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1. Catalytically inactive lecithin: cholesterol acyltransferase (LCAT) caused by a Gly 30 to Ser mutation in a family with LCAT deficiency

Author

X P Yang, A Inazu, A Honjo, I Koizumi, K Kajinami, J Koizumi, S M Marcovina, J J Albers, and H Mabuchi

Subjects
Biochemistry, QD415-436
Abstract

Plasma lecithin:cholesterol acyltransferase (LCAT) plays an important role in early steps of reverse cholesterol transport, i.e., cholesterol efflux from peripheral tissues and cholesterol esterification in HDL. However, structural and functional relationships of LCAT have not been fully elucidated. We described a missense mutation of Gly 30-to-Ser in a patient with classical LCAT deficiency. The proband was homozygous for the mutation and had a very low level of HDL cholesterol (2 mg/dl), with a half of normal LCAT mass (2.75 micrograms/ml), but no detectable or very low LCAT activity in endogenous and exogenous substrate assays. Both his mother and sister were heterozygous for the mutation, and had slightly decreased levels of HDL cholesterol (34 and 36 mg/dl, respectively). Transient expression study using COS cells indicated that mutant cDNA produces similar amounts of media protein as compared to wild type, but no detectable LCAT activity. The missense mutation may result in a near-native conformation without large effects on cellular secretion but a catalytically defective protein. Thus, the N-terminal domain appears crucial for enzymatic activity, in addition to the catalytically active consensus sequence of Gly179 to Gly183 and a putative sterol binding domain of Glu154 to Lys173.

