14 results on '"Lechner, Katharina"'
Search Results
2. Phase Ib study of BET inhibitor RO6870810 with venetoclax and rituximab in patients with diffuse large B-cell lymphoma
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Dickinson, Michael, Briones, Javier, Herrera, Alex F., Gonzalez Barca, Eva, Ghosh, Nilanjan, Cordoba, Raúl, Rutherford, Sarah C., Bournazou, Eirini, Labriola Tompkins, Emily, Franjkovic, Izolda, Chesne, Evelyne, Brouwer-Visser, Jurriaan, Lechner, Katharina, Brennan, Barbara, Nüesch, Eveline, Demario, Mark, Rüttinger, Dominik, Kornacker, Martin, and Hutchings, Martin
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Limfomes ,hemic and lymphatic diseases ,Proteins ,Lymphomas ,Proteïnes - Abstract
Bromodomain and extraterminal (BET) proteins are transcriptional activators for multiple oncogenic processes in diffuse large B-cell lymphoma (DLBCL), including MYC, BCL2, E2F, and toll-like receptor signaling. We report results of a phase 1b dose-escalation study of the novel, subcutaneous BET inhibitor RO6870810 (RO) combined with the BCL-2 inhibitor venetoclax, and rituximab, in recurrent/refractory DLBCL. RO was delivered for 14 days of a 21-day cycle, whereas venetoclax was delivered continuously. A 3 + 3 escalation design was used to determine the safety of the RO+venetoclax doublet; rituximab was added in later cohorts. Thirty-nine patients were treated with a median of 2.8 cycles (range, 1-11). Dose-limiting toxicities included grade 3 febrile neutropenia, grade 4 diarrhea, and hypomagnesemia for the doublet; and grade 3 hyperbilirubinemia and grade 4 diarrhea when rituximab was added. The doublet maximum tolerated dose (MTD) was determined to be 0.65 mg/kg RO+600 mg venetoclax; for RO+venetoclax+rituximab, the MTDs were 0.45 mg/kg, 600 mg, and 375 mg/m2, respectively. The most frequent grade 3 and 4 adverse events were neutropenia (28%) and anemia and thrombocytopenia (23% each). Responses were seen in all cohorts and molecular subtypes. Sustained decreases in CD11b on monocytes indicated pharmacodynamic activity of RO. Overall response rate according to modified Lugano criteria was 38.5%; 48% of responses lasted for ≥180 days. Complete response was observed in 8 patients (20.5%). Optimization of the treatment schedule and a better understanding of predictors of response would be needed to support broader clinical use. This trial is registered on www.clinicaltrials.gov as NCT03255096.
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- 2021
3. High-Risk Atherosclerosis and Metabolic Phenotype: The Roles of Ectopic Adiposity, Atherogenic Dyslipidemia, and Inflammation
- Author
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Lechner, Katharina, McKenzie, Amy L, Kränkel, Nicolle, Von Schacky, Clemens, Worm, Nicolai, Nixdorff, Uwe, Lechner, Benjamin, Scherr, Johannes, Weingärtner, Oliver, Krauss, Ronald M, University of Zurich, and Lechner, Katharina
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lifestyle ,dyslipidemia ,Medical Biotechnology ,Clinical Sciences ,610 Medicine & health ,metabolic syndrome ,2712 Endocrinology, Diabetes and Metabolism ,Endocrinology & Metabolism ,2724 Internal Medicine ,inflammation ,ectopic adipose tissue ,Public Health and Health Services ,10046 Balgrist University Hospital, Swiss Spinal Cord Injury Center ,atherosclerosis - Abstract
Current algorithms for assessing risk of atherosclerotic cardiovascular disease (ASCVD) and, in particular, the reliance on low-density lipoprotein (LDL) cholesterol in conditions where this measurement is discordant with apoB and LDL-particle concentrations fail to identify a sizeable part of the population at high risk for adverse cardiovascular events. This results in missed opportunities for ASCVD prevention, most notably in those with metabolic syndrome, prediabetes, and diabetes. There is substantial evidence that accumulation of ectopic fat and associated metabolic traits are markers for and pathogenic components of high-risk atherosclerosis. Conceptually, the subset of advanced lesions in high-risk atherosclerosis that triggers vascular complications is closely related to a set of coordinated high-risk traits clustering around a distinct metabolic phenotype. A key feature of this phenotype is accumulation of ectopic fat, which, coupled with age-related muscle loss, creates a milieu conducive for the development of ASCVD: atherogenic dyslipidemia, nonresolving inflammation, endothelial dysfunction, hyperinsulinemia, and impaired fibrinolysis. Sustained vascular inflammation, a hallmark of high-risk atherosclerosis, impairs plaque stabilization in this phenotype. This review describes how metabolic and inflammatory processes that are promoted in large measure by ectopic adiposity, as opposed to subcutaneous adipose tissue, relate to the pathogenesis of high-risk atherosclerosis. Clinical biomarkers indicative of these processes provide incremental information to standard risk factor algorithms and advanced lipid testing identifies atherogenic lipoprotein patterns that are below the discrimination level of standard lipid testing. This has the potential to enable improved identification of high-risk patients who are candidates for therapeutic interventions aimed at prevention of ASCVD.
