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1,120 results on '"Laufs, Ulrich"'

2. Quality of life in patients with statin intolerance: a multicentre prospective registry study

Author

Baessler, A., Borucki, K., Heine, G., Hoh, G., Klingenberg, R., Koenig, W., Parhofer, K., Rettig-Ewen, V., Schettler, V., Schirmer, S., Seiler-Mußler, S., Stach-Jablonski, K., Taggeselle, J., Tamm, A., Vogt, A., Stürzebecher, Paulina E., Gouni-Berthold, Ioanna, Mateev, Christina, Frenzel, Ole, Erbe, Stephan, Boeckel, Jes-Niels, Scholz, Markus, Schatz, Ulrike, Weingärtner, Oliver, Kassner, Ursula, and Laufs, Ulrich

Published
2024
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5. Leptin treatment has vasculo-protective effects in lipodystrophic mice

Author

Stürzebecher, Paulina Elena, Kralisch, Susan, Schubert, Marie Ruth, Filipova, Vanina, Hoffmann, Annett, Oliveira, Fabiana, Sheikh, Bilal N., Blüher, Matthias, Kogel, Alexander, Scholz, Markus, Kokot, Karoline Elizabeth, Erbe, Stephan, Kneuer, Jasmin Marga, Ebert, Thomas, Fasshauer, Mathias, Miehle, Konstanze, Laufs, Ulrich, Tonjes, Anke, and Boeckel, Jes-Niels

Published
2022

7. Hepatocyte pyroptosis and release of inflammasome particles induce stellate cell activation and liver fibrosis

Author

Gaul, Susanne, Leszczynska, Aleksandra, Alegre, Fernando, Kaufmann, Benedikt, Johnson, Casey D, Adams, Leon A, Wree, Alexander, Damm, Georg, Seehofer, Daniel, Calvente, Carolina J, Povero, Davide, Kisseleva, Tatiana, Eguchi, Akiko, McGeough, Matthew D, Hoffman, Hal M, Pelegrin, Pablo, Laufs, Ulrich, and Feldstein, Ariel E

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Chronic Liver Disease and Cirrhosis, Digestive Diseases, Liver Disease, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Inflammatory and immune system, Good Health and Well Being, Animals, Caspase 1, Hepatic Stellate Cells, Hepatocytes, Humans, Inflammasomes, Interleukin-1beta, Liver Cirrhosis, Mice, Mice, Inbred NOD, NLR Family, Pyrin Domain-Containing 3 Protein, Non-alcoholic Fatty Liver Disease, Protein Translocation Systems, Pyroptosis, Reactive Oxygen Species, NLRP3, Inflammasome, Specks, ASC, Fibrosis, NASH, Liver, Public Health and Health Services, Gastroenterology & Hepatology, Clinical sciences
Abstract

Background & aimsIncreased hepatocyte death contributes to the pathology of acute and chronic liver diseases. However, the role of hepatocyte pyroptosis and extracellular inflammasome release in liver disease is unknown.MethodsWe used primary mouse and human hepatocytes, hepatocyte-specific leucine 351 to proline Nlrp3KICreA mice, and GsdmdKO mice to investigate pyroptotic cell death in hepatocytes and its impact on liver inflammation and damage. Extracellular NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasomes were isolated from mutant NLRP3-YFP HEK cells and internalisation was studied in LX2 and primary human hepatic stellate cells. We also examined a cohort of 154 adult patients with biopsy-proven non-alcoholic fatty liver disease (Sir Charles Gairdner Hospital, Nedlands, Western Australia).ResultsWe demonstrated that primary mouse and human hepatocytes can undergo pyroptosis upon NLRP3 inflammasome activation with subsequent release of NLRP3 inflammasome proteins that amplify and perpetuate inflammasome-driven fibrogenesis. Pyroptosis was inhibited by blocking caspase-1 and gasdermin D activation. The activated form of caspase-1 was detected in the livers and in serum from patients with non-alcoholic steatohepatitis and correlated with disease severity. Nlrp3KICreA mice showed spontaneous liver fibrosis under normal chow diet, and increased sensitivity to liver damage and inflammation after treatment with low dose lipopolysaccharide. Mechanistically, hepatic stellate cells engulfed extracellular NLRP3 inflammasome particles leading to increased IL-1β secretion and α-smooth muscle actin expression. This effect was abrogated when cells were pre-treated with the endocytosis inhibitor cytochalasin B.ConclusionsThese results identify hepatocyte pyroptosis and release of inflammasome components as a novel mechanism to propagate liver injury and liver fibrosis development.Lay summaryOur findings identify a novel mechanism of inflammation in the liver. Experiments in cell cultures, mice, and human samples show that a specific form of cell death, called pyroptosis, leads to the release of complex inflammatory particles, the NLRP3 inflammasome, from inside hepatocytes into the extracellular space. From there they are taken up by other cells and thereby mediate inflammatory and pro-fibrogenic stress signals. The discovery of this mechanism may lead to novel treatments for chronic liver diseases in the future.