Published
1997
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2. Abstracts

Author

V. Dunet, A. Dabiri, G. Allenbach, A. Goyeneche Achigar, B. Waeber, F. Feihl, R. Heinzer, J. O. Prior, J. E. Van Velzen, J. D. Schuijf, F. R. De Graaf, M. A. De Graaf, M. J. Schalij, L. J. Kroft, A. De Roos, J. W. Jukema, E. E. Van Der Wall, J. J. Bax, E. Lankinen, A. Saraste, T. Noponen, R. Klen, M. Teras, T. Kokki, S. Kajander, M. Pietila, H. Ukkonen, J. Knuuti, A. P. Pazhenkottil, R. N. Nkoulou, J. R. Ghadri, B. A. Herzog, R. R. Buechel, S. M. Kuest, M. Wolfrum, O. Gaemperli, L. Husmann, P. A. Kaufmann, D. Andreini, G. Pontone, S. Mushtaq, L. Antonioli, E. Bertella, A. Formenti, S. Cortinovis, G. Ballerini, C. Fiorentini, M. Pepi, A. S. Koh, J. S. Flores, F. Y. J. Keng, R. S. Tan, T. S. J. Chua, A. D. Annoni, G. Tamborini, M. Fusari, A. L. Bartorelli, S. H. Ewe, A. C. T. Ng, V. Delgado, J. Schuijf, F. Van Der Kley, A. Colli, A. De Weger, N. A. Marsan, K. H. Yiu, A. C. Ng, S. A. J. Timmer, P. Knaapen, T. Germans, P. A. Dijkmans, M. Lubberink, J. M. Ten Berg, F. J. Ten Cate, I. K. Russel, A. A. Lammertsma, A. C. Van Rossum, Y. Y. Wong, G. Ruiter, P. Raijmakers, W. J. Van Der Laarse, N. Westerhof, A. Vonk-Noordegraaf, G. Youssef, E. Leung, G. Wisenberg, C. Marriot, K. Williams, J. Etele, R. A. Dekemp, J. Dasilva, D. Birnie, R. S. B. Beanlands, R. C. Thompson, A. H. Allam, L. S. Wann, A. H. Nureldin, G. Adelmaksoub, I. Badr, M. L. Sutherland, J. D. Sutherland, M. I. Miyamoto, G. S. Thomas, H. J. Harms, S. De Haan, M. C. Huisman, R. C. Schuit, A. D. Windhorst, C. Allaart, A. J. Einstein, T. Khawaja, C. Greer, A. Chokshi, M. Jones, K. Schaefle, K. Bhatia, D. Shimbo, P. C. Schulze, A. Srivastava, R. Chettiar, J. Moody, C. Weyman, D. Natale, W. Bruni, Y. Liu, E. Ficaro, A. J. Sinusas, A. Peix, E. Batista, L. O. Cabrera, K. Padron, L. Rodriguez, B. Sainz, V. Mendoza, R. Carrillo, Y. Fernandez, E. Mena, A. Naum, T. Bach-Gansmo, N. Kleven-Madsen, M. Biermann, B. Johnsen, J. Aase Husby, S. Rotevatn, J. E. Nordrehaug, J. Schaap, R. M. Kauling, M. C. Post, B. J. W. M. Rensing, J. F. Verzijlbergen, J. Sanchez, G. Giamouzis, N. Tziolas, P. Georgoulias, G. Karayannis, A. Chamaidi, N. Zavos, K. Koutrakis, G. Sitafidis, J. Skoularigis, F. Triposkiadis, S. Radovanovic, A. Djokovic, D. V. Simic, M. Krotin, A. Savic-Radojevic, M. Pljesa-Ercegovac, M. Zdravkovic, J. Saponjski, S. Jelic, T. Simic, R. Eckardt, B. J. Kjeldsen, L. I. Andersen, T. Haghfelt, P. Grupe, A. Johansen, B. Hesse, H. Pena, G. Cantinho, M. Wilk, Y. Srour, F. Godinho, N. Zafrir, A. Gutstein, I. Mats, A. Battler, A. Solodky, E. Sari, N. Singh, A. Vara, A. M. Peters, A. De Belder, S. Nair, N. Ryan, R. James, S. Dizdarevic, G. Depuey, M. Friedman, R. Wray, R. Old, H. Babla, B. Chuanyong, J. Maddahi, E. Tragardh Johansson, K. Sjostrand, L. Edenbrandt, S. Aguade-Bruix, G. Cuberas-Borros, M. N. Pizzi, M. Sabate-Fernandez, G. De Leon, D. Garcia-Dorado, J. Castell-Conesa, J. Candell-Riera, D. Casset-Senon, M. Edjlali-Goujon, D. Alison, A. Delhommais, P. Cosnay, C. S. Low, A. Notghi, J. O'brien, A. C. Tweddel, N. Bingham, P. O Neil, M. Harbinson, O. Lindner, W. Burchert, M. Schaefers, C. Marcassa, R. Campini, P. Calza, O. Zoccarato, A. Kisko, J. Kmec, M. Babcak, M. Vereb, M. Vytykacova, J. Cencarik, P. Gazdic, J. Stasko, A. Abreu, E. Pereira, L. Oliveira, P. Colarinha, V. Veloso, I. Enriksson, G. Proenca, P. Delgado, L. Rosario, J. Sequeira, I. Kosa, I. Vassanyi, C. S. Egyed, G. Y. Kozmann, S. Morita, M. Nanasato, I. Nanbu, Y. Yoshida, H. Hirayama, A. Allam, A. Sharef, I. Shawky, M. Farid, M. Mouden, J. P. Ottervanger, J. R. Timmer, M. J. De Boer, S. Reiffers, P. L. Jager, S. Knollema, G. M. Nasr, M. Mohy Eldin, M. Ragheb, I. Casans-Tormo, R. Diaz-Exposito, F. J. Hurtado-Mauricio, R. Ruano, M. Diego, F. Gomez-Caminero, C. Albarran, A. Martin De Arriba, A. Rosero, R. Lopez, C. Martin Luengo, J. R. Garcia-Talavera, I. E. K. Laitinen, M. Rudelius, E. Weidl, G. Henriksen, H. J. Wester, M. Schwaiger, X. B. Pan, T. Schindler, A. Quercioli, H. Zaidi, O. Ratib, J. M. Declerck, E. Alexanderson Rosas, R. Jacome, M. Jimenez-Santos, E. Romero, M. A. Pena-Cabral, A. Meave, J. Gonzalez, F. Rouzet, L. Bachelet, J. M. Alsac, M. Suzuki, L. Louedec, A. Petiet, F. Chaubet, D. Letourneur, J. B. Michel, D. Le Guludec, A. Aktas, A. Cinar, G. Yaman, T. Bahceci, K. Kavak, A. Gencoglu, A. Jimenez-Heffernan, E. Sanchez De Mora, J. Lopez-Martin, R. Lopez-Aguilar, C. Ramos, C. Salgado, A. Ortega, C. Sanchez-Gonzalez, J. Roa, A. Tobaruela, S. V. Nesterov, O. Turta, M. Maki, C. Han, D. Daou, M. Tawileh, S. O. Chamouine, C. Coaguila, E. Mariscal-Labrador, N. Kisiel-Gonzalez, P. De Araujo Goncalves, P. J. Sousa, H. Marques, J. O'neill, J. Pisco, R. Cale, J. Brito, A. Gaspar, F. P. Machado, J. Roquette, M. Martinez, G. Melendez, E. Kimura, J. M. Ochoa, A. M. Alessio, A. Patel, R. Lautamaki, F. M. Bengel, J. B. Bassingthwaighte, J. H. Caldwell, K. Rahbar, H. Seifarth, M. Schafers, L. Stegger, T. Spieker, A. Hoffmeier, D. Maintz, H. Scheld, O. Schober, M. Weckesser, H. Aoki, I. Matsunari, K. Kajinami, M. Martin Fernandez, M. Barreiro Perez, O. V. Fernandez Cimadevilla, D. Leon Duran, E. Velasco Alonso, J. P. Florez Munoz, L. H. Luyando, C. Templin, C. E. Veltman, J. H. C. Reiber, S. Venuraju, A. Yerramasu, S. Atwal, A. Lahiri, T. Kunimasa, M. Shiba, K. Ishii, J. Aikawa, E. S. J. Kroner, K. T. Ho, Q. W. Yong, K. C. Chua, C. Panknin, C. J. Roos, J. M. Van Werkhoven, A. J. Witkowska-Grzeslo, M. J. Boogers, D. V. Anand, D. Dey, D. Berman, F. Mut, R. Giubbini, L. Lusa, T. Massardo, A. Iskandrian, M. Dondi, A. Sato, Y. Kakefuda, E. Ojima, T. Adachi, A. Atsumi, T. Ishizu, Y. Seo, M. Hiroe, K. Aonuma, M. Kruk, R. Pracon, C. Kepka, J. Pregowski, A. Kowalewska, M. Pilka, M. Opolski, I. Michalowska, Z. Dzielinska, M. Demkow, V. Stoll, N. Sabharwal, A. Chakera, O. Ormerod, H. Fernandes, M. Bernardes, E. Martins, P. Oliveira, T. Vieira, G. Terroso, A. Oliveira, T. Faria, F. Ventura, J. Pereira, S. Fukuzawa, M. Inagaki, J. Sugioka, A. Ikeda, S. Okino, J. Maekawa, T. Uchiyama, N. Kamioka, S. Ichikawa, M. Afshar, R. Alvi, N. Aguilar, R. Ippili, H. Shaqra, J. Bella, N. Bhalodkar, A. Dos Santos, M. Daicz, L. O. Cendoya, H. G. Marrero, J. Casuscelli, M. Embon, G. Vera Janavel, E. Duronto, E. P. Gurfinkel, C. M. Cortes, Y. Takeishi, K. Nakajima, Y. Yamasaki, T. Nishimura, K. Hayes Brown, F. Collado, M. Alhaji, J. Green, S. Alexander, R. Vashistha, S. Jain, F. Aldaas, J. Shanes, R. Doukky, K. Ashikaga, Y. J. Akashi, M. Uemarsu, R. Kamijima, K. Yoneyama, K. Omiya, Y. Miyake, Y. Brodov, U. Raval, A. Berezin, V. Seden, E. Koretskaya, T. A. Panasenko, S. Matsuo, S. Kinuya, J. Chen, R. J. Van Bommel, B. Van Der Hiel, P. Dibbets-Schneider, E. V. Garcia, I. Rutten-Vermeltfoort, M. M. J. Gevers, B. Verhoeven, A. B. Dijk Van, E. Raaijmakers, P. G. H. M. Raijmakers, J. E. Engvall, M. Gjerde, J. De Geer, E. Olsson, P. Quick, A. Persson, M. Mazzanti, M. Marini, L. Pimpini, G. P. Perna, C. Marciano, P. Gargiulo, M. Galderisi, C. D'amore, G. Savarese, L. Casaretti, S. Paolillo, A. Cuocolo, P. Perrone Filardi, M. Al-Amoodi, E. C. Thompson, K. Kennedy, K. A. Bybee, A. I. Mcghie, J. H. O'keefe, T. M. Bateman, R. L. F. Van Der Palen, A. M. Mavinkurve-Groothuis, B. Bulten, L. Bellersen, H. W. M. Van Laarhoven, L. Kapusta, L. F. De Geus-Oei, P. P. Pollice, M. B. Bonifazi, F. P. Pollice, I. P. Clements, D. O. Hodge, C. G. Scott, M. De Ville De Goyet, B. Brichard, T. Pirotte, S. Moniotte, R. A. Tio, A. Elvan, R. A. I. O. Dierckx, R. H. J. A. Slart, T. Furuhashi, M. Moroi, H. Hase, N. Joki, H. Masai, R. Nakazato, H. Fukuda, K. Sugi, K. Kryczka, E. Kaczmarska, J. Petryka, L. Mazurkiewicz, W. Ruzyllo, P. Smanio, E. Vieira Segundo, M. Siqueira, J. Kelendjian, J. Ribeiro, J. Alaca, M. Oliveira, F. Alves, I. Peovska, J. Maksimovic, M. Vavlukis, N. Kostova, D. Pop Gorceva, V. Majstorov, M. Zdraveska, S. Hussain, M. Djearaman, E. Hoey, L. Morus, O. Erinfolami, A. Macnamara, M. P. Opolski, A. Witkowski, V. Berti, F. Ricci, R. Gallicchio, W. Acampa, G. Cerisano, C. Vigorito, R. Sciagra', A. Pupi, H. Sliem, F. M. Collado, S. Schmidt, A. Maheshwari, R. Kiriakos, V. Mwansa, S. Ljubojevic, S. Sedej, M. Holzer, G. Marsche, V. Marijanski, J. Kockskaemper, B. Pieske, A. Ricalde, G. Alexanderson, A. Mohani, P. Khanna, A. Sinusas, F. Lee, V. A. Pinas, B. L. F. Van Eck-Smit, H. J. Verberne, C. M. De Bruin, G. Guilhermina, L. Jimenez-Angeles, O. Ruiz De Jesus, O. Yanez-Suarez, E. Vallejo, E. Reyes, M. Chan, M. L. Hossen, S. R. Underwood, A. Karu, S. Bokhari, V. Pineda, L. M. Gracia-Sanchez, A. Garcia-Burillo, K. Zavadovskiy, Y. U. Lishmanov, W. Saushkin, I. Kovalev, A. Chernishov, A. Annoni, M. Tarkia, T. Saanijoki, V. Oikonen, T. Savunen, M. A. Green, M. Strandberg, A. Roivainen, M. C. Gaeta, C. Artigas, J. Deportos, L. Geraldo, A. Flotats, V. La Delfa, I. Carrio, W. J. Laarse, M. M. Izquierdo Gomez, J. Lacalzada Almeida, A. Barragan Acea, A. De La Rosa Hernandez, R. Juarez Prera, G. Blanco Palacios, J. A. Bonilla Arjona, J. J. Jimenez Rivera, J. L. Iribarren Sarrias, I. Laynez Cerdena, A. Dedic, A. Rossi, G. J. R. Ten Kate, A. Dharampal, A. Moelker, T. W. Galema, N. Mollet, P. J. De