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- 2020
4. The Effect of Exercise Intensity and Volume on Metabolic Phenotype in Patients with Metabolic Syndrome: A Randomized Controlled Trial
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von Korn, Pia, Keating, Shelley, Mueller, Stephan, Haller, Bernhard, Kraenkel, Nicolle, Dinges, Sophia, Duvinage, André, Scherr, Johannes, Wisløff, Ulrik, Tjønna, Arnt Erik, Halle, Martin, Lechner, Katharina, and University of Zurich
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610 Medicine & health ,10046 Balgrist University Hospital, Swiss Spinal Cord Injury Center - Published
- 2021
5. Turning back the clock on aging? A perspective on selected mechanisms and therapeutic avenues [Den alterungsprozess verlangsamen? Eine perspektive über ausgewählte mechanismen und therapeutische möglichkeiten]
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Stiebler, Marvin, Müller, Patrick, Bock, Matthias, Lechner, Benjamin, and Lechner, Katharina
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ddc:610 - Abstract
Increasing life expectancy has resulted in a growing number of individuals living with chronic, age-related conditions. This challenges healthcare systems worldwide and results in loss of quality of life in individuals living with chronic conditions. Strategies to promote healthy aging are thus gaining attention.Lifestyle factors such as caloric restriction, carbohydrate restriction and physical activity specifically modify a number of biological pathways associated with aging. One central shared mechanism seems to be the upregulating of maintenance pathways such as the AMPK signaling pathway, triggered by a low cellular energy status, as well as downregulation of anabolic pathways such as the insulin/IGF-1 signaling pathway. The transient energy deficit evoked by (intermittent) caloric restriction or vigorous physical activity – or the phenotypic imitation of this physiological state by dietary carbohydrate restriction – might offer some biologic plausibility for the observation of the benefits of these lifestyle factors. Largely independent of these mechanisms, physical activity directly impacts on downstream adaptive cellular responses via muscle-tissue crosstalk through myokines, i.e. hormone-like substances secreted by skeletal muscle in response to exercise. It is worth noting that distinct pharmaceuticals such as metformin, SGLT2-inhibitors and statins have the potential to complement lifestyle factors by directly modifying these longevity-associated pathways.Lifestyle factors are relevant determinants of health- and potentially of lifespan. Recent findings have significantly advanced our understanding of the mechanisms involved. This narrative review provides a perspective on selected modifiable determinants of healthspan and furthermore elucidates therapeutic avenues that have the potential to attenuate premature aging and to refine personalized preventive care.
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- 2021
6. Additional file 1 of Impact of a 2-year trial of nutritional ketosis on indices of cardiovascular disease risk in patients with type 2 diabetes
- Author
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Athinarayanan, Shaminie J., Hallberg, Sarah J., McKenzie, Amy L., Lechner, Katharina, King, Sarah, McCarter, James P., Volek, Jeff S., Phinney, Stephen D., and Krauss, Ronald M.