Published
2021

8. The German CaRe high registry for familial hypercholesterolemia – Sex differences, treatment strategies, and target value attainment

Author

März, Winfried, Schmidt, Nina, an Haack, Ira, Dressel, Alexander, Grammer, Tanja B., Kleber, Marcus E., Baessler, Andrea, Beil, F. Ulrich, Gouni-Berthold, Ioanna, Julius, Ulrich, Kassner, Ursula, Katzmann, Julius L., Klose, Gerald, König, Christel, Koenig, Wolfgang, Koschker, Ann-Cathrin, Laufs, Ulrich, Merkel, Martin, Otte, Britta, Parhofer, Klaus G., Hengstenberg, Wibke, Schunkert, Heribert, Stach-Jablonski, Ksenija, Steinhagen-Thiessen, Elisabeth, Olivier, Christoph B., Hahmann, Harry, Krzossok, Stefan, Vogt, Anja, Müller-Wieland, Dirk, and Schatz, Ulrike

Published
2023
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9. Treatment gaps in the implementation of LDL cholesterol control among high- and very high-risk patients in Europe between 2020 and 2021: the multinational observational SANTORINI study

Author

Ray, Kausik K., Haq, Inaam, Bilitou, Aikaterini, Manu, Marius C., Burden, Annie, Aguiar, Carlos, Arca, Marcello, Connolly, Derek L., Eriksson, Mats, Ferrières, Jean, Laufs, Ulrich, Mostaza, Jose M., Nanchen, David, Rietzschel, Ernst, Strandberg, Timo, Toplak, Hermann, Visseren, Frank L.J., and Catapano, Alberico L.

Published
2023
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14. Adverse effects of statin therapy: perception vs. the evidence – focus on glucose homeostasis, cognitive, renal and hepatic function, haemorrhagic stroke and cataract

Author

Mach, François, Ray, Kausik K, Wiklund, Olov, Corsini, Alberto, Catapano, Alberico L, Bruckert, Eric, De Backer, Guy, Hegele, Robert A, Hovingh, G Kees, Jacobson, Terry A, Krauss, Ronald M, Laufs, Ulrich, Leiter, Lawrence A, März, Winfried, Nordestgaard, Børge G, Raal, Frederick J, Roden, Michael, Santos, Raul D, Stein, Evan A, Stroes, Erik S, Thompson, Paul D, Tokgözoğlu, Lale, Vladutiu, Georgirene D, Gencer, Baris, Stock, Jane K, Ginsberg, Henry N, and Chapman, M John

Subjects
Aging, Brain Disorders, Prevention, Patient Safety, Liver Disease, Clinical Trials and Supportive Activities, Digestive Diseases, Stroke, Clinical Research, Evaluation of treatments and therapeutic interventions, Aetiology, 2.1 Biological and endogenous factors, 6.1 Pharmaceuticals, Cataract, Cerebral Hemorrhage, Chemical and Drug Induced Liver Injury, Cognition Disorders, Glucose, Homeostasis, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Kidney Diseases, European Atherosclerosis Society Consensus Panel, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology
Abstract

AimsTo objectively appraise evidence for possible adverse effects of long-term statin therapy on glucose homeostasis, cognitive, renal and hepatic function, and risk for haemorrhagic stroke or cataract.Methods and resultsA literature search covering 2000-2017 was performed. The Panel critically appraised the data and agreed by consensus on the categorization of reported adverse effects. Randomized controlled trials (RCTs) and genetic studies show that statin therapy is associated with a modest increase in the risk of new-onset diabetes mellitus (about one per thousand patient-years), generally defined by laboratory findings (glycated haemoglobin ≥6.5); this risk is significantly higher in the metabolic syndrome or prediabetes. Statin treatment does not adversely affect cognitive function, even at very low levels of low-density lipoprotein cholesterol and is not associated with clinically significant deterioration of renal function, or development of cataract. Transient increases in liver enzymes occur in 0.5-2% of patients taking statins but are not clinically relevant; idiosyncratic liver injury due to statins is very rare and causality difficult to prove. The evidence base does not support an increased risk of haemorrhagic stroke in individuals without cerebrovascular disease; a small increase in risk was suggested by the Stroke Prevention by Aggressive Reduction of Cholesterol Levels study in subjects with prior stroke but has not been confirmed in the substantive evidence base of RCTs, cohort studies and case-control studies.ConclusionLong-term statin treatment is remarkably safe with a low risk of clinically relevant adverse effects as defined above; statin-associated muscle symptoms were discussed in a previous Consensus Statement. Importantly, the established cardiovascular benefits of statin therapy far outweigh the risk of adverse effects.

Published
2018

15. SLM2 Is A Novel Cardiac Splicing Factor Involved in Heart Failure due to Dilated Cardiomyopathy

Author

Boeckel, Jes-Niels, Möbius-Winkler, Maximilian, Müller, Marion, Rebs, Sabine, Eger, Nicole, Schoppe, Laura, Tappu, Rewati, Kokot, Karoline E., Kneuer, Jasmin M., Gaul, Susanne, Bordalo, Diana M., Lai, Alan, Haas, Jan, Ghanbari, Mahsa, Drewe-Boss, Philipp, Liss, Martin, Katus, Hugo A., Ohler, Uwe, Gotthardt, Michael, Laufs, Ulrich, Streckfuss-Bömeke, Katrin, and Meder, Benjamin

Published
2022
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19. Evaluation of contemporary treatment of high- and very high-risk patients for the prevention of cardiovascular events in Europe – Methodology and rationale for the multinational observational SANTORINI study

Author

Ray, Kausik K., Haq, Inaam, Bilitou, Aikaterini, Aguiar, Carlos, Arca, Marcello, Connolly, Derek L., Eriksson, Mats, Ferrières, Jean, Hildebrandt, Per, Laufs, Ulrich, Mostaza, Jose M., Nanchen, David, Rietzschel, Ernst, Strandberg, Timo, Toplak, Hermann, Visseren, Frank L.J., and Catapano, Alberico L.