Feyter, K. Nieman, D. Trabattoni, A. Broersen, M. Frenay, M. M. Boogers, P. H. Kitslaar, J. Dijkstra, D. A. Annoni, M. Muratori, N. Johki, M. Tokue, A. S. Dharampal, A. C. Weustink, L. A. E. Neefjes, S. L. Papadopoulou, C. Chen, N. R. A. Mollet, E. H. Boersma, G. P. Krestin, J. A. Purvis, D. Sharma, S. M. Hughes, D. S. Berman, R. Taillefer, J. Udelson, M. Devine, J. Lazewatsky, G. Bhat, D. Washburn, D. Patel, T. Mazurek, S. Tandon, S. Bansal, S. Inzucchi, L. Staib, J. Davey, D. Chyun, L. Young, F. Wackers, M. T. Harbinson, G. Wells, J. Dougan, S. Borges-Neto, H. Phillips, A. Farzaneh-Far, Z. Starr, L. K. Shaw, M. Fiuzat, C. O'connor, M. Henzlova, W. L. Duvall, A. Levine, U. Baber, L. Croft, S. Sahni, S. Sethi, L. Hermann, A. Nureldin, A. Gomaa, M. A. T. Soliman, H. A. R. Hany, F. De Graaf, A. Pazhenkottil, H. M. J. Siebelink, J. H. Reiber, M. Ayub, T. Naveed, M. Azhar, A. Van Tosh, T. L. Faber, J. R. Votaw, N. Reichek, B. Pulipati, C. Palestro, K. J. Nichols, K. Okuda, Y. Kirihara, T. Ishikawa, J. Taki, M. Yoshita, M. Yamada, A. Salacata, S. Keavey, V. Chavarri, J. Mills, H. Nagaraj, P. Bhambhani, D. E. Kliner, P. Soman, J. Heo, A. E. Iskandrian, M. Jain, B. Lin, A. Walker, C. Nkonde, S. Bond, A. Baskin, J. Declerck, M. E. Soto, G. Mendoza, M. Aguilar, S. P. Williams, G. Colice, J. R. Mcardle, A. Lankford, D. K. Kajdasz, C. R. Reed, L. Angelini, F. Angelozzi, G. Ascoli, A. Jacobson, H. J. Lessig, M. C. Gerson, M. D. Cerqueira, J. Narula, M. Uematsu, K. Kida, K. Suzuki, P. E. Bravo, K. Fukushima, M. Chaudhry, J. Merrill, A. Alonso Tello, J. F. Rodriguez Palomares, G. Marti Aguasca, S. Aguade Bruix, V. Aliaga, P. Mahia, T. Gonzalez-Alujas, J. Candell, A. Evangelista, R. Mlynarski, A. Mlynarska, M. Sosnowski, B. Zerahn, P. Hasbak, C. E. Mortensen, H. F. Mathiesen, M. Andersson, D. Nielsen, L. Ferreira Santos, M. J. Ferreira, D. Ramos, D. Moreira, M. J. Cunha, A. Albuquerque, A. Moreira, J. Oliveira Santos, G. Costa, L. A. Providencia, Y. Arita, S. Kihara, N. Mitsusada, M. Miyawaki, H. Ueda, H. Hiraoka, Y. Matsuzawa, J. Askew, M. O'connor, L. Jordan, R. Ruter, R. Gibbons, T. Miller, L. Emmett, A. Ng, N. Sorensen, R. Mansberg, L. Kritharides, T. Gonzalez, H. Majmundar, N. P. Coats, S. Vernotico, J. H. Doan, T. M. Hernandez, M. Evini, A. D. Hepner, T. K. Ip, W. A. Chalela, A. M. Falcao, L. O. Azouri, J. A. F. Ramires, J. C. Meneghetti, F. Manganelli, M. Spadafora, P. Varrella, G. Peluso, R. Sauro, E. Di Lorenzo, F. Rotondi, S. Daniele, P. Miletto, A. J. M. Rijnders, B. W. Hendrickx, W. Van Der Bruggen, Y. G. C. J. America, P. J. Thorley, F. U. Chowdhury, C. J. Dickinson, S. I. Sazonova, I. Y. U. Proskokova, A. M. Gusakova, S. M. Minin, Y. U. B. Lishmanov, V. V. Saushkin, G. Rodriguez, F. Roffe, H. Ilarraza, D. Bialostozky, A. N. Kitsiou, P. Arsenos, I. Tsiantis, S. Charizopoulos, S. Karas, R. C. Vidal Perez, M. Garrido, V. Pubul, S. Argibay, C. Pena, M. Pombo, A. B. Ciobotaru, A. Sanchez-Salmon, A. Ruibal Morell, J. R. Gonzalez-Juanatey, E. Rodriguez-Gomez, B. Martinez, D. Pontillo, F. Benvissuto, F. Fiore Melacrinis, S. Maccafeo, E. V. Scabbia, R. Schiavo, Y. Golzar, C. Gidea, J. Golzar, D. Pop-Gorceva, M. Zdravkovska, S. Stojanovski, L. J. Georgievska-Ismail, T. Katsikis, A. Theodorakos, A. Kouzoumi, M. Koutelou, Y. Yoshimura, T. Toyama, H. Hoshizaki, S. Ohshima, M. Inoue, T. Suzuki, A. Uitterdijk, M. Dijkshoorn, M. Van Straten, W. J. Van Der Giessen, D. J. Duncker, D. Merkus, G. Platsch, J. Sunderland, C. Tonge, P. Arumugam, T. Dey, H. Wieczorek, R. Bippus, R. L. Romijn, B. E. Backus, T. Aach, M. Lomsky, L. Johansson, J. Marving, S. Svensson, J. L. Pou, F. P. Esteves, P. Raggi, R. Folks, Z. Keidar, J. W. Askew, L. Verdes, L. Campos, V. Gulyaev, A. Pankova, J. Santos, S. Carmona, I. Henriksson, A. Prata, M. Carrageta, A. I. Santos, K. Yoshinaga, M. Naya, C. Katoh, O. Manabe, S. Yamada, H. Iwano, S. Chiba, H. Tsutsui, N. Tamaki, I. Vassiliadis, E. Despotopoulos, O. Kaitozis, E. Hatzistamatiou, R. Thompson, J. Hatch, M. Zink, B. S. Gu, G. D. Bae, C. M. Dae, G. H. Min, E. J. Chun, S. I. Choi, M. Al-Mallah, K. Kassem, O. Khawaja, D. Goodman, D. Lipkin, L. Christiaens, B. Bonnet, J. Mergy, D. Coisne, J. Allal, N. Dias Ferreira, D. Leite, J. Rocha, M. Carvalho, D. Caeiro, N. Bettencourt, P. Braga, V. Gama Ribeiro, U. S. Kristoffersen, A. M. Lebech, H. Gutte, R. S. Ripa, N. Wiinberg, C. L. Petersen, G. Jensen, A. Kjaer, C. Bai, R. Conwell, R. D. Folks, L. Verdes-Moreiras, D. Manatunga, A. F. Jacobson, D. Belzer, Y. Hasid, M. Rehling, R. H. Poulsen, L. Falborg, J. T. Rasmussen, L. N. Waehrens, C. W. Heegaard, J. M. U. Silvola, S. Forsback, J. O. Laine, S. Heinonen, S. Ylaherttuala, A. Broisat, M. Ruiz, N. C. Goodman, J. Dimastromatteo, D. K. Glover, F. Hyafil, F. Blackwell, G. Pavon-Djavid, L. Sarda-Mantel, L. J. Feldman, A. Meddahi-Pelle, V. Tsatkin, Y.- H. Liu, R. De Kemp, P. J. Slomka, R. Klein, G. Germano, R. S. Beanlands, A. Rohani, V. Akbari, J. G. J. Groothuis, M. Fransen, A. M. Beek, S. L. Brinckman, M. R. Meijerink, M. B. M. Hofman, C. Van Kuijk, S. Kogure, E. Yamashita, J. Murakami, R. Kawaguchi, H. Adachi, S. Oshima, S. Minin, S. Popov, Y. U. Saushkina, G. Savenkova, D. Lebedev, E. Alexandridis, D. Rovithis, C. Parisis, I. Sazonova, V. Saushkin, V. Chernov, L. Zaabar, H. Bahri, S. Hadj Ali, A. Sellem, I. Slim, N. El Kadri, H. Slimen, H. Hammami, S. Lucic, A. Peter, S. Tadic, K. Nikoletic, R. Jung, M. Lucic, K. Tagil, D. Jakobsson, S.- E. Svensson, P. Wollmer, L. Leccisotti, L. Indovina, L. Paraggio, M. L. Calcagni, A. Giordano, M. Kapitan, A. Paolino, M. Nunez, J. Sweeny, N. Kulkarni, K. Guma, Y. Akashi, M. Takano, M. Takai, S. Koh, F. Miyake, N. Torun, G. Durmus Altun, A. Altun, E. Kaya, H. Saglam, D. T. Matsuoka, A. Sanchez, C. Bartolozzi, D. Padua, G. Ponta, A. Ponte, A. Carneiro, A. Thom, R. Ashrafi, P. Garg, G. Davis, A. Falcao, M. Costa, F. Bussolini, J. A. C. Meneghetti, M. Tobisaka, E. Correia, J. W. Jansen, P. A. Van Der Vleuten, T. P. Willems, F. Zijlstra, M. Sato, K. Taniguchi, M. Kurabayashi, D. Pop Gjorcheva, M. Zdraveska-Kochovska, K. Moriwaki, A. Kawamura, K. Watanabe, T. Omura, S. Sakabe, T. Seko, A. Kasai, M. Ito, M. Obana, T. Akasaka, C. Hruska, D. Truong, C. Pletta, D. Collins, C. Tortorelli, D. Rhodes, M. El-Prince, A. Martinez-Moeller, M. Marinelli, S. Weismueller, C. Hillerer, B. Jensen, S. G. Nekolla, H. Wakabayashi, K. Tsukamoto, S. M. E. A. Baker, K. M. H. S. Sirajul Haque, A. Siddique, S. Krishna Banarjee, A. Ahsan, F. Rahman, M. Mukhlesur Rahman, T. Parveen, M. Lutfinnessa, F. Nasreen, H. Sano, S. Naito, M. L. De Rimini, G. Borrelli, F. Baldascino, P. Calabro, C. Maiello, A. Russo, C. Amarelli, P. Muto, I. Danad, P. G. Raijmakers, Y. E. Appelman, O. S. Hoekstra, J. T. Marcus, A. Boonstra, D. V. Ryzhkova, T. V. Kuzmina, O. S. Borodina, M. A. Trukshina, I. S. Kostina, H. Hommel, G. Feuchtner, O. Pachinger, G. Friedrich, A. M. Stel, J. W. Deckers, V. Gama, A. Ciarka, L. A. Neefjes, N. R. Mollet, E. J. Sijbrands, J. Wilczek, C. Llibre Pallares, O. Abdul-Jawad Altisent, H. Cuellar Calabria, P. Mahia Casado, M. T. Gonzalez-Alujas, A. Evangelista Masip, D. Garcia-Dorado Garcia, Y. Tekabe, X. Shen, Q. Li, J. Luma, D. Weisenberger, A. M. Schmidt, R. Haubner, L. Johnson, L. Sleiman, S. Thorn, M. Hasu, M. Thabet, J. N. Dasilva, S. C. Whitman, D. Genovesi, A. Giorgetti, A. Gimelli, G. Cannizzaro, F. Bertagna, G. Fagioli, M. Rossi, R. Bonini, P. Marzullo, C. A. Paterson, S. A. Smith, A. D. Small, N. E. R. Goodfield, W. Martin, S. Nekolla, H. Sherif, S. Reder, M. Yu, A. Kusch, D. Li, J. Zou, M. S. Lloyd, K. Cao, D. W. Motherwell, A. Rice, G. M. Mccurrach, S. M. Cobbe, M. C. Petrie, I. Al Younis, E. Van Der Wall, T. Mirza, M. Raza, H. Hashemizadeh, L. Santos, B. A. Krishna, F. Perna, M. Lago, M. Leo, G. Pelargonio, G. Bencardino, M. L. Narducci, M. Casella, F. Bellocci, S. Kirac, O. Yaylali, M. Serteser, T. Yaylali, A. Okizaki, Y. Urano, M. Nakayama, S. Ishitoya, J. Sato, Y. Ishikawa, M. Sakaguchi, N. Nakagami, T. Aburano, S. V. Solav, R. Bhandari, S. Burrell, S. Dorbala, I. Bruno, C. Caldarella, A. Collarino, M. V. Mattoli, A. Stefanelli, A. Cannarile, F. Maggi, V. Soukhov, S. Bondarev, A. Yalfimov, M. Khan, P. P. Priyadharshan, G. Chandok, T. Aziz, M. Avison, R. A. Smith, D. S. Bulugahapitya, T. Vakhtangadze, F. Todua, M. Baramia, G. Antelava, N.- C. Roche, P. Paule, S. Kerebel, J.- M. Gil, L. Fourcade, A. Tzonevska, K. Tzvetkov, M. Atanasova, V. Parvanova, A. Chakarova, E. Piperkova, B. Kocabas, H. Muderrisoglu, C. P. Allaart, E. Entok, S. Simsek, B. Akcay, I. Ak, E. Vardareli, M. Stachura, P. J. Kwasiborski, G. J. Horszczaruk, E. Komar, A. Cwetsch, B. Zraik, R. Morales Demori, A. D. J. Almeida, M. E. Siqueira, E. Vieira, I. Balogh, G. Kerecsen, E. Marosi, Z. S. Szelid, A. Sattar, T. Swadia, J. Chattahi, W. Qureshi, F. Khalid, A. Gonzalez, S. Hechavarria, K. Takamura, S. Fujimoto, R. Nakanishi, S. Yamashina, A. Namiki, J. Yamazaki, K. Koshino, Y. Hashikawa, N. Teramoto, M. Hikake, S. Ishikane, T. Ikeda, H. Iida, Y. Takahashi, N. Oriuchi, H. Higashino, K. Endo, T. Mochizuki, K. Murase, A. Baali, R. Moreno, M. Chau, H. Rousseau, F. Nicoud, P. Dolliner, L. Brammen, G. Steurer, T. Traub-Weidinger, P. Ubl, P. Schaffarich, G. Dobrozemsky, A. Staudenherz, M. Ozgen Kiratli, B. Temelli, N. B. Kanat, T. Aksoy, G. A. Slavich, G. Piccoli, M. Puppato, S. Grillone, D. Gasparini, S. Perruchoud, C. Poitry-Yamate, M. Lepore, R. Gruetter, T. Pedrazzini, D. Anselm, A. Anselm, H. Atkins, J. Renaud, R. Dekemp, I. Burwash, A. Guo, R. Beanlands, C. Glover, I. Vilardi, B. Zangheri, L. Calabrese, P. Romano, A. Bruno, O. C. Fernandez Cimadevilla, V. A. Uusitalo, M. Luotolahti, M. Wendelin-Saarenhovi, J. Sundell, O. Raitakari, S. Huidu, R. Gadiraju, M. Ghesani, Q. Uddin, B. Wosnitzer, N. Takahashi, E. Alhaj, A. Legasto, B. Abiri, K. Elsaban, T. El Khouly, T. El Kammash, A. Al Ghamdi, B. Kyung Deok, K. Bon Seung, Y. Sang Geun, D. Chang Min, and M. Gwan Hong

