22 results on '"Sampietro, T."'
Search Results
2. Coronary microcirculatory blood flow significantly increases upon acute and chronic cholesterol lowering. Evaluation by cadmium-zinc-telluride cardiac imaging stress test
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Sampietro, T., primary, Sbrana, F., additional, Pino, B. Dal, additional, Bigazzi, F., additional, Ripoli, A., additional, Marzullo, P., additional, and Gimelli, A., additional
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- 2022
- Full Text
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3. Long-term efficacy of lipoprotein apheresis and lomitapide in the treatment of homozygous familial hypercholesterolemia (HoFH): a cross-national retrospective survey
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Tiziana Sampietro, Marcello Arca, Paolo Calabrò, Olga Kalmykova, Livia Pisciotta, Stefano Bertolini, Gabriella Iannuzzo, Francesco Sbrana, Fabio Nota, Antonio Gallo, Carlo Sabbà, Patrizia Suppressa, Arturo Cesaro, Giuliana Fortunato, Randa Bittar, Arturo Puja, Marco Bucci, Katia Bonomo, Angelo B. Cefalù, Samir Saheb, Maurizio Averna, Tiziana Montalcini, Alessio Buonaiuto, Sergio D'Addato, Alain Carrié, Chiara Pavanello, Sophie Béliard, Alessia Di Costanzo, S. Palmisano, Eric Bruckert, Giovanni Battista Vigna, Antonina Giammanco, Laura Calabresi, Fabio Fimiani, Laura D'Erasmo, D'Erasmo L., Gallo A., Cefalu A.B., Di Costanzo A., Saheb S., Giammanco A., Averna M., Buonaiuto A., Iannuzzo G., Fortunato G., Puja A., Montalcini T., Pavanello C., Calabresi L., Vigna G.B., Bucci M., Bonomo K., Nota F., Sampietro T., Sbrana F., Suppressa P., Sabba C., Fimiani F., Cesaro A., Calabro P., Palmisano S., D'Addato S., Pisciotta L., Bertolini S., Bittar R., Kalmykova O., Beliard S., Carrie A., Arca M., Bruckert E., D'Erasmo, L., Gallo, A., Cefalu, A. B., Di Costanzo, A., Saheb, S., Giammanco, A., Averna, M., Buonaiuto, A., Iannuzzo, G., Fortunato, G., Puja, A., Montalcini, T., Pavanello, C., Calabresi, L., Vigna, G. B., Bucci, M., Bonomo, K., Nota, F., Sampietro, T., Sbrana, F., Suppressa, P., Sabba, C., Fimiani, F., Cesaro, A., Calabro, Paolo, Palmisano, S., D'Addato, S., Pisciotta, L., Bertolini, S., Bittar, R., Kalmykova, O., Beliard, S., Carrie, A., Arca, M., Bruckert, E., Calabro, P., Università degli Studi di Roma 'La Sapienza' = Sapienza University [Rome] (UNIROMA), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Sorbonne Université (SU), Laboratoire d'Imagerie Biomédicale [Paris] (LIB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Università degli studi di Palermo - University of Palermo, University of Naples Federico II = Università degli studi di Napoli Federico II, CEINGE - Biotecnologie Avanzate, Università degli Studi 'Magna Graecia' di Catanzaro = University of Catanzaro (UMG), Università degli Studi di Milano = University of Milan (UNIMI), Università degli Studi di Ferrara = University of Ferrara (UniFE), Università degli studi 'G. d'Annunzio' Chieti-Pescara [Chieti-Pescara] (Ud'A), Ospedale San Luigi Gonzaga, Fondazione Toscana Gabriele Monasterio, University of the Study of Campania Luigi Vanvitelli, Policlinico S. Orsola-malpighi, Alma Mater Studiorum Università di Bologna [Bologna] (UNIBO)-Servizio sanitario regionale Emilia-Romagna, Università degli studi di Genova = University of Genoa (UniGe), Ospedale Policlinico San Martino [Genoa], Unité de Recherche sur les Maladies Cardiovasculaires, du Métabolisme et de la Nutrition = Research Unit on Cardiovascular and Metabolic Diseases (ICAN), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut de Cardiométabolisme et Nutrition = Institute of Cardiometabolism and Nutrition [CHU Pitié Salpêtrière] (IHU ICAN), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-CHU Pitié-Salpêtrière [AP-HP], Centre recherche en CardioVasculaire et Nutrition = Center for CardioVascular and Nutrition research (C2VN), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), and Hôpital de la Conception [CHU - APHM] (LA CONCEPTION)
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medicine.medical_specialty ,Settore MED/09 - Medicina Interna ,[SDV]Life Sciences [q-bio] ,Lipoproteins ,Genetic disease ,Therapeutics ,Familial hypercholesterolemia ,Disease ,Lipoprotein apheresi ,LDL ,Hyperlipoproteinemia Type II ,chemistry.chemical_compound ,Lipoprotein apheresis ,Retrospective survey ,Internal medicine ,Cholesterol burden ,Homozygous hypercholesterolemia ,Lomitapide ,Benzimidazoles ,Homozygote ,Humans ,Retrospective Studies ,Anticholesteremic Agents ,Blood Component Removal ,medicine ,Pharmacology (medical) ,Genetics (clinical) ,medicine.diagnostic_test ,business.industry ,Research ,General Medicine ,medicine.disease ,cholesterol burden ,genetic disease ,homozygous hypercholesterolemia ,lipoprotein apheresis ,lomitapide ,therapeutics ,chemistry ,Cohort ,Medicine ,Lipid profile ,business ,Cross national - Abstract
Abstract Background Homozygous familial hypercholesterolemia (HoFH) is a rare life-threatening condition that represents a therapeutic challenge. The vast majority of HoFH patients fail to achieve LDL-C targets when treated with the standard protocol, which associates maximally tolerated dose of lipid-lowering medications with lipoprotein apheresis (LA). Lomitapide is an emerging therapy in HoFH, but its place in the treatment algorithm is disputed because a comparison of its long-term efficacy versus LA in reducing LDL-C burden is not available. We assessed changes in long-term LDL-C burden and goals achievement in two independent HoFH patients’ cohorts, one treated with lomitapide in Italy (n = 30) and the other with LA in France (n = 29). Results The two cohorts differed significantly for genotype (p = 0.004), baseline lipid profile (p padj = 0.004). Yearly on-treatment LDL-C padj = 0.002). A trend towards fewer total cardiovascular events was observed in the Lomitapide than in the LA cohort. Conclusions In comparison with LA, lomitapide appears to provide a better control of LDL-C in HoFH. Further studies are needed to confirm this data and establish whether this translates into a reduction of cardiovascular risk.
