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1. Rationale and design of the CV-PREVITAL study: an Italian multiple cohort randomised controlled trial investigating innovative digital strategies in primary cardiovascular prevention

Author: Baldassarre, D, Iacoviello, L, Baetta, R, Roncaglioni, M, Condorelli, G, Remuzzi, G, Gensini, G, Frati, L, Ricciardi, W, Conaldi, P, Uccelli, A, Blandini, F, Bosari, S, Scambia, G, Fini, M, Di Malta, A, Amato, M, Veglia, F, Bonomi, A, Klersy, C, Colazzo, F, Pengo, M, Gorini, F, Auteri, L, Ferrante, G, Baviera, M, Ambrosio, G, Catapano, A, Gialluisi, A, Malavazos, A, Castelvecchio, S, Corsi-Romanelli, M, Cardani, R, La Rovere, M, Agnese, V, Pane, B, Prati, D, Spinardi, L, Liuzzo, G, Arbustini, E, Volterrani, M, Visconti, M, Werba, J, Genovese, S, Bilo, G, Invitti, C, Di Blasio, A, Lombardi, C, Faini, A, Rosa, D, Ojeda-Fernandez, L, Foresta, A, De Curtis, A, Di Castelnuovo, A, Scalvini, S, Pierobon, A, Gorini, A, Valenti, L, Luzi, L, Racca, A, Bandi, M, Tremoli, E, Menicanti, L, Parati, G, Pompilio, G, Colombo, G, Vavassori, C, Biondi, M, Frigerio, B, Ravani, A, Sansaro, D, Coggi, D, Romandini, A, Giroli, M, Giuliani, M, Bonmi, A, Rondinelli, M, Trudu, C, Cinieri, C, Monturano, M, Colazo, F, Inviti, C, Di Blasi, A, Torlasco, C, Gilardini, L, Soranna, D, Zambon, A, Perger, E, Zanotti, L, Badano, L, Cova, L, Gentilini, D, Grappiolo, L, Condoreli, G, Ferante, G, Papa, L, Savevski, V, Ieva, F, Romano, I, Remzzi, G, Ojeda, L, Clerici, F, Palumbo, A, Genini, G, Catpano, A, Mattioli, R, Longhi, E, Mantovani, L, Madotto, F, Bonaccio, M, Gianfagna, F, Ghulam, A, Magnacca, S, Noro, F, Costanzo, S, Esposito, S, Orlandi, S, Persichillo, M, Bracone, F, Panzera, T, Ruggiero, E, Parisi, R, Franciosa, S, Morelli, M, De Rita, F, Cerletti, C, de Gaetano, G, Donati, M, Mencanti, L, Romanelli, M, Cerri, A, Dubini, C, Trevisan, M, Renna, L, Milani, V, Boveri, S, Giubbilini, P, Ramputi, L, Baroni, I, De Angeli, G, Riciardi, W, Olmetti, F, Bussotti, M, Gaetano, C, Baiardi, P, Bachetti, T, Balbi, M, Comini, L, Lorenzoni, M, Olivares, A, Traversi, E, Garre, C, Sideri, R, Clemenza, F, Gentile, G, Caruana, G, Cuscino, N, Di Gesaro, G, Greco, A, Loddo, I, Tuzzolino, F, Ucelli, A, Palombo, D, Spinella, G, Mozzetta, G, Ameri, P, Zoppoli, G, Finotello, A, Porto, I, Pratesi, G, Bladini, F, Spnardi, L, Clerici, M, Pelusi, S, Bianco, C, Carpani, R, Periti, G, Margarita, S, Lanza, G, Severino, A, Pedicino, D, D'Amario, D, D'Aiello, A, Vinci, R, Bonanni, A, Brecciaroli, M, Filomia, S, Pastorino, R, Boccia, S, Urbani, A, Sanguinetti, M, Santoliquido, A, Proto, L, Tarquini, D, Grimaldi, M, Leonardi, S, Elia, A, Currao, A, Urtis, M, Di Toro, A, Giuliani, L, Caminiti, G, Marcolongo, F, Sposato, B, Guadagni, F, Morsella, V, Marziale, A, Protti, G, Baldassarre D., Iacoviello L., Baetta R., Roncaglioni M. C., Condorelli G., Remuzzi G., Gensini G., Frati L., Ricciardi W., Conaldi P. G., Uccelli A., Blandini F., Bosari S., Scambia G., Fini M., Di Malta A., Amato M., Veglia F., Bonomi A., Klersy C., Colazzo F., Pengo M., Gorini F., Auteri L., Ferrante G., Baviera M., Ambrosio G., Catapano A., Gialluisi A., Malavazos A. E., Castelvecchio S., Corsi-Romanelli M. M., Cardani R., La Rovere M. T., Agnese V., Pane B., Prati D., Spinardi L., Liuzzo G., Arbustini E., Volterrani M., Visconti M., Werba J. P., Genovese S., Bilo G., Invitti C., Di Blasio A., Lombardi C., Faini A., Rosa D., Ojeda-Fernandez L., Foresta A., De Curtis A., Di Castelnuovo A., Scalvini S., Pierobon A., Gorini A., Valenti L., Luzi L., Racca A., Bandi M., Tremoli E., Menicanti L., Parati G., Pompilio G., Colombo G., Vavassori C., Biondi M. L., Frigerio B., Ravani A., Sansaro D., Coggi D., Romandini A., Giroli M., Giuliani M., Bonmi A., Rondinelli M., Trudu C., Cinieri C., Monturano M., Colazo F., Inviti C., Di Blasi A., Torlasco C., Gilardini L., Soranna D., Zambon A., Perger E., Zanotti L., Badano L., Cova L., Gentilini D., Grappiolo L., Condoreli G., Ferante G., Papa L., Savevski V., Ieva F., Romano I., Remzzi G., Ojeda L., Clerici F., Palumbo A., Genini G. F., Catpano A., Mattioli R., Longhi E., Mantovani L. G., Madotto F., Bonaccio M., Gianfagna F., Ghulam A., Magnacca S., Noro F., Costanzo S., Esposito S., Orlandi S., Persichillo M., Bracone F., Panzera T., Ruggiero E., Parisi R., Franciosa S., Morelli M., De Rita F., Cerletti C., de Gaetano G., Donati M. B., Mencanti L., Romanelli M. M. C., Cerri A., Dubini C., Trevisan M. B., Renna L. V., Milani V., Boveri S., Giubbilini P., Ramputi L., Baroni I., De Angeli G., Riciardi W., Olmetti F., Bussotti M., Gaetano C., Baiardi P., Bachetti T., Balbi M., Comini L., Lorenzoni M., Olivares A., Traversi E., Garre C., Sideri R., Clemenza F., Gentile G., Caruana G., Cuscino N., Di Gesaro G., Greco A., Loddo I., Tuzzolino F., Ucelli A., Palombo D., Spinella G., Mozzetta G., Ameri P., Zoppoli G., Finotello A., Porto I., Pratesi G., Bladini F., Spnardi L., Clerici M., Pelusi S., Bianco C., Carpani R., Periti G., Margarita S., Lanza G. A., Severino A., Pedicino D., D'Amario D., D'Aiello A., Vinci R., Bonanni A., Brecciaroli M., Filomia S., Pastorino R., Boccia S., Urbani A., Sanguinetti M., Santoliquido A., Proto L., Tarquini D., Grimaldi M. C., Leonardi S., Elia A., Currao A., Urtis M., Di Toro A., Giuliani L., Caminiti G., Marcolongo F., Sposato B., Guadagni F., Morsella V., Marziale A., Protti G., Baldassarre, D, Iacoviello, L, Baetta, R, Roncaglioni, M, Condorelli, G, Remuzzi, G, Gensini, G, Frati, L, Ricciardi, W, Conaldi, P, Uccelli, A, Blandini, F, Bosari, S, Scambia, G, Fini, M, Di Malta, A, Amato, M, Veglia, F, Bonomi, A, Klersy, C, Colazzo, F, Pengo, M, Gorini, F, Auteri, L, Ferrante, G, Baviera, M, Ambrosio, G, Catapano, A, Gialluisi, A, Malavazos, A, Castelvecchio, S, Corsi-Romanelli, M, Cardani, R, La Rovere, M, Agnese, V, Pane, B, Prati, D, Spinardi, L, Liuzzo, G, Arbustini, E, Volterrani, M, Visconti, M, Werba, J, Genovese, S, Bilo, G, Invitti, C, Di Blasio, A, Lombardi, C, Faini, A, Rosa, D, Ojeda-Fernandez, L, Foresta, A, De Curtis, A, Di Castelnuovo, A, Scalvini, S, Pierobon, A, Gorini, A, Valenti, L, Luzi, L, Racca, A, Bandi, M, Tremoli, E, Menicanti, L, Parati, G, Pompilio, G, Colombo, G, Vavassori, C, Biondi, M, Frigerio, B, Ravani, A, Sansaro, D, Coggi, D, Romandini, A, Giroli, M, Giuliani, M, Bonmi, A, Rondinelli, M, Trudu, C, Cinieri, C, Monturano, M, Colazo, F, Inviti, C, Di Blasi, A, Torlasco, C, Gilardini, L, Soranna, D, Zambon, A, Perger, E, Zanotti, L, Badano, L, Cova, L, Gentilini, D, Grappiolo, L, Condoreli, G, Ferante, G, Papa, L, Savevski, V, Ieva, F, Romano, I, Remzzi, G, Ojeda, L, Clerici, F, Palumbo, A, Genini, G, Catpano, A, Mattioli, R, Longhi, E, Mantovani, L, Madotto, F, Bonaccio, M, Gianfagna, F, Ghulam, A, Magnacca, S, Noro, F, Costanzo, S, Esposito, S, Orlandi, S, Persichillo, M, Bracone, F, Panzera, T, Ruggiero, E, Parisi, R, Franciosa, S, Morelli, M, De Rita, F, Cerletti, C, de Gaetano, G, Donati, M, Mencanti, L, Romanelli, M, Cerri, A, Dubini, C, Trevisan, M, Renna, L, Milani, V, Boveri, S, Giubbilini, P, Ramputi, L, Baroni, I, De Angeli, G, Riciardi, W, Olmetti, F, Bussotti, M, Gaetano, C, Baiardi, P, Bachetti, T, Balbi, M, Comini, L, Lorenzoni, M, Olivares, A, Traversi, E, Garre, C, Sideri, R, Clemenza, F, Gentile, G, Caruana, G, Cuscino, N, Di Gesaro, G, Greco, A, Loddo, I, Tuzzolino, F, Ucelli, A, Palombo, D, Spinella, G, Mozzetta, G, Ameri, P, Zoppoli, G, Finotello, A, Porto, I, Pratesi, G, Bladini, F, Spnardi, L, Clerici, M, Pelusi, S, Bianco, C, Carpani, R, Periti, G, Margarita, S, Lanza, G, Severino, A, Pedicino, D, D'Amario, D, D'Aiello, A, Vinci, R, Bonanni, A, Brecciaroli, M, Filomia, S, Pastorino, R, Boccia, S, Urbani, A, Sanguinetti, M, Santoliquido, A, Proto, L, Tarquini, D, Grimaldi, M, Leonardi, S, Elia, A, Currao, A, Urtis, M, Di Toro, A, Giuliani, L, Caminiti, G, Marcolongo, F, Sposato, B, Guadagni, F, Morsella, V, Marziale, A, Protti, G, Baldassarre D., Iacoviello L., Baetta R., Roncaglioni M. C., Condorelli G., Remuzzi G., Gensini G., Frati L., Ricciardi W., Conaldi P. G., Uccelli A., Blandini F., Bosari S., Scambia G., Fini M., Di Malta A., Amato M., Veglia F., Bonomi A., Klersy C., Colazzo F., Pengo M., Gorini F., Auteri L., Ferrante G., Baviera M., Ambrosio G., Catapano A., Gialluisi A., Malavazos A. E., Castelvecchio S., Corsi-Romanelli M. M., Cardani R., La Rovere M. T., Agnese V., Pane B., Prati D., Spinardi L., Liuzzo G., Arbustini E., Volterrani M., Visconti M., Werba J. P., Genovese S., Bilo G., Invitti C., Di Blasio A., Lombardi C., Faini A., Rosa D., Ojeda-Fernandez L., Foresta A., De Curtis A., Di Castelnuovo A., Scalvini S., Pierobon A., Gorini A., Valenti L., Luzi L., Racca A., Bandi M., Tremoli E., Menicanti L., Parati G., Pompilio G., Colombo G., Vavassori C., Biondi M. L., Frigerio B., Ravani A., Sansaro D., Coggi D., Romandini A., Giroli M., Giuliani M., Bonmi A., Rondinelli M., Trudu C., Cinieri C., Monturano M., Colazo F., Inviti C., Di Blasi A., Torlasco C., Gilardini L., Soranna D., Zambon A., Perger E., Zanotti L., Badano L., Cova L., Gentilini D., Grappiolo L., Condoreli G., Ferante G., Papa L., Savevski V., Ieva F., Romano I., Remzzi G., Ojeda L., Clerici F., Palumbo A., Genini G. F., Catpano A., Mattioli R., Longhi E., Mantovani L. G., Madotto F., Bonaccio M., Gianfagna F., Ghulam A., Magnacca S., Noro F., Costanzo S., Esposito S., Orlandi S., Persichillo M., Bracone F., Panzera T., Ruggiero E., Parisi R., Franciosa S., Morelli M., De Rita F., Cerletti C., de Gaetano G., Donati M. B., Mencanti L., Romanelli M. M. C., Cerri A., Dubini C., Trevisan M. B., Renna L. V., Milani V., Boveri S., Giubbilini P., Ramputi L., Baroni I., De Angeli G., Riciardi W., Olmetti F., Bussotti M., Gaetano C., Baiardi P., Bachetti T., Balbi M., Comini L., Lorenzoni M., Olivares A., Traversi E., Garre C., Sideri R., Clemenza F., Gentile G., Caruana G., Cuscino N., Di Gesaro G., Greco A., Loddo I., Tuzzolino F., Ucelli A., Palombo D., Spinella G., Mozzetta G., Ameri P., Zoppoli G., Finotello A., Porto I., Pratesi G., Bladini F., Spnardi L., Clerici M., Pelusi S., Bianco C., Carpani R., Periti G., Margarita S., Lanza G. A., Severino A., Pedicino D., D'Amario D., D'Aiello A., Vinci R., Bonanni A., Brecciaroli M., Filomia S., Pastorino R., Boccia S., Urbani A., Sanguinetti M., Santoliquido A., Proto L., Tarquini D., Grimaldi M. C., Leonardi S., Elia A., Currao A., Urtis M., Di Toro A., Giuliani L., Caminiti G., Marcolongo F., Sposato B., Guadagni F., Morsella V., Marziale A., and Protti G.
Abstract: Introduction Prevention of cardiovascular disease (CVD) is of key importance in reducing morbidity, disability and mortality worldwide. Observational studies suggest that digital health interventions can be an effective strategy to reduce cardiovascular (CV) risk. However, evidence from large randomised clinical trials is lacking. Methods and analysis The CV-PREVITAL study is a multicentre, prospective, randomised, controlled, open-label interventional trial designed to compare the effectiveness of an educational and motivational mobile health (mHealth) intervention versus usual care in reducing CV risk. The intervention aims at improving diet, physical activity, sleep quality, psycho-behavioural aspects, as well as promoting smoking cessation and adherence to pharmacological treatment for CV risk factors. The trial aims to enrol approximately 80 000 subjects without overt CVDs referring to general practitioners' offices, community pharmacies or clinics of Scientific Institute for Research, Hospitalization and Health Care (Italian acronym IRCCS) affiliated with the Italian Cardiology Network. All participants are evaluated at baseline and after 12 months to assess the effectiveness of the intervention on short-term endpoints, namely improvement in CV risk score and reduction of major CV risk factors. Beyond the funded life of the study, a long-term (7 years) follow-up is also planned to assess the effectiveness of the intervention on the incidence of major adverse CV events. A series of ancillary studies designed to evaluate the effect of the mHealth intervention on additional risk biomarkers are also performed. Ethics and dissemination This study received ethics approval from the ethics committee of the coordinating centre (Monzino Cardiology Center; R1256/20-CCM 1319) and from all other relevant IRBs and ethics committees. Findings are disseminated through scientific meetings and peer-reviewed journals and via social media. Partners are informed about the study's
Published: 2023

