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1. N-3 fatty acids in patients with multiple cardiovascular risk factors

Author

Roncaglioni, Maria Carla, Avanzini, Fausto, Barlera, Simona, Marzona, Irene, Milani, Valentina, Tombesi, Massimo, Caimi, Vittorio, Longoni, Paolo, Silletta, Maria Giuseppina, Tognoni, Gianni, Marchioli, Avanzini F, Roberto., Caimi, V, Longoni, P, Marchioli, R, Roncaglioni, Mc, Silletta, Mg, Tognoni, G, Tombesi, M, Barlera, S, Milani, V, Nicolis, Eb, Casola, C, Marzona, I, Massa, E, Marrocco, W, Micalella, M, Avanzini, F, Franzosi, Mg, Geraci, E, Giansiracusa, N, Rocchetti, L, Decarli, A, Satolli, R, Alli, C, Beghi, E, Bertele', V, Volpi, A, Baviera, M, Monesi, L, Pangrazzi, I, Nicolis, E, Clerici, F, Palumbo, A, Sgaroni, G, Pioggiarella, R, Scarano, M, Marfisi, Rm, Flamminio, A, Macino, L, Ferri, B, Pera, C, Polidoro, A, Abbatino, D, Acquati, M, Addorisio, G, Adinolfi, D, Adreani, L, Agistri, Mr, Agneta, A, Agnolio, Ml, Agostini, N, Agostino, G, Airò, A, Alaimo, N, Albano, M, Albano, N, Alecci, G, Alemanno, S, Alexanian, A, Alfarano, M, Alfè, L, Alonzo, N, Alvino, S, Ancora, A, Andiloro, S, Andreatta, E, Angeli, S, Angiari, F, Angilletti, V, Annicchiarico, C, Anzivino, M, Aprea, R, Aprile, A, Aprile, E, Aprile, I, Aprile, L, Armellani, V, Arnetoli, M, Aronica, A, Autiero, V, Bacca, G, Baccalaro, Am, Bacci, M, Baglio, G, Bagnani, M, Baiano, A, Baldari, A, Ballarini, L, Banchi, G, Bandera, R, Bandini, F, Baratella, M, Barbieri, A, Barbieri Vita, A, Bardi, M, Barlocchi, M, Baron, P, Bartoli, M, Basile, A, Basile, F, Basile, S, Battaggia, A, Battaglia, A, Baù, A, Beconcini, G, Beggio, R, Belfiore, Pa, Belicchi, M, Bellamoli, S, Bellini, C, Bellomo, M, Benetollo, C, Benetti, R, Beretta, E, Bertalero, P, Bertaso, Fg, Bertolani, U, Bettelli, G, Biagiotti, G, Bianchi, S, Bianco, G, Biccari, F, Bigioli, F, Bindi, M, Bisanti, G, Bitetti, Em, Blasetti, Mp, Blesi, F, Boato, V, Boga, S, Boidi, E, Boldrin, G, Bollati, A, Bolzan, L, Bolzonella, S, Bonardi, P, Bonato, Gb, Bonci, M, Bonfitto, G, Bonincontro, E, Boninsegna, F, Bonissone, D, Bono, L, Bonollo, E, Borghi, M, Borioli, N, Borsatto, M, Bosco, T, Bosisio Pioltelli, M, Botarelli, C, Botassis, S, Bottini, F, Bottos, C, Bova, G, Bova, V, Bozzani, A, Bozzetto, Rm, Braga, Vt, Braglia, M, Bramati, E, Brazzoli, C, Breglia, G, Brescia, A, Briganti, D, Brigato, G, Brocchi, A, Brosio, Fa, Bruni, E, Buscaglia, E, Bussini, Md, Bussotti, A, Buzzaccarini, F, Buzzatti, A, Caccamo, G, Cacciavillani, C, Caggiano, G, Calciano, Fp, Calderisi, M, Calienno, S, Caltagirone, P, Calzolari, I, Cammisa, M, Campanaro, M, Campanella, Gb, Campese, F, Canali, G, Candiani, De, Canepa, R, Canini, D, Canino, A, Cantoro, Ea, Capilupi, V, Capotosto, P, Cappelli, B, Capraro, G, Carafa, Fa, Carano, Q, Carcaterra, V, Carriero, D, Carrozzo, G, Cartanese, M, Casalena, M, Casarola, M, Caso, C, Casotto, M, Castaldi, F, Castegnaro, R, Castellani, G, Castri, S, Catalano, E, Catinello, N, Caturano, G, Cavallaro, R, Cavallo, Am, Cavallo, G, Cavion, Mt, Cavirani, G, Cazzaniga, F, Cazzetta, D, Cecconi, V, Cefalo, A, Celebrano, M, Celora, A, Centonze, P, Cerati, D, Cesaretti, D, Checchia, G, Checchin, A, Cherubini, M, Chianese, L, Chiappa, A, Chiappa, Mv, Chiariello, G, Chiavini, G, Chicco, M, Chiumeo, F, Ciacciarelli, A, Ciaci, D, Ciancaglini, R, Cicale, C, Cicale, S, Cipolla, A, Ciruolo, A, Citeri, Al, Citterio, G, Clerici, M, Coazzoli, E, Collecchia, G, Colletta, F, Colombo, I, Colorio, P, Coluccia, S, Comerio, M, Comoretto, P, Compagni, M, Conte, O, Contri, S, Contrisciani, A, Coppetti, T, Corasaniti, F, Corradi, Mt, Corsano, A, Corsini, A, Corti, N, Costantini, G, Costantino, A, Cotroneo, S, Cozzi, D, Cravello, Mg, Cristiano, E, Cucchi, R, Cusmai, L, D' Errico GB, D'Agostino, P, Dal Bianco, L, Dal Mutto, U, Dal Pozzo, G, Dallapiccola, P, Dallatorre, G, Dalle Molle, G, Dalloni, E, D'Aloiso, A, D'Amicis, G, Danese, R, Danieli, D, Danisi, G, D'Anna, Ma, Danti, G, D'Ascanio, S, Davidde, G, De Angeli, D, De Bastiani, R, De Battisti, A, De Bellis, A, De Berardinis, G, De Carlo, F, De Giorgi, D, De Gobbi, R, De Lorenzis, E, De Luca, P, De Martini, G, De Marzi, M, De Matteis, D, De Padova, S, De Polo, P, De Sabato, N, De Stefano, T, De Vita MT, De