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- 2021
4. Worldwide experience of homozygous familial hypercholesterolaemia:retrospective cohort study
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Tycho R Tromp, Merel L Hartgers, G Kees Hovingh, Antonio J Vallejo-Vaz, Kausik K Ray, Handrean Soran, Tomas Freiberger, Stefano Bertolini, Mariko Harada-Shiba, Dirk J Blom, Frederick J Raal, Marina Cuchel, Tycho R. Tromp, Merel L. Hartgers, G. Kees Hovingh, Antonio J. Vallejo-Vaz, Kausik K. Ray, Stefano A. Bertolini, Jing Pang, Gerald F. Watts, Susanne Greber-Platzer, Martin Mäser, Thomas M. Stulnig, Christoph F. Ebenbichler, Khalid Bin Thani, David Cassiman, Olivier S. Descamps, Daisy Rymen, Peter Witters, Raul D. Santos, Liam R. Brunham, Gordon A. Francis, Jacques Genest, Robert A. Hegele, Brooke A. Kennedy, Isabelle Ruel, Mark H. Sherman, Long Jiang, Luya Wang, Željko Reiner, Vladimir Blaha, Richard Ceska, Jana Dvorakova, Lubomir Dlouhy, Pavel Horak, Vladimir Soska, Lukas Tichy, Robin Urbanek, Helena Vaverkova, Michal Vrablik, Stanislav Zemek, Lukas Zlatohlavek, Sameh Emil, Tarek Naguib, Ashraf Reda, Sophie Béliard, Eric Bruckert, Antonio Gallo, Moses S. Elisaf, Genovefa Kolovou, Hofit Cohen, Ronen Durst, Eldad J. Dann, Avishay Elis, Osama Hussein, Eran Leitersdorf, Daniel Schurr, Nitika Setia, Ishwar C. Verma, Mohammed D. Alareedh, Mutaz Al-Khnifsawi, Ali F. Abdalsahib Al-Zamili, Sabah H. Rhadi, Foaad K. Shaghee, Marcello Arca, Maurizio Averna, Andrea Bartuli, Marco Bucci, Paola S. Buonuomo, Paolo Calabrò, Sebastiano Calandra, Manuela Casula, Alberico L. Catapano, Angelo B. Cefalù, Arrigo F.G. Cicero, Sergio D'Addato, Laura D'Erasmo, Alessia Di Costanzo, Tommaso Fasano, Marta Gazzotti, Antonina Giammanco, Gabriella Iannuzzo, Anastasia Ibba, Emanuele A. Negri, Andrea Pasta, Chiara Pavanello, Livia Pisciotta, Claudio Rabacchi, Carlo Ripoli, Tiziana Sampietro, Francesco Sbrana, Fulvio Sileo, Patrizia Suppressa, Patrizia Tarugi, Chiara Trenti, Maria G. Zenti, Mika Hori, Mahmoud H. Ayesh, Sami T. Azar, Fadi F. Bitar, Akl C. Fahed, Elie M. Moubarak, Georges Nemer, Hapizah M. Nawawi, Ramón Madriz, Roopa Mehta, Arjen J. Cupido, Joep C. Defesche, M. Doortje Reijman, Jeanine E. Roeters-van Lennep, Erik S.G. Stroes, Albert Wiegman, Linda Zuurbier, Khalid Al-Waili, Fouzia Sadiq, Krzysztof Chlebus, Mafalda Bourbon, Isabel M. Gaspar, Katarina S. Lalic, Marat V. Ezhov, Andrey V. Susekov, Urh Groselj, Min-Ji Charng, Weerapan Khovidhunkit, Melih Aktan, Bulent B. Altunkeser, Sinan Demircioglu, Melis Kose, Cumali Gokce, Osman Ilhan, Meral Kayikcioglu, Leyla G. Kaynar, Irfan Kuku, Erdal Kurtoglu, Harika Okutan, Osman I. Ozcebe, Zafer Pekkolay, Saim Sag, Osman Z. Salcioglu, Ahmet Temizhan, Mustafa Yenercag, Mehmet Yilmaz, Hamiyet Yilmaz Yasar, Olena Mitchenko, Alexander R.M. Lyons, Christophe A.T. Stevens, Julie A. Brothers, Lisa C. Hudgins, Christina Nguyen, Rano Alieva, Aleksandr Shek, Doan-Loi Do, Ngoc-Thanh Kim, Hong-An Le, Thanh-Tung Le, Mai-Ngoc T. Nguyen, Thanh-Huong Truong, Dirk J. Blom, Frederick J. Raal, VU University medical center, Tromp T.R., Hartgers M.L., Hovingh G.K., Vallejo-Vaz A.J., Ray K.K., Soran H., Freiberger T., Bertolini S., Harada-Shiba M., Blom D.J., Raal F.J., Cuchel M., Bertolini S.A., Pang J., Watts G.F., Greber-Platzer S., Maser M., Stulnig T.M., Ebenbichler C.F., Bin Thani K., Cassiman D., Descamps O.S., Rymen D., Witters P., Santos R.D., Brunham L.R., Francis G.A., Genest J., Hegele R.A., Kennedy B.A., Ruel I., Sherman M.H., Jiang L., Wang L., Reiner Z., Blaha V., Ceska R., Dvorakova J., Dlouhy L., Horak P., Soska V., Tichy L., Urbanek R., Vaverkova H., Vrablik M., Zemek S., Zlatohlavek L., Emil S., Naguib T., Reda A., Beliard S., Bruckert E., Gallo A., Elisaf M.S., Kolovou G., Cohen H., Durst R., Dann E.J., Elis A., Hussein O., Leitersdorf E., Schurr D., Setia N., Verma I.C., Alareedh M.D., Al-Khnifsawi M., Abdalsahib Al-Zamili A.F., Rhadi S.H., Shaghee F.K., Arca M., Averna M., Bartuli