Subjects
Cardiology and Cardiovascular Medicine
Published
2011
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3. Management of Patients with Statin Intolerance in Japan, South Korea and Taiwan: Comparison of Results From A Clinician Survey

Author

K Kajinami, HM Wieffer, J McKendrick, A.L. Catapano, Shravanthi R. Gandra, Ricardo Dent, L Cheng, GK Hovingh, Erik S.G. Stroes, Robert S. Rosenson, and Paul Oh

Subjects
medicine.medical_specialty, Statin, business.industry, medicine.drug_class, Health Policy, Family medicine, Public Health, Environmental and Occupational Health, Medicine, business
Published
2016
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4. Serum lipoprotein lipid concentration and composition in homozygous and heterozygous patients with cholesteryl ester transfer protein deficiency

Author

Junji Koizumi, Hiroshi Mabuchi, Ichiro Koizumi, Susumu Miyamoto, Alan R. Tall, P. Moulin, Kunimasa Yagi, K. Kajinami, Akihiro Inazu, and Yoshihide Uno

Subjects
Adult, Male, Heterozygote, medicine.medical_specialty, Very low-density lipoprotein, Lipoproteins, chemistry.chemical_compound, Internal medicine, Cholesterylester transfer protein, medicine, Humans, Triglycerides, Glycoproteins, Intermediate-density lipoprotein, Triglyceride, biology, Chemistry, Cholesterol, Homozygote, Radioimmunoassay, Heterozygote advantage, Middle Aged, Cholesterol Ester Transfer Proteins, Endocrinology, biology.protein, Female, lipids (amino acids, peptides, and proteins), Cholesterol Esters, Carrier Proteins, Cardiology and Cardiovascular Medicine, Lipoprotein
Abstract

Six homozygous, 10 heterozygous and 8 unaffected subjects in a CETP deficient family confirmed by CETP gene analysis were studied to characterize serum lipoproteins separated by ultracentrifugation, and to examine the relations between CETP levels and lipoprotein lipid concentration and composition. The serum CETP levels were measured by radioimmunoassay using 125I-labeled monoclonal antibodies (TP2). The serum CETP levels in the homozygotes were undetectable and those in the heterozygotes were significantly lower than those in the unaffected subjects (1.5 +/- 0.1 vs. 2.2 +/- 0.5 microgram/ml, P less than 0.01). In the HDL fraction, esterified cholesterol (EC) levels in the homozygotes were significantly increased (P less than 0.01), and those in the heterozygotes were slightly increased (n.s.), in comparison with those in the unaffected and the normolipidemic controls. The EC levels in the IDL fractions were lower in the homozygotes than in the normolipidemic controls. The EC/triglyceride (TG) molar ratios in IDL, the fraction obtained from the homo- and heterozygotes, were lower than those from the unaffected subjects (P less than 0.01 and less than 0.01, respectively), and the EC/TG ratios in the HDL fraction obtained from the homo- and heterozygotes were higher than those from the unaffected subjects (P less than 0.01 and n.s., respectively). Linear regression analysis showed that positive correlates of the serum CETP levels in all subjects were: IDL-EC (r = 0.463), HDL-TG (r = 0.603) and VLDL- and IDL-EC/TG ratio (r = 0.698 and 0.843).(ABSTRACT TRUNCATED AT 250 WORDS)

Published
1991
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5. Apolipoprotein composition of HDL in cholesteryl ester transfer protein deficiency

Author

Akihiro Inazu, Marcelo Costa Batista, Katalin V. Horvath, Hiroshi Mabuchi, Chorthip Nartsupha, K. Kajinami, Ernst J. Schaefer, Bela F. Asztalos, and Caitlin E. Cox

Subjects
Apolipoprotein E, Adult, Male, medicine.medical_specialty, Apolipoprotein B, Genotype, QD415-436, Compound heterozygosity, Biochemistry, Endocrinology, Internal medicine, Cholesterylester transfer protein, medicine, polycyclic compounds, Humans, Apolipoproteins A, Glycoproteins, Gel electrophoresis, biology, Apolipoprotein A-I, Chemistry, Reverse cholesterol transport, nutritional and metabolic diseases, Heterozygote advantage, Cell Biology, Middle Aged, reverse cholesterol transport, Cholesterol Ester Transfer Proteins, lipoproteins, Apolipoproteins, biology.protein, lipids (amino acids, peptides, and proteins), Female, Carrier Proteins, Lipoproteins, HDL, high density lipoprotein subpopulations, Apolipoprotein A-II, Biomarkers, Metabolism, Inborn Errors
Abstract

Our purpose was to compare HDL subpopulations, as determined by nondenaturing two-dimensional gel electrophoresis followed by immunoblotting for apolipoprotein A-I (apoA-I), apoA-II, apoA-IV, apoCs, and apoE in heterozygous, compound heterozygous, and homozygous subjects for cholesteryl ester transfer protein (CETP) deficiency and controls. Heterozygotes, compound heterozygotes, and homozygotes had CETP masses that were 30, 63, and more than 90% lower and HDL-cholesterol values that were 64, 168, and 203% higher than those in controls, respectively. Heterozygotes had approximately 50% lower pre-beta-1 and more than 2-fold higher levels of alpha-1 and pre-alpha-1 particles than controls. Three of the five heterozygotes' alpha-1 particles also contained apoA-II, which was not seen in controls. Compound heterozygotes and homozygotes had very large particles not observed in controls and heterozygotes. These particles contained apoA-I, apoA-II, apoCs, and apoE. However, these subjects did not have decreased pre-beta-1 levels. Our data indicate that CETP deficiency results in the formation of very large HDL particles containing all of the major HDL apolipoproteins except for apoA-IV. We hypothesize that the HDL subpopulation profile of heterozygous CETP-deficient patients, especially those with high levels of alpha-1 containing apoA-I but no apoA-II, represent an improved anti-atherogenic state, although this might not be the case for compound heterozygotes and homozygotes with very large, undifferentiated HDL particles.

Published
2003

6. Hyperhomocysteinemia, diabetes mellitus, and carotid atherosclerosis independently increase atherosclerotic vascular disease outcome in Japanese patients with end-stage renal disease

Author

T, Haraki, T, Takegoshi, C, Kitoh, K, Kajinami, T, Wakasugi, J, Hirai, T, Shimada, M, Kawashiri, A, Inazu, J, Koizumi, and H, Mabuchi

Subjects
Adult, Carotid Artery Diseases, Male, Oxidoreductases Acting on CH-NH Group Donors, Polymorphism, Genetic, Genotype, Arteriosclerosis, Hyperhomocysteinemia, Middle Aged, Diabetes Complications, Carotid Arteries, Japan, Risk Factors, Case-Control Studies, Outcome Assessment, Health Care, Humans, Kidney Failure, Chronic, Female, Prospective Studies, Homocysteine, Methylenetetrahydrofolate Reductase (NADPH2), Aged, Follow-Up Studies, Ultrasonography
Abstract

Patients with end-stage renal disease (ESRD) have high mortality from atherosclerotic/atherothrombotic vascular disease (AVD). However, the role of an elevated plasma total homocysteine (tHcy) level as a risk factor is uncertain in ESRD.We enrolled 55 ESRD patients in a prospective follow-up study in order to evaluate the prognostic significance of their tHcy levels, common methylenetetrahydrofolate reductase (MTHFR) gene polymorphism, and other atherosclerotic risk factors, in combination with the results of B mode ultrasound for carotid arteries.Mean intima-media thickness of the common carotid artery (CCA-IMT) in ESRD patients was thicker than that in 102 age- and sex-matched healthy controls. Carotid plaque was more frequently present in patients compared with controls, as was calcified plaque more common in patients (p0.001). Plasma tHcy levels (mean +/- SD) in patients (39.1 +/- 27.2 nmol/ml) were higher than that (8.8 +/- 2.7 nmol/ml) in controls (p0.001). Folic acid was the major determinant of elevated tHcy levels in ESRD patients. During the follow-up period of 31 +/- 3 months, 14 patients had one or more AVD complications, and 10 consequently died from AVD causes. Proportional hazards modeling showed that 5-year intervals of age (relative risk of 2.95, 95% CI 1.62 - 5.37), 10 nmol/ml intervals of tHcy levels (relative risk of 2.31, 95% CI 1.31 - 4.08), and presence of diabetes mellitus (relative risk of 6.62, 95% CI 1.07 +/- 40.8) were independent predictors of future AVD events, and tHcy levels (relative risk of 2.67, 95% CI 1.29 - 5.52) and age (relative risk of 2.10, 95% CI 1.15 - 3.83) were those of AVD mortality. We also found a significant association between carotid plaque prevalence and AVD events (X(2) = 11.6, p = 0.001).Hyperhomocysteinemia, diabetes mellitus, and carotid atherosclerosis appeared to contribute independently to increase the risk of AVD outcome in Japanese patients with ESRD.