Vita, U, De Zolt, V, Debernardi, F, Del Carlo, A, Del Re, G, Del Zotti, F, D'Elia, R, Della Giovanna, P, Dell'Acqua, L, Dell'Orco, Rl, Demaria, G, Di Benedetto MG, Di Chiara, G, Di Corcia, V, Di Domizio, O, Di Donato, P, Di Donato, S, Di Fermo, G, Di Franco, M, Di Giovannantonio, G, Di Lascio, G, Di Lecce, G, Di Lorenzo, N, Di Maro, T, Di Mattia, Q, Di Michele, E, Di Modica RS, Di Murro, D, Di Noi MC, Di Paoli, V, Di Santi, M, Di Sanzo, A, Di Turi, C, Diazzi, A, Dileo, I, D'Ingianna, Ap, Dolci, A, Donà, G, Donato, C, Donato, P, Donini, A, Donna, Me, Donvito, Tv, Esposito, L, Esposito, N, Evangelista, M, Faita, G, Falco, M, Falcone, Da, Falorni, F, Fanciullacci, A, Fanton, L, Fasolo, L, Fassina, R, Fassone, A, Fatarella, P, Fedele, F, Fera, I, Fera, L, Ferioli, S, Ferlini, Mg, Ferlino, R, Ferrante, G, Ferrara, Fn, Ferrarese, Mf, Ferrari, G, Ferrari, O, Ferreri, A, Ferroni, M, Fezzi, G, Figaroli, C, Fina, Mg, Fioretta, A, Fiorucci, C, Firrincieli, R, Fischetti, M, Fischietti, G, Fiume, Dc, Flecchia, G, Forastiere, G, Fossati, B, Franceschi, Pl, Franchi, L, Franzoso, F, Frapporti, G, Frasca, G, Frisotti, A, Fumagalli, G, Fusco, D, Gabriele, P, Gabrieli, A, Gagliano, D, Galimberti, G, Galli, A, Gallicchio, N, Gallio, F, Gallipoli, T, Gallo, P, Galopin, T, Gambarelli, L, Garbin, A, Garozzo, Gm, Gasparri, R, Gastaldo, M, Gatti, E, Gazzaniga, P, Gennachi, N, Gentile, Rv, Germani, P, Gesualdi, F, Gherardi, E, Ghezzi, C, Ghidini, Mg, Ghionda, F, Giacci, L, Gialdini, D, Giampaolo, C, Giancane, R, Giannanti, A, Giannese, S, Giannini, L, Giaretta, M, Giaretta, R, Giavardi, L, Giordano, P, Giordano, E, Giordano, B, Gioria, Gm, Giugliano, R, Grassi, Ea, Greco, A, Greco, L, Grilletti, N, Grimaldi, N, Grisetti, G, Groppelli, G, Gualtieri, L, Guarducci, M, Guastella, G, Guerra, M, Guerrini, F, Guglielmini, A, Guido, A, Gulotta, P, Iacono, E, Iadarola, G, Ianiro, G, Iarussi, V, Ieluzzi, Ml, Ierardi, C, Ingaldi, F, Interlandi, S, Iocca, M, Iorno, A, Ioverno, E, Iurato, R, La Pace, L, La Piscopia, C, La Selva, R, Lafratta, M, Lamparelli, M, Lanaro, G, Lancerotto, R, Larcher, M, Lassandro, M, Lattuada, G, Laurino, P, Lefons, C, Legrottaglie, F, Lemma, A, Leone, D, Leone, F, Leso, A, Leuzzi, G, Levato, G, Libardi, L, Libralesso, N, Licini, Pi, Licursi, G, Lidonnici, F, Lillo, C, Liveri, L, Livio, A, Loiero, Ra, Loison, M, Lombardo, G, Lombardo, T, Lomunno, V, Lomuscio, S, Lonedo, A, Longo, E, Lora, L, Lotterio, A, Lucatello, L, Luongo, A, Lupoli, M, Macchia, C, Macri, G, Mafessanti, M, Maggialetti, V, Maggioni, A, Magnani, M, Maiellaro, G, Mancuso, A, Maniglio, Ar, Mannari, Gl, Manni, A, Manocchio, B, Mao, M, Maranò, A, Maraone, E, Marascio, D, Marcheselli, P, Marchetto, B, Marchetto, S, Marchi, A, Marchi, Gl, Mariano, C, Marinacci, S, Marinelli, S, Marini, G, Marra, Vc, Marrali, F, Marseglia, C, Martello, G, Martino, C, Martino, G, Martino, M, Marulli, Cf, Maruzzi, G, Marzotti, A, Mascheroni, G, Mascolo, P, Masoch, G, Masone, R, Massa, L, Massafra, M, Massi, M, Massignani, Dm, Matarese, Am, Matini, G, Mauro, R, Mazzi, M, Mazzillo, A, Mazzocato, E, Mazzoleni, Ns, Mazzone, A, Melacci, A, Mele, E, Meliota, P, Menaspà, S, Meneghello, F, Merola, G, Merone, L, Metrucci, A, Mezzina, V, Micchi, A, Michielon, A, Migliore, N, Minero, G, Minotta, F, Mirandola, C, Mistrorigo, S, Modafferi, L, Moitre, R, Mola, E, Monachese, C, Mongiardini, C, Montagna, F, Montani, M, Montemurno, I, Montolli, R, Montorsi, S, Montresor, M, Monzani, Mg, Morabito, F, Mori, G, Moro, A, Mosca, Mf, Motti, F, Muddolon, L, Mugnai, M, Muscas, F, Naimoli, F, Nanci, G, Nargi, E, Nasorri, R, Nastrini, G, Negossi, M, Negrini, A, Negroni, A, Neola, V, Niccolini, F, Niro, Cm, Nosengo, C, Novella, G, Nuti, C, Obici, F, Olita, C, Oliverio, Ss, Olivieri, I, Oriente, S, Orlando, G, Paci, C, Pagano, G, Pagliara, C, Paita, G, Paladini, G, Paladino, G, Palano, T, Palatella, A, Palermo, P, Palmisano, M, Pando, P, Panessa, P, Panigo, F, Panozzo, G, Panvini, F, Panzieri, F, Panzino, A, Panzitta, F, Paoli, N, Papagna, R, Papaleo, Mg, Papalia, G, Parisi, R, Parotti, N, Parravicini, D, Passarella, P, Pastore, Ga, Patafio, M, Pavone, P, Pedroli, W, Pedroni, M, Pelligra, G, Pellizzari, M, Penati, A, Perlot, M, Perrone, A, Perrone, G, Peruzzi, P, Peselli, C, Petracchini, L, Petrera, L, Petrone, S, Peverelli, C, Pianorsi, F, Piazza, Gp, Piazzolla, G, Picci, A, Pienabarca, G, Pietronigro, Tp, Pignocchino, P, Pilone, R, Pinto, D, Pirovano, E, Pirrotta, D, Pisante, V, Pitotto, P, Pittari, L, Piva, A, Pizzoglio, A, Plantera, Or, Plebani, W, Plessi, S, Podrecca, D, Poerio, V, Poggiani, F, Pogliani, W, Poli, L, Poloni, Fg, Porcelli, R, Porto, S, Pranzo, L, Prevedello, C, Profeta, C, Profico, D, Punzi, A, Quaglia, Gm, Racano, M, Raccone, A, Radice, F, Raho, Ca, Raimondi, R, Rainò, M, Ramponi, R, Ramunni, A, Ramunni, Al, Ravasio, F, Ravera, M, Re