A., Bucci M., Buonuomo P.S., Calabro P., Calandra S., Casula M., Catapano A.L., Cefalu A.B., Cicero A.F.G., D'Addato S., D'Erasmo L., Di Costanzo A., Fasano T., Gazzotti M., Giammanco A., Iannuzzo G., Ibba A., Negri E.A., Pasta A., Pavanello C., Pisciotta L., Rabacchi C., Ripoli C., Sampietro T., Sbrana F., Sileo F., Suppressa P., Tarugi P., Trenti C., Zenti M.G., Hori M., Ayesh M.H., Azar S.T., Bitar F.F., Fahed A.C., Moubarak E.M., Nemer G., Nawawi H.M., Madriz R., Mehta R., Cupido A.J., Defesche J.C., Reijman M.D., Roeters-van Lennep J.E., Stroes E.S.G., Wiegman A., Zuurbier L., Al-Waili K., Sadiq F., Chlebus K., Bourbon M., Gaspar I.M., Lalic K.S., Ezhov M.V., Susekov A.V., Groselj U., Charng M.-J., Khovidhunkit W., Aktan M., Altunkeser B.B., Demircioglu S., Kose M., Gokce C., Ilhan O., Kayikcioglu M., Kaynar L.G., Kuku I., Kurtoglu E., Okutan H., Ozcebe O.I., Pekkolay Z., Sag S., Salcioglu O.Z., Temizhan A., Yenercag M., Yilmaz M., Yilmaz Yasar H., Mitchenko O., Lyons A.R.M., Stevens C.A.T., Brothers J.A., Hudgins L.C., Nguyen C., Alieva R., Shek A., Do D.-L., Kim N.-T., Le H.-A., Le T.-T., Nguyen M.-N.T., Truong T.-H., University of Amsterdam, University of Pennsylvania, European Atherosclerosis Society, Experimental Vascular Medicine, Graduate School, Vascular Medicine, ACS - Atherosclerosis & ischemic syndromes, Human Genetics, Paediatric Metabolic Diseases, ACS - Diabetes & metabolism, AGEM - Amsterdam Gastroenterology Endocrinology Metabolism, ACS - Heart failure & arrhythmias, R Tromp, Tycho, L Hartgers, Merel, Kees Hovingh, G, J Vallejo-Vaz, Antonio, K Ray, Kausik, Soran, Handrean, Freiberger, Toma, A Bertolini, Stefano, Harada-Shiba, Mariko, Pang, Jing, F Watts, Gerald, Greber-Platzer, Susanne, Mäser, Martin, M Stulnig, Thoma, F Ebenbichler, Christoph, Bin Thani, Khalid, Cassiman, David, S Descamps, Olivier, Rymen, Daisy, Witters, Peter, D Santos, Raul, R Brunham, Liam, A Francis, Gordon, Genest, Jacque, A Hegele, Robert, A Kennedy, Brooke, Ruel, Isabelle, H Sherman, Mark, Jiang, Long, Wang, Luya, Reiner, Željko, Blaha, Vladimir, Ceska, Richard, Dvorakova, Jana, Dlouhy, Lubomir, Horak, Pavel, Soska, Vladimir, Tichy, Luka, Urbanek, Robin, Vaverkova, Helena, Vrablik, Michal, Zemek, Stanislav, Zlatohlavek, Luka, Emil, Sameh, Naguib, Tarek, Reda, Ashraf, Béliard, Sophie, Bruckert, Eric, Gallo, Antonio, S Elisaf, Mose, Kolovou, Genovefa, Cohen, Hofit, Durst, Ronen, J Dann, Eldad, Elis, Avishay, Hussein, Osama, Leitersdorf, Eran, Schurr, Daniel, Setia, Nitika, C Verma, Ishwar, D Alareedh, Mohammed, Al-Khnifsawi, Mutaz, F Abdalsahib Al-Zamili, Ali, H Rhadi, Sabah, K Shaghee, Foaad, Arca, Marcello, Averna, Maurizio, Bartuli, Andrea, Bucci, Marco, S Buonuomo, Paola, Calabrò, Paolo, Calandra, Sebastiano, Casula, Manuela, L Catapano, Alberico, B Cefalù, Angelo, G Cicero, Arrigo F, D'Addato, Sergio, D'Erasmo, Laura, Di Costanzo, Alessia, Fasano, Tommaso, Gazzotti, Marta, Giammanco, Antonina, Iannuzzo, Gabriella, Ibba, Anastasia, A Negri, Emanuele, Pasta, Andrea, Pavanello, Chiara, Pisciotta, Livia, Rabacchi, Claudio, Ripoli, Carlo, Sampietro, Tiziana, Sbrana, Francesco, Sileo, Fulvio, Suppressa, Patrizia, Tarugi, Patrizia, Trenti, Chiara, G Zenti, Maria, Hori, Mika, H Ayesh, Mahmoud, T Azar, Sami, F Bitar, Fadi, C Fahed, Akl, M Moubarak, Elie, Nemer, George, M Nawawi, Hapizah, Madriz, Ramón, Mehta, Roopa, J Cupido, Arjen, C Defesche, Joep, Doortje Reijman, M, E Roeters-van Lennep, Jeanine, G Stroes, Erik S, Wiegman, Albert, Zuurbier, Linda, Al-Waili, Khalid, Sadiq, Fouzia, Chlebus, Krzysztof, Bourbon, Mafalda, M Gaspar, Isabel, S Lalic, Katarina, V Ezhov, Marat, V Susekov, Andrey, Groselj, Urh, Charng, Min-Ji, Khovidhunkit, Weerapan, Aktan, Melih, B Altunkeser, Bulent, Demircioglu, Sinan, Kose, Meli, Gokce, Cumali, Ilhan, Osman, Kayikcioglu, Meral, G Kaynar, Leyla, Kuku, Irfan, Kurtoglu, Erdal, Okutan, Harika, I Ozcebe, Osman, Pekkolay, Zafer, Sag, Saim, Z Salcioglu, Osman, Temizhan, Ahmet, Yenercag, Mustafa, Yilmaz, Mehmet, Yilmaz Yasar, Hamiyet, Mitchenko, Olena, M Lyons, Alexander R, T Stevens, Christophe A, A Brothers, Julie, C Hudgins, Lisa, Nguyen, Christina, Alieva, Rano, Shek, Aleksandr, Do, Doan-Loi, Kim, Ngoc-Thanh, Le, Hong-An, Le, Thanh-Tung, T Nguyen, Mai-Ngoc, Truong, Thanh-Huong, J Blom, Dirk, J Raal, Frederick, and Cuchel, Marina