Published
2021
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21. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel

Author

Ference, Brian A, Ginsberg, Henry N, Graham, Ian, Ray, Kausik K, Packard, Chris J, Bruckert, Eric, Hegele, Robert A, Krauss, Ronald M, Raal, Frederick J, Schunkert, Heribert, Watts, Gerald F, Borén, Jan, Fazio, Sergio, Horton, Jay D, Masana, Luis, Nicholls, Stephen J, Nordestgaard, Børge G, van de Sluis, Bart, Taskinen, Marja-Riitta, Tokgözoğlu, Lale, Landmesser, Ulf, Laufs, Ulrich, Wiklund, Olov, Stock, Jane K, Chapman, M John, and Catapano, Alberico L

Subjects
Cardiovascular, Atherosclerosis, Clinical Trials and Supportive Activities, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Anticholesteremic Agents, Cholesterol, HDL, Cholesterol, LDL, Consensus, Epidemiologic Methods, Ezetimibe, Genetic Predisposition to Disease, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hyperlipidemias, Lipoproteins, LDL, PCSK9 Inhibitors, Cardiovascular disease, Causality, Clinical trials, Low-density lipoprotein, Mendelian randomization, PCSK9, Recommendations, Statin, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology
Abstract

AimsTo appraise the clinical and genetic evidence that low-density lipoproteins (LDLs) cause atherosclerotic cardiovascular disease (ASCVD).Methods and resultsWe assessed whether the association between LDL and ASCVD fulfils the criteria for causality by evaluating the totality of evidence from genetic studies, prospective epidemiologic cohort studies, Mendelian randomization studies, and randomized trials of LDL-lowering therapies. In clinical studies, plasma LDL burden is usually estimated by determination of plasma LDL cholesterol level (LDL-C). Rare genetic mutations that cause reduced LDL receptor function lead to markedly higher LDL-C and a dose-dependent increase in the risk of ASCVD, whereas rare variants leading to lower LDL-C are associated with a correspondingly lower risk of ASCVD. Separate meta-analyses of over 200 prospective cohort studies, Mendelian randomization studies, and randomized trials including more than 2 million participants with over 20 million person-years of follow-up and over 150 000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. Both the naturally randomized genetic studies and the randomized intervention trials consistently demonstrate that any mechanism of lowering plasma LDL particle concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C, provided that the achieved reduction in LDL-C is concordant with the reduction in LDL particle number and that there are no competing deleterious off-target effects.ConclusionConsistent evidence from numerous and multiple different types of clinical and genetic studies unequivocally establishes that LDL causes ASCVD.

Published
2017

22. ASC speck serum concentrations, a component of sterile cellular inflammation, are associated with individual cardiopulmonary capacity.

Author

Kogel, Alexander, Voßhage, Nell, Behzadi, Amirhossein, Laufs, Ulrich, and Fikenzer, Sven

Subjects
MARATHON running, EXERCISE tests, BODY composition, HEART beat, INFLAMMASOMES
Abstract

Aims: Exercise-induced cellular stress and sterile inflammation are of increasing interest. ASC specks are a component of the intracellular NLRP3-inflammasome and can be released into the blood. For example, serum ASC specks are increased after marathon running. We therefore tested whether ASC specks are potentially associated with the individual response to physical training and cardiopulmonary capacity. Methods: We performed a prospective study in 45 healthy athletes. Blood samples were taken before and after cardiopulmonary exercise testing (CPET). ASC speck concentrations were quantitated using flow cytometry. Results: Baseline ASC speck levels correlated with clinical parameters of body composition (height, weight, BMI) and parameters of cardiopulmonary performance (peak VO2, peak oxygen pulse, heart rate after exercise). Athletes with lowest baseline ASC speck concentrations have a significantly lower BMI (22.0 ± 1.8 vs. 24.9 ± 1.6 kg/m2), higher heart rate at rest (72 ± 10 vs. 58 ± 10 beats/min), lower peak VO2 (2692 ± 629 vs. 3404 ± 747 mL/min) and lower peak oxygen pulse (15.6 ± 3.4 vs. 20.7 ± 3.5 mL/heart rate). Overall, ASC speck concentrations showed no significant change after CPET (7.0 ± 4.5 vs. 8.0 ± 5.4 ASC specks/µL, p = 0.3). However, subgroup analysis revealed a significant increase in circulating ASC specks in athletes with the lowest baseline values (2.37 ± 0.84 vs. 8.43 ± 7.52 ASC specks/µL, p < 0.05). Athletes with an increase in ASC speck concentrations in response to CPET had a lower peak oxygen pulse compared to those with a decrease (17.1 ± 4.2 vs. 19.8 ± 4.1, p < 0.05). Conclusion: Low ASC speck baseline values as well as an increase in response to exercise are associated with lower peak oxygen pulse in healthy athletes. [ABSTRACT FROM AUTHOR]

Published
2024
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24. Apolipoprotein B, Residual Cardiovascular Risk After Acute Coronary Syndrome, and Effects of Alirocumab