2. Biological profiling in the spectrum of acute coronary syndrome: characterizing patients from MINOCA to NSTEMI with different features of the culprit plaque

Author: D'aiello, A, primary, Pedicino, D, additional, Bonanni, A, additional, Vinci, R, additional, Severino, A, additional, Ponzo, M, additional, Conte, C, additional, Cribari, F, additional, Filomia, S, additional, Brecciaroli, M, additional, Grimaldi, M C, additional, Montone, R A, additional, Massetti, M, additional, Crea, F, additional, and Liuzzo, G, additional
Published: 2023
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3. Transcatheter versus surgical aortic valve replacement in patients with aortic stenosis: molecular pathways and correlation with clinical and echocardiographic parameters

Author: Pedicino, D, primary, D'aiello, A, additional, Bonanni, A, additional, Vinci, R, additional, Severino, A, additional, Pasquini, A, additional, Burzotta, F, additional, Trani, C, additional, Ciampi, P, additional, Aurigemma, C, additional, Bruno, P, additional, Russo, G, additional, Massetti, M, additional, Crea, F, additional, and Liuzzo, G, additional
Published: 2023
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4. Challenges and future perspectives of transcatheter tricuspid valve interventions: adopt old strategies or adapt to new opportunities?

Author: Russo, G, Taramasso, M, Pedicino, D, Gennari, M, Gavazzoni, M, Pozzoli, A, Muraru, D, Badano, L, Metra, M, Maisano, F, Russo G., Taramasso M., Pedicino D., Gennari M., Gavazzoni M., Pozzoli A., Muraru D., Badano L. P., Metra M., Maisano F., Russo, G, Taramasso, M, Pedicino, D, Gennari, M, Gavazzoni, M, Pozzoli, A, Muraru, D, Badano, L, Metra, M, Maisano, F, Russo G., Taramasso M., Pedicino D., Gennari M., Gavazzoni M., Pozzoli A., Muraru D., Badano L. P., Metra M., and Maisano F.
Abstract: Tricuspid regurgitation (TR) is a highly prevalent valvular heart disease and is associated with an increased risk of cardiovascular events and death at long-term follow-up. Functional TR accounts for over 90% of TR and is mainly due to annular or right ventricular dilatation. Most often, TR is observed in patients with left-sided valvular heart disease (with or without previous surgical correction) and pulmonary hypertension. Isolated TR is less frequent, though burdened by high surgical mortality. This, together with an incomplete understanding of the disease, has brought to a significant undertreatment in spite of the growing evidence of the impact of severe TR on mortality. Moreover, uncertainties about the appropriate timing for intervention and the predictors of procedural success have contributed to limit TR treatment. Transcatheter tricuspid valve replacement or repair interventions represent novel and less invasive alternatives to surgery and have shown early promising results. The purpose of this review is to provide a complete and updated overview of TR pathology with a special focus on current percutaneous treatment options, future challenges and directions.
Published: 2022

5. Molecular Hallmarks of Ischemia with Non-Obstructive Coronary Arteries: The “INOCA versus Obstructive CCS” Challenge

Author: Bonanni, A., D'aiello, A., Pedicino, D., Di Sario, M., Vinci, R., Ponzo, M., Ciampi, P., Curto, D. L., Conte, C., Cribari, F., Canonico, F., Russo, G., Montone, R. A., Trani, C., Severino, A., Crea, F., Liuzzo, G., Bonanni A., Pedicino D., Di Sario M., Vinci R., Ponzo M., Ciampi P., Conte C., Cribari F., Canonico F. (ORCID:0000-0001-6936-4548), Montone R. A., Trani C. (ORCID:0000-0001-9777-013X), Severino A., Crea F. (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Bonanni, A., D'aiello, A., Pedicino, D., Di Sario, M., Vinci, R., Ponzo, M., Ciampi, P., Curto, D. L., Conte, C., Cribari, F., Canonico, F., Russo, G., Montone, R. A., Trani, C., Severino, A., Crea, F., Liuzzo, G., Bonanni A., Pedicino D., Di Sario M., Vinci R., Ponzo M., Ciampi P., Conte C., Cribari F., Canonico F. (ORCID:0000-0001-6936-4548), Montone R. A., Trani C. (ORCID:0000-0001-9777-013X), Severino A., Crea F. (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)
Abstract: Up to 4 million patients with signs of myocardial ischemia have no obstructive coronary artery disease (CAD). The absence of precise guidelines for diagnosis and treatment in non-obstructive CAD encourages the scientific community to fill the gap knowledge, to provide non-invasive and less expensive diagnostic tools. The aim of our study was to explore the biological profile of Ischemia with Non-Obstructive Coronary Arteries (INOCA) patients with microvascular dysfunction compared to patients presenting with obstructive chronic coronary syndrome (ObCCS) in order to find specific hallmarks of each clinical condition. We performed a gene expression array from peripheral blood mononuclear cells (PBMCs) isolated from INOCA (n = 18) and ObCCS (n = 20) patients. Our results showed a significantly reduced gene expression of molecules involved in cell adhesion, signaling, vascular motion, and inflammation in INOCA as compared to the ObCCS group. In detail, we found lower expression of Platelet and Endothelial Cell Adhesion Molecule 1 (CD31, p < 0.0001), Intercellular Adhesion Molecule-1 (ICAM1, p = 0.0004), Tumor Necrosis Factor (TNF p = 0.0003), Transferrin Receptor (TFRC, p = 0.002), and Vascular Endothelial Growth Factor A (VEGFA, p = 0.0006) in the INOCA group compared with ObCCS. Meanwhile, we observed an increased expression of Hyaluronidase (HYAL2, p < 0.0001) in INOCA patients in comparison to ObCCS. The distinct expression of molecular biomarkers might allow an early and non-invasive differential diagnosis between ObCCS and INOCA, improving clinical management and treatment options, in the era of personalized medicine.
Published: 2022

6. Characteristics and outcomes of patients with atrial versus ventricular secondary tricuspid regurgitation undergoing tricuspid transcatheter edge-to-edge repair - Results from the TriValve registry

Author: Russo, G, Badano, L, Adamo, M, Alessandrini, H, Andreas, M, Braun, D, Connelly, K, Denti, P, Estevez-Loureiro, R, Fam, N, Gavazzoni, M, Hahn, R, Harr, C, Hausleiter, J, Himbert, D, Kalbacher, D, Ho, E, Latib, A, Lubos, E, Ludwig, S, Lurz, P, Monivas, V, Nickenig, G, Pedicino, D, Pedrazzini, G, Pozzoli, A, Marafon, D, Pastorino, R, Praz, F, Rodes-Cabau, J, Besler, C, Schofer, J, Scotti, A, Piayda, K, Sievert, H, Tang, G, Thiele, H, Schlotter, F, von Bardeleben, R, Webb, J, Windecker, S, Leon, M, Maisano, F, Metra, M, Taramasso, M, Connelly, KA, Hahn, RT, Marafon, DP, Tang, GHL, von Bardeleben, RS, Russo, G, Badano, L, Adamo, M, Alessandrini, H, Andreas, M, Braun, D, Connelly, K, Denti, P, Estevez-Loureiro, R, Fam, N, Gavazzoni, M, Hahn, R, Harr, C, Hausleiter, J, Himbert, D, Kalbacher, D, Ho, E, Latib, A, Lubos, E, Ludwig, S, Lurz, P, Monivas, V, Nickenig, G, Pedicino, D, Pedrazzini, G, Pozzoli, A, Marafon, D, Pastorino, R, Praz, F, Rodes-Cabau, J, Besler, C, Schofer, J, Scotti, A, Piayda, K, Sievert, H, Tang, G, Thiele, H, Schlotter, F, von Bardeleben, R, Webb, J, Windecker, S, Leon, M, Maisano, F, Metra, M, Taramasso, M, Connelly, KA, Hahn, RT, Marafon, DP, Tang, GHL, and von Bardeleben, RS
Abstract: Aim Functional or secondary tricuspid regurgitation (STR) is the most common phenotype of tricuspid regurgitation (TR) with atrial STR (ASTR) and ventricular STR (VSTR) being recently identified as two distinct entities. Data on tricuspid transcatheter edge-to-edge repair (T-TEER) in patients with STR according to phenotype (i.e. ASTR vs. VSTR) are lacking. The aim of this study was to assess characteristics and outcomes of patients with ASTR versus VSTR undergoing T-TEER. Methods and results Patients with STR undergoing T-TEER were selected from the Transcatheter Tricuspid Valve Therapies (TriValve) registry. ASTR was defined by (i) left ventricular ejection fraction >= 50%, (ii) atrial fibrillation, and (iii) systolic pulmonary artery pressure <50 mmHg. Patients not matching these criteria were classified as VSTR. Patients with primary TR and cardiac implantable electronic device were excluded. Key endpoints included procedural success and survival at follow-up. A total of 298 patients were enrolled in the study: 65 (22%) with ASTR and 233 (78%) with VSTR. Procedural success was similar in the two groups (80% vs. 83% for ASTR vs. VSTR, p = 0.56) and TEER was effective in reducing TR in both groups (from 97% of patients with baseline TR >= 3+ to 23% in ASTR and to 15% in VSTR, all p = 0.001). At 12-month follow-up, survival was significantly higher in the ASTR versus VSTR cohort (91% vs. 72%, log-rank p = 0.02), with VSTR being an independent predictor of mortality at multivariable analysis (hazard ratio 4.75). Conclusions In a real-world, multicentre registry, T-TEER was effective in reducing TR grade in both ASTR and VSTR. At 12-month follow-up, ASTR showed better survival than VSTR.
Published: 2023