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lipids (amino acids, peptides, and proteins) - Abstract
Additional file 1: Figure S1. Change in lipids and lipoprotein subclasses in CCI at baseline, one and two years. Table S1. Baseline characteristics. Table S2. Adjusted means and changes in lipids, blood pressure and CIMT over time by treatment group among completers. Table S3. Lipid lowering and anti-hypertensive medication use over time among completers. Table S4. Adjusted means and changes in lipids, lipoproteins, apoproteins, blood pressure, and CIMT over time by treatment group (intent-to-treat analysis). Table S5. Principal Components and Respective Loading of Each Lipoprotein/Lipid from Baseline and Two-year Follow-up Data. Table S6. Estimated mean proportions and standard errors in the change of LDL phenotype patterns from baseline to two years. Table S7. Multivariate analysis of variance (MANOVA) of lipoprotein subclasses in LDL-C hypo- versus hyper-responders. Table S8. Multivariate analysis of variance (MANOVA) of lipoprotein subclasses in ApoB hypo- versus hyper-responders. Table S9. Relationships between change in BMI and central abdominal fat with lipids and lipoproteins. Table S10. Association between frequency of participants reporting BHB ≥ 0.5mM with change in lipids and lipoproteins from baseline to 2 years. Table S11. LDL phenotype conversions and their associations with frequency of participants reporting BHB ≥ 0.5mM from baseline to 2 years.
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- 2020
- Full Text
- View/download PDF
7. The McCAVE Trial: Vanucizumab plus mFOLFOX‐6 Versus Bevacizumab plus mFOLFOX‐6 in Patients with Previously Untreated Metastatic Colorectal Carcinoma (mCRC)
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Bendell, Johanna C., Sauri, Tamara, Gracián, Antonio Cubillo, Alvarez, Rafael, López López, Carlos, García Alfonso, Pilar, Hussein, Maen, Limon Miron, Maria Luisa, Cervantes, Andrés, Montagut Viladot, Clara, Santos, Cristina, Bessudo, Alberto, Plezia, Patricia, Moons, Veerle, Andel, Johannes, Bennouna, Jaafar, Westhuizen, Andre, Samuel, Leslie, Rossomanno, Simona, Boetsch, Christophe, Lahr, Angelika, Franjkovic, Izolda, Heil, Florian, Lechner, Katharina, Krieter, Oliver, Hurwitz, Herbert, and McCAVE Study Group
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0301 basic medicine ,Oncology ,Cancer Research ,medicine.medical_specialty ,VEGF‐A ,Vanucizumab ,Bevacizumab ,Angiopoetin-2 ,Organoplatinum Compounds ,Colorectal cancer ,Leucovorin ,Phases of clinical research ,First‐line metastatic colorectal cancer ,Antibodies, Monoclonal, Humanized ,VEGF-A ,Disease-Free Survival ,Metastasis ,03 medical and health sciences ,Folinic acid ,0302 clinical medicine ,Metàstasi ,Càncer colorectal ,Internal medicine ,Gastrointestinal Cancer ,Antineoplastic Combined Chemotherapy Protocols ,medicine ,Clinical endpoint ,Humans ,Neoplasm Metastasis ,Angiopoetin‐2 ,business.industry ,Hazard ratio ,medicine.disease ,Oxaliplatin ,030104 developmental biology ,Fluorouracil ,030220 oncology & carcinogenesis ,Camptothecin ,business ,Colorectal Neoplasms ,First-line metastatic colorectal cancer ,medicine.drug - Abstract
Background Bevacizumab, a VEGF‐A inhibitor, in combination with chemotherapy, has proven to increase progression‐free survival (PFS) and overall survival in multiple lines of therapy of metastatic colorectal cancer (mCRC). The angiogenic factor angiopoetin‐2 (Ang‐2) is associated with poor prognosis in many cancers, including mCRC. Preclinical models demonstrate improved activity when inhibiting both VEGF‐A and Ang‐2, suggesting that the dual VEGF‐A and Ang‐2 blocker vanucizumab (RO5520985 or RG‐7221) may improve clinical outcomes. This phase II trial evaluated the efficacy of vanucizumab plus modified (m)FOLFOX‐6 (folinic acid (leucovorin), fluorouracil (5‐FU) and oxaliplatin) versus bevacizumab/mFOLFOX‐6 for first‐line mCRC. Patients and Methods All patients received mFOLFOX‐6 and were randomized 1:1 to also receive vanucizumab 2,000 mg or bevacizumab 5 mg/kg every other week. Oxaliplatin was given for eight cycles; other