Author

Hagström, Emil, Steg, P. Gabriel, Szarek, Michael, Bhatt, Deepak L., Bittner, Vera A., Danchin, Nicolas, Diaz, Rafael, Goodman, Shaun G., Harrington, Robert A., Jukema, J. Wouter, Liberopoulos, Evangelos, Marx, Nikolaus, McGinniss, Jennifer, Manvelian, Garen, Pordy, Robert, Scemama, Michel, White, Harvey D., Zeiher, Andreas M., Schwartz, Gregory G., Schwartz, Gregory G., Bhatt, Deepak L., Bittner, Vera A., Diaz, Rafael, Goodman, Shaun G., Harrington, Robert A., Jukema, J. Wouter, Szarek, Michael, White, Harvey D., Zeiher, Andreas M., Tricoci, Pierluigi, Roe, Matthew T., Mahaffey, Kenneth W., Edelberg, Jay M., Hanotin, Corinne, Lecorps, Guillaume, Moryusef, Angèle, Pordy, Robert, Sasiela, William J., Tamby, Jean-François, Diaz, Rafael, Aylward, Philip E, Drexel, Heinz, Sinnaeve, Peter, Dilic, Mirza, Lopes, Renato D., Gotcheva, Nina N, Goodman, Shaun G., Prieto, Juan-Carlos, Yong, Huo, López-Jaramillo, Patricio, Pećin, Ivan, Reiner, Zeljko, Ostadal, Petr, Poulsen, Steen Hvitfeldt, Viigimaa, Margus, Nieminen, Markku S, Danchin, Nicolas, Chumburidze, Vakhtang, Marx, Nikolaus, Liberopoulos, Evangelos, Carlos, Pablo, Valdovinos, Montenegro, Tse, Hung-Fat, Kiss, Robert Gabor, Xavier, Denis, Zahger, Doron, Valgimigli, Marco, Kimura, Takeshi, Kim, Hyo Soo, Kim, Sang-Hyun, Erglis, Andrejs, Laucevicius, Aleksandras, Kedev, Sasko, Yusoff, Khalid, Ramos López, Gabriel Arturo, Alings, Marco, White, Harvey D., Halvorsen, Sigrun, Correa Flores, Roger M, Sy, Rody G., Budaj, Andrzej, Morais, Joao, Dorobantu, Maria, Karpov, Yuri, Ristic, Arsen D., Chua, Terrance, Murin, Jan, Fras, Zlatko, Dalby, Anthony J, Tuñón, José, de Silva, H. Asita, Hagström, Emil, Landmesser, Ulf, Müller, Christian, Chiang, Chern-En, Sritara, Piyamitr, Guneri, Sema, Parkhomenko, Alexander, Ray, Kausik K., Moriarty, Patrick M., Roe, Matthew T., Vogel, Robert, Chaitman, Bernard, Kelsey, Sheryl F., Olsson, Anders G., Rouleau, Jean-Lucien, Simoons, Maarten L., Alexander, Karen, Meloni, Chiara, Rosenson, Robert, Sijbrands, Eric J.G., Tricoci, Pierluigi, Alexander, John H., Armaganijan, Luciana, Bagai, Akshay, Bahit, Maria Cecilia, Brennan, J. Matthew, Clifton, Shaun, DeVore, Adam D., Deloatch, Shalonda, Dickey, Sheila, Dombrowski, Keith, Ducrocq, Grégory, Eapen, Zubin, Endsley, Patricia, Eppinger, Arleen, Harrison, Robert W., Hess, Connie Ng, Hlatky, Mark A., Jordan, Joseph Dedrick, Knowles, Joshua W., Kolls, Bradley J., Kong, David F., Leonardi, Sergio, Lillis, Linda, Lopes, Renato D., Maron, David J., Mahaffey, Kenneth W., Marcus, Jill, Mathews, Robin, Mehta, Rajendra H., Mentz, Robert J., Moreira, Humberto Graner, Patel, Chetan B., Pereira, Sabrina Bernardez, Perkins, Lynn, Povsic, Thomas J., Puymirat, Etienne, Roe, Matthew T., Jones, William Schuyler, Shah, Bimal R., Sherwood, Matthew W., Stringfellow, Kenya, Sujjavanich, Darin, Toma, Mustafa, Trotter, Charlene, van Diepen, Sean F.P., Wilson, Matthew D., Tze-Kay Yan, Andrew, Schiavi, Lilia B, Garrido, Marcelo, Alvarisqueta, Andrés F, Sassone, Sonia A, Bordonava, Anselmo P, Alves De Lima, Alberto E, Schmidberg, Jorge M, Duronto, Ernesto A, Caruso, Orlando C, Novaretto, Leonardo P, Hominal, Miguel Angel, Montaña, Oscar R, Caccavo, Alberto, Gomez Vilamajo, Oscar A, Lorenzatti, Alberto J, Cartasegna, Luis R, Paterlini, Gustavo A, Mackinnon, Ignacio J, Caime, Guillermo D, Amuchastegui, Marcos, Salomone, Oscar, Codutti, Oscar R, Jure, Horacio O, Bono, Julio OE, Hrabar, Adrian D, Vallejos, Julio A, Ahuad Guerrero, Rodolfo A, Novoa, Federico, Patocchi, Cristian A, Zaidman, Cesar J, Giuliano, Maria