7. Left atrial strain analysis improves left ventricular filling pressures non-invasive estimation in the acute phase of Takotsubo syndrome

Author: Iannaccone, G, Graziani, F, Del Buono, M, Camilli, M, Lillo, R, Caffè, A, Moroni, F, La Vecchia, G, Pedicino, D, Sanna, T, Trani, C, Lombardo, A, Lanza, G, Massetti, M, Crea, F, Montone, R, Iannaccone, Giulia, Graziani, Francesca, Del Buono, Marco Giuseppe, Camilli, Massimiliano, Lillo, Rosa, Caffè, Andrea, Moroni, Francesco, La Vecchia, Giulia, Pedicino, Daniela, Sanna, Tommaso, Trani, Carlo, Lombardo, Antonella, Lanza, Gaetano Antonio, Massetti, Massimo, Crea, Filippo, Montone, Rocco A, Iannaccone, G, Graziani, F, Del Buono, M, Camilli, M, Lillo, R, Caffè, A, Moroni, F, La Vecchia, G, Pedicino, D, Sanna, T, Trani, C, Lombardo, A, Lanza, G, Massetti, M, Crea, F, Montone, R, Iannaccone, Giulia, Graziani, Francesca, Del Buono, Marco Giuseppe, Camilli, Massimiliano, Lillo, Rosa, Caffè, Andrea, Moroni, Francesco, La Vecchia, Giulia, Pedicino, Daniela, Sanna, Tommaso, Trani, Carlo, Lombardo, Antonella, Lanza, Gaetano Antonio, Massetti, Massimo, Crea, Filippo, and Montone, Rocco A
Abstract: Aims The aim of our study is to assess the ability of left atrial (LA) strain values to improve left ventricular and diastolic pressure (LVEDP) non-invasive estimation as compared with traditional echocardiographic indexes in the acute phase of Takotsubo syndrome (TTS) and to predict adverse in-hospital outcomes in this population. Methods and results Consecutive TTS patients were prospectively enrolled. Left ventricular and diastolic pressure was measured at the time of catheterization. Transthoracic echocardiography was performed within 48 h from hospital admission. In-hospital complications (acute heart failure, death from any cause, and life-threatening arrhythmias) were collected. A total of 62 patients were analysed (72.2 ± 10.1 years, female 80%) and in-hospital complications occurred in 25 (40.3%). Left ventricular and diastolic pressure mean value was 24.53 ± 7.92 mmHg. Left atrial reservoir and pump strain values presented higher correlation with LVEDP (r −0.859, P < 0.001 and r −0.848, P < 0.001, respectively) in comparison with E/e ′ ratio, left atrial volume index (LAVi), and tricuspid regurgitation (TR) peak velocity. In addition, at receiver-operating characteristic curve analysis, LA reservoir and pump strain resulted to be better predictors of LVEDP above the mean of our population [0.909 (95% CI 0.818-0.999, P < 0.001) and 0.889 (95% CI 0.789-0.988, P < 0.001)], respectively] as compared with E/e′ ratio, LAVi, and TR peak velocity. Finally, LA reservoir strain resulted to be an independent predictor of worse in-hospital outcomes, together with LVEDP and left ventricular ejection fraction (all P < 0.001). Conclusion In our study, lower LA reservoir and pump strain values were better predictors of LVEDP as compared with traditional echocardiographic indexes in the acute phase of TTS syndrome. Moreover, LA reservoir strain was an independent predict- or of adverse in-hospital outcomes.
Published: 2023

8. Left atrial strain analysis improves non-invasive estimation of left ventricular filling pressures in takotsubo syndrome

Author: Iannaccone, G, primary, Graziani, F, additional, Del Buono, M G, additional, Camilli, M, additional, Lillo, R, additional, Caffe', A, additional, La Vecchia, G, additional, Rinaldi, R, additional, Pedicino, D, additional, Sanna, T, additional, Trani, C, additional, Lombardo, A, additional, Lanza, G A, additional, Montone, R A, additional, and Crea, F, additional
Published: 2022
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9. A methylation-dependent checkpoint by SETD7 promotes myocardial ischemic injury in mice and men

Author: Ambrosini, S, primary, Montecucco, F, additional, Koljin, D, additional, Akhmedov, A, additional, Pedicino, D, additional, Mohammed, S A, additional, Kiss, A, additional, Beltrami, A P, additional, Luscher, T F, additional, Crea, F, additional, Ruschitzka, F, additional, Hamdani, N, additional, Costantino, S, additional, and Paneni, F, additional
Published: 2022
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10. Incessant pericarditis following the second dose of SARS-CoV-2 mRNA vaccine successfully treated with anakinra: a case report

Author: Conte, C, primary, Princi, G, additional, D’Amario, D, additional, Sanna, T, additional, Pedicino, D, additional, and Liuzzo, G, additional
Published: 2022
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11. Personalized clinical phenotyping through systems medicine and artificial intelligence

Author: Cesario, A, D'Oria, M, Bove, F, Privitera, G, Boskoski, I, Pedicino, D, Boldrini, L, Erra, C, Loreti, C, Liuzzo, G, Crea, F, Armuzzi, A, Gasbarrini, A, Calabresi, P, Padua, L, Costamagna, G, Antonelli, M, Valentini, V, Auffray, C, Scambia, G, Cesario A., D'oria M., Bove F., Privitera G., Boskoski I., Pedicino D., Boldrini L., Erra C., Loreti C., Liuzzo G., Crea F., Armuzzi A., Gasbarrini A., Calabresi P., Padua L., Costamagna G., Antonelli M., Valentini V., Auffray C., Scambia G., Cesario, A, D'Oria, M, Bove, F, Privitera, G, Boskoski, I, Pedicino, D, Boldrini, L, Erra, C, Loreti, C, Liuzzo, G, Crea, F, Armuzzi, A, Gasbarrini, A, Calabresi, P, Padua, L, Costamagna, G, Antonelli, M, Valentini, V, Auffray, C, Scambia, G, Cesario A., D'oria M., Bove F., Privitera G., Boskoski I., Pedicino D., Boldrini L., Erra C., Loreti C., Liuzzo G., Crea F., Armuzzi A., Gasbarrini A., Calabresi P., Padua L., Costamagna G., Antonelli M., Valentini V., Auffray C., and Scambia G.
Abstract: Personalized Medicine (PM) has shifted the traditional top-down approach to medicine based on the identification of single etiological factors to explain diseases, which was not suitable for explaining complex conditions. The concept of PM assumes several interpretations in the literature, with particular regards to Genetic and Genomic Medicine. Despite the fact that some disease-modifying genes affect disease expression and progression, many complex conditions cannot be understood through only this lens, especially when other lifestyle factors can play a crucial role (such as the environment, emotions, nutrition, etc.). Personalizing clinical phenotyping becomes a challenge when different pathophysiological mechanisms underlie the same manifestation. Brain disorders, cardiovascular and gastroentero-logical diseases can be paradigmatic examples. Experiences on the field of Fondazione Policlinico Gemelli in Rome (a research hospital recognized by the Italian Ministry of Health as national leader in “Personalized Medicine” and “Innovative Biomedical Technologies”) could help understanding which techniques and tools are the most performing to develop potential clinical phenotypes person-alization. The connection between practical experiences and scientific literature highlights how this potential can be reached towards Systems Medicine using Artificial Intelligence tools.
Published: 2021

12. Use of Levosimendan as bridge therapy to surgical correction of post-infarction ventricular septal defect: a case report

Author: Camilli, M., Ciampi, P., Pedicino, D., D'Aiello, A., Mazza, A., Montone, R. A., Sanna, T., Rebuzzi, A. G., Massetti, M., Crea, F., Liuzzo, G., Camilli M., Ciampi P., Pedicino D., Montone R. A., Sanna T. (ORCID:0000-0002-5760-6885), Rebuzzi A. G. (ORCID:0000-0002-9873-957X), Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Camilli, M., Ciampi, P., Pedicino, D., D'Aiello, A., Mazza, A., Montone, R. A., Sanna, T., Rebuzzi, A. G., Massetti, M., Crea, F., Liuzzo, G., Camilli M., Ciampi P., Pedicino D., Montone R. A., Sanna T. (ORCID:0000-0002-5760-6885), Rebuzzi A. G. (ORCID:0000-0002-9873-957X), Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)
Abstract: – OBJECTIVE: Ventricular septal defect (VSD) is an uncommon but frequently fatal complication following acute myocardial infarction. In medically treated patients, mortality rates exceed 90%, while the surgical repair is associated with better outcomes, even though optimal surgical timing is still under debate. CASE REPORT: We present the case of a 78-years-old man with no previous remarkable cardiological history admitted to our Emergency Department with the diagnosis of anteri- or ST-elevation myocardial infarction and significant reduction of left ventricular ejection fraction. The emergency coronary angiography showed sub-occlusion of the left anterior descending coronary artery, treated with stent implantation. The post-procedural echocardiography unveiled the presence of an apical VSD with a large left-to-right shunt, significant right ventricular overload and dysfunction. An intra-aortic balloon pump (IABP) was positioned and, after Heart Team evaluation, a delayed surgical approach was planned. As a bridge to the intervention Levosimendan infusion was administered, on top of IABP support, and a significant improvement in bi-ventricular function and pressure profiles was obtained. Cardiac surgery was successfully performed 9 days after the admission without periprocedural complications. CONCLUSIONS: This unique case supports the use of Levosimendan as a valid pharmacological strategy for perioperative management of VSD.
Published: 2021

13. From angiotensin-converting enzyme 2 disruption to thromboinflammatory microvascular disease: A paradigm drawn from COVID-19

Author: Vinci, R., Pedicino, D., Andreotti, F., Russo, G., D'Aiello, A., De Cristofaro, R., Crea, F., Liuzzo, G., Vinci R., Pedicino D., Andreotti F. (ORCID:0000-0002-1456-6430), Russo G., De Cristofaro R. (ORCID:0000-0002-8066-8849), Crea F. (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Vinci, R., Pedicino, D., Andreotti, F., Russo, G., D'Aiello, A., De Cristofaro, R., Crea, F., Liuzzo, G., Vinci R., Pedicino D., Andreotti F. (ORCID:0000-0002-1456-6430), Russo G., De Cristofaro R. (ORCID:0000-0002-8066-8849), Crea F. (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)
Abstract: We concisely review clinical, autopsy, experimental and molecular data of 2019 coronavirus disease (COVID-19). Angiotensin-converting enzyme 2 disruption and thromboinflammatory microangiopathy emerge as distinctive features. Briefly, entry of the virus into microvessels can profoundly disrupt the local renin-angiotensin system, cause endothelial injury, activate the complement cascade and induce powerful thromboinflammatory reactions, involving, in particular, von Willebrand factor, that, if widespread, may lead to microvascular plugging, ischemia and, ultimately, organ failure. We believe the current COVID-19 data consolidate a widely unrecognised paradigm of potentially fatal thromboinflammatory microvascular disease.
Published: 2021