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Adult ,Male ,Homozygous Familial Hypercholesterolemia ,Adolescent ,retrospective study ,CHILDREN ,Doenças Cardio e Cérebro-vasculares ,Cohort Studies ,Young Adult ,Medicine, General & Internal ,General & Internal Medicine ,Cardiovascular Disease ,Humans ,Registries ,LIPOPROTEIN-APHERESIS ,Child ,11 Medical and Health Sciences ,Retrospective Studies ,Homozygous Familial Hypercholesterolaemia International Clinical Collaborators ,Science & Technology ,GUIDANCE ,clinical characteristic ,EVOLOCUMAB ,Homozygous familial hypercholesterolemia ,Worldwide ,Therapies ,Cardiovascular disease ,General Medicine ,CARE ,OPEN-LABEL ,EFFICACY ,INSIGHTS ,Child, Preschool ,outcome ,Female ,genetic ,Familial Hypercholesterolaemia ,Life Sciences & Biomedicine - Abstract
[Background]: Homozygous familial hypercholesterolaemia (HoFH) is a rare inherited disorder resulting in extremely elevated low-density lipoprotein cholesterol levels and premature atherosclerotic cardiovascular disease (ASCVD). Current guidance about its management and prognosis stems from small studies, mostly from high-income countries. The objective of this study was to assess the clinical and genetic characteristics, as well as the impact, of current practice on health outcomes of HoFH patients globally., [Methods]: The HoFH International Clinical Collaborators registry collected data on patients with a clinical, or genetic, or both, diagnosis of HoFH using a retrospective cohort study design. This trial is registered with ClinicalTrials.gov, NCT04815005., [Findings]: Overall, 751 patients from 38 countries were included, with 565 (75%) reporting biallelic pathogenic variants. The median age of diagnosis was 12∙0 years (IQR 5∙5–27∙0) years. Of the 751 patients, 389 (52%) were female and 362 (48%) were male. Race was reported for 527 patients; 338 (64%) patients were White, 121 (23%) were Asian, and 68 (13%) were Black or mixed race. The major manifestations of ASCVD or aortic stenosis were already present in 65 (9%) of patients at diagnosis of HoFH. Globally, pretreatment LDL cholesterol levels were 14∙7 mmol/L (IQR 11∙6–18∙4). Among patients with detailed therapeutic information, 491 (92%) of 534 received statins, 342 (64%) of 534 received ezetimibe, and 243 (39%) of 621 received lipoprotein apheresis. On-treatment LDL cholesterol levels were lower in high-income countries (3∙93 mmol/L, IQR 2∙6–5∙8) versus non-highincome countries (9∙3 mmol/L, 6∙7–12∙7), with greater use of three or more lipid-lowering therapies (LLT; highincome 66% vs non-high-income 24%) and consequently more patients attaining guideline-recommended LDL cholesterol goals (high-income 21% vs non-high-income 3%). A first major adverse cardiovascular event occurred a decade earlier in non-high-income countries, at a median age of 24∙5 years (IQR 17∙0–34∙5) versus 37∙0 years (29∙0–49∙0) in high-income countries (adjusted hazard ratio 1∙64, 95% CI 1∙13–2∙38)., [Interpretation]: Worldwide, patients with HoFH are diagnosed too late, undertreated, and at high premature ASCVD risk. Greater use of multi-LLT regimens is associated with lower LDL cholesterol levels and better outcomes. Significant global disparities exist in treatment regimens, control of LDL cholesterol levels, and cardiovascular event-free survival, which demands a critical re-evaluation of global health policy to reduce inequalities and improve outcomes for all patients with HoFH., Amsterdam University Medical Centers, Location Academic Medical Center; Perelman School of Medicine at the University of Pennsylvania; and European Atherosclerosis Society