Sartò, G, Rebustello, G, Regazzoli, S, Restelli, C, Rezzonico, M, Ricchiuto, F, Rigo, S, Rigon, G, Rigon, R, Rinaldi, Ov, Rinaldi, M, Risplendente, Pg, Rispoli, M, Riundi, R, Riva, Mg, Rizzi, Al, Rizzi, D, Rizzo, Ld, Rocchi, L, Rondinone, B, Rosa, B, Rosati, F, Roselli, F, Rossetti, A, Rossetti, C, Rossi, R, Rossi, Pr, Rossi, A, Rossi, Cl, Rossitto, A, Ruffini, R, Ruffo, A, Ruggio, S, Ruo, M, Russo, B, Russo, L, Russo, R, Russo, S, Russo, U, Russo, V, Ruta, G, Sacchi, F, Sacco Botto, F, Saia, A, Salladini, G, Salmoiraghi, S, Saluzzo, F, Salvatore, C, Salvatori, E, Salvio, G, Sandri, P, Sandrini, T, Sangermano, V, Santoni, N, Saracino, Ad, Saracino, A, Sarasin, P, Sardo Infirri, C, Sarrì, B, Sartori, G, Sartori, N, Sauro, C, Scaglioni, M, Scalfi, C, Scamardella, Am, Scandale, G, Scandone, L, Scannavini, G, Scarati, R, Scardi, A, Scarpa, Fm, Scazzi, P, Schifone, A, Schirosa, G, Scigliano, G, Scilla, A, Sciortino, M, Scolaro, G, Scollo, E, Scorretti, G, Sellitti, R, Selmo, A, Selvaggio, G, Sempio, A, Seren, F, Serio, L, Serra, C, Serra, L, Siciliano, D, Sideri, A, Sighele, M, Signore, R, Siliberto, F, Silvestro, M, Simioni, G, Simmini, G, Simonato, L, Sinchetto, F, Sizzano, E, Smajato, G, Smaldone, M, Sola, G, Sordillo, L, Sovran, Cs, Spagnul, P, Spanò, F, Sproviero, S, Squintani, A, Stella, L, Stilo, V, Stocchiero, B, Stornello, Mc, Stracka, G, Strada, S, Stranieri, G, Stucci, N, Stufano, N, Suppa, A, Susca, Vg, Sutti, M, Taddei, M, Tagliabue, E, Tagliente, G, Talato, F, Talerico, P, Talia, R, Taranto, R, Tartaglia, M, Tauro, N, Tedesco, A, Tieri, P, Tirelli, M, Tocci, L, Todesco, P, Tognolo, M, Tomba, A, Tonello, P, Tonon, R, Toscano, L, Tosi, A, Tosi, G, Toso, S, Travaglio, P, Tremul, L, Tresso, C, Triacchini, P, Triggiano, L, Trigilio, A, Trimeloni, J, Tripicchio, G, Tritto, Gs, Trono, F, Trotta, E, Trotta, G, Tubertini, A, Turri, C, Turri, L, Tuttolani, Mp, Urago, M, Ursini, G, Valcanover, F, Valente, L, Valenti, M, Valentini, F, Vallone, G, Valz, P, Valzano, L, Vanin, V, Vatteroni, M, Vegetti, L, Vendrame, D, Veramonti, I, Veronelli, G, Vesco, A, Vicariotto, G, Vignale, G, Villa, Pl, Vinciguerra, R, Visco, A, Visentin, G, Visonà, E, Vitali, E, Vitali, S, Vitti, F, Volpone, Da, Zambon, N, Zammarrelli, A, Zanaboni, A, Zane, D, Zanetti, B, Zanibellato, R, Zappetti, M, Zappone, P, Zerilli, G, Zirino, V, Zoccali, R, Zuin, F, Altomonte, M, Anelli, N, Angiò, F, Annale, P, Antonacci, S, Anzilotta, R, Bano, F, Basadonna, O, Beduschi, L, Becagli, P, Bellotti, G, Blotta, C, Bruno, G, Cappuccini, A, Caramatti, S, Cariolato, Mp, Castellana, M, Castellani, L, Catania, R, Chielli, A, Chinellato, A, Ciaccia, A, Clerici, E, Cocci, A, Costanzo, G, D'Ercole, F, De Stefano, G, Decè, F, Di Cicco, N, Di Marco, A, Donati Sarti, C, Draghi, E, Dusi, G, Esposito, V, Ferraro, L, Ferretti, A, Ferri, E, Foggetti, L, Foglia, A, Fonzi, E, Frau, G, Fuoco, Mr, Furci, G, Gallo, L, Garra, V, Giannini, A, Gris, A, Iacovino, R, Interrigi, R, Joppi, R, Laner, B, La Fortezza, G, La Padula, A, Lista, Mr, Lupi, G, Maffei, D, Maggioni, G, Magnani, L, Marrazzo, E, Marcon, L, Marinò, V, Maroni, A, Martinelli, C, Mastandrea, E, Mastropierro, F, Meo, At, Mero, P, Minesso, E, Moschetta, V, Mosele, E, Nanni, C, Negretti, A, Nisticò, C, Orsini, A, Osti, M, Pacilli, Mc, Pennestre, C, Picerno, G, Piol, K, Pivano, L, Pizzuti, E, Poggi, L, Poidomani, I, Pozzetto, M, Presti, Ml, Ravani, R, Recalenda, V, Romagnuolo, F, Rossignoli, S, Rossin, E, Sabatella, C, Sacco, F, Sanità, F, Sansone, E, Servadei, F, Sisto, Mt, Sorio, A, Sorrentino, A, Spinelli, E, Spolaor, A, Squillacioti, A, Stella, P, Talerico, A, Todisco, C, Vadino, M, and Zuliani, C.