14. Transcatheter versus surgical aortic valve replacement in patients with aortic stenosis: characterization of molecular pathways before and after treatment

Author: Bonanni, A, primary, Pedicino, D, additional, D'aiello, A, additional, Vinci, R, additional, Severino, A, additional, Russo, G, additional, Cribari, F, additional, Conte, C, additional, Filomia, S, additional, Bruno, P, additional, Burzotta, F, additional, Trani, C, additional, Massetti, M, additional, Crea, F, additional, and Liuzzo, G, additional
Published: 2022
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15. Restricted T-Cell Repertoire in the Epicardial Adipose Tissue of Non-ST Segment Elevation Myocardial Infarction Patients

Author: Pedicino, Daniela, Severino, Anna, Di Sante, Gabriele, De Rosa, Maria Cristina, Pirolli, Davide, Vinci, Ramona, Pazzano, V., Giglio, A. F., Trotta, F., Russo, G., Ruggio, A., Pisano, Eugenia, D'Aiello, Alessia, Canonico, Francesco, Ciampi, P., Cianflone, D., Cianfanelli, L., Grimaldi, Maria Chiara, Filomia, Simone, Luciani, Nicola, Glieca, Franco, Bruno, Piergiorgio, Massetti, Massimo, Ria, Francesco, Crea, Filippo, Liuzzo, Giovanna, Pedicino D., Severino A., Di Sante G. (ORCID:0000-0001-6608-3388), De Rosa M. C., Pirolli D. (ORCID:0000-0003-2303-2577), Vinci R., Pisano E., d'Aiello A., Canonico F. (ORCID:0000-0001-6936-4548), Grimaldi M. C., Filomia S., Luciani N. (ORCID:0000-0002-9407-0303), Glieca F. (ORCID:0000-0003-3645-7152), Bruno P. (ORCID:0000-0002-1075-5808), Massetti M. (ORCID:0000-0002-7100-8478), Ria F. (ORCID:0000-0002-8444-0307), Crea F. (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Pedicino, Daniela, Severino, Anna, Di Sante, Gabriele, De Rosa, Maria Cristina, Pirolli, Davide, Vinci, Ramona, Pazzano, V., Giglio, A. F., Trotta, F., Russo, G., Ruggio, A., Pisano, Eugenia, D'Aiello, Alessia, Canonico, Francesco, Ciampi, P., Cianflone, D., Cianfanelli, L., Grimaldi, Maria Chiara, Filomia, Simone, Luciani, Nicola, Glieca, Franco, Bruno, Piergiorgio, Massetti, Massimo, Ria, Francesco, Crea, Filippo, Liuzzo, Giovanna, Pedicino D., Severino A., Di Sante G. (ORCID:0000-0001-6608-3388), De Rosa M. C., Pirolli D. (ORCID:0000-0003-2303-2577), Vinci R., Pisano E., d'Aiello A., Canonico F. (ORCID:0000-0001-6936-4548), Grimaldi M. C., Filomia S., Luciani N. (ORCID:0000-0002-9407-0303), Glieca F. (ORCID:0000-0003-3645-7152), Bruno P. (ORCID:0000-0002-1075-5808), Massetti M. (ORCID:0000-0002-7100-8478), Ria F. (ORCID:0000-0002-8444-0307), Crea F. (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)
Abstract: Aims: Human epicardial adipose tissue, a dynamic source of multiple bioactive factors, holds a close functional and anatomic relationship with the epicardial coronary arteries and communicates with the coronary artery wall through paracrine and vasocrine secretions. We explored the hypothesis that T-cell recruitment into epicardial adipose tissue (EAT) in patients with non-ST segment elevation myocardial infarction (NSTEMI) could be part of a specific antigen-driven response implicated in acute coronary syndrome onset and progression. Methods and Results: We enrolled 32 NSTEMI patients and 34 chronic coronary syndrome (CCS) patients undergoing coronary artery bypass grafting (CABG) and 12 mitral valve disease (MVD) patients undergoing surgery. We performed EAT proteome profiling on pooled specimens from three NSTEMI and three CCS patients. We performed T-cell receptor (TCR) spectratyping and CDR3 sequencing in EAT and peripheral blood mononuclear cells of 29 NSTEMI, 31 CCS, and 12 MVD patients. We then used computational modeling studies to predict interactions of the TCR beta chain variable region (TRBV) and explore sequence alignments. The EAT proteome profiling displayed a higher content of pro-inflammatory molecules (CD31, CHI3L1, CRP, EMPRINN, ENG, IL-17, IL-33, MMP-9, MPO, NGAL, RBP-4, RETN, VDB) in NSTEMI as compared to CCS (P < 0.0001). CDR3-beta spectratyping showed a TRBV21 enrichment in EAT of NSTEMI (12/29 patients; 41%) as compared with CCS (1/31 patients; 3%) and MVD (none) (ANOVA for trend P < 0.001). Of note, 11/12 (92%) NSTEMI patients with TRBV21 perturbation were at their first manifestation of ACS. Four patients with the first event shared a distinctive TRBV21-CDR3 sequence of 178 bp length and 2/4 were carriers of the human leukocyte antigen (HLA)-A*03:01 allele. A 3D analysis predicted the most likely epitope able to bind HLA-A3*01 and interact with the TRBV21-CDR3 sequence of 178 bp length, while the alignment results were consistent wit
Published: 2022

16. Monocyte-Platelet Aggregates Triggered by CD31 Molecule in Non-ST Elevation Myocardial Infarction: Clinical Implications in Plaque Rupture

Author: Vinci, Ramona, Pedicino, Daniela, Bonanni, Alice, D'Aiello, A., Pisano, Eugenia, Ponzo, Myriana, Severino, Anna, Ciampi, Pellegrino, Canonico, Francesco, Russo, Giulio, Di Sario, Marianna, Vergallo, Rocco, Filomia, Simone, Montone, Rocco Antonio, Flego, Davide, Stefanini, L., Piacentini, Roberto, Conte, C., Cribari, Francesco, Massetti, Massimo, Crea, Filippo, Liuzzo, Giovanna, Vinci R., Pedicino D., Bonanni A., Pisano E., Ponzo M., Severino A., Ciampi P., Canonico F. (ORCID:0000-0001-6936-4548), Russo G., Di Sario M., Vergallo R., Filomia S., Montone R. A., Flego D., Piacentini R. (ORCID:0000-0003-4215-1643), Cribari F., Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Vinci, Ramona, Pedicino, Daniela, Bonanni, Alice, D'Aiello, A., Pisano, Eugenia, Ponzo, Myriana, Severino, Anna, Ciampi, Pellegrino, Canonico, Francesco, Russo, Giulio, Di Sario, Marianna, Vergallo, Rocco, Filomia, Simone, Montone, Rocco Antonio, Flego, Davide, Stefanini, L., Piacentini, Roberto, Conte, C., Cribari, Francesco, Massetti, Massimo, Crea, Filippo, Liuzzo, Giovanna, Vinci R., Pedicino D., Bonanni A., Pisano E., Ponzo M., Severino A., Ciampi P., Canonico F. (ORCID:0000-0001-6936-4548), Russo G., Di Sario M., Vergallo R., Filomia S., Montone R. A., Flego D., Piacentini R. (ORCID:0000-0003-4215-1643), Cribari F., Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)
Abstract: Despite the recent innovations in cardiovascular care, atherothrombosis is still a major complication of acute coronary syndromes (ACS). We evaluated the involvement of the CD31 molecule in thrombotic risk through the formation of monocyte-platelet (Mo-Plt) aggregates in patients with ACS with no-ST-segment elevation myocardial infarction (NSTEMI) on top of dual anti-platelet therapy (DAPT). We enrolled 19 control (CTRL) subjects, 46 stable angina (SA), and 86 patients with NSTEMI, of which, 16 with Intact Fibrous Cap (IFC) and 19 with Ruptured Fibrous Cap (RFC) as assessed by the Optical Coherence Tomography (OCT). The expression of CD31 on monocytes and platelets was measured. Following the coronary angiography, 52 NSTEMIs were further stratified according to thrombus grade (TG) evaluation. Finally, a series of ex vivo experiments verified whether the CD31 participates in Mo-Plt aggregate formation. In patients with NSTEMI, CD31 was reduced on monocytes and was increased on platelets, especially in NSTEMI presented with RFC plaques compared to those with IFC lesions, and in patients with high TG compared to those with zero/low TG. Ex vivo experiments documented an increase in Mo-Plt aggregates among NSTEMI, which significantly decreased after the CD31 ligation, particularly in patients with RFC plaques. In NSTEMI, CD31 participates in Mo-Plt aggregate formation in spite of optimal therapy and DAPT, suggesting the existence of alternative thrombotic pathways, as predominantly displayed in patients with RFC.
Published: 2022

17. Transcatheter aortic valve implantation in pure aortic regurgitation: Hemodynamic and echocardiographic findings in bioprosthesis vs. native valve

Author: Paraggio, L., Burzotta, Francesco, Graziani, Francesca, Aurigemma, Cristina, Romagnoli, Elisa, Pedicino, Daniela, Locorotondo, Gabriella, Mencarelli, E., Lillo, Rosa, Bruno, Piergiorgio, Laezza, Domenico, Giambusso, N., Lombardo, Antonella, Trani, Carlo, Burzotta F. (ORCID:0000-0002-6569-9401), Graziani F. (ORCID:0000-0002-4520-5689), Aurigemma C., Romagnoli E., Pedicino D., Locorotondo G., Lillo R., Bruno P. (ORCID:0000-0002-1075-5808), Laezza D., Lombardo A. (ORCID:0000-0003-3162-1830), Trani C. (ORCID:0000-0001-9777-013X), Paraggio, L., Burzotta, Francesco, Graziani, Francesca, Aurigemma, Cristina, Romagnoli, Elisa, Pedicino, Daniela, Locorotondo, Gabriella, Mencarelli, E., Lillo, Rosa, Bruno, Piergiorgio, Laezza, Domenico, Giambusso, N., Lombardo, Antonella, Trani, Carlo, Burzotta F. (ORCID:0000-0002-6569-9401), Graziani F. (ORCID:0000-0002-4520-5689), Aurigemma C., Romagnoli E., Pedicino D., Locorotondo G., Lillo R., Bruno P. (ORCID:0000-0002-1075-5808), Laezza D., Lombardo A. (ORCID:0000-0003-3162-1830), and Trani C. (ORCID:0000-0001-9777-013X)
Abstract: Objective: The objective of this study is to compare hemodynamic and echocardiographic findings between valve-in-valve (VIV) and native-valve (NV) patients submitted to transcatheter aortic valve implantation (TAVI) due to pure aortic regurgitation (AR). Background: Patients with severe AR are surgically treated with variable postinterventional left-ventricular (LV) “reverse remodeling.” TAVI might be considered in selected AR patients. Methods: Twenty-eight patients with pure severe AR caused by either degenerated bioprosthesis or NV disease were successfully treated by TAVI at our institution. LV catheterization before and after TAVI and echocardiography before, after (24–72 h), and at follow-up (3–12 months) were performed. Results: Baseline clinical, hemodynamic, and echocardiographic characteristics were comparable between the two study groups, except for a younger age, higher proto-diastolic LV pressure, and higher LV end-systolic diameter in the NV group. At catheterization, an immediate hemodynamic impact of TAVI in both groups was noticed, with a trend toward better postprocedural residual regurgitation index and significantly lower LV dP/dT values (666.0 ± 177.9 vs. 883.5 ± 259.7 mmHg/s, p = 0.04) in VIV. At echocardiography, both NV and VIV patients showed favorable (early and sustained) post-TAVI echocardiographically detectable reverse remodeling. VIV patients also showed more pronounced early reduction in indexed LV end-diastolic volume (68.1 ± 27.4 vs. 86.5 ± 28.9 ml/m2 in VIV, p < 0.001 and 81.0 ± 29.0 vs. 95.2 ± 37.8 ml/m2 in NV, p = 0.043). Conclusions: Successful TAVI induces a striking hemodynamic impact with major structural (reverse remodeling) consequences in patients with pure AR caused by both bioprosthesis degeneration or NV disease. In the immediate postrelease phase, VIV patients might exhibit a more pronounced early LV contractile and structural benefit.
Published: 2022

