5 results on '"Winterfield JR"'
Search Results
2. Acute Hemodynamic Effects of Pacing in Patients Supported by a Heartmate 3 Durable Left Ventricular Assist Device.
- Author
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Akdogan RE, Silverman D, Rofael M, Fu S, Kozaily E, Atkins J, Jackson GR, Inampudi C, Griffin JM, Rao VN, Gregoski MJ, Hajj JM, Winterfield JR, Kilic A, Houston BA, Tedford RJ, and Carnicelli AP
- Subjects
- Humans, Male, Middle Aged, Female, Cardiac Pacing, Artificial, Ventricular Function, Left physiology, Aged, Treatment Outcome, Heart-Assist Devices, Heart Failure physiopathology, Heart Failure therapy, Hemodynamics physiology
- Abstract
Competing Interests: Dr Carnicelli reports research support from Acorai. Dr Hajj reports consulting for Abbott and Medtronic. Dr Kilic reports speaker/consultant fees from Abbott, Abiomed, 3ive, and LivaNova. Dr Tedford reports no direct conflicts of interest related to this article. He is co-chair of the Pulmonary Hypertension Due to Left Heart Disease Task Force for Seventh World Symposium on Pulmonary Hypertension. He reports general disclosures to include consulting relationships with Abbott, Acorai, Aria CV Inc, Acceleron/Merck, Alleviant, Boston Scientific, Cytokinetics, Edwards LifeSciences, Endotronix, Gradient, Medtronic, Morphic Therapeutics, Restore Medical, and United Therapeutics. Dr Tedford serves on steering committee for Merck, Edwards, Endotronix, and Abbott as well as a research advisory board for Abiomed. He also does hemodynamic core laboratory work for Merck. The other authors report no relevant disclosures.
- Published
- 2024
- Full Text
- View/download PDF
3. Dilated cardiomyopathy.
- Author
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Lakdawala NK, Winterfield JR, and Funke BH
- Subjects
- Animals, Cardiomyopathy, Dilated diagnosis, Cardiomyopathy, Dilated pathology, Cardiomyopathy, Dilated physiopathology, Cardiomyopathy, Dilated therapy, Death, Sudden, Cardiac pathology, Death, Sudden, Cardiac prevention & control, Defibrillators, Implantable, Electric Countershock instrumentation, Genetic Predisposition to Disease, Genetic Testing, Heart Failure genetics, Heart Failure pathology, Heart Failure physiopathology, Heart Failure therapy, Humans, Phenotype, Treatment Outcome, Cardiomyopathy, Dilated genetics
- Published
- 2013
- Full Text
- View/download PDF
4. Altered desmosomal proteins in granulomatous myocarditis and potential pathogenic links to arrhythmogenic right ventricular cardiomyopathy.
- Author
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Asimaki A, Tandri H, Duffy ER, Winterfield JR, Mackey-Bojack S, Picken MM, Cooper LT, Wilber DJ, Marcus FI, Basso C, Thiene G, Tsatsopoulou A, Protonotarios N, Stevenson WG, McKenna WJ, Gautam S, Remick DG, Calkins H, and Saffitz JE
- Subjects
- Adolescent, Adult, Aged, Animals, Arrhythmias, Cardiac blood, Arrhythmias, Cardiac etiology, Autopsy, Biopsy, Cardiomyopathies blood, Cardiomyopathies etiology, Case-Control Studies, Cells, Cultured, Chemokine CCL2 blood, Chemokine CCL4 blood, Child, Female, Humans, Intercellular Junctions drug effects, Intercellular Junctions metabolism, Interleukin-17 metabolism, Interleukin-17 pharmacology, Interleukin-6 metabolism, Interleukin-6 pharmacology, Interleukin-8 blood, Male, Middle Aged, Models, Animal, Myocarditis pathology, Myocytes, Cardiac drug effects, Myocytes, Cardiac metabolism, Rats, Rats, Wistar, Sarcoidosis metabolism, Sarcoidosis physiopathology, Signal Transduction physiology, Tumor Necrosis Factor-alpha metabolism, Tumor Necrosis Factor-alpha pharmacology, Ventricular Dysfunction, Right blood, Ventricular Dysfunction, Right etiology, Young Adult, Arrhythmias, Cardiac physiopathology, Cardiomyopathies physiopathology, Desmosomes metabolism, Myocarditis metabolism, Myocarditis physiopathology, Ventricular Dysfunction, Right physiopathology, gamma Catenin metabolism