Subjects
Male, medicine.medical_specialty, General Practice, Kaplan-Meier Estimate, Placebo, Double-Blind Method, Risk Factors, Internal medicine, Fatty Acids, Omega-3, Clinical endpoint, medicine, Humans, Myocardial infarction, Treatment Failure, Aged, Proportional Hazards Models, chemistry.chemical_classification, Omega-3, business.industry, Proportional hazards model, Medicine (all), Hazard ratio, Fatty Acids, General Medicine, Middle Aged, medicine.disease, Hospitalization, Primary Prevention, chemistry, Cardiovascular Diseases, Heart failure, Cohort, Female, business, Polyunsaturated fatty acid
Abstract

Background Trials have shown a beneficial effect of n-3 polyunsaturated fatty acids in patients with a previous myocardial infarction or heart failure. We evaluated the potential benefit of such therapy in patients with multiple cardiovascular risk factors or atherosclerotic vascular disease who had not had a myocardial infarction. Methods In this double-blind, placebo-controlled clinical trial, we enrolled a cohort of patients who were followed by a network of 860 general practitioners in Italy. Eligible patients were men and women with multiple cardiovascular risk factors or atherosclerotic vascular disease but not myocardial infarction. Patients were randomly assigned to n-3 fatty acids (1 g daily) or placebo (olive oil). The initially specified primary end point was the cumulative rate of death, nonfatal myocardial infarction, and nonfatal stroke. At 1 year, after the event rate was found to be lower than anticipated, the primary end point was revised as time to death from cardiovascular causes or admission to the hospital for cardiovascular causes. Results Of the 12,513 patients enrolled, 6244 were randomly assigned to n-3 fatty acids and 6269 to placebo. With a median of 5 years of follow-up, the primary end point occurred in 1478 of 12,505 patients included in the analysis (11.8%), of whom 733 of 6239 (11.7%) had received n-3 fatty acids and 745 of 6266 (11.9%) had received placebo (adjusted hazard ratio with n-3 fatty acids, 0.97; 95% confidence interval, 0.88 to 1.08; P=0.58). The same null results were observed for all the secondary end points. Conclusions In a large general-practice cohort of patients with multiple cardiovascular risk factors, daily treatment with n-3 fatty acids did not reduce cardiovascular mortality and morbidity. (Funded by Societa Prodotti Antibiotici and others; ClinicalTrials.gov number, NCT00317707.).

Published
2013

2. Quantitative trait genetic linkage analysis of body mass index in familial coronary artery disease

Author

Specchia, Claudia, Barlera, S, Chiodini, Bd, Nicolis, Eb, Farrall, M, Peden, J, Collins, R, Watkins, H, Tognoni, G, Franzosi, Mg, and Procardis, Consortium

Subjects
Male, Genetic Linkage, Quantitative Trait Loci, Coronary Artery Disease, Biology, Quantitative trait locus, Body Mass Index, Cohort Studies, Coronary artery disease, Genetic linkage, Genetic linkage analysis, Genetics, medicine, Humans, Obesity, Genetics (clinical), Aged, Analysis of Variance, Chromosomes, Human, Pair 13, Body Weight, Chromosome Mapping, Middle Aged, medicine.disease, Female, Analysis of variance, Lod Score, Body mass index, Cohort study
Abstract

Objective: Body mass index (BMI) is one of the most reproducible and commonly used proxies for obesity and is known to be influenced by many environmental causes as well as genetic factors. Identification of susceptibility genes for BMI regulation has been difficult. Reasons for these inconclusive results are both methodological and related to obesity aetiology. A genome-wide linkage analysis was performed to localise Quantitative trait loci influencing BMI in a large cohort collected in the PROCARDIS coronary heart disease study consisting of 1,812 informative families. Methods: Multipoint linkage analysis for BMI was conducted using both a variance component approach and a model-free regression method, and the resulting LOD scores were compared. Results: The strongest evidence for linkage was detected on chromosomes 13 (LOD 1.6). Other regions showing a LOD score greater than 1 were observed on chromosomes 3, 5, 11, 12 and 15. These results were mainly confirmed by the three different approaches used in the analysis. Conclusion: Our study did not find any locus with strongly supporting evidence for linkage to BMI even in such a large sample. Our results confirm the substantial genetic heterogeneity influencing BMI regulation that has emerged from the majority of genome scans so far published.

Published
2008

3. Patient-reported outcome measures in patients with familial cerebral cavernous malformations: results from the Treat_CCM trial.

Author

Meessen JMTA, Abete-Fornara G, Zarino B, Castori M, Tassi L, Carriero MR, D'Alessandris QG, Al-Shahi Salman R, Blanda A, Nicolis EB, Novelli D, Caruana M, Vasamì A, Lanfranconi S, and Latini R

Abstract

Background: The Phase 1/2 Treat_CCM randomized controlled trial for people with familial cerebral cavernous malformations (FCCMs) confirmed the safety of propranolol and suggested beneficial effects on intracerebral hemorrhage or new focal neurological deficits, but the effects on patient-reported outcome measures have not been reported., Methods: Participants completed self-reported questionnaires at baseline, 1 and 2 years. Depression was assessed with the Beck Depression Inventory-II (BDI-2); Anxiety with the State-Trait Anxiety Inventory X1 and X2 (STAI X-1 and STAI X-2); and Quality of Life with the Short Form 36 (SF-36), split into the physical and mental component scales (PCS and MCS). Differences between treatment groups and the general population were assessed. Change over time by treatment was assessed by means of mixed models., Results: In total, 71 participants (48 propranolol and 23 standard care) were enrolled, of whom 61 (73%) completed questionnaires at baseline and 2-year FU. At baseline, no differences between treatment groups for any of the questionnaires were present. Twenty (31.7%) patients were considered depressed at baseline, while this proportion was lower in the propranolol group after 2 years (28.6% vs. 55.5%, p  = 0.047). The STAI X-1 and X-2 scores were stable over time. PCS was lower in FCCM patients as compared with the general Italian population, while the MCS was similar to the general population. No effect of propranolol was found for both PCS and MCS., Conclusion: Depression is common among patients with FCCM. Patients randomized to propranolol had a lower proportion of participants with depression after 2 years. Clinical trial registration : https://clinicaltrials.gov/, identifier (NCT03589014)., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Meessen, Abete-Fornara, Zarino, Castori, Tassi, Carriero, D'Alessandris, Al-Shahi Salman, Blanda, Nicolis, Novelli, Caruana, Vasamì, Lanfranconi and Latini.)