18. Right ventricle systolic function and right ventricle-pulmonary artery coupling in patients with severe aortic stenosis and the early impact of TAVI

Author: Lillo, Rosa, Graziani, Francesca, Ingrasciotta, Gessica, Przbybylek, B., Iannaccone, Giulia, Locorotondo, Gabriella, Pedicino, Daniela, Aurigemma, Cristina, Romagnoli, Elisa, Trani, Carlo, Lanza, Gaetano Antonio, Lombardo, Antonella, Burzotta, Francesco, Massetti, Massimo, Lillo R., Graziani F. (ORCID:0000-0002-4520-5689), Ingrasciotta G., Iannaccone G., Locorotondo G., Pedicino D., Aurigemma C., Romagnoli E., Trani C. (ORCID:0000-0001-9777-013X), Lanza G. A. (ORCID:0000-0003-2187-6653), Lombardo A. (ORCID:0000-0003-3162-1830), Burzotta F. (ORCID:0000-0002-6569-9401), Massetti M. (ORCID:0000-0002-7100-8478), Lillo, Rosa, Graziani, Francesca, Ingrasciotta, Gessica, Przbybylek, B., Iannaccone, Giulia, Locorotondo, Gabriella, Pedicino, Daniela, Aurigemma, Cristina, Romagnoli, Elisa, Trani, Carlo, Lanza, Gaetano Antonio, Lombardo, Antonella, Burzotta, Francesco, Massetti, Massimo, Lillo R., Graziani F. (ORCID:0000-0002-4520-5689), Ingrasciotta G., Iannaccone G., Locorotondo G., Pedicino D., Aurigemma C., Romagnoli E., Trani C. (ORCID:0000-0001-9777-013X), Lanza G. A. (ORCID:0000-0003-2187-6653), Lombardo A. (ORCID:0000-0003-3162-1830), Burzotta F. (ORCID:0000-0002-6569-9401), and Massetti M. (ORCID:0000-0002-7100-8478)
Abstract: Few data are available on the prevalence of right ventricle (RV) systolic dysfunction, assessed including RV strain, and RV to pulmonary artery (PA) coupling in patients with aortic stenosis (AS) submitted to TAVI and the early effect of the procedure. We performed standard and speckle tracking echocardiography in 80 patients with severe AS the day before TAVI and within 48 h after TAVI. In all patients we measured TAPSE/PASP (cut-off for RV-PA uncoupling 0.31) and in 60/80 we were able to analyze RV global longitudinal strain (RV-GLS) and RV free wall strain (RV-FWS). RVFAC and TAPSE were impaired in 8.3% while RV-GLS and RV-FWS in 45% and 33.3% respectively before TAVI. TAPSE/PASP < 0.31 was documented in 7/80 patients (8.7%) before TAVI. These subjects differed from patients with TAPSE/PASP ≥ 0.31 for: enlarged left ventricular (LV) end-diastolic and end-systolic volumes (p < 0.001), worst LV ejection fraction (p < 0.001) and RVFAC (p < 0.001), worst RV-GLS and RV-FWS (p = 0.01 and p = 0.03) and bigger right atrium (RA) area (p < 0.001). After TAVI, RV systolic function did not improve while PASP significantly decreased (p = 0.005) driving the improvement of TAPSE/PASP (p = 0.01). Patients with TAPSE/PASP improvement (51%) differed from the others for worst pre-TAVI diastolic function (E/eʹ p = 0.045), RVFAC (p = 0.042), RV-GLS (p = 0.049) and RA area (p = 0.02). RV-GLS unveils RV systolic dysfunction in as much as 45% of patients with AS vs only 8.3% revealed by conventional echocardiography. RV systolic function does not significantly improve early after TAVI while RV-PA coupling does. Patients with lower TAPSE/PASP at baseline have worst LV and RV systolic function as well as larger RA. Patients who improve TAPSE/PASP after TAVI are those with worst diastolic function, RV systolic function and larger RA at baseline.
Published: 2022

19. Left ventricular end-diastolic pressure predicts in-hospital outcomes in Takotsubo syndrome

Author: Montone, R.A, primary, Del Buono, M, additional, Meucci, M.C, additional, La Vecchia, G, additional, Camilli, M, additional, Pedicino, D, additional, Trani, C, additional, Sanna, T, additional, Niccoli, G, additional, and Crea, F, additional
Published: 2021
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20. Targeting the methyltransferase setd7 prevents myocardial ischemic injury: a translational study

Author: Ambrosini, S, primary, Montecucco, F, additional, Kolijn, D, additional, Akhmedov, A, additional, Pedicino, D, additional, Mohammed, S, additional, Kiss, A, additional, Beltrami, A, additional, Crea, F, additional, Luescher, T, additional, Hamdani, N, additional, Costantino, S, additional, and Paneni, F, additional
Published: 2021
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21. Takotsubo syndrome: a way to reach a straightforward diagnosis

Author: Bonanni, A, primary, Pedicino, D, additional, Vinci, R, additional, D'Aiello, A, additional, Ponzo, M, additional, Ciampi, P, additional, Pisano, E, additional, Canonico, F, additional, Di Sario, M, additional, Conte, C, additional, Cribari, F, additional, Grimaldi, M C, additional, Severino, A, additional, Crea, F, additional, and Liuzzo, G, additional
Published: 2021
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22. Brain-derived neurotrophic factor in patients with acute coronary syndrome

Author: Montone, Rocco Antonio, Camilli, Massimiliano, Del Buono, Marco Giuseppe, Russo, Michele, Rinaldi, R., Canonico, Francesco, Pedicino, Daniela, Severino, Anna, D'Amario, Domenico, Trani, Carlo, Liuzzo, Giovanna, Crea, Filippo, Niccoli, Giampaolo, Montone R. A., Camilli M., Del Buono M. G., Russo M., Canonico F. (ORCID:0000-0001-6936-4548), Pedicino D., Severino A., D'Amario D., Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), Niccoli G. (ORCID:0000-0002-3187-6262), Montone, Rocco Antonio, Camilli, Massimiliano, Del Buono, Marco Giuseppe, Russo, Michele, Rinaldi, R., Canonico, Francesco, Pedicino, Daniela, Severino, Anna, D'Amario, Domenico, Trani, Carlo, Liuzzo, Giovanna, Crea, Filippo, Niccoli, Giampaolo, Montone R. A., Camilli M., Del Buono M. G., Russo M., Canonico F. (ORCID:0000-0001-6936-4548), Pedicino D., Severino A., D'Amario D., Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), and Niccoli G. (ORCID:0000-0002-3187-6262)
Abstract: Brain-derived neurotrophic factor (BDNF) is a neurotrophic factor highly expressed in coronary plaques, particularly in macrophages, and in activated platelets. Thus, a possible role in the pathogenesis of acute coronary syndrome (ACS) has been suggested. We evaluated systemic BDNF levels according to the different clinical presentations of ACS. Moreover, we assessed the relationship between BDNF levels and the presence of optical coherence tomography (OCT)-defined macrophage infiltrates (MØI) and healed plaques along the culprit vessel. We enrolled consecutive patients presenting with ST-elevation myocardial infarction (STEMI) or non-ST-elevation (NSTE)-ACS. Serum BDNF levels were assessed by enzyme-linked immunosorbent assay. Plaque characteristics of the culprit vessel were assessed by OCT. Among 126 ACS patients (median age 68.00, interquartile range [IQR] 59.75–75.25 years, male 74.6%, 71 (56.3%) were NSTE-ACS and 55 (43.7%) were STEMI. BDNF levels were higher in STEMI patients compared to NSTE-ACS. OCT assessment was performed in 53 (42.1%) patients. Patients with MØI (n = 27) had higher BDNF levels compared to patients without MØI. Furthermore, patients with healed plaques (n = 13) had lower BDNF levels than patients without healed plaques. At multivariate regression analysis BDNF levels independently predicted the presence of MØI (odds ratio [OR] = 2.856; 95% confidence interval [CI] [1.151–7.090], P = 0.024) and the absence of healed plaques (OR = 0.438, 95% CI [0.185–0.992], P= 0.050). Among ACS patients, BDNF levels were higher in patients with STEMI. Moreover, BDNF levels were independently associated with MØI and with the absence of healed plaques along the culprit vessel, suggesting a possible role of BDNF in promoting plaque inflammation, destabilization and occlusive thrombosis.
Published: 2021

23. Personalized clinical phenotyping through systems medicine and artificial intelligence

Author: Cesario, Alfredo, D'Oria, M., Bove, F., Privitera, G., Boskoski, Ivo, Pedicino, Daniela, Boldrini, Luca, Erra, Carmen, Loreti, Claudia, Liuzzo, Giovanna, Crea, Filippo, Armuzzi, Alessandro, Gasbarrini, Antonio, Calabresi, Paolo, Padua, Luca, Costamagna, Guido, Antonelli, Massimo, Valentini, Vincenzo, Auffray, C., Scambia, Giovanni, Cesario A. (ORCID:0000-0003-4687-0709), Boskoski I. (ORCID:0000-0001-8194-2670), Pedicino D., Boldrini L., Erra C., Loreti C., Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), Armuzzi A. (ORCID:0000-0003-1572-0118), Gasbarrini A. (ORCID:0000-0002-7278-4823), Calabresi P. (ORCID:0000-0003-0326-5509), Padua L. (ORCID:0000-0003-2570-9326), Costamagna G. (ORCID:0000-0002-8100-2731), Antonelli M. (ORCID:0000-0003-3007-1670), Valentini V. (ORCID:0000-0003-4637-6487), Scambia G. (ORCID:0000-0003-2758-1063), Cesario, Alfredo, D'Oria, M., Bove, F., Privitera, G., Boskoski, Ivo, Pedicino, Daniela, Boldrini, Luca, Erra, Carmen, Loreti, Claudia, Liuzzo, Giovanna, Crea, Filippo, Armuzzi, Alessandro, Gasbarrini, Antonio, Calabresi, Paolo, Padua, Luca, Costamagna, Guido, Antonelli, Massimo, Valentini, Vincenzo, Auffray, C., Scambia, Giovanni, Cesario A. (ORCID:0000-0003-4687-0709), Boskoski I. (ORCID:0000-0001-8194-2670), Pedicino D., Boldrini L., Erra C., Loreti C., Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), Armuzzi A. (ORCID:0000-0003-1572-0118), Gasbarrini A. (ORCID:0000-0002-7278-4823), Calabresi P. (ORCID:0000-0003-0326-5509), Padua L. (ORCID:0000-0003-2570-9326), Costamagna G. (ORCID:0000-0002-8100-2731), Antonelli M. (ORCID:0000-0003-3007-1670), Valentini V. (ORCID:0000-0003-4637-6487), and Scambia G. (ORCID:0000-0003-2758-1063)
Abstract: Personalized Medicine (PM) has shifted the traditional top-down approach to medicine based on the identification of single etiological factors to explain diseases, which was not suitable for explaining complex conditions. The concept of PM assumes several interpretations in the literature, with particular regards to Genetic and Genomic Medicine. Despite the fact that some disease-modifying genes affect disease expression and progression, many complex conditions cannot be understood through only this lens, especially when other lifestyle factors can play a crucial role (such as the environment, emotions, nutrition, etc.). Personalizing clinical phenotyping becomes a challenge when different pathophysiological mechanisms underlie the same manifestation. Brain disorders, cardiovascular and gastroentero-logical diseases can be paradigmatic examples. Experiences on the field of Fondazione Policlinico Gemelli in Rome (a research hospital recognized by the Italian Ministry of Health as national leader in “Personalized Medicine” and “Innovative Biomedical Technologies”) could help understanding which techniques and tools are the most performing to develop potential clinical phenotypes person-alization. The connection between practical experiences and scientific literature highlights how this potential can be reached towards Systems Medicine using Artificial Intelligence tools.
Published: 2021

24. Clinical predictors and prognostic role of high Killip class in patients with a first episode of anterior ST-segment elevation acute myocardial infarction