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- 2022
5. PCSK9 and leptin plasma levels in anorexia nervosa.
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Bigazzi F, De Pasquale CF, Maestro S, Corciulo C, Dal Pino B, Sbrana F, and Sampietro T
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- Female, Adolescent, Humans, Cholesterol, LDL, Leptin, Proprotein Convertases metabolism, Serine Endopeptidases metabolism, Proprotein Convertase 9, Anorexia Nervosa
- Abstract
Aim: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a regulator of low-density-lipoprotein cholesterol (LDL-C), a major risk factor for cardiovascular (CV) disease. Since the hormone leptin has been suggested as having a role in CV risk regulation, possibly by modulating LDL receptor expression through the PCSK9 pathway, nutritional status may represent a potential regulator. Thus, evaluation of PCSK9 levels in human eating disorders appears to be of interest. In this report, we evaluate the lipoprotein profile, PCSK9, and leptin levels in subjects affected by anorexia nervosa (AN) to improve our understanding of the metabolic alterations in this disease., Methods and Results: We designed a case-control observational study, enrolling 20 anorexic adolescent females and 20 adolescent females without AN as the control group, age- and sex-matched. Subjects affected by AN showed lower BMI, total cholesterol, and LDL-C in comparison to the control group, with lipoprotein levels in the normal range. Furthermore, adolescent girls with AN show significantly higher PCSK9 (+24%, p < 0.005) and lower leptin levels (-43%, p < 0.01), compared to the control group., Conclusions: The findings of increased levels of PCSK9 and reduced leptin levels among AN subjects warrant further research in order to unravel the role of the liver and adipose tissue in the management of PCSK9/LDL metabolism in adolescents affected by AN., (© 2023. The Author(s), under exclusive licence to Hellenic Endocrine Society.)
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- 2024
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6. Comorbidity in lipoprotein apheresis: Their role in the era of new lipid-lowering therapies.
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Sbrana F, Pianelli M, Luciani R, Bigazzi F, Corciulo C, Ripoli A, Sampietro T, and Dal Pino B
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- Humans, Male, Middle Aged, Retrospective Studies, Cholesterol, LDL, Comorbidity, Treatment Outcome, Lipoprotein(a), Blood Component Removal adverse effects
- Abstract
Background: Despite advance in pharmacotherapy of lipid disorders, lipoprotein apheresis (LA) plays a leading role in the management of severe hypercholesterolemia and in atherosclerosis prevention., Methods: Aim of this study was to retrospectively evaluate Charlson Comorbidity Index (CCI), presence of major comorbidity, and/or concomitant polypharmacy (definite as 5+ drugs daily) in patients with inherited dyslipidemias on chronic LA., Results: Since 1994, we performed more than 500 LA treatment/year and followed a total of 83 patients (age 56 [47-65] years, male 75%). In subjects with more than 5 years of LA treatment (38 patients, age 54 [45-62] years, male 66%), at the end of the observation time (9 [7-16] years), patients had higher CCI, polypharmacy, anemia, heart failure, peptic ulcer disease, and benign prostatic hyperplasia., Discussion: Even in the era of new lipid-lowering therapies, the LA treatment established itself as a safe and lifesaving intervention. Patients on chronic LA require a multidisciplinary approach to address their comorbidity and the apheresis unit's medical staff (doctors and nurses) play a pivotal role creating a bridge toward the general practitioner and other specialists for overcoming clinical issues., (© 2023 Wiley Periodicals LLC.)
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- 2024
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7. Widespread xanthomas regression by personalized lipid lowering therapy in heterozygous familial hypercholesterolemia.
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Sbrana F, Pino BD, Bigazzi F, and Sampietro T
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- Humans, Female, Aged, Cholesterol, LDL, Ezetimibe therapeutic use, Hyperlipoproteinemia Type II drug therapy, Hypercholesterolemia, Xanthomatosis etiology, Anticholesteremic Agents pharmacology, Anticholesteremic Agents therapeutic use
- Abstract
"The lower, the better" is the recommended approach in the management of high LDL cholesterol. Unfortunately, this does not always achieve as in the case of a 69-year-old woman referred to our Institute for her lipid profile (LDL cholesterol 412mg/dl), bilateral xanthelasma and cutaneous xanthomas. With a maximized and personalized lipid-lowering therapies (rosuvastatin, ezetimibe, PCSK9i and lipoprotein apheresis), after only six months, the patient showed an impressive regression in her cutaneous xanthomas., (Copyright © 2023 Sociedad Española de Arteriosclerosis. Publicado por Elsevier España, S.L.U. All rights reserved.)
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- 2024
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8. Major cardiovascular events increase in long-term proprotein convertase subtilisin/kexin type 9 inhibitors therapy: the Tuscany cost-effective study.