agents were continued until disease progression or unacceptable toxicity for a maximum of 24 months. The primary endpoint was investigator‐assessed PFS. Results One hundred eighty‐nine patients were randomized (vanucizumab, n = 94; bevacizumab, n = 95). The number of PFS events was comparable (vanucizumab, n = 39; bevacizumab, n = 43). The hazard ratio was 1.00 (95% confidence interval, 0.64–1.58; p = .98) in a stratified analysis based on number of metastatic sites and region. Objective response rate was 52.1% and 57.9% in the vanucizumab and bevacizumab arm, respectively. Baseline plasma Ang‐2 levels were prognostic in both arms but not predictive for treatment effects on PFS of vanucizumab. The incidence of adverse events of grade ≥3 was similar between treatment arms (83.9% vs. 82.1%); gastrointestinal perforations (10.8% vs. 8.4%) exceeded previously reported rates in this setting. Hypertension and peripheral edema were more frequent in the vanucizumab arm. Conclusion Vanucizumab/mFOLFOX‐6 did not improve PFS and was associated with increased rates of antiangiogenic toxicity compared with bevacizumab/mFOLFOX‐6. Our results suggest that Ang‐2 is not a relevant therapeutic target in first‐line mCRC. Implications for Practice This randomized phase II study demonstrates that additional angiopoietin‐2 (Ang‐2) inhibition does not result in superior benefit over anti–VEGF‐A blockade alone when each added to standard chemotherapy. Moreover, the performed pharmacokinetic and pharmacodynamic analysis revealed that vanucizumab was bioavailable and affected its intended target, thereby strongly suggesting that Ang‐2 is not a relevant therapeutic target in the clinical setting of treatment‐naïve metastatic colorectal cancer. As a result, the further clinical development of the dual VEGF‐A and Ang‐2 inhibitor vanucizumab was discontinued., This phase II trial evaluated the efficacy of vanucizumab plus mFOLFOX‐6 versus bevacizumab/mFOLFOX‐6 in the first‐line setting of metastatic colorectal cancer.
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- 2019
8. Veränderungen des Lipoproteinprofils unter kurzzeitiger Mirtazapineinnahme bei gesunden Probanden
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Lechner, Katharina
- Subjects
FOS: Medical and Health Sciences ,Mirtazapin, Lipoproteine, Körpergewicht, Appetit - Abstract
Mirtazapin ist ein noradrenerges und spezifisch serotonerges Antidepressivum, das seit seiner Erstzulassung im Jahre 1996 routinemäßig zur Therapie von schweren depressiven Störungen eingesetzt wird. Eine medikamentöse Behandlung mit Mirtazapin wird in vielen Studien mit Störungen der Appetitregulation, einer erheblichen Zunahme von Körpergewicht sowie Lipidstoffwechselstörungen in Verbindung gebracht. Da es durch die Einnahme von Mirtazapin meist zu einer erheblichen Gewichtszunahme kommt, bleibt unklar, ob Lipidstoffwechselstörungen erst sekundär durch die Gewichtszunahme entstehen oder primär als Medikamentennebenwirkung auftreten. Bis dato wurde noch kein gewichtsunabhängiger Effekt von Mirtazapin auf den Lipidstoffwechsel beschrieben. Dies hat uns dazu veranlasst zu prüfen, ob sich in einem hoch standardisierten Studiensetting in Bezug auf Ernährung, Bewegung und Schlaf-Wach-Rhythmus bei psychisch und körperlich gesunden Probanden durch eine 7-tägige Gabe von 30 mg/d Mirtazapin systematische Veränderungen des Lipoproteinprofils, des Körpergewichts, der Waist to Hip Ratio und des Appetits ergeben. In einer Längsschnitterhebung mit mehreren Messzeitpunkten wurde der Einfluss einer 7-tägigen oralen Einnahme von 30 mg/d Mirtazapin auf den Fettstoffwechsel, das Körpergewicht, die Waist to Hip Ratio sowie das Appetitempfinden von 12 gesunden, kaukasischen, männlichen Probanden im Alter zwischen 20 und 25 Jahren überprüft. Um die Einflussgrößen der Ernährung und Bewegung auf Fettstoffwechsel und Körpergewicht konstant zu halten, wurde diese Studie in einem hochstandardisierten Studiensetting durchgeführt. Die Datenerhebung erfolgte von Dezember 2008 bis April 2010. Die 7-tägige Einnahme von Mirtazapin verursachte in unserer Studienpopulation sowohl eine