Published
2024
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4. Circulating biomarkers in familial cerebral cavernous malformation.

Author

Lazzaroni F, Meessen JMTA, Sun Y, Lanfranconi S, Scola E, D'Alessandris QG, Tassi L, Carriero MR, Castori M, Marino S, Blanda A, Nicolis EB, Novelli D, Calabrese R, Agnelli NM, Bottazzi B, Leone R, Mazzola S, Besana S, Catozzi C, Nezi L, Lampugnani MG, Malinverno M, Grdseloff N, Rödel CJ, Rezai Jahromi B, Bolli N, Passamonti F, Magnusson PU, Abdelilah-Seyfried S, Dejana E, and Latini R

Subjects
Animals, Humans, Male, Female, Proto-Oncogene Proteins genetics, Microtubule-Associated Proteins genetics, Zebrafish metabolism, Biomarkers, Seizures, Antigens, Neoplasm, Cell Adhesion Molecules, Hemangioma, Cavernous, Central Nervous System etiology, Hemangioma, Cavernous, Central Nervous System genetics
Abstract

Background: Cerebral Cavernous Malformation (CCM) is a rare cerebrovascular disease, characterized by the presence of multiple vascular malformations that may result in intracerebral hemorrhages (ICHs), seizure(s), or focal neurological deficits (FND). Familial CCM (fCCM) is due to loss of function mutations in one of the three independent genes KRIT1 (CCM1), Malcavernin (CCM2), or Programmed Cell death 10 (PDCD10/CCM3). The aim of this study was to identify plasma protein biomarkers of fCCM to assess the severity of the disease and predict its progression., Methods: Here, we have investigated plasma samples derived from n = 71 symptomatic fCCM patients (40 female/31 male) and n = 17 healthy donors (HD) (9 female/8 male) of the Phase 1/2 Treat_CCM trial, using multiplexed protein profiling approaches., Findings: Biomarkers as sCD14 (p = 0.00409), LBP (p = 0.02911), CXCL4 (p = 0.038), ICAM-1 (p = 0.02013), ANG2 (p = 0.026), CCL5 (p = 0.00403), THBS1 (p = 0.0043), CRP (p = 0.0092), and HDL (p = 0.027), were significantly different in fCCM compared to HDs. Of note, sENG (p = 0.011), THBS1 (p = 0.011) and CXCL4 (p = 0.011), were correlated to CCM genotype. sROBO4 (p = 0.014), TM (p = 0.026) and CRP (p = 0.040) were able to predict incident adverse clinical events, such as ICH, FND or seizure. GDF-15, FLT3L, CXCL9, FGF-21 and CDCP1, were identified as predictors of the formation of new MRI-detectable lesions over 2-year follow-up. Furthermore, the functional relevance of ang2, thbs1, robo4 and cdcp1 markers was validated by zebrafish pre-clinical model of fCCM., Interpretation: Overall, our study identifies a set of biochemical parameters to predict CCM progression, suggesting biological interpretations and potential therapeutic approaches to CCM disease., Funding: Italian Medicines Agency, Associazione Italiana per la Ricerca sul Cancro (AIRC), ERC, Leducq Transatlantic Network of Excellence, Swedish Research Council., Competing Interests: Declaration of interests B.B is inventor of patents on PTX3 and obtains royalties on PTX3-related reagents. N.B. serves on Advisory Board and Speakers Bureau for Celgene and Janssen, and on Speakers Bureau for Takeda, Amgen., (Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.)

Published
2024
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5. LIPCAR Is Increased in Chronic Symptomatic HF Patients. A Sub-Study of the GISSI-HF Trial.

Author

Meessen JMTA, Bär C, di Dona FM, Staszewsky LI, Di Giulio P, Di Tano G, Costa A, Leonardy J, Novelli D, Nicolis EB, Masson S, Pinet F, Thum T, and Latini R

Subjects
Biomarkers, Chronic Disease, Female, Humans, Male, Quality of Life, Ventricular Remodeling, Heart Failure, RNA, Long Noncoding
Abstract

Background: The long noncoding RNA LIPCAR (Long Intergenic noncoding RNA Predicting CARdiac remodeling) has emerged as a promising biomarker in cardiac disease and cardiac remodeling. To determine whether LIPCAR levels help for a molecular phenotyping of chronic heart failure (HF) patients, this study assessed the association of LIPCAR with severity of the disease and its progression, and with risk of death or hospitalization in HF patients., Methods: LIPCAR was measured in plasma of 967 HF patients with symptomatic heart failure participating in the Gruppo Italiano per lo Studio della Sopravvivenza nell'Insufficienza Cardiaca - Heart Failure (GISSI-HF) biohumoral sub-study., Results: Plasma levels of LIPCAR were significantly associated with functional impairment as assessed by the New York Heart Association (NYHA) class, kidney function as reflected by estimated glomerular filtration rate, and creatinine, hemoglobin and mitral insufficiency. In females, these associations were more marked as compared to males. LIPCAR plasma levels were significantly related to the two cardiac markers, N-terminal pro-B type natriuretic peptide and high-sensitivity cardiac troponin T, but not to inflammatory markers such as high sensitivity C-reactive protein and pentraxin-3, nor to patient reported outcomes such as depression and quality of life. HF patients with high LIPCAR levels univariately showed significantly higher incidence of cardiovascular hospitalizations but not of death; after adjusting for covariates, no significant effects of LIPCAR were found for cardiovascular hospitalizations., Conclusion: The circulating long noncoding RNA LIPCAR was increased in HF patients with higher NYHA class, impaired kidney function, and lower hemoglobin, which are indicators of patients' overall state., (© American Association for Clinical Chemistry 2021. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Published
2021
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6. Circulating biomarkers and cardiac function over 3 years after chemotherapy with anthracyclines: the ICOS-ONE trial.