E, Dran, Ricardo D, Vico, Marisa L, Carnero, Gabriela S, Guzman, Pablo N, Medrano Allende, Juan C, Garcia Brasca, Daniela F, Bustamante Labarta, Miguel H, Nani, Sebastian, Blumberg, Eduardo DS, Colombo, Hugo R, Liberman, Alberto, Fuentealba, Victorino, Luciardi, Hector L, Waisman, Gabriel D, Berli, Mario A, Garcia Duran, Ruben O, Cestari, Horacio G, Luquez, Hugo A, Giordano, Jorge A, Saavedra, Silvia S, Zapata, Gerardo, Costamagna, Osvaldo, Llois, Susana, Waites, Jonathon H, Collins, Nicholas, Soward, Allan, Aylward, Philip E, Hii, Chris LS, Aylward, Philip E, Shaw, James, Arstall, Margaret A, Horowitz, John, Ninio, Daniel, Rogers, James F, Colquhoun, David, Oqueli Flores, Romulo E, Roberts-Thomson, Philip, Raffel, Owen, Lehman, Sam J, Aroney, Constantine, Coverdale, Steven GM, Garrahy, Paul J, Starmer, Gregory, Sader, Mark, Carroll, Patrick A, Dick, Ronald, Zweiker, Robert, Hoppe, Uta, Drexel, Heinz, Huber, Kurt, Berger, Rudolf, Delle-Karth, Georg, Frey, Bernhard, Weidinger, Franz, Faes, Dirk, Hermans, Kurt, Pirenne, Bruno, Leone, Attilio, Hoffer, Etienne, Sinnaeve, Peter, Vrolix, Mathias CM, Wolf, Luc De, Wollaert, Bart, Castadot, Marc, Dujardin, Karl, Beauloye, Christophe, Vervoort, Geert, Striekwold, Harry, Convens, Carl, Roosen, John, Barbato, Emanuele, Claeys, Marc, Cools, Frank, Terzic, Ibrahim, Barakovic, Fahir, Midzic, Zlatko, Pojskic, Belma, Fazlibegovic, Emir, Dilic, Mirza, Durak-Nalbantic, Azra, Kulić, Mehmed, Vulic, Dusko, Muslibegovic, Adis, Goronja, Boris, Reis, Gilmar, Sousa, Luciano, Nicolau, Jose C, Giorgeto, Flavio E, Silva, Ricardo P, Maia, Lilia Nigro, Rech, Rafael, Rossi, Paulo RF, Cerqueira, Maria José AG, Duda, Norberto, Kalil, Renato, Kormann, Adrian, Abrantes, José Antonio M, Filho, Pedro Pimentel, Soggia, Ana Priscila, de Santos, Mayler ON, Neuenschwander, Fernando, Bodanese, Luiz C, Michalaros, Yorghos L, Eliaschewitz, Freddy G, Vidotti, Maria H, Leaes, Paulo E, Botelho, Roberto V, Kaiser, Sergio, Manenti, Euler Roberto F Fernandes, Precoma, Dalton B, Moura Jorge, Jose C, Silva, Pedro, Silveira, Jose A, Saporito, Wladmir, Neto, Jose A Marin, Feitosa, Gilson S, Ritt, Luiz Eduardo F, de Souza, Juliana A, Costa, Fernando, Souza, Weimar KSB, Reis, Helder JL, Lopes, Renato D., Machado, Leandro, Aidar Ayoub, José Carlos, Todorov, Georgi V, Nikolov, Fedya P, Velcheva, Elena S, Tzekova, Maria L, Benov, Haralambi O, Petranov, Stanislav L, Tumbev, Haralin S, Shehova-Yankova, Nina S, Markov, Dimitar T, Raev, Dimitar H, Mollov, Mihail N, Kichukov, Kostadin N, Ilieva- Pandeva, Katya A, Gotcheva, Nina N, Ivanova, Raya, Gospodinov, Maryana, Mincheva, Valentina M, Lazov, Petar V, Dimov, Bojidar I, Senaratne, Manohara, Stone, James, Kornder, Jan, Pearce, Stephen, Dion, Danielle, Savard, Daniel, Pesant, Yves, Pandey, Amritanshu, Robinson, Simon, Gosselin, Gilbert, Vizel, Saul, Hoag, Gordon, Bourgeois, Ronald, Morisset, Anne, Sabbah, Eric, Sussex, Bruce, Kouz, Simon, MacDonald, Paul, Diaz, Ariel, Michaud, Nicolas, Fell, David, Leung, Raymond, Vuurmans, Tycho, Lai, Christopher, Nigro, Frank, Davies, Richard, Nogareda, Gustavo, Vijayaraghavan, Ram, Ducas, John, Lepage, Serge, Mehta, Shamir, Cha, James, Dupuis, Robert, Fong, Peter, Lutchmedial, Sohrab, Rodes-Cabau, Josep, Fadlallah, Hussein, Cleveland, David, Huynh, Thao, Bata, Iqbal, Hameed, Adnan, Pincetti, Cristian, Potthoff, Sergio, Prieto, Juan C, Acevedo, Monica, Aguirre, Arnoldo, Vejar, Margarita, Yañez, Mario, Araneda, Guillermo, Fernandez, Mauricio, Perez, Luis, Varleta, Paola, Florenzano, Fernando, Huidobro, Laura, Raffo, Carlos