Published
2001

7. [Assay for LDL receptor activity]

Author

K, Kajinami and N, Takekoshi

Subjects
Hyperlipoproteinemia Type II, Cholesterol, Receptors, LDL, Humans, Lymphocytes, Flow Cytometry, Lipoproteins, HDL
Published
2001

8. [Atorvastatin]

Author

K, Kajinami and N, Takekoshi

Subjects
Arteriosclerosis, Heptanoic Acids, Anticholesteremic Agents, Hypercholesterolemia, Atorvastatin, Animals, Humans, Coronary Disease, Pyrroles, Cholesterol, LDL, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Randomized Controlled Trials as Topic
Published
2001

9. Effects of NK-104, a new hydroxymethylglutaryl-coenzyme reductase inhibitor, on low-density lipoprotein cholesterol in heterozygous familial hypercholesterolemia. Hokuriku NK-104 Study Group

Author

K, Kajinami, J, Koizumi, K, Ueda, S, Miyamoto, T, Takegoshi, and H, Mabuchi

Subjects
Hyperlipoproteinemia Type II, Lipoproteins, LDL, Male, Heterozygote, Quinolines, Humans, Female, Hydroxymethylglutaryl CoA Reductases, Middle Aged, Lipids
Abstract

The clinical efficacy of NK-104, a novel and totally synthetic hydroxymethylglutaryl-coenzyme A reductase inhibitor, was assessed in 30 patients (men/women = 15/15, mean age 51 years) with heterozygous familial hypercholesterolemia. After a placebo phase of4 weeks, NK-104 was given at an initial dose of 2 mg/day for 8 weeks, which was increased to 4 mg/day for a further 8 weeks. As a result of 2 mg/day of NK-104 treatment, mean +/- SD of total and low-density lipoprotein cholesterol levels decreased significantly (p0.0001) from baseline, namely from 8.80+/-1.38 to 6.11+/-1.09 mmol/L (-31%) and from 6.81+/-1.52 to 4.09+/-1.03 mmol/L (-40%), respectively. They decreased further (p0.0001) as a result of 4-mg/day administration, to 5.52+/-0.81 mmol/L (-37%) and 3.55+/-0.85 mmol/L (-48%), respectively. Changes in high-density lipoprotein cholesterol levels failed to reach statistical significance. Serum triglyceride levels decreased significantly (p0.0001) from baseline as a result of 4 mg/day of NK-104, from 1.99+/-1.72 to 1.35+/-0.90 mmol/L (-23%). Serum apolipoprotein B, CII, CIII, and E levels significantly decreased: mean changes from baseline at the end of the study were -41% (p0.0001), -27% (p0.0001), -19% (p = 0.002), and -37% (p0.0001), respectively. On the other hand, apolipoprotein AI and All levels significantly increased as a result of the treatment: + 10% (p = 0.002) and +6% (p = 0.008), respectively. There were no adverse events observed in either clinical or laboratory findings that could be attributed to the treatment. These results suggest that the potency of NK-104 appears to be dose-dependent, and that NK-104 is safe and well tolerated in the treatment of patients with heterozygous familial hypercholesterolemia, and thus also provides a new therapeutic choice for subjects requiring lipid-modifying therapy.

Published
2000

10. Duplication of the middle cerebral artery associated with an unruptured aneurysm

Author

Motohiro Nomura, Daisuke Kita, Shinya Kida, Junkoh Yamashita, T. Yamashima, and K Kajinami

Subjects
Intracranial Arteriovenous Malformations, medicine.medical_specialty, Middle Cerebral Artery, Aneurysm, medicine.artery, Gene duplication, medicine, Humans, Neuroradiology, medicine.diagnostic_test, business.industry, Vascular disease, Interventional radiology, Intracranial Aneurysm, Middle Aged, medicine.disease, Prognosis, Surgery, Cerebral Angiography, Middle cerebral artery, Female, Neurology (clinical), Neurosurgery, business, Cerebral angiography
Published
2000

11. [Genotype-phenotype correlations in familial hypercholesterolemia]

Author

K, Kajinami

Subjects
Hyperlipoproteinemia Type II, Phenotype, Asian People, Genotype, Japan, Receptors, LDL, Humans
Abstract

The low-density lipoprotein (LDL) receptor gene mutations cause familial hypercholesterolemia (FH), which was characterized by increased levels of LDL cholesterol and premature coronary atherosclerosis. Molecular genetic study of FH showed extreme heterogeneity in their underlying LDL receptor gene mutations, and suggested that this heterogeneity is responsible for the variability of its clinical manifestations. Since 1988, we have identified 11 mutations (10 novel and 1 previously reported) in the LDL receptor gene among 201 unrelated FH families in Hokuriku district, Japan. However, they explained only 38.8% of the patients suggesting that a more efficient mutation screening method should be developed. Through mutation detection, a genetically-determined mild type of FH (homozygotes with relative longevity and normocholesterolemic heterozygotes) was found in a case in which exons 2 and 3 were eliminated by a 10 kb deletion (Tonami-2). In addition, cholesterol-lowering drug therapy was significantly more effective in heterozygous patients with the P664L mutation (Kanazawa-2) compared to those with a 6 kb deletion including exon 15 (Tonami-1). These observations indicate that FH patients should be managed based on the results of their gene analyses.

Published
2000

12. Coronary ectasia in familial hypercholesterolemia: histopathologic study regarding matrix metalloproteinases

Author

K, Kajinami, S, Kasashima, Y, Oda, J, Koizumi, S, Katsuda, and H, Mabuchi

Subjects
Adult, Male, Anticholesteremic Agents, Macrophages, Plasma Cells, Metalloendopeptidases, Tissue Inhibitor of Metalloproteinases, Coronary Artery Disease, Coronary Angiography, Coronary Vessels, Muscle, Smooth, Vascular, Hyperlipoproteinemia Type II, Humans, Lymphocytes, Dilatation, Pathologic
Abstract

A 39-year-old male heterozygous familial hypercholesterolemia patient with marked ectasia over the entire coronary artery tree had been treated with several kinds of lipid-lowering single or combined drug therapies using clofibrate, compactin, cholestyramine, probucol, and pravastatin, and LDL-apheresis. During the 19-year follow-up, he suffered myocardial infarction three times and some of the ectatic coronary segments became enlarged, others narrowed, and one of them occluded in spite of the treatment. At the age of 58, he died after a fourth cardiac attack and subsequent cardiogenic shock. The autopsy indicated that his three coronary arteries showed diffuse ectatic changes and the largest lumen diameter of the left anterior descending artery was 25 mm, of the circumflex artery 12 mm, and of the right coronary artery 13 mm. The ectatic artery wall was not thick and the major part of the lumen was occupied by organized thrombi. Microscopic examinations showed that the larger the diameter of the lumen, the more severe the structural damage of the intima and tunica media and the larger the number of infiltrated cells, including lymphocytes, macrophages, and plasma cells. Immunoreactivity against matrix metalloproteinase (MMP)-1, and MMP-2 was observed in smooth muscle cells, macrophages, lymphocytes, and endothelial cells of the vasa vasorum or neovasculature. MMP-9 immunoreactivity was also localized in intimal foamy macrophages and round cells (macrophages and lymphocytes) of the media and adventitia. MMP-1 increased with the lumen diameter of the ectatic arteries. The ratio of immunoreactivity against both MMP-2 and MMP-9 to that against tissue inhibitor of metalloproteinase (TIMP)-2 also increased with the lumen diameter, but it no longer increased when the diameter was over 10 mm. These observations suggest that the MMP-TIMP system appears to play a significant role in the development of coronary ectasia

Published
2000

13. Long-term efficacy of low-density lipoprotein apheresis on coronary heart disease in familial hypercholesterolemia. Hokuriku-FH-LDL-Apheresis Study Group

Author

H, Mabuchi, J, Koizumi, M, Shimizu, K, Kajinami, S, Miyamoto, K, Ueda, and T, Takegoshi

Subjects
Male, Anticholesteremic Agents, Coronary Disease, Middle Aged, Coronary Angiography, Disease-Free Survival, Hyperlipoproteinemia Type II, Lipoproteins, LDL, Treatment Outcome, Blood Component Removal, Humans, Female, Longitudinal Studies, Aged
Abstract

Familial hypercholesterolemia (FH) is characterized by severe hypercholesterolemia and premature coronary heart disease (CHD). The lower the plasma cholesterol level, the more likely it is that CHD can be prevented or retarded; aggressive cholesterol-lowering therapies may be indicated for FH patients with CHD. This study describes the long-term (6 years) safety and efficacy of intensive cholesterol-lowering therapies with low-density lipoprotein (LDL) apheresis in heterozygous FH patients with CHD. One hundred thirty heterozygous FH patients with CHD documented by coronary angiography had been treated by cholesterol-lowering drug therapy alone (n=87) or LDL apheresis combined with cholesterol-lowering drugs (n=43). Serum lipid levels and outcomes in each treatment group were compared after approximately 6 years. Both treatment groups had significant reductions in serum cholesterol, LDL cholesterol, and high density lipoprotein cholesterol levels. LDL apheresis significantly reduced LDL cholesterol levels from 7.42+/-1.73 to 3.13+/-0.80 mmol/L (58%) compared with group taking drug therapy, from 6.03+/-1.32 to 4.32+/-1.53 mmol/L (28%). With Kaplan-Meier analyses of the coronary events including nonfatal myocardial infarction, percutaneous transluminal coronary angioplasty, coronary artery bypass grafting, and death from CHD, the rate of total coronary events was 72% lower in the LDL-apheresis group (10%) than in drug therapy group (36%) (p=0.0088). It is concluded that LDL-apheresis is effective as treatment of CHD in FH heterozygotes, and may become the therapy of choice in severe types of FH.