Author: Del Buono, Marco Giuseppe, Montone, Rocco Antonio, Rinaldi, R., Gurgoglione, Filippo Luca, Meucci, Maria Chiara, Camilli, Massimiliano, Iannaccone, Giulia, Sanna, Tommaso, Pedicino, Daniela, Trani, Carlo, Niccoli, Giampaolo, Crea, Filippo, Del Buono M. G., Montone R. A., Gurgoglione F. L., Meucci M. C., Camilli M., Iannaccone G., Sanna T. (ORCID:0000-0002-5760-6885), Pedicino D., Trani C. (ORCID:0000-0001-9777-013X), Niccoli G. (ORCID:0000-0002-3187-6262), Crea F. (ORCID:0000-0001-9404-8846), Del Buono, Marco Giuseppe, Montone, Rocco Antonio, Rinaldi, R., Gurgoglione, Filippo Luca, Meucci, Maria Chiara, Camilli, Massimiliano, Iannaccone, Giulia, Sanna, Tommaso, Pedicino, Daniela, Trani, Carlo, Niccoli, Giampaolo, Crea, Filippo, Del Buono M. G., Montone R. A., Gurgoglione F. L., Meucci M. C., Camilli M., Iannaccone G., Sanna T. (ORCID:0000-0002-5760-6885), Pedicino D., Trani C. (ORCID:0000-0001-9777-013X), Niccoli G. (ORCID:0000-0002-3187-6262), and Crea F. (ORCID:0000-0001-9404-8846)
Abstract: AIMS: Killip classification is a simple and fast clinical tool for risk stratification of patients presenting with acute coronary syndrome (ACS). However, the clinical features and predictors of high Killip class at admission, and its prognostic impact in patients presenting with anterior ST elevation MI (STEMI) as first clinical cardiovascular event are still poorly known. The aim of this study was to identify the predictors of high Killip class and its impact on in-hospital and follow-up outcomes. METHODS: We prospectively enrolled patients with unheralded anterior STEMI because of proximal or mid left anterior descending (LAD) artery categorized according to Killip classification. Patients' characteristics, in-hospital complications and major adverse cardiovascular events (MACEs; composite of all-cause death, heart failure hospitalization and new-onset ACS) at follow-up were collected. RESULTS: We enrolled 147 patients [age 66.16±13.33, 113 male patients (76.9%)]. Killip class III--IV occurred in 22 (15%) patients. The median duration of follow-up was 12 [6--15.1] months. At multivariate analysis age [hazard ratio 1.137, 95% CI (1.068--1.209), P < 0.001], prehospital cardiac arrest [hazard ratio 12.145, 95% CI (1.710--86.254), P = 0.013] and proximal LAD lesion [hazard ratio 5.066, 95% CI (1.400--18.334), P = 0.013] were predictive of Killip class III--IV at admission. At multivariate analysis, Killip class III--IV was an independent predictor of in-hospital mortality [hazard ratio 7.790, 95% CI (1.024--59.276], P = 0.047 and of MACEs [hazard ratio 4.155 (1.558--11.082), P = 0.004) at follow-up. CONCLUSION: Killip classification performed at the time of admission is a simple and useful clinical marker of a high risk of early and late adverse cardiovascular events.
Published: 2021

25. Platelet hyaluronidase 2 enrichment in acute coronary syndromes: a conceivable role in monocyte-platelet aggregate formation

Author: Vinci, Ramona, Pedicino, Daniela, D'Aiello, A., Ciampi, Pellegrino, Ponzo, Myriana, Bonanni, Alice, Russo, G., Montone, Rocco Antonio, Massetti, Massimo, Crea, Filippo, Liuzzo, Giovanna, Vinci R., Pedicino D., Ciampi P., Ponzo M., Bonanni A., Montone R. A., Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), Liuzzo G. (ORCID:0000-0002-5714-0907), Vinci, Ramona, Pedicino, Daniela, D'Aiello, A., Ciampi, Pellegrino, Ponzo, Myriana, Bonanni, Alice, Russo, G., Montone, Rocco Antonio, Massetti, Massimo, Crea, Filippo, Liuzzo, Giovanna, Vinci R., Pedicino D., Ciampi P., Ponzo M., Bonanni A., Montone R. A., Massetti M. (ORCID:0000-0002-7100-8478), Crea F. (ORCID:0000-0001-9404-8846), and Liuzzo G. (ORCID:0000-0002-5714-0907)
Abstract: Acute Coronary Syndromes (ACS) with plaque erosion display dysregulated hyaluronan metabolism, with increased hyaluronidase-2 (HYAL2) expression. However, the expression and the role of this enzyme on platelets has never been explored. We evaluated the platelet’s HYAL2 (pltHYAL2) levels on I) stable angina (SA) and II) ACS patients, furtherly sub-grouped in Intact-Fibrous-Cap (IFC) and Ruptured-Fibrous-Cap (RFC), according to Optical Coherence Tomography. We assessed the HYAL2 role through an in vitro model setting of co-cultured monocytes and platelets, before and after treatment with low-molecular-weight hyaluronic acid (HA) as pro-inflammatory stimulus and with or without HYAL2-antibody to inhibit HYAL2 activity. ACS patients exhibit higher pltHYAL2 levels comparing to SA, with the higher expression for IFC group. The addition of HYAL2-antibody significantly reduced the percentage of monocyte-platelet binding, suggesting that pltHYAL2 enrichment at the site of the culprit lesion is a key mediator in the systemic thrombo-inflammatory status of ACS presenting with plaque erosion.
Published: 2021

26. Levosimendan for acute right heart failure in COVID-19: another arrow in our quiver?

Author: CRIBARI, F., CONTE, C., RUGGIO, A., NARDUCCI, M. L., PEDICINO, D., BIASUCCI, L. M., and LIUZZO, G.
Abstract: OBJECTIVE: SARS-CoV-2 infection is associated with a higher risk of acute right heart failure (RHF) due to primary right ventricle (RV) dilation and systemic inflammatory response, which in turn lead to microvascular and cardiomyocytes dysfunction, local hypoxia and multi-organ failure. In this clinical setting, levosimendan could be a viable therapy thanks to its right-heart tropism and its additional pleiotropic properties. CASE REPORT: We present the case of a 72 years-old man with positive nasopharyngeal swab for SARS-CoV-2 infection, mild pulmonary involvement and clinical signs of new-onset RHF. We started a 12-hour levosimendan cycle to improve RV performance and reduce cardiac filling pressures. RESULTS: We obtained a net clinical benefit in terms of acute RHF-related signs and symptoms, progressive renal and liver function improvement and concomitant reduction of high-sensitivity C-Reactive Protein and Interleukin-6 (IL-6) levels. CONCLUSIONS: Acute RHF during SARSCoV-2 infection could be related to a convergent widespread systemic inflammatory response. Thanks to its anti-inflammatory and anti-remodeling properties, levosimendan might represent a viable therapy in this clinical setting, contributing to the dampening of the inflammatory response. [ABSTRACT FROM AUTHOR]
Published: 2022

27. From angiotensin-converting enzyme 2 disruption to thromboinflammatory microvascular disease: A paradigm drawn from COVID-19

Author: Vinci, R., primary, Pedicino, D., additional, Andreotti, F., additional, Russo, G., additional, D'Aiello, A., additional, De Cristofaro, R., additional, Crea, F., additional, and Liuzzo, G., additional
Published: 2021
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28. Brain-derived neurotrophic factor in patients with acute coronary syndrome

Author: Montone, Rocco Antonio, Camilli, Massimiliano, Del Buono, Marco Giuseppe, Russo, M., Rinaldi, R., Canonico, Francesco, Pedicino, Daniela, Severino, Anna, D'Amario, Domenico, Trani, Carlo, Liuzzo, Giovanna, Crea, Filippo, Niccoli, Giampaolo, Montone R. A., Camilli M., Del Buono M. G., Canonico F. (ORCID:0000-0001-6936-4548), Pedicino D., Severino A., D'Amario D., Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), Niccoli G. (ORCID:0000-0002-3187-6262), Montone, Rocco Antonio, Camilli, Massimiliano, Del Buono, Marco Giuseppe, Russo, M., Rinaldi, R., Canonico, Francesco, Pedicino, Daniela, Severino, Anna, D'Amario, Domenico, Trani, Carlo, Liuzzo, Giovanna, Crea, Filippo, Niccoli, Giampaolo, Montone R. A., Camilli M., Del Buono M. G., Canonico F. (ORCID:0000-0001-6936-4548), Pedicino D., Severino A., D'Amario D., Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Crea F. (ORCID:0000-0001-9404-8846), and Niccoli G. (ORCID:0000-0002-3187-6262)
Abstract: Brain-derived neurotrophic factor (BDNF) is a neurotrophic factor highly expressed in coronary plaques, particularly in macrophages, and in activated platelets. Thus, a possible role in the pathogenesis of acute coronary syndrome (ACS) has been suggested. We evaluated systemic BDNF levels according to the different clinical presentations of ACS. Moreover, we assessed the relationship between BDNF levels and the presence of optical coherence tomography (OCT)-defined macrophage infiltrates (MØI) and healed plaques along the culprit vessel. We enrolled consecutive patients presenting with ST-elevation myocardial infarction (STEMI) or non-ST-elevation (NSTE)-ACS. Serum BDNF levels were assessed by enzyme-linked immunosorbent assay. Plaque characteristics of the culprit vessel were assessed by OCT. Among 126 ACS patients (median age 68.00, interquartile range [IQR] 59.75–75.25 years, male 74.6%, 71 (56.3%) were NSTE-ACS and 55 (43.7%) were STEMI. BDNF levels were higher in STEMI patients compared to NSTE-ACS. OCT assessment was performed in 53 (42.1%) patients. Patients with MØI (n = 27) had higher BDNF levels compared to patients without MØI. Furthermore, patients with healed plaques (n = 13) had lower BDNF levels than patients without healed plaques. At multivariate regression analysis BDNF levels independently predicted the presence of MØI (odds ratio [OR] = 2.856; 95% confidence interval [CI] [1.151–7.090], P = 0.024) and the absence of healed plaques (OR = 0.438, 95% CI [0.185–0.992], P= 0.050). Among ACS patients, BDNF levels were higher in patients with STEMI. Moreover, BDNF levels were independently associated with MØI and with the absence of healed plaques along the culprit vessel, suggesting a possible role of BDNF in promoting plaque inflammation, destabilization and occlusive thrombosis.
Published: 2020

29. Early Hemodynamic and Structural Impact of Transcatheter Aortic Valve Replacement in Pure Aortic Regurgitation

Author: Graziani, Francesca, Mencarelli, E., Burzotta, Francesco, Paraggio, L., Aurigemma, Cristina, Romagnoli, Elisa, Pedicino, Daniela, Locorotondo, G., Lombardo, Antonella, Leone, Antonio Maria, Laezza, Domenico, Crea, Filippo, Trani, Carlo, Graziani F. (ORCID:0000-0002-4520-5689), Burzotta F. (ORCID:0000-0002-6569-9401), Aurigemma C., Romagnoli E., Pedicino D., Lombardo A. (ORCID:0000-0003-3162-1830), Leone A. M. (ORCID:0000-0002-1276-9883), Laezza D., Crea F. (ORCID:0000-0001-9404-8846), Trani C. (ORCID:0000-0001-9777-013X), Graziani, Francesca, Mencarelli, E., Burzotta, Francesco, Paraggio, L., Aurigemma, Cristina, Romagnoli, Elisa, Pedicino, Daniela, Locorotondo, G., Lombardo, Antonella, Leone, Antonio Maria, Laezza, Domenico, Crea, Filippo, Trani, Carlo, Graziani F. (ORCID:0000-0002-4520-5689), Burzotta F. (ORCID:0000-0002-6569-9401), Aurigemma C., Romagnoli E., Pedicino D., Lombardo A. (ORCID:0000-0003-3162-1830), Leone A. M. (ORCID:0000-0002-1276-9883), Laezza D., Crea F. (ORCID:0000-0001-9404-8846), and Trani C. (ORCID:0000-0001-9777-013X)
Abstract: N/A
Published: 2020

30. CD8 lymphocytes and plaque erosion: A new piece in the jigsaw

Author: Liuzzo, Giovanna, Pedicino, Daniela, Vinci, Ramona, Crea, Filippo, Liuzzo G. (ORCID:0000-0002-5714-0907), Pedicino D., Vinci R., Crea F. (ORCID:0000-0001-9404-8846), Liuzzo, Giovanna, Pedicino, Daniela, Vinci, Ramona, Crea, Filippo, Liuzzo G. (ORCID:0000-0002-5714-0907), Pedicino D., Vinci R., and Crea F. (ORCID:0000-0001-9404-8846)
Abstract: N/A
Published: 2020