- Abstract
Background: Immunoreactive signal for the desmosomal protein plakoglobin (γ-catenin) is reduced at cardiac intercalated disks in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC), a highly arrhythmogenic condition caused by mutations in genes encoding desmosomal proteins. Previously, we observed a false-positive case in which plakoglobin signal was reduced in a patient initially believed to have ARVC but who actually had cardiac sarcoidosis. Sarcoidosis can masquerade clinically as ARVC but has not been previously associated with altered desmosomal proteins., Methods and Results: We observed marked reduction in immunoreactive signal for plakoglobin at cardiac myocyte junctions in patients with sarcoidosis and giant cell myocarditis, both highly arrhythmogenic forms of myocarditis associated with granulomatous inflammation. In contrast, plakoglobin signal was not depressed in lymphocytic (nongranulomatous) myocarditis. To determine whether cytokines might promote dislocation of plakoglobin from desmosomes, we incubated cultures of neonatal rat ventricular myocytes with selected inflammatory mediators. Brief exposure to low concentrations of interleukin (IL)-17, tumor necrosis factor-α (TNF-α), and IL-6 (cytokines implicated in granulomatous myocarditis) caused translocation of plakoglobin from cell-cell junctions to intracellular sites, whereas other potent cytokines implicated in nongranulomatous myocarditis had no effect, even at much higher concentrations. We also observed myocardial expression of IL-17 and TNF-α and elevated levels of serum inflammatory mediators, including IL-6R, IL-8, monocyte chemoattractant protein 1, and macrophage inflammatory protein 1β, in patients with ARVC (all P<0.0001 compared with controls)., Conclusions: The results suggest novel disease mechanisms involving desmosomal proteins in granulomatous myocarditis and implicate cytokines, perhaps derived in part from the myocardium, in disruption of desmosomal proteins and arrhythmogenesis in ARVC.
- Published
- 2011
- Full Text
- View/download PDF
5. Intractable cardiac arrest due to lidocaine toxicity successfully resuscitated with lipid emulsion.
- Author
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Dix SK, Rosner GF, Nayar M, Harris JJ, Guglin ME, Winterfield JR, Xiong Z, and Mudge GH Jr
- Subjects
- Humans, Male, Middle Aged, Treatment Outcome, Anesthetics, Local adverse effects, Fat Emulsions, Intravenous therapeutic use, Heart Arrest chemically induced, Lidocaine adverse effects, Resuscitation methods
- Abstract
Objective: Demonstrate a case report involving successful use of lipid emulsion therapy for intractable cardiac arrest due to lidocaine toxicity., Data Source: Lipid emulsion therapy has been shown to be effective in treating the cardiotoxic effects of such drugs as bupivacaine, verapamil, propranolol, and clomipramine as mentioned in a 2009 editorial in Critical Care Medicine by Jeffrey Bent. The mechanism of action of lipid emulsion therapy is not well defined and has been postulated to work by both a "lipid sink," decreasing circulating amounts of drugs to the periphery, or through a direct "energy source" to the myocardium. We present a case report of a patient successfully resuscitated with lipid emulsion therapy after prolonged and intractable lidocaine toxicity. Lidocaine is generally considered much less cardiotoxic than other local anesthetics and is used commonly as infusions for intractable ventricular arrhythmias., Conclusion: This case demonstrates the need to consider lipid emulsion therapy in the advanced cardiac life support algorithm for lidocaine toxicity as well as other lipid soluble drug intoxications.
- Published
- 2011
- Full Text
- View/download PDF
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