A, Olivares, Claudia, Nahuelpan, Leonardo, Montecinos, Humberto, Chen, Jiyan, Dong, Yugang, Huang, Weijian, Wang, Jianzhong, Huang, Shi’An, Yao, Zhuhua, Li, Xiang, Cui, Lan, Lin, Wenhua, Sun, Yuemin, Wang, Jingfeng, Li, Jianping, Zhang, Xuelian, Zhu, Hong, Chen, Dandan, Huang, Lan, Dong, Shaohong, Su, Guohai, Xu, Biao, Su, Xi, Cheng, Xiaoshu, Lin, Jinxiu, Zong, Wenxia, Li, Huanming, Feng, Yi, Xu, Dingli, Yang, Xinchun, Ke, Yuannan, Lin, Xuefeng, Zhang, Zheng, Zheng, Zeqi, Luo, Zhurong, Chen, Yundai, Ding, Chunhua, Zhong, Yi, Zheng, Yang, Li, Xiaodong, Peng, Daoquan, Zhao, Shuiping, Li, Ying, Liu, Xuebo, Wei, Meng, Liu, Shaowen, Yu, Yihua, Qu, Baiming, Jiang, Weihong, Zhou, Yujie, Zhao, Xingsheng, Yuan, Zuyi, Guo, Ying, Xu, Xiping, Shi, Xubo, Ge, Junbo, Fu, Guosheng, Bai, Feng, Fang, Weiyi, Shou, Xiling, Yang, Xiangjun, Wang, Jian’An, Xiang, Meixiang, Sun, Yingxian, Lu, Qinghua, Zhang, Ruiyan, Zhu, Jianhua, Xu, Yizhou, Fan, Zhongcai, Li, Tianchang, Wu, Chun, Jaramillo, Nicolas, Vallejo, Gregorio Sanchez, Luna Botia, Diana C, Lopez, Rodrigo Botero, De Salazar, Dora I Molina, Bonfanti, Alberto J Cadena, Aroca, Carlos Cotes, Higuera, Juan Diego, Blanquicett, Marco, Barrera Silva, Sandra I, Garcia Lozada, Henry J, Coronel Arroyo, Julian A, Accini Mendoza, Jose L, Fernandez Ruiz, Ricardo L, Quintero Ossa, Alvaro M., Manzur Jatin, Fernando G, Sotomayor Herazo, Aristides, Parada, Jeffrey Castellanos, Arambula, Rafael Suarez, Urina Triana, Miguel A, Trujillo, Angela M Fernandez, Strozzi, Maja, Car, Siniša, Miličić, Davor, Lovrić Benčić, Martina, Pintarić, Hrvoje, Prvulović, Đeiti, Šikić, Jozica, Peršić, Viktor, Mileta, Dean, Štambuk, Kresimir, Babić, Zdravko, Tomulic, Vjekoslav, Lukenda, Josip, Mejic-Krstulovic, Stanka, Starcevic, Boris, Spinar, Jindrich, Horak, David, Velicka, Zdenek, Alan, David, Machova, Vilma, Linhart, Ales, Novotny, Vojtech, Kaucak, Vladimir, Rokyta, Richard, Naplava, Robert, Coufal, Zdenek, Adamkova, Vera, Podpera, Ivo, Zizka, Jiri, Motovska, Zuzana, Marusincova, Ivana, Ostadal, Petr, Heinc, Petr, Kuchar, Jiri, Povolny, Petr, Matuska, Jiri, Poulsen, Steen H, Raungaard, Bent, Clemmensen, Peter, Bang, Lia E, May, Ole, Bøttcher, Morten, Hove, Jens D, Frost, Lars, Gislason, Gunnar, Larsen, John, Johansen, Peter Betton, Hald, Flemming, Johansen, Peter, Jeppesen, Jørgen, Nielsen, Tonny, Kristensen, Kjeld S, Walichiewicz, Piotr Maria, Lomholdt, Jens D, Klausen, Ib C, Nielsen, Peter Kaiser, Davidsen, Flemming, Videbaek, Lars, Viigimaa, Margus, Soots, Mai, Vahula, Veiko, Hedman, Anu, Soopõld, Üllar, Märtsin, Kaja, Jurgenson, Tiina, Kristjan, Arved, Nieminen, Markku S, Vikman, Saila, Huikuri, Heikki, Airaksinen, Juhani, Coste, Pierre, Ferrari, Emile, Danchin, Nicolas, Morel, Olivier, Montalescot, Gilles, Machecourt, Jacques, Barone-Rochette, Gilles, Mansourati, Jacques, Cottin, Yves, Steg, Ph. 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Mladen, Knutson, Thomas, Friedman, Dennis, Chaleff, Fred, Loussararian, Arthur, Rozeman, Phillip, Kimmelstiel, Carey, Kuvin, Jeffrey, Silver, Kevin, Foster, Malcolm, Tonnessen, Glen, Espinoza, Andrey, Amlani, Mohamadali, Wali, Andreas, Malozzi, Christopher, Jong, Geert T, Massey, Clara, Wattanakit, Keattiyoat, O’Donnell, Philip J., Singal, Dinesh, Jaffrani, Naseem, Banuru, Sridhar, Fisher, Daniel, Xenakis, Mark, Perlmutter, Neal, Bhagwat, Ravi, Strader, James, Blonder, Ronald, Akyea-Djamson, Ayim, Labroo, Ajay, Lee, Kwan, Marais, H. John, Claxton, Edmund, Weiss, Robert, Kathryn, Rohr, Berk, Martin, Rossi, Peter, Joshi, Parag, Khera, Amit, Khaira, Ajit