31. Non invasive ventilation and right ventricle function in cardiogenic pulmonary edema: an echocardiographic perspective to select the "right" ventilatory support

Author: Pedicino, D, primary, Angelini, A, additional, Russo, G, additional, D"aiello, A, additional, Rocco, E, additional, Ciampi, P, additional, Ponzo, M, additional, Graziani, F, additional, Locorotondo, G, additional, Sanna, T, additional, Rebuzzi, AG, additional, Lombardo, A, additional, Massetti, M, additional, Liuzzo, G, additional, and Crea, F, additional
Published: 2021
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32. Plaque instability in acute coronary syndromes: a possible pathogenic role of gut microbial communities

Author: Pisano, E, primary, Severino, A, additional, Bugli, F, additional, Pedicino, D, additional, Paroni Sterbini, F, additional, Martini, C, additional, Vinci, R, additional, Canonico, F, additional, Bonanni, A, additional, D'Aiello, A, additional, Ciampi, P, additional, Ponzo, M, additional, Sanguinetti, M, additional, Crea, F, additional, and Liuzzo, G, additional
Published: 2020
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33. Early haemodynamic and structural impact of transcatheter aortic valve replacement in pure aortic regurgitation

Author: Graziani, F, primary, Mencarelli, E, additional, Burzotta, F, additional, Paraggio, L, additional, Aurigemma, C, additional, Romagnoli, E, additional, Pedicino, D, additional, Locorotondo, G, additional, Lombardo, A, additional, Leone, A.M, additional, Laezza, D, additional, Crea, F, additional, and Trani, C, additional
Published: 2020
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34. Meta-inflammation in monocytes of patients with Acute Coronary Syndrome

Author: Canonico, F, primary, Vinci, R, additional, Pedicino, D, additional, Pisano, E, additional, Ciampi, P, additional, Bonanni, A, additional, Ponzo, M, additional, D'Aiello, A, additional, Di Sario, M, additional, Severino, A, additional, D'Amario, D, additional, Niccoli, G, additional, Biasucci, L.M, additional, Crea, F, additional, and Liuzzo, G, additional
Published: 2020
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35. Fluid-dynamics and biological features of unstable plaques: different shear stress for different plaques

Author: Russo, G, primary, Pedicino, D, additional, Burzotta, F, additional, Lodi Rizzini, M, additional, Genuardi, L, additional, Vinci, R, additional, Bologna, M, additional, D'Aiello, A, additional, Gallo, D, additional, Chiastra, C, additional, Aurigemma, C, additional, Bonanni, A, additional, Trani, C, additional, Liuzzo, G, additional, and Crea, F, additional
Published: 2020
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36. Coronary slow flow is associated with a worse clinical outcome in patients with Takotsubo syndrome

Author: Montone, Rocco Antonio, Galiuto, Leonarda, Meucci, Maria Chiara, Del Buono, Marco Giuseppe, Vergni, F., Camilli, Massimiliano, Sanna, Tommaso, Pedicino, Daniela, Buffon, Antonino Maria Tommaso, D'Amario, Domenico, Giraldi, Luca, Trani, Carlo, Liuzzo, Giovanna, Rebuzzi, Antonio Giuseppe, Niccoli, Giampaolo, Crea, Filippo, Montone R. A., Galiuto L. (ORCID:0000-0002-6831-479X), Meucci M. C., Del Buono M. G., Camilli M., Sanna T. (ORCID:0000-0002-5760-6885), Pedicino D., Buffon A. (ORCID:0000-0002-6910-8357), D'Amario D., Giraldi L., Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Rebuzzi A. G. (ORCID:0000-0002-9873-957X), Niccoli G. (ORCID:0000-0002-3187-6262), Crea F. (ORCID:0000-0001-9404-8846), Montone, Rocco Antonio, Galiuto, Leonarda, Meucci, Maria Chiara, Del Buono, Marco Giuseppe, Vergni, F., Camilli, Massimiliano, Sanna, Tommaso, Pedicino, Daniela, Buffon, Antonino Maria Tommaso, D'Amario, Domenico, Giraldi, Luca, Trani, Carlo, Liuzzo, Giovanna, Rebuzzi, Antonio Giuseppe, Niccoli, Giampaolo, Crea, Filippo, Montone R. A., Galiuto L. (ORCID:0000-0002-6831-479X), Meucci M. C., Del Buono M. G., Camilli M., Sanna T. (ORCID:0000-0002-5760-6885), Pedicino D., Buffon A. (ORCID:0000-0002-6910-8357), D'Amario D., Giraldi L., Trani C. (ORCID:0000-0001-9777-013X), Liuzzo G. (ORCID:0000-0002-5714-0907), Rebuzzi A. G. (ORCID:0000-0002-9873-957X), Niccoli G. (ORCID:0000-0002-3187-6262), and Crea F. (ORCID:0000-0001-9404-8846)
Abstract: Objective: Patients with Takotsubo syndrome (TTS) present an acute microvascular dysfunction that leads to an impaired myocardial perfusion and, in more severe forms, an impaired epicardial flow. However, clinical relevance of a delayed coronary flow, the coronary slow flow (CSF), has never been investigated. We studied the prognostic value of CSF occurring in the acute phase of TTS. Methods: This cohort study prospectively evaluated patients with a diagnosis of TTS. CSF was defined as angiographically non-obstructive coronary arteries with thrombolysis in myocardial infarction-2 flow. The incidence of overall mortality and major adverse cardiovascular events (MACEs), defined as the composite of TTS recurrence, cardiac rehospitalisation, cerebrovascular events and mortality, was assessed at follow-up. Results: We enrolled 101 patients (mean age 71.0±11.1 years, 86 (85.1%) female); CSF occurred in 18 (17.8%) patients. At admission, patients with CSF presented more frequently with Killip class III/IV, moderate-to-severe left ventricle systolic dysfunction and right ventricle dysfunction. During the index admission, patients with CSF had a higher rate of intrahospital complications (12 (66.7%) vs 28 (33.7%), p=0.01). At long-term follow-up, patients with CSF had a significantly higher occurrence of overall mortality (9 (50%) vs 19 (22.9%), p=0.011), mainly due to non-cardiac causes (89.3%), and a higher rate of MACE (10 (55.5%) vs 27 (32.5%), p=0.06). At multivariable Cox regression, CSF was independently associated with death from any causes. Conclusions: Patients with TTS presenting with CSF have a worse clinical presentation with a higher rate of intrahospital complications and a poor long-term clinical outcome.
Published: 2019

37. Inflammasome, T Lymphocytes and Innate-Adaptive Immunity Crosstalk: Role in Cardiovascular Disease and Therapeutic Perspectives

Author: Pedicino, Daniela, Giglio, Ada Francesca, Ruggio, Aureliano, Massaro, G, D'Aiello, Alessia, Trotta, Francesco, Lucci, Claudia, Graziani, Francesca, Biasucci, Luigi Marzio, Crea, Filippo, Liuzzo, Giovanna, Pedicino D, Giglio AF, Ruggio A, Trotta F, Lucci C, Graziani F (ORCID:0000-0002-4520-5689), Biasucci LM (ORCID:0000-0002-6921-6497), Crea F (ORCID:0000-0001-9404-8846), Liuzzo G (ORCID:0000-0002-5714-0907), Pedicino, Daniela, Giglio, Ada Francesca, Ruggio, Aureliano, Massaro, G, D'Aiello, Alessia, Trotta, Francesco, Lucci, Claudia, Graziani, Francesca, Biasucci, Luigi Marzio, Crea, Filippo, Liuzzo, Giovanna, Pedicino D, Giglio AF, Ruggio A, Trotta F, Lucci C, Graziani F (ORCID:0000-0002-4520-5689), Biasucci LM (ORCID:0000-0002-6921-6497), Crea F (ORCID:0000-0001-9404-8846), and Liuzzo G (ORCID:0000-0002-5714-0907)
Abstract: Over the past few decades, lot of evidences have shown atherosclerosis as a chronic progressive disease with an exquisite inflammatory feature. More recently, the role of innate immune response in the onset and progression of coronary artery disease (CAD) and an adaptive immunity imbalance, mostly involving T cell sub-sets, have been documented. Therefore, like in many other inflammatory and autoimmune disorders, an altered innate-adaptive immunity crosstalk could represent the key of the inflammatory burden leading to atherosclerotic plaque formation and progression and to the breakdown of plaque stability. In this review, we will address the role of inflammasome in innate immunity and in the imbalance of adaptive immunity. We will discuss how this altered immune crosstalk is related to CAD onset and progression. We will also discuss how unravelling the key molecular mechanisms is of paramount importance in the development of therapeutic tools to delay the chronic progression and prevent the acute destabilization of atherosclerotic plaque.
Published: 2018

38. Poorly differentiated thyroid carcinoma with cardiac metastasis and pulmonary embolism as first clinical presentation: Case report and review of the literature

Author: Pazzano, V., Narducci, M. L., Santangeli, P., Pedicino, D., Glieca, F., Rota, C. A., Novello, M., Pontecorvi, A., Lauriola, L., and Crea, F.
Published: 2011
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39. P2672A role for glucose metabolism in adaptive immunity dysregulation in patients with acute coronary syndromes

Author: Flego, D, primary, Canonico, F, additional, Vinci, R, additional, Pisano, E, additional, Angelini, G, additional, Pedicino, D, additional, Ruggio, A, additional, Russo, G, additional, Lucci, C, additional, Severino, A, additional, Crea, F, additional, and Liuzzo, G, additional
Published: 2018
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40. P1692Increased expression of CD31 on platelets from patients with Non-ST segment Elevation Myocardial Infarction and its role in platelets-monocytes interaction

Author: Vinci, R, primary, Pedicino, D, additional, Pisano, E, additional, Flego, D, additional, Giglio, A F, additional, Trotta, F, additional, Lucci, C, additional, Ruggio, A, additional, Ponzo, M, additional, D'Aiello, A, additional, Canonico, F, additional, Severino, A, additional, Biasucci, L M, additional, Liuzzo, G, additional, and Crea, F, additional
Published: 2018
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41. 15HYAL2 and CD44v6: towards new molecular signatures of plaque instability

Author: Vinci, R, primary, Pedicino, D, additional, Pisano, E, additional, Porto, I, additional, Vergallo, R, additional, Ruggio, A, additional, Flego, D, additional, Severino, A, additional, Liuzzo, G, additional, and Crea, F, additional
Published: 2018
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42. P524Low molecular weight-hyaluronan (LMW-HA) tones down the expression of monocytes-CD31 from ACS patients in subset-dependent manner

Author: Vinci, R, primary, Pedicino, D, additional, Ruggio, A, additional, Flego, D, additional, Vergallo, R, additional, Annibali, G, additional, Angelini, G, additional, D'amario, D, additional, Liuzzo, G, additional, and Crea, F, additional
Published: 2018
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43. Where Does Inflammation Fit?