Published
1999

14. [Abnormal apolipoprotein B]

Author

K, Kajinami, A, Nohara, Y, Tohdoh, and H, Mabuchi

Subjects
Diagnosis, Differential, Genetic Variation, Humans, Prognosis, Lipid Metabolism, Inborn Errors, Apolipoproteins B
Published
1998

15. [Familial hypercholesterolemia]

Author

K, Kajinami and H, Mabuchi

Subjects
Diagnosis, Differential, Hyperlipoproteinemia Type II, Genotype, Receptors, LDL, Blood Component Removal, Humans, Ion Exchange Resins, Hydroxymethylglutaryl-CoA Reductase Inhibitors
Published
1998

16. Images in cardiology. Non-invasive detection of quadricuspid aortic valve

Author

Noboru Takekoshi, K. Kajinami, and Hiroshi Mabuchi

Subjects
Aortic valve, Aortic valve disease, medicine.medical_specialty, Aortic Valve Insufficiency, Internal medicine, medicine, Humans, Aged, Pulmonary Valve, medicine.diagnostic_test, business.industry, Non invasive, Hypertrophic cardiomyopathy, Magnetic resonance imaging, medicine.disease, Magnetic Resonance Imaging, medicine.anatomical_structure, Quadricuspid aortic valve, Echocardiography, Pulmonary valve, Aortic Valve, Cardiology, Female, Cardiology and Cardiovascular Medicine, business, Research Article
Published
1997

17. Enhanced cholesteryl ester transfer protein activities and abnormalities of high density lipoproteins in familial hypercholesterolemia

Author

K. Kajinami, Ryoyu Takeda, Junji Koizumi, Akihiro Inazu, and Hiroshi Mabuchi

Subjects
Adult, Male, medicine.medical_specialty, Apolipoprotein B, Endocrinology, Diabetes and Metabolism, Clinical Biochemistry, Familial hypercholesterolemia, Biochemistry, Hyperlipoproteinemia Type II, chemistry.chemical_compound, Endocrinology, Internal medicine, Cholesterylester transfer protein, medicine, Humans, Glycoproteins, Triglyceride, biology, Cholesterol, Biochemistry (medical), Cholesterol, HDL, General Medicine, Middle Aged, medicine.disease, Cholesterol Ester Transfer Proteins, Apolipoproteins, chemistry, biology.protein, Cholesteryl ester, lipids (amino acids, peptides, and proteins), Female, Cholesterol Esters, Carrier Proteins, Lipoprotein
Abstract

Cholesteryl ester transfer protein may play a role in the cholesteryl ester metabolism between high density lipoproteins (HDL) and apolipoprotein B-containing lipoproteins. To investigate relationship between HDL and cholesteryl ester transfer protein (CETP) activity in the development of atherosclerosis, the present study has focused on CETP activity in the patients with familial hypercholesterolemia (GH). HDL-C and HDL-C/apo A-I mass ratio in heterozygous FH were lower than those in normolipidemic controls. There was a 2-fold increase in total CETP activity in incubated FH serum compared with normolipidemic controls. Assays for CETP activity in the lipoprotein deficient serum (d greater than 1.215 g/ml) were carried out by measuring the transfer of radioactive cholesteryl ester from HDL (1.125 less than d less than 1.21 g/ml) to LDL (1.019 less than d less than 1.060 g/ml). CETP activities in heterozygous FH (79 +/- 4 nmol/ml/h) was significantly higher than those in normolipidemic controls (54 +/- 6 nmol/ml/h). The increased total cholesteryl ester transfer mainly results from increased CETP activity in the d greater than 1.215 g/ml, possibly reflecting an increase in CETP mass in serum. Increased CETP activity in the d greater than 1.215 g/ml was correlated positively with IDL-cholesterol/triglyceride mass ratio (r = 0.496, p less than 0.01), and negatively with HDL-cholesterol/apo A-I mass ratio (r = -0.334, p less than 0.05). These results indicate that the enhanced CETP activities may contribute to increase risk for developing atherosclerosis in FH by changing the distribution of cholesteryl ester in serum lipoproteins.

Published
1992

18. A family of familial hypercholesterolemia with cerebral infarction and without coronary heart disease. An unusual case with corneal opacity, polyneuropathy and carpal tunnel syndrome in the family: therapy with probucol and tocopherol nicotinate

Author

Y, Ihara, K, Nobukuni, R, Namba, K, Kamisaka, M, Kibata, K, Kajinami, H, Fujita, H, Mabuchi, T, Shirabe, and K, Ohshima

Subjects
Free Radicals, Arteriosclerosis, Mosaicism, Superoxide Dismutase, CD4-CD8 Ratio, Nicotinic Acids, Turner Syndrome, Cerebral Infarction, Middle Aged, Carpal Tunnel Syndrome, Axons, Hyperlipoproteinemia Type II, Lipoproteins, LDL, Corneal Opacity, Probucol, Humans, Vitamin E, Female, Schwann Cells, Hereditary Sensory and Motor Neuropathy
Abstract

A study is presented of a 48-year-old female patient and her three siblings with familial hypercholesterolemia. The family members had episodes of cerebral infarction and apparently had atherosclerosis of the internal carotid artery, but no coronary heart disease due to their almost normal level of cholesterol. The laboratory studies of the family members revealed the elevations of serum lipid peroxides, serum lipoprotein(a), leukotriene C4 in blood, the thromboxane B2/6-keto-prostaglandin F1 alpha ratio in plasma and serum hydroxyl radical. Therefore, it is suspected that these factors accelerating atherosclerotic process caused the cerebral infarction. The patient demonstrated corneal opacities, palpebral xanthomas, thickened Achilles tendons, polyneuropathy and the carpal tunnel syndrome. Laboratory studies revealed an elevation in the OKT4/8 ratio, monocyte dysfunction with respect to phagocytosis and chemotaxis, and the presence of the 46XX/45XO mosaic chromosome. Lipid deposits were observed in the Achilles tendon, the transverse carpal ligament, the Schwann's cells and axons of the sural nerve, and in the keratocytes and stroma of the cornea. Following the administration of tocopherol nicotinate and probucol, the patient's serum lipid peroxide normalized and there was improvement in her palpebral xanthomas, thickening of the Achilles tendons and polyneuropathy. We conclude that the lipid deposits in this patient were due to the abnormal oxidative metabolism of low-density lipoprotein and a disturbance of the scavenger pathway due to the monocyte dysfunction.

Published
1991

20. [Primary hypercholesterolemia]

Author

K, Kajinami and H, Mabuchi

Subjects
Male, Heterozygote, Hyperlipoproteinemias, Homozygote, Hyperlipidemia, Familial Combined, Coronary Disease, Coronary Artery Disease, Hyperlipoproteinemia Type II, Lipoproteins, LDL, Receptors, LDL, Risk Factors, Xanthomatosis, Humans, Female
Published
1990

23. RELATIONSHIP OF INSUUN RESISTANCE TO CAROTID ARTERIOSCLEROSIS, CARDIAC HYPERTROPHY/CARDIAC FUNCTION, AND COAGULATION/FIBRINOLYSIS FACTORS IN HYPERTENSIVE PATIENTS

Author

N. Tada, N. Takekoshi, H. Tsugawa, S. Okubo, S. Kanemitu, K. Kajinami, S. Matsui, N. Satou, I. Kitagawa, and Hiroshi Masuya

Subjects
Cardiac function curve, medicine.medical_specialty, Physiology, business.industry, Arteriosclerosis, medicine.disease, Internal medicine, Cardiac hypertrophy, Internal Medicine, medicine, Cardiology, Coagulation fibrinolysis, Cardiology and Cardiovascular Medicine, business
Published
2004
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24. Long-term effects of fluvastatin on serum lipids and apolipoprotein levels in patients with familial hypercholesterolemia

Author

Mitsuaki Takeda, Junji Koizumi, M. Ota, K. Ueda, Yoshihide Uno, Akihiro Inazu, Ryoyu Takeda, Kunimasa Yagi, Hiroshi Mabuchi, Susumu Miyamoto, Tatsuo Haraki, K. Kajinami, and Tadayoshi Takegoshi

Subjects
medicine.medical_specialty, Apolipoprotein B, biology, business.industry, Blood lipids, Familial hypercholesterolemia, medicine.disease, Endocrinology, Internal medicine, medicine, biology.protein, In patient, Cardiology and Cardiovascular Medicine, business, Fluvastatin, medicine.drug
Published
1994
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25. Denaturing gradient gel electrophoresis analysis of the low density lipoprotein receptor gene and the apolipoprotein B-100 gene in Japanese patients with familial hypercholesterolemia

Author

Junji Koizumi, K. Kajinami, Akihiro Inazu, Hiroshi Mabuchi, and A. Nohara

Subjects
Apolipoprotein B, biology, Chemistry, biology.protein, medicine, Familial hypercholesterolemia, Low Density Lipoprotein Receptor Gene, Cardiology and Cardiovascular Medicine, medicine.disease, Gene, Molecular biology, Temperature gradient gel electrophoresis
Published
1999
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26. 4.P.37 Coronary calcification and regression of coronary atherosclerosis by long-term LDL-apheresis in patients with heterozygous familial hypercholesterolemia

Author

Toshinori Higashikata, K. Kajinami, K. Ueda, Hiroshi Mabuchi, Junji Koizumi, and M. Noto

Subjects
medicine.medical_specialty, LDL apheresis, business.industry, Internal medicine, Coronary artery calcification, medicine, Cardiology, In patient, Familial hypercholesterolemia, Cardiology and Cardiovascular Medicine, medicine.disease, business, Coronary atherosclerosis
Published
1997
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27. 1.P.248 Variety of low-density-lipoprotein-receptor gene mutations and expression of coronary artery disease in heterozygous familial hypercholesterolemia

