, are providing valuable new insight into the mechanism and quantification of mitral valve dysfunction. In this review we discuss important applications of 3D volumetric leaflet imaging with emphasis on the distinction between organic and functional mitral regurgitation. We also discuss the added benefit of current and emerging 3D color Doppler methods for the quantification of mitral regurgitation severity. The limitations of the 2D proximal isovelocity surface area method are discussed, along with potential solutions provided by 3D color Doppler imaging methods that do not require assumptions about the converging flow geometry. Methods to directly measure the vena contracta area of a regurgitant jet are presented along with recent validation studies comparing this method to a reference standard of cardiac MRI. In brief, we review the established and emerging applications of 3D color Doppler techniques for the quantification of mitral regurgitation severity. © 2011 Springer Science+Business Media, LLC.
Estep J.D.,The Methodist key Heart and Vascular Center
JACC. Cardiovascular imaging | Year: 2010
Recent advances in the field of left ventricular device support have led to an increased use of left ventricular assist devices (LVADs) in patients with end stage heart disease. The primary imaging modality to monitor patients with LVADs has been echocardiography. The purpose of this review is to highlight the clinical role of echo and other noninvasive imaging modalities in the assessment of cardiac structure and function in patients with pulsatile and continuous flow LVADs. In addition, we discuss the role of imaging with emphasis on echo to detect LVAD dysfunction and device related complications. Copyright © 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
High proportion of patients with end-stage heart failure regardless of aetiology demonstrates anti-cardiac antibody deposition in failing myocardium: humoral activation, a potential contributor of disease progression
PubMed | The Methodist key Heart and Vascular Center
Type: Journal Article | Journal: European heart journal | Year: 2014
Various reports have raised the possibility of humoral immune responses as contributors for the progression of heart failure. Previous studies, however, have focused on the analysis of serum and documented circulating antibodies against a variety of cardiac proteins. However, there is little evidence on whether anti-cardiac antibodies are deposited in end-stage failing myocardium. Our objective was to determine whether or not there was evidence of deposition of anti-cardiac antibodies and/or activated complement components in end-stage failing human myocardium.Myocardial samples were obtained from 100 end-stage heart failure patients and 40 donor control biopsies. Sections were cut and stained using standard fluorescent immunohistochemistry techniques with anti-human immunoglobulin G (IgG), IgG3, and C3c. Gel electrophoresis and protein identification by mass spectrometry were used to confirm the presence of IgG and its antigen. Immunoglobulin G was localized to the sarcolemma in 71% of patients, 48% of those being positive for the subtype IgG3. The proportion of patients with ischaemic heart disease that was positive for IgG was 65% and among those with non-ischaemic aetiologies was 76%. In a subgroup analysis, the presence of IgG and its subunits were confirmed by mass spectrometry and adenosine triphosphate synthase subunit identified as an antigen. Complement was activated in 31% of all patients. The presence of IgG, IgG3, and C3c was directly correlated with the length of disease (r = 0.451, P = 0.006).Evidence of anti-cardiac antibodies and complement activation was found in a large number of patients with end-stage cardiomyopathy regardless of the aetiology. Adenosine triphosphate synthase appears to be a new prominent antigenic stimulus; but more interestingly, the simultaneous co-existence of activated complement components suggests that this humoral mechanism may participate in disease progression.