quantitative Veränderung des Gesamtcholesterins als auch erhebliche qualitative Veränderungen der einzelnen Lipidfraktionen. Das Gesamtcholesterin zeigte nach 7 Tagen eine statistisch signifikante Verminderung von 8%, das LDL-Cholesterin verminderte sich um statistisch signifikante 9% und das HDL-Cholesterin sank ebenfalls statistisch signifikant um 9%. Die Triglyzeride zeigten einen statistisch signifikanten Anstieg von 9%. Die Einzelverläufe der Lipidwerte zeigten in unserer Studienpopulation einen insgesamt sehr homogenen Verlauf. Unter Beibehaltung der standardisierten Diät der 3-wöchigen Vorbereitungsphase kam es durch die 7-tägige Einnahme von 30mg/d Mirtazapin zu einer statistisch signifikanten Abnahme des Körpergewichts. Die Waist to Hip Ratio nahm zu, jedoch ohne statistische Signifikanz. Hinsichtlich des subjektiven Hungergefühls zeigte sich ein statistisch höchst signifikanter Anstieg von 44% als akute Reaktion auf die Einnahme des Studienpräparats innerhalb von 12 Stunden. Am 3. Tag erreichte das Appetitempfinden ein Maximum, ebenso waren der Appetit auf süße sowie auf fettige Speisen an Tag 3 gegenüber dem Baselinewert statistisch signifikant erhöht. Insgesamt gesehen deuten die Ergebnisse der vorliegenden Studie darauf hin, dass Mirtazapin zu einer Konstellation der Blutfettwerte führt, wie sie häufig im Rahmen des Typ 2 Diabetes mellitus beobachtet wird. Diese Konstellation eines erniedrigten HDL-Cholesterins sowie erhöhten Triglyzeridwerten scheint eine besonders aggressive endothelschädigende Potenz an den Blutgefäßen zu haben. Veränderungen des Lipoproteinprofils durch die Einnahme von Mirtazapin ergeben sich in der vorliegenden Studie unabhängig von Veränderungen des Körpergewichts. Dies steht im Gegensatz zu der bisher gängigen Theorie, dass Störungen im Lipidstoffwechsel nicht primär durch das Medikament, sondern eher durch die pharmakainduzierte Gewichtszunahme verursacht werden. Ein Erklärungsansatz hierfür könnte die, bisher nur in Zellkulturen beobachtete, mirtazapininduzierte Aktivierung von SREBP Transkriptionsfaktoren, die die Cholesterin- und Fettsäurebiosynthese kontrollieren, sein. Durch ein besseres Verständnis der Wirkmechanismen von Mirtazapin könnten die Ergebnisse dieser Studie klinische Auswirkungen auf dessen Anwendungsbereich haben. Bei bereits vorliegendem metabolischen Syndrom sowie dessen Einzelkomponenten sollte bei der Behandlung depressiver Sörungen von Medikamenten wie Mirtazapin, die sich nachteilig auf das kardiovaskuläre Risikoprofil auswirken könnten, möglicherweise besser abgesehen werden
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- 2013
9. Regulierungstendenzen öffentlichen Raums und daraus folgende Konsequenzen für die Sozialarbeit
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Lechner, Katharina
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Öffentlicher Raum ,Sozialraum ,Sozialarbeit - Abstract
vorgelegt von: Katharina Lechner Zsfassung in engl. Sprache FH Campus Wien, Fachhochschulstudiengang Sozialarbeit, Dipl.-Arb., 2010
- Published
- 2010
10. Différences culturelles entre l'Autriche et la France en theórie
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Lechner, Katharina
- Abstract
Grundsätzlich erheben sich keine tiefgründigen Unterschiede zwischen Österreichern und Franzosen und ihre Zusammenarbeit oder allgemeine Interaktionen erweisen sich nicht sehr konfliktreich. Trotzdem können jedoch auch nur kleine Verhaltensunterschiede Missverständnisse oder Frustration hervorrufen. Die vorliegende Arbeit hat zum Ziel ein Mittel zum besseren Verständnis des Verhaltens von Franzosen und Österreichern darzustellen und somit zu einer besseren Vorbereitung auf interkulturelle Zusammentreffen beizutragen. Zu diesem Zwick werden die kulturellen Unterschiede zuerst anhand von vorliegenden interkulturellen Theorien präsentiert und danach mit den Ergebnissen der durchgeführten empirischen Studie verglichen. Die Befragung, stützt sich auf 18 Interviews und erhebt die Kulturstandards in Frankreich, das heißt die Unterschiede, die von Österreichern, mit der französischen Kultur vertraut, wahrgenommen werden.