Author

H. Matsushita, Toshinori Higashikata, K. Kajinami, Kunimasa Yagi, Hiroshi Mabuchi, Junji Koizumi, Akihiro Inazu, and A. Nohara

Subjects
Coronary artery disease, medicine.medical_specialty, Endocrinology, business.industry, Internal medicine, medicine, Familial hypercholesterolemia, Low Density Lipoprotein Receptor Gene, Cardiology and Cardiovascular Medicine, medicine.disease, business
Published
1997
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28. 1.P.189 Ldl-receptor genotype dependent response to cholesterol-lowering therapy in patients with heterozygous familial hypercholesterolemia

Author

K. Kajinami, Toshinori Higashikata, Akihiro Inazu, Kunimasa Yagi, Hiroshi Mabuchi, and Junji Koizumi

Subjects
medicine.medical_specialty, Endocrinology, business.industry, Internal medicine, LDL receptor, Genotype, medicine, Cholesterol lowering, In patient, Familial hypercholesterolemia, Cardiology and Cardiovascular Medicine, medicine.disease, business
Published
1997
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29. 3.P.344 Coronary artery calcification and coronary atherosclerosis in familial hypercholesterolemia: Electron beam computed tomographic study

Author

K. Kajinami, A. Nohara, Hiroshi Mabuchi, and Noboru Takekoshi

Subjects
medicine.medical_specialty, business.industry, Internal medicine, Coronary artery calcification, Cardiology, medicine, Familial hypercholesterolemia, Cardiology and Cardiovascular Medicine, medicine.disease, business, Coronary atherosclerosis, Computed tomographic
Published
1997
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31. New LDL-receptor gene mutant in two homozygous familial hypercholesterolemia sisters showing relative longevity

Author

A. Nohara, Junji Koizumi, Ryoyu Takeda, M. Kitatani, Toshinori Higashikata, Tatsuo Haraki, Akihiro Inazu, K. Kajinami, H. Matsushita, H. Mukaida, Kunimasa Yagi, Hiroshi Mabuchi, T. Sawada, and K. Maruhama

Subjects
Ldl receptor gene, medicine.medical_specialty, Endocrinology, media_common.quotation_subject, Internal medicine, Mutant, Longevity, medicine, Familial hypercholesterolemia, Biology, Cardiology and Cardiovascular Medicine, medicine.disease, media_common
Published
1994
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33. 16% of familial hypercholesterolemia in the Hokuriku District of Japan can be explained by seven mutants of LDL-receptor gene

Author

A. Nohara, K. Kajinami, Toshinori Higashikata, M. Kitatani, Tatsuo Haraki, Akihiro Inazu, Kunimasa Yagi, Ryoyu Takeda, Hiroshi Mabuchi, H. Matsushita, and Junji Koizumi

Subjects
Ldl receptor gene, medicine.medical_specialty, Endocrinology, Internal medicine, Mutant, medicine, Familial hypercholesterolemia, Biology, Cardiology and Cardiovascular Medicine, medicine.disease
Published
1994
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37. Initial decrease in the lipoprotein(a) level is a novel prognostic biomarker in patients with acute coronary syndrome.

Author

Saeki Y, Sawaguchi J, Akita S, Takamura TA, Fujibayashi K, Wakasa M, Akao H, Kitayama M, Kawai Y, and Kajinami K

Abstract

Background: Lipoprotein(a) [Lp(a)] is a causal risk factor for atherosclerotic cardiovascular diseases; however, its role in acute coronary syndrome (ACS) remains unclear., Aim: To investigate the hypothesis that the Lp(a) levels are altered by various conditions during the acute phase of ACS, resulting in subsequent cardiovascular events., Methods: From September 2009 to May 2016, 377 patients with ACS who underwent emergent coronary angiography, and 249 who completed ≥ 1000 d of follow-up were enrolled. Lp(a) levels were measured using an isoform-independent assay at each time point from before percutaneous coronary intervention (PCI) to 48 h after PCI. The primary endpoint was the occurrence of major adverse cardiac events (MACE; cardiac death, other vascular death, ACS, and non-cardiac vascular events)., Results: The mean circulating Lp(a) level decreased significantly from pre-PCI (0 h) to 12 h after (19.0 mg/dL to 17.8 mg/dL, P < 0.001), and then increased significantly up to 48 h after (19.3 mg/dL, P < 0.001). The changes from 0 to 12 h [Lp(a)Δ0-12] significantly correlated with the basal levels of creatinine [Spearman's rank correlation coefficient (SRCC): -0.181, P < 0.01] and Lp(a) (SRCC: -0.306, P < 0.05). Among the tertiles classified according to Lp(a)Δ0-12, MACE was significantly more frequent in the lowest Lp(a)Δ0-12 group than in the remaining two tertile groups (66.2% vs 53.6%, P = 0.034). A multivariate analysis revealed that Lp(a)Δ0-12 [hazard ratio (HR): 0.96, 95% confidence interval (95%CI): 0.92-0.99] and basal creatinine (HR: 1.13, 95%CI: 1.05-1.22) were independent determinants of subsequent MACE., Conclusion: Circulating Lp(a) levels in patients with ACS decreased significantly after emergent PCI, and a greater decrease was independently associated with a worse prognosis., Competing Interests: Conflict-of-interest statement: There are no conflicts of interest to disclose., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

Published
2024
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38. Efficacy, Safety, and Pharmacokinetics of Inclisiran in Japanese Patients: Results from ORION-15.

Author

Yamashita S, Kiyosue A, Maheux P, Mena-Madrazo J, Lesogor A, Shao Q, Tamaki Y, Nakamura H, Akahori M, and Kajinami K

Subjects
Aged, Female, Humans, Male, Middle Aged, Double-Blind Method, East Asian People, Hyperlipoproteinemia Type II drug therapy, Japan epidemiology, Proprotein Convertase 9, RNA, Small Interfering, Treatment Outcome, Cholesterol, LDL blood, Hypercholesterolemia drug therapy
Abstract

Aim: To evaluate the efficacy, safety, and pharmacokinetics (PK) of inclisiran in Japanese patients with high cardiovascular risk and elevated low-density lipoprotein cholesterol (LDL-C)., Methods: ORION-15 was a phase 2, double-blind, placebo-controlled randomized trial. Patients with hypercholesterolemia, including heterozygous familial hypercholesterolemia (HeFH), were randomized to inclisiran sodium 100, 200, or 300 mg, or placebo and dosed subcutaneously on Days 1, 90, and 270. The primary endpoint was the percentage change from baseline to Day 180 to demonstrate the superiority of inclisiran vs. placebo. Patients who consented to the PK substudy had additional study procedures for blood collection and safety assessment., Results: Overall, 312 patients (mean age, 63.6 years; male, 74.4%; baseline LDL-C, 114.0 mg/dL) were randomized. Baseline characteristics were well balanced among the groups. At Day 180, inclisiran at all doses demonstrated significant LDL-C and proprotein convertase subtilisin/kexin type 9 (PCSK9) reductions (p＜0.0001 for both), which showed a dose-response relationship. The greatest reductions (LDL-C, 65.3%; PCSK9, 79.2%) were with inclisiran sodium 300 mg. At Day 180, ＞86% of the patients receiving inclisiran achieved the Japan Atherosclerosis Society 2017 lipid management targets compared to 8.9% for placebo. The mean (SD) plasma half-life for inclisiran was 6.8 (2.0)-7.6 (0.8) h. The incidence of adverse events with inclisiran was similar to that with placebo., Conclusion: Inclisiran sodium 100, 200, and 300 mg demonstrated clinically meaningful and statistically significant LDL-C and PCSK9 reductions at Day 180, which were consistent over 12 months. Inclisiran was effective and well tolerated in Japanese patients with hypercholesterolemia, including HeFH.

Published
2024
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39. Marchiafava-Bignami disease: Prompt diagnosis made by magnetic resonance brain imaging.

Author

Akita S, Takakuwa T, and Kajinami K

Abstract

Key Clinical Message: Marchiafava-Bignami disease, a rare condition often associated with alcoholism, shows myelin degeneration with tissue necrosis specifically in the corpus callosum. Urgent application of magnetic resonance imaging could lead to prompt diagnosis., Abstract: A 66-year-old male with habitual alcohol drink complained acute deterioration of left-side muscle weakness as initial presentation. On the arrival, the patient was confused, with stable vital sign and unremarkable pyramidal sign. Although several potential diagnoses could be considered, brain computed tomography did not provide diagnostic information, and subsequently-performed magnetic resonance imaging revealed hyperintense lesions on T2-flair images in corpus callosum, suggesting MBD as clinical diagnosis. Prompt diagnosis enabled us to introduce thiamine administration with subsequent favorable neurological outcome., Competing Interests: The authors have no pertinent conflicts of interest to report for this manuscript., (© 2024 The Authors. Clinical Case Reports published by John Wiley & Sons Ltd.)

Published
2024
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40. Thrombotic Microangiopathy after a 15-year Treatment with Interferon Beta-1b in a Patient with Multiple Sclerosis: A Case Report and Review of Literature.

Author

Akita S, Fujibayashi K, Ueno EI, Wakasa M, Kawai Y, and Kajinami K

Subjects
Female, Humans, Middle Aged, Interferon beta-1b adverse effects, Interferon-beta adverse effects, Multiple Sclerosis complications, Multiple Sclerosis drug therapy, Multiple Sclerosis chemically induced, Thrombotic Microangiopathies chemically induced, Hypertension complications
Abstract

A 54-year-old woman with multiple sclerosis treated with interferon-β (IFN-β)-1b for 15 years presented with sustained hypertension (240/124 mmHg) and retinal bleeding. She had proteinuria, anemia, thrombocytopenia, elevated serum creatinine levels, and haptoglobin depletion. Intravenous nicardipine stabilized her blood pressure, but her renal function and platelet count deteriorated. The initial disintegrin-like metalloprotease with thrombospondin type 1 motifs 13 (ADAMTS13) activity was 28% of normal without its inhibitor. The subsequent peripheral appearance of schistocytes suggested thrombotic microangiopathy (TMA). After IFN-β-1b cessation, the platelet count increased, and the blood pressure stabilized. The ADAMTS13 activity normalized, although the creatinine level did not. TMA may develop after the long-term use of IFN-β without adverse events.