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Sbrana F, Dal Pino B, Bigazzi F, Ripoli A, Corciulo C, Lo Surdo G, Biagini S, and Sampietro T
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- Aged, Humans, Male, Middle Aged, Carotid Intima-Media Thickness, Cholesterol, LDL, Cost-Benefit Analysis, PCSK9 Inhibitors, Proprotein Convertase 9, Subtilisins, Anticholesteremic Agents adverse effects, Cardiovascular Diseases chemically induced
- Abstract
Background: Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) represent a breakthrough in the treatment of hypercholesterolemia. The aim of this study was to perform a multicentre prospective analysis on the effects of PCSK9i since their distribution in Italy., Methods: During the study period (July 2017 to February 2022) 246 patients (mean age 61 ± 11 years, male 73%) who were evolocumab (142/246) or alirocumab (104/246) new users were enrolled in the CERTI (Costo Efficacia Regione Toscana Inibitori PCSK9) study. Lipid value, adverse events (AEs), major cardiovascular events (MACEs) and intima-media thickness were analysed., Results: PCSK9i therapy allowed a significant improvement in patients' lipid profile [total cholesterol -35%, P < 0.001; triglycerides -9%, P < 0.05; low-density lipoprotein (LDL) cholesterol -51%, P < 0.001; Lp(a) levels -4%, P < 0.05], maintained during the follow-up. No significant variations in intima-media thickness were observed. In the subgroup of patients with more than 1 year of PCSK9i therapy (165/246 patients) we highlighted: a 66% reduction in MACEs compared with the year before recruitment; a progressive increase in MACEs during the follow-up (MACEs event/rate at first year 0.08 vs. MACEs event/rate at year 5: 0.47); a patients cluster with late MACEs older, with higher prevalence of hypertension, smoking habit and peripheral vascular disease. During the follow-up, we recorded AEs in 31% of patients, which mainly resulted in reduction/discontinuation of lipid-lowering therapy for 50 patients or in discontinuation/shift of PCSK9i (respectively 8 and 6 cases)., Conclusion: Our data agree with the large evidence on the effectiveness/tolerability of PCSK9i therapy; however, although PCSK9i represents a good cholesterol-lowering therapeutic option, our study shows a progressive increase in MACEs during the late follow-up that deserve further research., (Copyright © 2023 Italian Federation of Cardiology - I.F.C. All rights reserved.)
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- 2023
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9. Consensus document on Lipoprotein(a) from the Italian Society for the Study of Atherosclerosis (SISA).
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Chiesa G, Zenti MG, Baragetti A, Barbagallo CM, Borghi C, Colivicchi F, Maggioni AP, Noto D, Pirro M, Rivellese AA, Sampietro T, Sbrana F, Arca M, Averna M, and Catapano AL
- Subjects
- Humans, Lipoprotein(a) genetics, Proprotein Convertase 9, Consensus, Atherosclerosis diagnosis, Atherosclerosis epidemiology, Atherosclerosis genetics, Aortic Valve Stenosis
- Abstract
Aims: In view of the consolidating evidence on the causal role of Lp(a) in cardiovascular disease, the Italian Society for the Study of Atherosclerosis (SISA) has assembled a consensus on Lp(a) genetics and epidemiology, together with recommendations for its measurement and current and emerging therapeutic approaches to reduce its plasma levels. Data on the Italian population are also provided., Data Synthesis: Lp(a) is constituted by one apo(a) molecule and a lipoprotein closely resembling to a low-density lipoprotein (LDL). Its similarity with an LDL, together with its ability to carry oxidized phospholipids are considered the two main features making Lp(a) harmful for cardiovascular health. Plasma Lp(a) concentrations vary over about 1000 folds in humans and are genetically determined, thus they are quite stable in any individual. Mendelian Randomization studies have suggested a causal role of Lp(a) in atherosclerotic cardiovascular disease (ASCVD) and aortic valve stenosis and observational studies indicate a linear direct correlation between cardiovascular disease and Lp(a) plasma levels. Lp(a) measurement is strongly recommended once in a patient's lifetime, particularly in FH subjects, but also as part of the initial lipid screening to assess cardiovascular risk. The apo(a) size polymorphism represents a challenge for Lp(a) measurement in plasma, but new strategies are overcoming these difficulties. A reduction of Lp(a) levels can be currently attained only by plasma apheresis and, moderately, with PCSK9 inhibitor treatment., Conclusions: Awaiting the approval of selective Lp(a)-lowering drugs, an intensive management of the other risk factors for individuals with elevated Lp(a) levels is strongly recommended., Competing Interests: Declaration of competing interest APM received personal fees from AstraZeneca, Bayer, Novartis for the participation in study committees, outside the present work. M Arca has received research grant support and lecturing fees from Alfasigma, Amarin, Amgen, Amryt, IONIS/Akcea Therapeutics, Daiichi Sankyo, Novartis, Pfizer, Regeneron and Sanofi, SOBI. ALC in the last three years has received honoraria, lecture fees or research grants from Aegerion, Akcea Therapeutics, Amarin, Amgen, Amryt Pharma, AstraZeneca, Daiichi Sankyo, Esperion, Ionis Pharmaceutical, Medscape Education, Menarini, Merck, Mylan, Novartis, PeerVoice, Pfizer, Recordati, Regeneron, Sanofi, The Corpus, Viatris. GC, MGZ, AB, CMB, CB, FC, DN, MP, AAR, TS, FS, M Averna declare no competing interest., (Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.)
- Published
- 2023
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10. Skin microcirculation significantly increases after lipoprotein apheresis.
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Sbrana F, Dal Pino B, and Sampietro T
- Subjects
- Humans, Microcirculation, Lipoproteins, Lipoprotein(a), Treatment Outcome, Blood Component Removal
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- 2023
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11. Familial LCAT deficiency and cardiovascular disease: the game is not over. A case of dramatic multivessel atherosclerosis.
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Bigazzi F, Dal Pino B, Pavanello C, Sbrana F, Aquaro GD, Napoli V, Palmieri C, Barison A, Calabresi L, and Sampietro T
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- Humans, Mutation, Lecithin Cholesterol Acyltransferase Deficiency complications, Lecithin Cholesterol Acyltransferase Deficiency genetics, Cardiovascular Diseases etiology, Atherosclerosis genetics
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- 2023
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12. Lipid modification induced by lipoprotein apheresis could mirrored mid-regional-pro-adrenomedullin plasma levels?