S, Kumkumian, Greg, Lupovitch, Steven, Purow, Joshua, Welka, Stephen, Hoffman, David, Fischer, Stuart, Soroka, Eugene, Eagerton, Donald, Pancholy, Samir, Ray, Michael, Erenrich, Norman, Farrar, Michael, Pollock, Stewart, French, William J, Diamantis, Steve, Guy, Douglas, Gimple, Lawrence, Neustel, Mark, Schwartz, Steven, Pereira, Edward, Albert, Seals, Spriggs, Douglas, Strain, Janet, Mittal, Suneet, Vo, Anthony, Chane, Majed, Hall, Jason, Vijay, Nampalli, Lotun, Kapildeo, Lester, F. Martin, Nahhas, Ahed, Pope, Theodore, Nager, Paul, Vohra, Rakesh, Sharma, Mukesh, Bashir, Riyaz, Ahmed, Hinan, Berlowitz, Michael, Fishberg, Robert, Barrucco, Robert, Yang, Eric, Radin, Michael, Sporn, Daniel, Stapleton, Dwight, Eisenberg, Steven, Landzberg, Joel, Mcgough, Martin, Turk, Samir, Schwartz, Michael, Sundram, P. Sandy, Jain, Diwakar, Zainea, Mark, Bayron, Carlos, Karlsberg, Ronald, Dohad, Suhail, Lui, Henry, Keen, William, Westerhausen, Donald, Khurana, Sandeep, Agarwal, Himanshu, Birchem, Jessica, Penny, William, Chang, Mark, Murphy, Sherrill, Henry, John, Schifferdecker, Branislav, Gilbert, John M, Chalavarya, Gopal, Eaton, Charles, Schmedtje, John F, Christenson, Stuart, Dotani, Imran, Denham, Douglas, Macdonell, Alexander, Gibson, Paul, Rahman, Aref, Al Joundi, Tammam, Assi, Nizar, Conrad, Gary, Kotha, Purushotham, Love, Michael, Giesler, Gregory, Rubenstein, Howard, Gamil, Dawood, Akright, Laura, Krawczyk, Justine, Cobler, Joanne, Wells, Terry, Welker, James, Foster, Robert, Gilmore, Richard, Anderson, Jay, Jacoby, Douglas, Harris, Bill, Gardner, Geraldine, Dandillaya, Ramprasad, Vora, Kishor, Kostis, John, Hunter, John, Laxson, David, Ball, Eric, Anderson, Jay, Wells, Terry, Vora, Kishor, Ball, Eric, Welker, James, Lopes, Renato D., Egydio, Flavia, Kawakami, Anelise, Oliveira, Janaina, Goodman, Shaun G., Wozniak, Julianna, Matthews, Alexander, Ratky, Caroline, Valiris, Janine, Berdan, Lisa, Hepditch, Anita, Quintero, Kirby, Roe, Matthew T., Rorick, Tyrus, Westbrook, Melissa, Danchin, Nicolas, Bezault, Madeleine, Drouet, Elodie, Simon, Tabassome, White, Harvey D., Alsweiler, Caroline, Sinnaeve, Peter, Luyten, Anne, Aylward, Philip E, Butters, Julie, Griffith, Liddy, Shaw, Michelle, Hagström, Emil, Grunberg, Lena, Szarek, Michael, Islam, Shahidul, Brégeault, Marie-France, Bougon, Nathalie, Faustino, Douglas, Fontecave, Sylvie, Murphy, Judith, Tamby, Jean- Francois, Verrier, Melanie, Agnetti, Veronique, Andersen, Dorthe, Badreddine, Emmy, Bekkouche, Mhamed, Bouancheau, Cecile, Brigui, Imane, Brocklehurst, Maddy, Cianciarulo, Joseph, Devaul, Dawn, Domokos, Szilvia, Gache, Cecile, Gobillot, Caroline, Guillou, Severine, Healy, Jan, Heath, Megan, Jaiwal, Gayatri, Javierre, Carine, Labeirie, Julien, Monier, Myriam, Morales, Ulises, Mrabti, Asmaa, Mthombeni, Bicky, Okan, Betim, Smith, Lucile, Sheller, Jennifer, Sopena, Sebastien, Pellan, Valerie, Benbernou, Fadela, Bengrait, Nafissa, Lamoureux, Maud, Kralova, Katarina, Scemama, Michel, Bejuit, Raphael, Coulange, Anthony, Berthou, Christelle, Repincay, Jérôme, Lorenzato, Christelle, Etienne, Alexis, Gouet, Valerie, Lecorps, Guillaume, Loizeau, Virginie, Normand, Mickael, Ourliac, Anne, Rondel, Christelle, Adamo, Antony, Beltran, Pascale, Barraud, Pauline, Dubois-Gache, Helene, Halle, Benjamin, Metwally, Lamia, Mourgues, Maxime, Sotty, Marc, Vincendet, Marion, Cotruta, Raluca, Chengyue, Zhu, Fournie-Lloret, Dominique, Morrello, Christine, Perthuis, Aurelie, Picault, Patrick, Zobouyan, Isabelle, Colhoun, Helen M., Dempsey, Michael A., and McClanahan, Mark A.

