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12 results on '"Glantschnig, Theresa"'

1. Impact of the Timing of Mechanical Circulatory Support on the Outcomes in Myocardial Infarction-Related Cardiogenic Shock: Subanalysis of the PREPARE CS Registry

Author

Prunea, Dan M., primary, Bachl, Eva, additional, Herold, Lukas, additional, Kanoun Schnur, Sadeek S., additional, Pätzold, Sascha, additional, Altmanninger-Sock, Siegfried, additional, Sommer, Gudrun A., additional, Glantschnig, Theresa, additional, Kolesnik, Ewald, additional, Wallner, Markus, additional, Ablasser, Klemens, additional, Bugger, Heiko, additional, Buschmann, Eva, additional, Praschk, Andreas, additional, Fruhwald, Friedrich M., additional, Schmidt, Albrecht, additional, von Lewinski, Dirk, additional, and Toth, Gabor G., additional

Published
2024
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2. Impact of Mechanical Circulatory Support Timing on Outcomes in Myocardial Infarction-Related Cardiogenic Shock: Subanalysis of the PREPARE CS Registry

Author

Prunea, Dan Mihai, primary, Bachl, Eva, additional, Herold, Lukas, additional, Kanoun Schnur, Sadeek Sidney, additional, Pätzold, Sascha, additional, Altmanninger-Sock, Siegfried, additional, Sommer, Gudrun Angelika, additional, Glantschnig, Theresa, additional, Kolesnik, Ewald, additional, Wallner, Markus, additional, Ablasser, Klemens, additional, Bugger, Heiko, additional, Buschmann, Eva, additional, Praschk, Andreas, additional, Fruhwald, Friedrich M., additional, Schmidt, Albrecht, additional, Von Lewinski, Dirk, additional, and Toth-Gayor, Gabor, additional

Published
2024
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3. Outcomes of ECLS-SHOCK Eligibility Criteria Applied to a Real-World Cohort

Author

von Lewinski, Dirk, primary, Herold, Lukas, additional, Bachl, Eva, additional, Bugger, Heiko, additional, Glantschnig, Theresa, additional, Kolesnik, Ewald, additional, Verheyen, Nicolas, additional, Benedikt, Martin, additional, Wallner, Markus, additional, von Lewinski, Friederike, additional, Schmidt, Albrecht, additional, Harb, Stefan, additional, Ablasser, Klemens, additional, Sacherer, Michael, additional, Scherr, Daniel, additional, Manninger-Wünscher, Martin, additional, Pätzold, Sascha, additional, Gollmer, Johannes, additional, Zirlik, Andreas, additional, and Toth, Gabor G., additional

Published
2023
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6. May Measurement Month 2018–2019: an analysis of blood pressure screening results from Austria

Author

Glantschnig, Theresa, primary, Koppelstätter, Christian, additional, Zweiker, David, additional, Kolesnik, Ewald, additional, Niederl, Ella, additional, Kraler, Elisabeth, additional, Stoff, Ingrid, additional, Zweiker, Robert, additional, Weber, Thomas, additional, Horn, Sabine, additional, Weiss, Thomas, additional, Wang, Wei, additional, Beaney, Thomas, additional, Poulter, Neil R, additional, and Perl, Sabine, additional

Published
2022
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7. Left ventricular ejection fraction and cardiac biomarkers for dynamic prediction of cardiotoxicity in early breast cancer

Author

Posch, Florian, primary, Niedrist, Tobias, additional, Glantschnig, Theresa, additional, Firla, Saskia, additional, Moik, Florian, additional, Kolesnik, Ewald, additional, Wallner, Markus, additional, Verheyen, Nicolas, additional, Jost, Philipp J., additional, Zirlik, Andreas, additional, Pichler, Martin, additional, Balic, Marija, additional, and Rainer, Peter P., additional

Published
2022
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8. Cohort profile: ‘Biomarkers of Personalised Medicine’ (BioPersMed): a single-centre prospective observational cohort study in Graz/Austria to evaluate novel biomarkers in cardiovascular and metabolic diseases

Author

Haudum, Christoph Walter, primary, Kolesnik, Ewald, additional, Colantonio, Caterina, additional, Mursic, Ines, additional, Url-Michitsch, Marion, additional, Tomaschitz, Andreas, additional, Glantschnig, Theresa, additional, Hutz, Barbara, additional, Lind, Alice, additional, Schweighofer, Natascha, additional, Reiter, Clemens, additional, Ablasser, Klemens, additional, Wallner, Markus, additional, Tripolt, Norbert Joachim, additional, Pieske-Kraigher, Elisabeth, additional, Madl, Tobias, additional, Springer, Alexander, additional, Seidel, Gerald, additional, Wedrich, Andreas, additional, Zirlik, Andreas, additional, Krahn, Thomas, additional, Stauber, Rudolf, additional, Pieske, Burkert, additional, Pieber, Thomas R, additional, Verheyen, Nicolas, additional, Obermayer-Pietsch, Barbara, additional, and Schmidt, Albrecht, additional

Published
2022
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10. A novel LMNA nonsense mutation causes two distinct phenotypes of cardiomyopathy with high risk of sudden cardiac death in a large five-generation family

Author

Glöcklhofer, Christina R, primary, Steinfurt, Johannes, additional, Franke, Gerlind, additional, Hoppmann, Anselm, additional, Glantschnig, Theresa, additional, Perez-Feliz, Stefanie, additional, Alter, Svenja, additional, Fischer, Judith, additional, Brunner, Michael, additional, Rainer, Peter P, additional, Köttgen, Anna, additional, Bode, Christoph, additional, and Odening, Katja E, additional