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- 2008
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11. Dispvtatio Theologica De Ivre Et Ivstitia
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Lechner, Katharina
- Abstract
Quam sub Præsidio R. P. Gasparis Lechneri ... ; conscripsit & defendendam suscepit M. Ioannes Kraus ..., M. DC. XXVII. Ivnii, Dissertation Universität Dillingen 1627, Aus dem Vorbesitz des Klosters Rheinau
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- 1626
- Full Text
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12. Lifestyle factors and high-risk atherosclerosis: Pathways and mechanisms beyond traditional risk factors
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Ronald M. Krauss, Benjamin Lechner, Clemens von Schacky, Martin Halle, Amy L. McKenzie, Johannes Scherr, Uwe Nixdorff, Nicolle Kränkel, Katharina Lechner, Nicolai Worm, University of Zurich, and Lechner, Katharina
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Aging ,Epidemiology ,Vulnerability ,Adipose tissue ,610 Medicine & health ,adipose tissue phenotype ,030204 cardiovascular system & hematology ,Cardiovascular ,Bioinformatics ,Affect (psychology) ,Risk Assessment ,Full Research Paper ,2705 Cardiology and Cardiovascular Medicine ,03 medical and health sciences ,CVD Risk Factors ,0302 clinical medicine ,Risk Factors ,Humans ,2.1 Biological and endogenous factors ,Medicine ,Healthy Lifestyle ,030212 general & internal medicine ,Aetiology ,Life Style ,Nutrition ,business.industry ,novel lifestyle risk factors ,Prevention ,Stressor ,Cardiorespiratory fitness ,Protective Factors ,Risk factor (computing) ,Atherosclerosis ,n-3 fatty acids ,ddc ,Residual risk ,Sleep deprivation ,Good Health and Well Being ,Heart Disease Risk Factors ,Atherosclerotic cardiovascular disease ,plaque phenotype ,10046 Balgrist University Hospital, Swiss Spinal Cord Injury Center ,ketone body ß-hydroxybutyrate ,Patient Safety ,medicine.symptom ,Cardiology and Cardiovascular Medicine ,business ,Risk Reduction Behavior ,2713 Epidemiology - Abstract
Despite major efforts to reduce atherosclerotic cardiovascular disease (ASCVD) burden with conventional risk factor control, significant residual risk remains. Recent evidence on non-traditional determinants of cardiometabolic health has advanced our understanding of lifestyle–disease interactions. Chronic exposure to environmental stressors like poor diet quality, sedentarism, ambient air pollution and noise, sleep deprivation and psychosocial stress affect numerous traditional and non-traditional intermediary pathways related to ASCVD. These include body composition, cardiorespiratory fitness, muscle strength and functionality and the intestinal microbiome, which are increasingly recognized as major determinants of cardiovascular health. Evidence points to partially overlapping mechanisms, including effects on inflammatory and nutrient sensing pathways, endocrine signalling, autonomic function and autophagy. Of particular relevance is the potential of low-risk lifestyle factors to impact on plaque vulnerability through altered adipose tissue and skeletal muscle phenotype and secretome. Collectively, low-risk lifestyle factors cause a set of phenotypic adaptations shifting tissue cross-talk from a proinflammatory milieu conducive for high-risk atherosclerosis to an anti-atherogenic milieu. The ketone body ß-hydroxybutyrate, through inhibition of the NLRP-3 inflammasome, is likely to be an intermediary for many of these observed benefits. Adhering to low-risk lifestyle factors adds to the prognostic value of optimal risk factor management, and benefit occurs even when the impact on conventional risk markers is discouragingly minimal or not present. The aims of this review are (a) to discuss novel lifestyle risk factors and their underlying biochemical principles and (b) to provide new perspectives on potentially more feasible recommendations to improve long-term adherence to low-risk lifestyle factors.