Author

Meessen JMTA, Cardinale D, Ciceri F, Sandri MT, Civelli M, Bottazzi B, Cucchi G, Menatti E, Mangiavacchi M, Condorelli G, Barbieri E, Gori S, Colombo A, Curigliano G, Salvatici M, Pastori P, Ghisoni F, Bianchi A, Falci C, Cortesi P, Farolfi A, Monopoli A, Milandri C, Bregni M, Malossi A, Nassiacos D, Verusio C, Staszewsky L, Leone R, Novelli D, Balconi G, Nicolis EB, Franzosi MG, Masson S, Garlanda C, Mantovani A, Cipolla CM, and Latini R

Subjects
Biomarkers, Humans, Inducible T-Cell Co-Stimulator Protein, Natriuretic Peptide, Brain, Troponin I, Anthracyclines adverse effects, Ventricular Dysfunction, Left
Abstract

Aims: A multicentre trial, ICOS-ONE, showed increases above the upper limit of normality of cardiac troponin (cTn) in 27% of patients within 12 months after the end of cancer chemotherapy (CT) with anthracyclines, whether cardiac protection with enalapril was started at study entry in all (prevention arm) or only upon first occurrence on supra-normal cTn (troponin-triggered arm). The aims of the present post hoc analysis were (i) to assess whether anthracycline-based treatment could induce cardiotoxicity over 36 month follow-up and (ii) to describe the time course of three cardiovascular biomarkers (i.e. troponin I cTnI-Ultra, B-type natriuretic peptide BNP, and pentraxin 3 PTX3) and of left ventricular (LV) function up to 36 months., Methods and Results: Eligible patients were those prescribed first-in-life CT, without evidence of cardiovascular disease, normal cTn, LV ejection fraction (EF) >50%, not on renin-angiotensin aldosterone system antagonists. Patients underwent echocardiography and blood sampling at 24 and 36 months. No differences were observed in biomarker concentration between the two study arms, 'prevention' vs. 'troponin-triggered'. During additional follow-up 13 more deaths occurred, leading to a total of 23 (9.5%), all due to a non-cardiovascular cause. No new occurrences of LV-dysfunction were reported. Two additional patients were admitted to the hospital for cardiovascular causes, both for acute pulmonary embolism. No first onset of raised cTnI-Ultra was reported in the extended follow-up. BNP remained within normal range: at 36 months was 23.4 ng/L, higher (N.S.) than at baseline, 17.6 ng/L. PTX3 peaked at 5.2 ng/mL 1 month after CT and returned to baseline values thereafter. cTnI-Ultra peaked at 26 ng/L 1 month after CT and returned to 3 ng/L until the last measurement at 36 months. All echocardiographic variables remained stable during follow-up with a median LVEF of 63% and left atrial volume index about 24 mL/m 2 ., Conclusions: First-in-life CT with median cumulative dose of anthracyclines of 180 mg/m 2 does not seem to cause clinically significant cardiac injury, as assessed by circulating biomarkers and echocardiography, in patients aged 51 years (median), without pre-existing cardiac disease. This may suggest either a 100% efficacy of enalapril (given as preventive or troponin-triggered) or a reassuringly low absolute cardiovascular risk in this cohort of patients, which may not require intensive cardiologic follow-up., (© 2020 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology.)

Published
2020
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7. Propranolol for familial cerebral cavernous malformation (Treat_CCM): study protocol for a randomized controlled pilot trial.

Author

Lanfranconi S, Scola E, Bertani GA, Zarino B, Pallini R, d'Alessandris G, Mazzon E, Marino S, Carriero MR, Scelzo E, Faragò G, Castori M, Fusco C, Petracca A, d'Agruma L, Tassi L, d'Orio P, Lampugnani MG, Nicolis EB, Vasamì A, Novelli D, Torri V, Meessen JMTA, Al-Shahi Salman R, Dejana E, and Latini R

Subjects
Adrenergic beta-Antagonists administration & dosage, Adrenergic beta-Antagonists adverse effects, Adult, Animals, Anxiety epidemiology, Case-Control Studies, Depression epidemiology, Disease Progression, Female, Hemangioma, Cavernous, Central Nervous System diagnostic imaging, Hemangioma, Cavernous, Central Nervous System epidemiology, Humans, Intracranial Hemorrhages epidemiology, Italy epidemiology, Magnetic Resonance Imaging methods, Male, Mice, Models, Animal, Nervous System Diseases epidemiology, Propranolol administration & dosage, Propranolol adverse effects, Prospective Studies, Quality of Life, Safety, Severity of Illness Index, Treatment Outcome, Adrenergic beta-Antagonists therapeutic use, Hemangioma, Cavernous, Central Nervous System drug therapy, Propranolol therapeutic use
Abstract

Background: Cerebral cavernous malformations (CCMs) are vascular malformations characterized by clusters of enlarged leaky capillaries in the central nervous system. They may result in intracranial haemorrhage, epileptic seizure(s), or focal neurological deficits, and potentially lead to severe disability. Globally, CCMs represent the second most common intracranial vascular malformation in humans, and their familial form (FCCMs) accounts for one-fifth of cases. Neurosurgical excision, and perhaps stereotactic radiosurgery, is the only available therapeutic option. Case reports suggest that propranolol might modify disease progression., Methods: Treat_CCM is a prospective, randomized, open-label, blinded endpoint (PROBE), parallel-group trial involving six Italian clinical centres with central reading of brain magnetic resonance imaging (MRI) and adverse events. Patients with symptomatic FCCMs are randomized (2:1 ratio) either to propranolol (40-80 mg twice daily) in addition to standard care or to standard care alone (i.e. anti-epileptic drugs or headache treatments). The primary outcome is intracranial haemorrhage or focal neurological deficit attributable to CCMs. The secondary outcomes are MRI changes over time (i.e. de novo CCM lesions, CCM size and signal characteristics, iron deposition, and vascular leakage as assessed by quantitative susceptibility mapping and dynamic contrast enhanced permeability), disability, health-related quality of life, depression severity, and anxiety (SF-36, BDI-II, State-Trait Anxiety Inventory)., Discussion: Treat_CCM will evaluate the safety and efficacy of propranolol for CCMs following promising case reports in a randomized controlled trial. The direction of effect on the primary outcome and the consistency of effects on the secondary outcomes (even if none of them yield statistically significant differences) of this external pilot study may lead to a larger sample size in a definitive phase 2 trial., Trial Registration: ClinicalTrails.gov, NCT03589014. Retrospectively registered on 17 July 2018.