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Corciulo C, Dal Pino B, Visentini D, Bigazzi F, Ripoli A, Sozio E, Curcio F, Tascini C, Fabris M, Sampietro T, and Sbrana F
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- Humans, Lipoproteins, Biomarkers, Adrenomedullin, Blood Component Removal
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- 2023
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13. Acute Increase in Ocular Microcirculation Blood Flow Upon Cholesterol Removal. The Eyes Are the Window of the Heart.
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Sampietro T, Pino BD, Bigazzi F, Sbrana F, Ripoli A, Fontanelli E, Pianelli M, Luciani R, Lepri A, and Calzetti G
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- Humans, Microcirculation, Cholesterol, Lipoproteins
- Abstract
Background: Lipoprotein apheresis acutely increases coronary microvascular blood flow. However, measurement techniques are time-consuming, costly, and invasive. The ocular vasculature may be an appropriate surrogate and an easily accessible window to investigate the microcirculation. Recent advances in ocular imaging techniques enable quick, noninvasive quantification of ocular microcirculation blood flow. The insights from these techniques represent a significant opportunity to study the short-term changes in optic disk blood flow after lipoprotein apheresis for inherited hypercholesterolemia., Methods: This study was performed at the Italian Reference Center for Inherited Dyslipidemias in Tuscany. The study sample was comprised of 22 patients with inherited hypercholesterolemia who were previously studied for coronary microcirculation. Laser speckle flowgraphy (LSFG) was used to measure optic disk blood flow before and after lipoprotein apheresis. The main outcomes measures were average tissue blood flow (referred to as mean tissue) and arteriolar/venular average blood flow (referred to as mean vessel). Eyes were divided into 2 groups based on pre-lipoprotein apheresis optic disk blood flow values. P < .05 was considered statistically significant., Results: After each lipoprotein apheresis treatment resulting in the reduction of plasma lipids, there was a concurrent increase in all optic disk microcirculatory parameters. The increase was statistically significant in eyes with lower pre-apheresis optic disk blood flow values (mean tissue +7.0%, P < .005; mean vessel +7.2%, P < .05)., Conclusions: A single lipoprotein apheresis session resulted in a statistically significant short-term increase in optic disk blood flow. These findings together with previous coronary microcirculation data suggest a similar ocular and coronary blood flow response to lipoprotein apheresis. Ocular microcirculation may represent a versatile biomarker for evaluating systemic microcirculatory health, including coronary microcirculation. Hence, it is plausible that plasma lipoprotein levels may influence optic disk blood flow., (Copyright © 2022 Elsevier Inc. All rights reserved.)
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- 2023
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14. A place for bempedoic acid: an effective therapeutic cooperation.
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Sbrana F, Dal Pino B, Bigazzi F, and Sampietro T
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- Humans, Fatty Acids therapeutic use, Dicarboxylic Acids therapeutic use, Hypolipidemic Agents therapeutic use, Hypercholesterolemia drug therapy, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use
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- 2023
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15. Paradoxical effect of lipid lowering therapy in homozygous familial hypercholesterolemia: Atherosclerotic plaque calcifications and increased cardiovascular events.
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Sampietro T, Sbrana F, Bigazzi F, and Dal Pino B
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- 2022
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16. Coronary microcirculatory blood flow significantly increases upon acute and chronic cholesterol lowering: evaluation by cadmium-zinc-telluride cardiac imaging stress test.
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Sampietro T, Sbrana F, Dal Pino B, Bigazzi F, Ripoli A, Marzullo P, and Gimelli A
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- Cadmium, Cholesterol, LDL, Humans, Microcirculation, PCSK9 Inhibitors, Tellurium, Zinc, Anticholesteremic Agents, Exercise Test
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- 2022
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17. Lipoprotein(a) apheresis restores coronary microcirculation in refractory angina.
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Sbrana F, Dal Pino B, Aquaro GD, Bigazzi F, Vergaro G, and Sampietro T
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- 2022
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18. The management of heterozygous familial hypercholesterolaemia with high lipoprotein (a) and statin intolerance. The guidelines a mirage?
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Dal Pino B, Bigazzi F, Sbrana F, and Sampietro T
- Subjects
- Humans, Lipoprotein(a), Hydroxymethylglutaryl-CoA Reductase Inhibitors, Hyperlipoproteinemia Type II, Anticholesteremic Agents
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- 2021
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19. Is treating severe He FH so easy? A combined treatment between lipoprotein apheresis and PCSK9 inhibitors.
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Dal Pino B, Sbrana F, Bigazzi F, and Sampietro T
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- Aged, Humans, PCSK9 Inhibitors pharmacology, Blood Component Removal methods, Hyperlipoproteinemia Type II drug therapy, Hyperlipoproteinemia Type II therapy, Lipoproteins metabolism, PCSK9 Inhibitors therapeutic use
- Abstract
Despite advance in pharmacotherapy of lipid disorders, many heterozygous Familial Hypercholesterolemia patients do not achieve a desirable lipid target to significantly reduce the risk of atherosclerotic cardiovascular disease. The aim of the present work is to evaluate the interaction between Lipoprotein apheresis (LA) and PCSK9i in a small FH cohort in which the guidelines therapeutic target is not achieved. During one year, together with a complete adherence to PCSK9i therapy, we recorded a 3 to 5 LA sessions less per year in each patient. This therapeutic approach suggests: i) the possibility of increasing the number of patients treated with LA, ii) the improvement of their quality of life, and iii) the costs reduction for the single patient-treatment., (Copyright © 2021 Elsevier Ltd. All rights reserved.)
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- 2021
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20. Triglycerides and low HDL cholesterol predict coronary heart disease risk in patients with stable angina.