Published
2022
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25. Statin-associated muscle symptoms: impact on statin therapy—European Atherosclerosis Society Consensus Panel Statement on Assessment, Aetiology and Management

Author

Stroes, Erik S, Thompson, Paul D, Corsini, Alberto, Vladutiu, Georgirene D, Raal, Frederick J, Ray, Kausik K, Roden, Michael, Stein, Evan, Tokgözoğlu, Lale, Nordestgaard, Børge G, Bruckert, Eric, De Backer, Guy, Krauss, Ronald M, Laufs, Ulrich, Santos, Raul D, Hegele, Robert A, Hovingh, G Kees, Leiter, Lawrence A, Mach, Francois, März, Winfried, Newman, Connie B, Wiklund, Olov, Jacobson, Terry A, Catapano, Alberico L, Chapman, M John, Ginsberg, Henry N, Stroes, Erik, John Chapman, M, de Backer, Guy, Kees Hovingh, G, and Leiter, Lawrence

Subjects
Clinical Research, Cardiovascular, Atherosclerosis, 2.1 Biological and endogenous factors, Aetiology, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Cholesterol Ester Transfer Proteins, Complementary Therapies, Consensus, Creatine Kinase, Diet, Genetic Predisposition to Disease, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hypolipidemic Agents, Mitochondria, Muscle, Mitochondrial Diseases, Muscular Diseases, Proprotein Convertase 9, Proprotein Convertases, Risk Factors, Serine Endopeptidases, European Atherosclerosis Society Consensus Panel, Cholesterol, Consensus statement, Lipids, Mitochondrial, Muscle symptoms, Myalgia, Myopathy, Statin, Statin intolerance, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology
Abstract

Statin-associated muscle symptoms (SAMS) are one of the principal reasons for statin non-adherence and/or discontinuation, contributing to adverse cardiovascular outcomes. This European Atherosclerosis Society (EAS) Consensus Panel overviews current understanding of the pathophysiology of statin-associated myopathy, and provides guidance for diagnosis and management of SAMS. Statin-associated myopathy, with significant elevation of serum creatine kinase (CK), is a rare but serious side effect of statins, affecting 1 per 1000 to 1 per 10 000 people on standard statin doses. Statin-associated muscle symptoms cover a broader range of clinical presentations, usually with normal or minimally elevated CK levels, with a prevalence of 7-29% in registries and observational studies. Preclinical studies show that statins decrease mitochondrial function, attenuate energy production, and alter muscle protein degradation, thereby providing a potential link between statins and muscle symptoms; controlled mechanistic and genetic studies in humans are necessary to further understanding. The Panel proposes to identify SAMS by symptoms typical of statin myalgia (i.e. muscle pain or aching) and their temporal association with discontinuation and response to repetitive statin re-challenge. In people with SAMS, the Panel recommends the use of a maximally tolerated statin dose combined with non-statin lipid-lowering therapies to attain recommended low-density lipoprotein cholesterol targets. The Panel recommends a structured work-up to identify individuals with clinically relevant SAMS generally to at least three different statins, so that they can be offered therapeutic regimens to satisfactorily address their cardiovascular risk. Further research into the underlying pathophysiological mechanisms may offer future therapeutic potential.

Published
2015

31. Loss of Mitochondrial Ca2+ Uniporter Limits Inotropic Reserve and Provides Trigger and Substrate for Arrhythmias in Barth Syndrome Cardiomyopathy

Author

Bertero, Edoardo, Nickel, Alexander, Kohlhaas, Michael, Hohl, Mathias, Sequeira, Vasco, Brune, Carolin, Schwemmlein, Julia, Abeßer, Marco, Schuh, Kai, Kutschka, Ilona, Carlein, Christopher, Münker, Kai, Atighetchi, Sarah, Müller, Andreas, Kazakov, Andrey, Kappl, Reinhard, von der Malsburg, Karina, van der Laan, Martin, Schiuma, Anna-Florentine, Böhm, Michael, Laufs, Ulrich, Hoth, Markus, Rehling, Peter, Kuhn, Michaela, Dudek, Jan, von der Malsburg, Alexander, Prates Roma, Leticia, and Maack, Christoph

Published
2021
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49. Levels and dynamics of estimated glomerular filtration rate and recurrent vascular events and death in patients with minor stroke or transient ischemic attack

Author

Tütüncü, Serdar, Olma, Manuel C., Kunze, Claudia, Krämer, Michael, Dietzel, Joanna, Schurig, Johannes, Filser, Paula, Pfeilschifter, Waltraud, Hamann, Gerhard F., Büttner, Thomas, Heuschmann, Peter U., Kirchhof, Paulus, Laufs, Ulrich, Nabavi, Darius G., Röther, Joachim, Thomalla, Götz, Veltkamp, Roland, Eckardt, Kai‐Uwe, Haeusler, Karl Georg, and Endres, Matthias

Subjects
Stroke, Neurology, Ischemic Attack, Transient, Risk Factors, Atrial Fibrillation, Humans, ddc:610, Neurology (clinical), Glomerular Filtration Rate, Ischemic Stroke
Abstract

Background and purpose Impaired kidney function is associated with an increased risk of vascular events in acute stroke patients, when assessed by single measurements of estimated glomerular filtration rate (eGFR). It is unknown whether repeated measurements provide additional information for risk prediction. Methods The MonDAFIS (Systematic Monitoring for Detection of Atrial Fibrillation in Patients with Acute Ischemic Stroke) study randomly assigned 3465 acute ischemic stroke patients to either standard procedures or an additive Holter electrocardiogram. Baseline eGFR (CKD‐EPI formula) were dichotomized into values of < versus ≥60 ml/min/1.73 m\(^{2}\). eGFR dynamics were classified based on two in‐hospital values as “stable normal” (≥60 ml/min/1.73 m\(^{2}\)), “increasing” (by at least 15% from baseline, second value ≥ 60 ml/min/1.73 m\(^{2}\)), “decreasing” (by at least 15% from baseline of ≥60 ml/min/1.73 m\(^{2}\)), and “stable decreased” (

Published
2022
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