Published
2020
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8. Galectin-3 and the Mineralocorticoid Receptor Antagonist Canrenone in Mild Heart Failure.

Author

Clemenza F, Masson S, Conaldi PG, Di Carlo D, Boccanelli A, Mureddu GF, Gonzini L, Lucci D, Maggioni AP, Di Lenarda A, Nicolis EB, Vanasia M, and Latini R

Subjects
Aged, Biomarkers blood, Blood Proteins, Female, Fibrosis, Galectins, Heart Failure diagnosis, Humans, Male, Middle Aged, Mineralocorticoid Receptor Antagonists therapeutic use, Prognosis, Treatment Outcome, Canrenone therapeutic use, Galectin 3 blood, Heart Failure drug therapy
Abstract

Background: Galectin-3 (Gal-3) is involved in collagen deposition and inflammation and is a prognostic biomarker in heart failure (HF)., Methods and results: Gal-3 and other markers of fibrosis or cardiac stress were measured serially in 413 patients with mild HF randomized to the mineralocorticoid receptor antagonist canrenone or placebo to evaluate treatment effect and association with clinical outcome. Gal-3 increased slightly over 6 months in both arms of the study and was associated with clinical endpoints., Conclusions: Although Gal-3 showed prognostic value, the effect of canrenone on clinical outcomes was unaffected by baseline concentrations of biomarkers of fibrosis or cardiac stress.

Published
2017
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9. Raising standards in clinical research - The impact of the ECRIN data centre certification programme, 2011-2016.

Author

Ohmann C, Canham S, Demotes J, Chêne G, Lauritsen J, Martins H, Mendes RV, Nicolis EB, Svobodnik A, and Torres F

Abstract

The nature and the purpose of the ECRIN Data Centre Certification Programme are summarised, and a very brief description is given of the underlying standards (129 in total, divided into 19 separate lists). The certification activity performed so far is described. In a pilot phase 2 centres were certified in 2012. Calls in 2014 and 2015 resulted in a further 8 certified centres, with 2 certifications still in progress, and the 2016 call has generated several additional applications. The impact and benefits of the programme are listed, divided into a) the effects of the introduction of the standards, b) the effects of the certification programme in general, and c) the effects of the certification programme on individual units. The discussion emphasises the generally positive impact of the programme so far but stresses the need to better clarify the perspective and role of the programme.

Published
2017
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10. Characterization of the biological processes shaping the genetic structure of the Italian population.

Author

Parolo S, Lisa A, Gentilini D, Di Blasio AM, Barlera S, Nicolis EB, Boncoraglio GB, Parati EA, and Bione S

Subjects
Chromosomes, Human, Pair 13 genetics, Gene Ontology, Genetic Loci, Genome, Human, Humans, Italy, Principal Component Analysis, Selection, Genetic, Biological Phenomena, Genetics, Population
Abstract

Background: The genetic structure of human populations is the outcome of the combined action of different processes such as demographic dynamics and natural selection. Several efforts toward the characterization of population genetic architectures and the identification of adaptation signatures were recently made. In this study, we provide a genome-wide depiction of the Italian population structure and the analysis of the major determinants of the current existing genetic variation., Results: We defined and characterized 210 genomic loci associated with the first Principal Component calculated on the Italian genotypic data and correlated to the North-south genetic gradient. Using a gene-enrichment approach we identified the immune function as primarily involved in the Italian population differentiation and we described a locus on chromosome 13 showing combined evidence of North-south diversification in allele frequencies and signs of recent positive selection. In this region our bioinformatics analysis pinpointed an uncharacterized long intergenic non-coding (lincRNA), whose expression appeared specific for immune-related tissues suggesting its relevance for the immune function., Conclusions: Our study, combining population genetic analyses with biological insights provides a description of the Italian genetic structure that in future could contribute to the evaluation of complex diseases risk in the population context.

Published
2015
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11. Revising the ECRIN standard requirements for information technology and data management in clinical trials.

Author

Ohmann C, Canham S, Cornu C, Dreß J, Gueyffier F, Kuchinke W, Nicolis EB, and Wittenberg M

Subjects
Certification, Clinical Trials as Topic statistics & numerical data, Data Interpretation, Statistical, Guideline Adherence, Guidelines as Topic, Health Information Management statistics & numerical data, Humans, Information Storage and Retrieval statistics & numerical data, Medical Informatics statistics & numerical data, Program Development, Research Design statistics & numerical data, Terminology as Topic, Vocabulary, Controlled, Clinical Trials as Topic standards, Health Information Management standards, Information Storage and Retrieval standards, Medical Informatics standards, Research Design standards
Abstract

The pilot phase of the ECRIN (European Clinical Research Infrastructure Network) certification programme for European data centres, in late 2011, led to a substantial revision of the original ECRIN standards, completed by June 2012. The pilot phase, the conclusions drawn from it and the revised set of standards are described. Issues concerning the further development of standards and related material are discussed, as are the methods available to best support that development. A strategy is outlined based on short-lived specific task groups, established as necessary by a steering group drawn from ECRIN-ERIC. A final section discusses possible future developments.

Published
2013
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12. Influence of pentraxin 3 (PTX3) genetic variants on myocardial infarction risk and PTX3 plasma levels.