Author: Biasucci, Luigi Marzio, La Rosa, G., Pedicino, Daniela, D'Aiello, Alessia, Galli, Mattia, Liuzzo, Giovanna, Biasucci L. M. (ORCID:0000-0002-6921-6497), Pedicino D., D'Aiello A., Galli M., Liuzzo G. (ORCID:0000-0002-5714-0907), Biasucci, Luigi Marzio, La Rosa, G., Pedicino, Daniela, D'Aiello, Alessia, Galli, Mattia, Liuzzo, Giovanna, Biasucci L. M. (ORCID:0000-0002-6921-6497), Pedicino D., D'Aiello A., Galli M., and Liuzzo G. (ORCID:0000-0002-5714-0907)
Abstract: Purpose of Review: This review focuses on the complex relationship between inflammation and the onset of acute coronary syndrome and heart failure. Recent Findings: In the last few years, two important lines of research brought new and essential information to light in the pathogenesis of acute coronary syndrome: a) the understanding of the immune mediate mechanisms of inflammation in Ischemic Heart Disease (IHD) and b) evidence that the inflammatory mechanisms associated with atherosclerosis and its complications can be modulated by anti-inflammatory molecules. A large amount of data also suggests that inflammation is a major component in the development and exacerbation of heart failure (HF), in a symbiotic relationship. In particular, recent evidence underlies peculiar aspects of the phenomenon: oxidative stress and autophagy; DAMPS and TLR-4 signaling activation; different macrophages lineage and the contribution of NLRP-3 inflammasome; adaptive immune system. A possible explanation that could unify the pathogenic mechanism of these different conditions is the rising evidence that increased bowel permeability may allow translation of gut microbioma product into the circulation. Summary: These findings clearly establish the role of inflammation as the great trigger for two of the major cardiovascular causes of death and morbidity. Further studies are needed, to better clarify the issue and to define more targeted approaches to reduce pathological inflammation while preserving the physiological one.
Published: 2017

44. Reduced CD31 expression on CD14+CD16+ monocyte subset in acute coronary syndromes

Author: Flego, D., Severino, A., Trotta, F., Copponi, G., Manchi, M., Pedicino, D., Giglio, A.F., Crea, F., and Liuzzo, G.
Published: 2015
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45. P4669Pro-inflammatory effects of low-molecular weight hyaluronan in patients with Non-ST Elevation Myocardial Infarction: down-regulation of CD31 on circulating monocytes

Author: Vinci, R., primary, Pedicino, D., additional, Flego, D., additional, Giglio, A.F., additional, Pisano, E., additional, Trotta, F., additional, Ruggio, A., additional, Angelini, G., additional, Lucci, C., additional, Galante, D., additional, Severino, A., additional, Biasucci, L.M., additional, Liuzzo, G., additional, and Crea, F., additional
Published: 2017
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46. P4672Differential expression of HYAL2 and CD44 splicing variants in acute coronary syndromes, stable angina patients and healthy controls: correlation between hyaluronan-pathway and plaque erosion

Author: Pedicino, D., primary, Vinci, R., additional, Giglio, A.F., additional, Flego, D., additional, Trotta, F., additional, Pisano, E., additional, Ruggio, A., additional, Angelini, G., additional, Lucci, C., additional, Iaconelli, A., additional, Galante, D., additional, Severino, A., additional, Biasucci, L.M., additional, Liuzzo, G., additional, and Crea, F., additional
Published: 2017
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47. HIT Poster session 1P154Preclinical diastolic dysfunction is related to impaired endothelial function in patients with chronic kidney diseaseP155Early detection of left atrial and left ventricular abnormalities in hypertensive and obese womenP156Right ventricle preserved systolic function irrespective of right ventricular hypertrophy and disease severity in anderson fabry diseaseP157Left atrial volume and function in patients undergoing percutaneous mitral valve repairP158Impact of left ventricular dysfunction on outcomes of patients undergoing direct TAVI with a self-expanding bioprosthesisP159Anatomic Doppler spectrum – retrospective spectral tissue Doppler from ultra high frame rate tissue Doppler imaging for evaluation of tissue deformationP160Phasic dynamics of ischaemic mitral regurgitation after primary coronary intervention in acute myocardial infarction: serial echocardiographic assessment from emergency room to long-term follow-upP161Reproducibility of 3DE RV volumes - novel insights at a regional levelP162Pulmonary vascular capacitance as assessed by echocardiography in pulmonary arterial hypertensionP163Three-dimensional endocardial area strain: a novel parameter for quantitative assessment of global left ventricular systolic functionP164Role of exercise hemodynamics assessed by echocardiography on symptom reduction after MitraClipP165Early identification of ventricular dysfunction in patients with juvenile systemic sclerosisP166Heart failure with and without preserved ejection fraction - the role of biomarkers in the aspect of global longitudinal strainP167Complex systolic deformation of aortic root: insights from two dimensional speckle tracking imageP168Volumetric and deformational imaging usind 2d strain and 3d echocardiography in patients with pulmonary hypertensionP169Influence of pressure load and right ventricular morphology and function on tricuspid regurgitation in pulmonary arterial hypertensionP170Left ventricular myocardial diastolic deformation analysis by 2D speckle tracking echocardiography and relationship with conventional diastolic parameters in chronic aortic regurgitationP171Extracellular volume, and not native T1 time, distinguishes diffuse fibrosis in dilated or hypertrophic cardiomyopathy at 3TP172Left atrial strain is significantly reduced in arterial hypertensionP173Symptomatic severe secondary mitral regurgitation: LV enddiastolic diameter (LVEDD) as preferable parameter for risk stratificationP174Left ventricular mechanics in isolated left bundle branch block at rest and when exercising: exploration of the concept of conductive cardiomyopathyP175Assessment of myocardial scar by 2D contrast echocardiographyP176Chronic pericarditis - expression of a rare disease: Erdheim Chester diseaseP177Aortic arch mechanics with two-dimensional speckle tracking echocardiography to estimate the left ventricular remodelling in hypertensive patientsP178Strain analysis by tissue doppler imaging: comparison of conventional manual measurement with a semi-automated approachP179Distribution of extravascular lung water in heart failure patients assessed by lung ultrasoudP180Surrogate markers for obstructive coronary artery diseaseP181LA deformation and LV longitudinal strain by two-dimensional speckle tracking echocardiography as predictors of postoperative AF development after aortic valve replacement in ASP182Left ventricular diastolic dysfunction in type 2 diabetic patients with non alcoholic fatty liver diseaseP183Myocardial strain by speckle-tracking and evaluation of 3D ejection fraction in drug-induced cardiotoxicity's approach in breast cancer

Author: Gevaert, AB, primary, Borizanova, A, primary, Graziani, F, primary, Galuszka, O M, primary, Stathogiannis, K, primary, Lervik Nilsen, L C, primary, Nishino, S, primary, Willis, J, primary, Venner, C, primary, Luo, XX, primary, Van De Heyning, C M, primary, Castaldi, B, primary, Michalski, BW, primary, Wang, TL, primary, Aktemur, T, primary, Dorlet, S, primary, Verseckaite, R, primary, Amzulescu, MS, primary, Brecht, A, primary, Brand, M, primary, Galli, E, primary, Murzilli, R, primary, Bica, R, primary, Teixeira, R, primary, Schmid, J, primary, Miglioranza, MH, primary, Cherneva, ZH, primary, Gheghici, S, primary, Pernigo, M, primary, Rafael, D, primary, Van Craenenbroeck, AH, additional, Shivalkar, B, additional, Lemmens, K, additional, Vrints, CJ, additional, Van Craenenbroeck, EM, additional, Somleva, D, additional, Zlatareva- Gronkova, N, additional, Kinova, E, additional, Goudev, A, additional, Camporeale, A, additional, Pieroni, M, additional, Pedicino, D, additional, Laurito, MP, additional, Verrecchia, E, additional, Lanza, GA, additional, Manna, R, additional, Crea, F, additional, Reinthaler, M, additional, Rutschow, S, additional, Gross, M, additional, Landmesser, U, additional, Kasner, M, additional, Toutouzas, K, additional, Drakopoulou, M, additional, Latsios, G, additional, Synetos, A, additional, Kaitozis, O, additional, Trantalis, G, additional, Mastrokostopoulos, A, additional, Kotronias, R, additional, Tousoulis, D, additional, Brekke, BB, additional, Aase, SA, additional, Lonnebakken, MT, additional, Stensvag, D, additional, Amundsen, B, additional, Torp, H, additional, Stoylen, A, additional, Watanabe, N, additional, Kimura, T, additional, Nakama, T, additional, Furugen, M, additional, Koiwaya, H, additional, Ashikaga, K, additional, Kuriyama, N, additional, Shibata, Y, additional, Augustine, DX, additional, Knight, D, additional, Sparey, J, additional, Coghlan, G, additional, Easaw, J, additional, Huttin, O, additional, Voilliot, D, additional, Mercy, M, additional, Villemin, T, additional, Olivier, A, additional, Mandry, D, additional, Chaouat, A, additional, Juilliere, Y, additional, Selton-Suty, C, additional, Fang, F, additional, Li, S, additional, Zhang, ZH, additional, Yu, CM, additional, Bertrand, PB, additional, De Maeyer, C, additional, De Bock, D, additional, Paelinck, BP, additional, Claeys, MJ, additional, Reffo, E, additional, Balzarin, M, additional, Zulian, F, additional, Milanesi, O, additional, Miskowiec, D, additional, Kupczynska, K, additional, Peczek, L, additional, Nawrot, B, additional, Lipiec, P, additional, Kasprzak, JD, additional, Li, H, additional, Jin, XY, additional, Poci, N, additional, Kaymaz, C, additional, Venner, C, additional, Manenti, V, additional, Carillo, S, additional, Chabot, F, additional, Mizariene, V, additional, Rimkeviciute, D, additional, Bieseviciene, M, additional, Jonkaitiene, R, additional, Jurkevicius, R, additional, Roy, C, additional, Slimani, A, additional, Boileau, L, additional, De Meester, C, additional, Vancraeynest, D, additional, Pasquet, A, additional, Vanoverschelde, JL, additional, Pouleur, AC, additional, Gerber, BL, additional, Oertelt-Prigione, S, additional, Seeland, U, additional, Ruecke, M, additional, Regitz-Zagrosek, V, additional, Stangl, V, additional, Knebel, F, additional, Laux, D, additional, Roeing, J, additional, Butz, T, additional, Christ, M, additional, Grett, M, additional, Wennemann, R, additional, Trappe, H- J, additional, Fournet, M, additional, Leclercq, C, additional, Samset, E, additional, Daubert, J-C, additional, Donal, E, additional, Leo, LA, additional, Pasotti, E, additional, Klersy, C, additional, Moccetti, T, additional, Faletra, FF, additional, Dobre, D, additional, Darmon, S, additional, Dumitrescu, S, additional, Calistru, P, additional, Monteiro, R, additional, Ribeiro, M, additional, Garcia, J, additional, Cardim, N, additional, Goncalves, L, additional, Kaufmann, R, additional, Grubler, MR, additional, Verheyen, N, additional, Weidemann, F, additional, Binder, JS, additional, Santanna, RT, additional, Rover, MM, additional, Leiria, T, additional, Kalil, R, additional, Picano, E, additional, Gargani, L, additional, Kuneva, ZK, additional, Vasilev, DV, additional, Ianula, R, additional, Dasoveanu, M, additional, Calin, C, additional, Homentcovsci, C, additional, Siliste, R, additional, Bergamini, C, additional, Mantovani, A, additional, Bonapace, S, additional, Lipari, P, additional, Barbieri, E, additional, Bonora, E, additional, Targher, G, additional, Camarozano, AC, additional, Pereira Da Cunha, CL, additional, Padilha, SL, additional, Souza, AM, additional, and Freitas, AKE, additional
Published: 2015
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48. Interleukin-17 in atherosclerosis and cardiovascular disease: the good, the bad, and the unknown

Author: Liuzzo, Giovanna, Trotta, F, Pedicino, D., Liuzzo, Giovanna (ORCID:0000-0002-5714-0907), Liuzzo, Giovanna, Trotta, F, Pedicino, D., and Liuzzo, Giovanna (ORCID:0000-0002-5714-0907)
Abstract: Over the past few years our understanding of the importance of adaptive immunity in acute coronary syndromes (ACS) has considerably increased. Profound abnormalities have been observed in specific subsets of CD4+T cells, including type 1 helper T (Th1) cells, CD4+CD28nullT cells, and naturally occurring regulatory T cells (Treg cells). Recently a new lineage of CD4+T cells, type 17 helper T (Th17) cells producing the signature cytokines interleukin (IL)-17, IL-21, and IL-22, has been identified. This has fundamentally changed the Th1/Th2 dichotomy paradigm.
Published: 2013

49. Intrinsic abnormalities in the signaling machinery of acute coronary syndrome T-cells involving PTPN22 expression and Y-292 Zap70 phosphorylation

Author: Flego, D., primary, Severino, A., additional, Trotta, F., additional, Previtero, M., additional, Pedicino, D., additional, Massaro, G., additional, Ucci, S., additional, Crea, F., additional, and Liuzzo, G., additional
Published: 2013
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50. Activation of NALP3/inflammasome pathway in circulating monocytes and epicardial adipose tissue of patients with acute coronary syndromes

Author: Ucci, S., primary, Pedicino, D., additional, Flego, D., additional, Zara, C., additional, Severino, A., additional, Trotta, F., additional, Previtero, M., additional, Massaro, G., additional, Crea, F., additional, and Liuzzo, G., additional
Published: 2013
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