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Caselli C, De Caterina R, Smit JM, Campolo J, El Mahdiui M, Ragusa R, Clemente A, Sampietro T, Clerico A, Liga R, Pelosi G, Rocchiccioli S, Parodi O, Scholte A, Knuuti J, and Neglia D
- Subjects
- Biomarkers blood, Cardiomyopathies blood, Cardiomyopathies drug therapy, Cholesterol blood, Cholesterol, LDL blood, Coronary Angiography methods, Female, Humans, Hypolipidemic Agents pharmacology, Insulin Resistance physiology, Male, Metabolic Syndrome blood, Metabolic Syndrome drug therapy, Middle Aged, Risk Factors, Angina, Stable blood, Cholesterol, HDL blood, Coronary Artery Disease blood, Coronary Artery Disease etiology, Triglycerides blood
- Abstract
We assessed whether high triglycerides (TG) and low high-density lipoprotein cholesterol (HDL-C) levels, expressed by an increased TG/HDL-C ratio, predict coronary atherosclerotic disease (CAD) outcomes in patients with stable angina. We studied 355 patients (60 ± 9 years, 211 males) with stable angina who underwent coronary computed tomography angiography (CTA), were managed clinically and followed for 4.5 ± 0.9 years. The primary composite outcome was all-cause mortality and non-fatal myocardial infarction. At baseline, the proportion of males, patients with metabolic syndrome, diabetes and obstructive CAD increased across TG/HDL-C ratio quartiles, together with markers of insulin resistance, hepatic and adipose tissue dysfunction and myocardial damage, with no difference in total cholesterol or LDL-C. At follow-up, the global CTA risk score (HR 1.06, 95% confidence interval (CI) 1.03-1.09, P = 0.001) and the IV quartile of the TG/HDL-C ratio (HR 2.85, 95% CI 1.30-6.26, P < 0.01) were the only independent predictors of the primary outcome. The TG/HDL-C ratio and the CTA risk score progressed over time despite increased use of lipid-lowering drugs and reduction in LDL-C. In patients with stable angina, high TG and low HDL-C levels are associated with CAD related outcomes independently of LDL-C and treatments.Trial registration. EVINCI study: ClinicalTrials.gov NCT00979199, registered September 17, 2009; SMARTool study: ClinicalTrials.gov NCT04448691, registered June 26, 2020., (© 2021. The Author(s).)
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- 2021
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21. Long-term efficacy of lipoprotein apheresis and lomitapide in the treatment of homozygous familial hypercholesterolemia (HoFH): a cross-national retrospective survey.
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D'Erasmo L, Gallo A, Cefalù AB, Di Costanzo A, Saheb S, Giammanco A, Averna M, Buonaiuto A, Iannuzzo G, Fortunato G, Puja A, Montalcini T, Pavanello C, Calabresi L, Vigna GB, Bucci M, Bonomo K, Nota F, Sampietro T, Sbrana F, Suppressa P, Sabbà C, Fimiani F, Cesaro A, Calabrò P, Palmisano S, D'Addato S, Pisciotta L, Bertolini S, Bittar R, Kalmykova O, Béliard S, Carrié A, Arca M, and Bruckert E
- Subjects
- Benzimidazoles, Homozygote, Humans, Lipoproteins, Retrospective Studies, Anticholesteremic Agents therapeutic use, Blood Component Removal, Hyperlipoproteinemia Type II drug therapy, Hyperlipoproteinemia Type II genetics
- Abstract
Background: Homozygous familial hypercholesterolemia (HoFH) is a rare life-threatening condition that represents a therapeutic challenge. The vast majority of HoFH patients fail to achieve LDL-C targets when treated with the standard protocol, which associates maximally tolerated dose of lipid-lowering medications with lipoprotein apheresis (LA). Lomitapide is an emerging therapy in HoFH, but its place in the treatment algorithm is disputed because a comparison of its long-term efficacy versus LA in reducing LDL-C burden is not available. We assessed changes in long-term LDL-C burden and goals achievement in two independent HoFH patients' cohorts, one treated with lomitapide in Italy (n = 30) and the other with LA in France (n = 29)., Results: The two cohorts differed significantly for genotype (p = 0.004), baseline lipid profile (p < 0.001), age of treatment initiation (p < 0.001), occurrence of cardiovascular disease (p = 0.003) as well as follow-up duration (p < 0.001). The adjunct of lomitapide to conventional lipid-lowering therapies determined an additional 58.0% reduction of last visit LDL-C levels, compared to 37.1% when LA was added (p
adj = 0.004). Yearly on-treatment LDL-C < 70 mg/dl and < 55 mg/dl goals were only achieved in 45.5% and 13.5% of HoFH patients treated with lomitapide. The long-term exposure to LDL-C burden was found to be higher in LA than in Lomitapide cohort (13,236.1 ± 5492.1 vs. 11,656.6 ± 4730.9 mg/dL-year respectively, padj = 0.002). A trend towards fewer total cardiovascular events was observed in the Lomitapide than in the LA cohort., Conclusions: In comparison with LA, lomitapide appears to provide a better control of LDL-C in HoFH. Further studies are needed to confirm this data and establish whether this translates into a reduction of cardiovascular risk., (© 2021. The Author(s).)- Published
- 2021
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22. Acute coronary syndrome and lipid-lowering therapy in a realistic diagnostic-therapeutic care pathway.
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Sampietro T, Sbrana F, Dal Pino B, Bigazzi F, Palmieri C, and Berti S
- Subjects
- Critical Pathways, Humans, Hypolipidemic Agents therapeutic use, Lipids therapeutic use, Acute Coronary Syndrome drug therapy, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use
- Published
- 2021
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