Published
2018
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11. Unfolding Cardiac Amyloidosis - From Pathophysiology to Cure

Author

Klemens Ablasser, Theresa Glantschnig, Peter P. Rainer, Giulio Agnetti, Nicolas Verheyen, Ablasser, Klemen, Verheyen, Nicola, Glantschnig, Theresa, Agnetti, Giulio, and Rainer, Peter P

Subjects
medicine.medical_specialty, Heart Diseases, Pre-amyloid oligomer, Disease, 030204 cardiovascular system & hematology, Biochemistry, Transthyretin, Desmin, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Drug Discovery, medicine, Amyloidosi, Posttranslational Modification, Animals, Humans, Prealbumin, Immunoglobulin Light-chain Amyloidosis, 030304 developmental biology, Fibril, Pharmacology, Heart Failure, 0303 health sciences, Amyloid Neuropathies, Familial, biology, business.industry, Amyloidosis, Organic Chemistry, medicine.disease, Pathophysiology, Liver Transplantation, Amyloid deposition, Cardiac amyloidosis, Heart failure, Cardiology, biology.protein, cardiovascular system, Molecular Medicine, Immunoglobulin Light Chains, Immunotherapy, Immunoglobulin Light Chain, Protein Multimerization, business, Stem Cell Transplantation
Abstract

Deposition of amyloidogenic proteins leading to the formation of amyloid fibrils in the myocardium cause cardiac amyloidosis. Although any form of systemic amyloidosis can affect the heart, light-chain (AL) or transthyretin amyloidosis (ATTR) account for the majority of diagnosed cardiac amyloid deposition. The extent of cardiac disease independently predicts mortality. The reversal or arrest of adverse cardiac remodeling is the target of current therapies, as cardiac-related mortality worsens prognosis in patients where the underlying systemic amyloidosis was successfully treated. Here, we provide a condensed overview on the pathophysiology of AL and ATTR cardiac amyloidoses and describe treatments that are currently used or investigated in clinical or preclinical trials. We also briefly touch on acquired amyloid deposition in cardiovascular disease other than AL or ATTR.

Published
2019

12. A novel LMNA nonsense mutation causes two distinct phenotypes of cardiomyopathy with high risk of sudden cardiac death in a large five-generation family.

Author

Glöcklhofer CR, Steinfurt J, Franke G, Hoppmann A, Glantschnig T, Perez-Feliz S, Alter S, Fischer J, Brunner M, Rainer PP, Köttgen A, Bode C, and Odening KE

Subjects
Adult, Arrhythmias, Cardiac mortality, Arrhythmias, Cardiac physiopathology, Arrhythmias, Cardiac therapy, Cardiomyopathy, Dilated mortality, Cardiomyopathy, Dilated physiopathology, Cardiomyopathy, Dilated therapy, Death, Sudden, Cardiac prevention & control, Defibrillators, Implantable, Disease Progression, Electric Countershock instrumentation, Female, Genetic Predisposition to Disease, Heart Transplantation, Heredity, Humans, Male, Middle Aged, Pedigree, Phenotype, Prognosis, Risk Factors, Severity of Illness Index, Arrhythmias, Cardiac genetics, Cardiomyopathy, Dilated genetics, Codon, Nonsense, Death, Sudden, Cardiac etiology, Lamin Type A genetics
Abstract

Aims: Characterization of the cardiac phenotype associated with the novel LMNA nonsense mutation c.544C>T, p.Q182*, which we have identified in a large five-generation family., Methods and Results: A family tree was constructed. Clinical data [arrhythmia, syncope, sudden cardiac death (SCD), New York Heart Association (NYHA) class] were collected from living and deceased family members. DNA of 23 living family members was analysed for mutations in LMNA. Additionally, dilated cardiomyopathy multi-gene-panel testing and whole exome sequencing were performed in some family members to identify potential phenotype-modifiers. In this five-generation family (n = 65), 17 SCDs occurred at 49.3 ± 10.0 years. Furthermore, we identified eight additional mutation-carriers, seven symptomatic (44 ± 13 years), and one asymptomatic (44 years). First signs of disease [sinus bradycardia with atrioventricular (AV)-block I°] occurred at 36.5 ± 8.1 years. Paroxysmal atrial fibrillation (AF) (onset at 41.8 ± 5.7 years) rapidly progressed to permanent AF (46.2 ± 9.8 years). Subsequently, AV-conduction worsened, syncope, pacemaker-dependence, and non-sustained ventricular tachycardia (43.3 ± 8.2 years) followed. Ventricular arrhythmia caused SCD in patients without implantable cardioverter-defibrillator (ICD). Patients protected by ICD developed rapidly progressive heart failure (45.2 ± 10.6 years). A different phenotype was seen in a sub-family in three patients with early onset of rapidly decompensating heart failure and only minor prior arrhythmia-related symptoms. One patient received high-urgency heart transplantation (HTX) at 32 years, while two died prior to HTX. One of them developed lethal peripartum-associated heart failure. Possible disease-modifiers were identified in this 'heart failure sub-family'., Conclusion: The novel LMNA nonsense mutation c.544C>T causes a severe arrhythmogenic phenotype manifesting with high incidence of SCD in most patients; and in one sub-family, a distinct phenotype with fast progressing heart failure, indicating the need for early consideration of ICD-implantation and listing for heart-transplantation.

Published
2018
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