Author

Barbati E, Specchia C, Villella M, Rossi ML, Barlera S, Bottazzi B, Crociati L, d'Arienzo C, Fanelli R, Garlanda C, Gori F, Mango R, Mantovani A, Merla G, Nicolis EB, Pietri S, Presbitero P, Sudo Y, Villella A, and Franzosi MG

Subjects
Aged, Biomarkers analysis, Biomarkers blood, Biomarkers metabolism, Blood Chemical Analysis, Case-Control Studies, Female, Gene Frequency, Genetic Predisposition to Disease, Humans, Male, Middle Aged, Myocardial Infarction diagnosis, Osmolar Concentration, Polymorphism, Single Nucleotide, Prognosis, Risk Factors, C-Reactive Protein analysis, C-Reactive Protein genetics, Myocardial Infarction blood, Myocardial Infarction genetics, Serum Amyloid P-Component analysis, Serum Amyloid P-Component genetics
Abstract

PTX3 is a long pentraxin of the innate immune system produced by different cell types (mononuclear phagocytes, dendritic cells, fibroblasts and endothelial cells) at the inflammatory site. It appears to have a cardiovascular protective function by acting on the immune-inflammatory balance in the cardiovascular system. PTX3 plasma concentration is an independent predictor of mortality in patients with acute myocardial infarction (AMI) but the influence of PTX3 genetic variants on PTX3 plasma concentration has been investigated very little and there is no information on the association between PTX3 variations and AMI. Subjects of European origin (3245, 1751 AMI survivors and 1494 controls) were genotyped for three common PTX3 polymorphisms (SNPs) (rs2305619, rs3816527, rs1840680). Genotype and allele frequencies of the three SNPs and the haplotype frequencies were compared for the two groups. None of the genotypes, alleles or haplotypes were significantly associated with the risk of AMI. However, analysis adjusted for age and sex indicated that the three PTX3 SNPs and the corresponding haplotypes were significantly associated with different PTX3 plasma levels. There was also a significant association between PTX3 plasma concentrations and the risk of all-cause mortality at three years in AMI patients (OR 1.10, 95% CI: 1.01-1.20, p = 0.02). Our study showed that PTX3 plasma levels are influenced by three PTX3 polymorphisms. Genetically determined high PTX3 levels do not influence the risk of AMI, suggesting that the PTX3 concentration itself is unlikely to be even a modest causal factor for AMI. Analysis also confirmed that PTX3 is a prognostic marker after AMI.

Published
2012
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13. Left atrial remodeling and response to valsartan in the prevention of recurrent atrial fibrillation: the GISSI-AF echocardiographic substudy.

Author

Staszewsky L, Wong M, Masson S, Raimondi E, Gramenzi S, Proietti G, Bicego D, Emanuelli C, Pulitanò G, Taddei F, Nicolis EB, Correale E, Fabbri G, Bertocchi F, Franzosi MG, Maggioni AP, Tognoni G, Disertori M, and Latini R

Subjects
Aged, Analysis of Variance, Angiotensin II Type 1 Receptor Blockers administration & dosage, Atrial Fibrillation mortality, Atrial Fibrillation physiopathology, Dose-Response Relationship, Drug, Double-Blind Method, Drug Administration Schedule, Female, Follow-Up Studies, Humans, Italy, Male, Middle Aged, Proportional Hazards Models, Prospective Studies, Recovery of Function, Risk Assessment, Secondary Prevention, Severity of Illness Index, Survival Rate, Treatment Outcome, Valine administration & dosage, Valsartan, Atrial Fibrillation diagnostic imaging, Atrial Fibrillation drug therapy, Atrial Function, Left drug effects, Echocardiography, Doppler methods, Tetrazoles administration & dosage, Valine analogs & derivatives
Abstract

Background: Left atrial (LA) dilation precedes or appears early after the onset of atrial fibrillation (AF) and factors in perpetuating the arrhythmia. Angiotensin receptor blockers were proposed for reversing LA remodeling. We evaluated the effect of valsartan on LA remodeling in patients with a recent episode of AF and the effect of LA size on AF recurrence (AFr)., Methods and Results: LA and left ventricular (LV) echocardiographic variables were measured at baseline and 6 and 12 months in 340 patients from GISSI-AF, a trial testing valsartan prevention of AFr. Reversal of remodeling was considered as a decrease in LA size over 12 months. Changes in patients with and without recurrence and the relationship to duration of AFr were analyzed. Patients were 68.4±8.8 years old, with history of hypertension (85.3%) and cardioversion in the previous 2 weeks (87.4%) or ≥2 AFr in the previous 6 months (40.4%). Baseline LA maximal volume (LAVmax) was severely increased (>40 mL/m(2)); LV dimensions and function were relatively normal. Over 12 months, 54.4% of patients had AFr. LAVmax was unchanged by rhythm, time, or randomized treatment. Higher baseline LAVmax and lower LA emptying fraction were linearly related to increasing AFr duration during follow-up., Conclusions: GISSI-AF patients in sinus rhythm and history of AF showed severely increased LAVmax with mostly normal LV volume, mass, and systolic and diastolic function. Valsartan for 1 year did not reverse LA remodeling or prevent AFr. Half of the patients without AFr had severe LA dilation; therefore, mechanisms other than structural remodeling triggered recurrence.

Published
2011
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14. Multiple QTL influence the serum Lp(a) concentration: a genome-wide linkage screen in the PROCARDIS study.

Author

Barlera S, Specchia C, Farrall M, Chiodini BD, Franzosi MG, Rust S, Green F, Nicolis EB, Peden J, Assmann G, Collins R, Hamsten A, Tognoni G, and Watkins H

Subjects
Aged, Chromosome Mapping, Female, Genetic Testing, Genome, Human, Humans, Male, Middle Aged, Chromosomes, Human genetics, Genetic Linkage, Lipoprotein(a) blood, Quantitative Trait Loci
Abstract

The serum concentration of lipoprotein Lp (a) is known to be highly heritable and associated with cardiovascular risk. A genome-wide variance component linkage analysis was performed to localise quantitative trait loci (QTLs) influencing Lp(a) levels in a large cohort collected in the PROCARDIS coronary heart disease study. Highly significant linkage was detected at the previously described LP(a) locus on chromosome 6q27 (LOD 108). Taking into account the effect of the locus detected on chromosome 6, a highly significant LOD score was detected on chromosome 13q22-31 (LOD 7.0). Another significant region of linkage was observed on chromosomes 11p14-15 (LOD 3.5). The significant peak at 13q22-31 shows an essential overlap with a locus modulating cholesterol in familial hypercholesterolemia. If the gene underlying these loci is the same, it will be a promising candidate target for manipulating LDL-cholesterol and Lp(a). We also detected linkage at a previously identified locus influencing Lp(a) on chromosome 1q23 (LOD 1.5). Our findings provide new and confirmatory information about genomic regions involved in the quantitative variation of Lp(a) and serve as a basis for further studies of candidate genes in these regions.

Published
2007
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