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- 2019
13. Your athlete-patient has a high coronary artery calcification score-'Heart of Stone'. What should you advise? Is exercise safe?
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Johannes Scherr, Benjamin Lechner, Bianca Spanier, Katharina Lechner, University of Zurich, and Lechner, Katharina
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medicine.medical_specialty ,Heart disease ,Sports medicine ,Physical fitness ,Physical Therapy, Sports Therapy and Rehabilitation ,610 Medicine & health ,Disease ,Coronary Artery Disease ,Lower risk ,03 medical and health sciences ,0302 clinical medicine ,2732 Orthopedics and Sports Medicine ,Internal medicine ,medicine ,Humans ,Orthopedics and Sports Medicine ,cardiovascular diseases ,030212 general & internal medicine ,3612 Physical Therapy, Sports Therapy and Rehabilitation ,Exercise ,Coronary atherosclerosis ,Subclinical infection ,business.industry ,Heart ,030229 sport sciences ,General Medicine ,medicine.disease ,Blood pressure ,Athletes ,10046 Balgrist University Hospital, Swiss Spinal Cord Injury Center ,business - Abstract
Coronary artery calcification (CAC) is a strong marker of subclinical coronary atherosclerosis and leading authorities recommend CAC scoring to help inform patient management decisions in cardiovascular disease (CVD) prevention.1 2 This will result in an increasing number of athlete-patients with subclinical coronary atherosclerosis presenting to sport and exercise medicine physicians, raising questions about exercise recommendations in this subgroup. With a specific focus on the recent outcomes data of DeFina and colleagues3 we extend our recent discussion of the topic2 by focusing on how to manage athlete-patients with elevated CAC in the sport and exercise medicine setting. A breakthrough in reporting the association of CAC and mortality risk across different activity levels came from a recent study of 21 758 healthy male participants without prevalent CVD. Higher levels of leisure-time physical activity were associated with a lower risk of mortality at any given level of CAC.3 The authors reported a higher risk metabolic profile (ie, higher baseline blood pressure, higher glucose concentrations and higher triglycerides) in the high volume exercise group with elevated CAC ≥100 AU …
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- 2020
14. Exercise recommendations in athletes with coronary artery calcification
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Martin Halle, Johannes Scherr, Katharina Lechner, Jonathan A. Drezner, University of Zurich, and Lechner, Katharina
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medicine.medical_specialty ,Computed Tomography Angiography ,Epidemiology ,MEDLINE ,610 Medicine & health ,Coronary Artery Disease ,Coronary Angiography ,Risk Assessment ,2705 Cardiology and Cardiovascular Medicine ,Text mining ,Predictive Value of Tests ,Risk Factors ,Internal medicine ,medicine ,Humans ,Vascular Calcification ,Exercise ,Computed tomography angiography ,medicine.diagnostic_test ,biology ,business.industry ,Athletes ,Coronary arteriosclerosis ,Cardiovascular Agents ,Protective Factors ,Prognosis ,biology.organism_classification ,Death, Sudden, Cardiac ,Predictive value of tests ,Coronary artery calcification ,Cardiology ,10046 Balgrist University Hospital, Swiss Spinal Cord Injury Center ,Cardiology and Cardiovascular Medicine ,Risk assessment ,business ,Risk Reduction Behavior ,2713 Epidemiology - Published
- 2019
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