Published
2024
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41. A Novel Approach: Investigating the Intracellular Clearance Mechanism of Glyceraldehyde-Derived Advanced Glycation End-Products Using the Artificial Checkpoint Kinase 1 d270KD Mutant as a Substrate Model.

Author

Takeda K, Sakai-Sakasai A, Kajinami K, and Takeuchi M

Subjects
Proteasome Endopeptidase Complex, Checkpoint Kinase 1, Maillard Reaction, Ubiquitins, Glycation End Products, Advanced metabolism, Glyceraldehyde
Abstract

Advanced glycation end-products (AGEs), formed through glyceraldehyde (GA) as an intermediate in non-enzymatic reactions with intracellular proteins, are cytotoxic and have been implicated in the pathogenesis of various diseases. Despite their significance, the mechanisms underlying the degradation of GA-derived AGEs (GA-AGEs) remain unclear. In the present study, we found that N-terminal checkpoint kinase 1 cleavage products (CHK1-CPs) and their mimic protein, d270WT, were degraded intracellularly post-GA exposure. Notably, a kinase-dead d270WT variant (d270KD) underwent rapid GA-induced degradation, primarily via the ubiquitin-proteasome pathway. The high-molecular-weight complexes formed by the GA stimulation of d270KD were abundant in the RIPA-insoluble fraction, which also contained high levels of GA-AGEs. Immunoprecipitation experiments indicated that the high-molecular-weight complexes of d270KD were modified by GA-AGEs and that p62/SQSTM1 was one of its components. The knockdown of p62 or treatment with chloroquine reduced the amount of high-molecular-weight complexes in the RIPA-insoluble fraction, indicating its involvement in the formation of GA-AGE aggregates. The present results suggest that the ubiquitin-proteasome pathway and p62 play a role in the degradation and aggregation of intracellular GA-AGEs. This study provides novel insights into the mechanisms underlying GA-AGE metabolism and may lead to the development of novel therapeutic strategies for diseases associated with the accumulation of GA-AGEs.

Published
2023
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42. Increased plasma glutamate in non-smokers with vasospastic angina pectoris is associated with plasma cystine and antioxidant capacity.

Author

Oda M, Fujibayashi K, Wakasa M, Takano S, Fujita W, Kitayama M, Nakanishi H, Saito K, Kawai Y, and Kajinami K

Subjects
Antioxidants, Cystine metabolism, Endothelial Cells metabolism, Humans, Non-Smokers, Oxygen, Coronary Vasospasm, Glutamic Acid metabolism
Abstract

Objectives . Endothelial dysfunction caused by oxidative stress plays an important role in the development of vasospastic angina pectoris (VSAP). Glutamate causes endothelial dysfunction by generating oxidative stress, and it inhibits cystine import into endothelial cells via the cystine/glutamate antiporter (X C - ), which leads to depletion of antioxidant glutathione. However, whether glutamate and cystine are implicated in the pathogenesis of VSAP remains unclear. We investigated plasma glutamate and cystine levels, oxidative stress markers and antioxidant capacity in non-smoker patients with VSAP to determine whether glutamate and cystine are associated with the development of VSAP. We assessed 49 non-smokers assigned to groups with ( n  = 27) and without ( n  = 22) VSAP, and also measured plasma glutamate, cystine, nitrotyrosine, reactive oxygen metabolites and biological antioxidant potential. Results . Plasma glutamate and cystine values were significantly higher in the group with, than without VSAP (59.8 ± 25.7 vs. 43.5 ± 18.7 µmol/L, p  = .016 and 35.3 ± 14.2 vs. 25.2 ± 9.1 µmol/L, p  = .0056, respectively). Plasma glutamate and cystine values were significantly and positively associated ( r  = 0.32, p  = .027). Levels of the oxidative stress markers nitrotyrosine and reactive oxygen metabolites, and biological antioxidant potential of as a measure of antioxidant capacity, did not significantly differ between the two groups. However, glutamate and biological antioxidant potential values were significantly and negatively associated ( r  = -0.3, p  = .036). Conclusion . Plasma glutamate levels were increased in patients with VSAP who did not smoke, and they were positively associated with plasma cystine and negatively associated with the biological antioxidant potential levels.

Published
2022
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43. Glyceraldehyde-derived advanced glycation end-products are associated with left ventricular ejection fraction and brain natriuretic peptide in patients with diabetic adverse cardiac remodeling.

Author

Yasuda Y, Aoki H, Fujita W, Fujibayashi K, Wakasa M, Kawai Y, Nakanishi H, Saito K, Takeuchi M, and Kajinami K

Subjects
Glyceraldehyde, Humans, Natriuretic Peptide, Brain, Stroke Volume, Tumor Necrosis Factor-alpha, Ventricular Function, Left, Ventricular Remodeling, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 diagnosis, Heart Failure
Abstract

Objectives : Glyceraldehyde-derived advanced glycation end-products (Glycer-AGEs) have a strong binding affinity for their cognate receptor and elicit oxidative stress and inflammation. However, it remains unknown whether the levels of Glycer-AGEs correlate with the severity of cardiac function and heart failure in patients with diabetic adverse cardiac remodeling (DbCR). Fourteen heart failure patients with type 2 diabetes mellitus (DM) without other cardiac disorders (DbCR group) were enrolled. Another 14 patients with idiopathic dilated cardiomyopathy (DCM) without DM were served as a control (DCM group). All patients were assessed for serum Glycer-AGEs, nitrotyrosine (NT), and tumor necrosis factor alpha (TNFα) and for plasma brain natriuretic peptide (BNP). The left ventricular ejection fraction (LVEF) was evaluated by echocardiography. Results : The mean serum levels of Glycer-AGEs, NT, and TNFα in the DbCR group were significantly higher than those in the DCM group (for Glycer-AGEs, p  = .0073; for NT, p  = .005; for TNFα, p  < .0001, respectively). In the patients with DbCR, the levels of serum Glycer-AGEs and TNFα were closely associated with LVEF and BNP values. Conclusions : Both Glycer-AGEs and TNFα showed close associations with LVEF and the levels of BNP in patients with DbCR. Glycer-AGEs and TNFα may play a pathological role in the development of DbCR.

Published
2022
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44. A Case of Myopericarditis After the Second Dose of mRNA COVID-19 Vaccine in a Patient With a History of Myopericarditis.

Author

Fujibayashi K and Kajinami K

Abstract

Vaccination is important for the prevention of coronavirus-induced disease 2019 (COVID-19) caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) and to protect persons with a high risk for complications. There have been reports of myopericarditis following COVID-19 vaccination, especially in adolescent males and young adults. Breakthrough infections, such as the Delta or Omicron variant of SARS-CoV-2, have raised great concern about the necessity for repeated doses of the vaccine. A case of myopericarditis after the second dose of COVID-19 mRNA-1273 (Moderna) vaccine in a 23-year-old man with a prior episode of viral myopericarditis is presented. He received the second dose of the COVID-19 mRNA vaccine, after which he developed persistent midsternal chest pain and he was subsequently transferred to our emergency department. An echocardiogram showed a trivial inferior pericardial effusion with diffuse left ventricular systolic dysfunction. He was treated with colchicine from the first day of hospitalization with a diagnosis of myopericarditis. His chest pain had resolved by the third day, and left ventricular wall motion was dramatically improved by the seventh day of hospitalization. A strong response to the second vaccination in the present case suggests that the prior history of myopericarditis is evidence of strong congenital or acquired immunological features in this individual. Individuals with such a strong immune response may be more likely to develop myopericarditis after mRNA vaccination. Immunization against COVID-19 is currently recommended from a risk-benefit standpoint. We advised the patient to avoid additional COVID-19 mRNA vaccines because of this episode. The risk of COVID-19 weighed against myopericarditis associated with the mRNA vaccination should be considered on a case-by-case basis. This case may help us better understand the mechanism of myopericarditis following COVID-19 mRNA vaccination., Competing Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2022.)

Published
2022
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45. The circulating furin-cleaved/mature PCSK9 ratio has a potential prognostic significance in statin-naïve patients with acute ST elevation myocardial infarction.

Author

Sawaguchi J, Saeki Y, Oda M, Takamura TA, Fujibayashi K, Wakasa M, Akao H, Kitayama M, Kawai Y, and Kajinami K

Abstract

Background and Aims: Proprotein convertase subtilisin/kexin type 9 (PCSK9) circulates as mature and furin-cleaved forms, but their biological functions are uncertain. We investigated whether their levels associate with prognosis in patients with acute ST elevation myocardial infarction (STEMI)., Methods: We enrolled 160 statin-naïve patients with acute STEMI and followed for 3 years. PCSK9 subtype levels were determined by an enzyme-linked immunosorbent assay before and at five timepoints up to 48 h after emergent coronary intervention. The occurrence of coronary and cardiac events was compared between subjects stratified by the PCSK9 level., Results: One hundred and twenty-six patients completed 3 years of follow-up. In the acute phase, both PCSK9 subtype levels decreased, and thereafter increased from 6 to 48 h (mature: from 198 ± 67 to 334 ± 116 ng/mL, furin-cleaved: from 20 ± 7 to 39 ± 16 ng/mL, both p  < 0.01). Major cardiac events occurred in 46 patients. The furin-cleaved/mature PCSK9 ratio at 48 h after coronary intervention predicted the likelihood of experiencing of events; patients in the third tertile had lower event-free survival than those in the first and second tetiles in Kaplan-Meier analysis ( p  = 0.004). Multivariate Cox regression analysis revealed that this ratio had a greater impact (HR: 1.92; 95% CI: 1.06-3.45, p  = 0.03) on events than other known atherosclerosis risk factors., Conclusions: The furin-cleaved/mature PCSK9 ratio was associated with 3-year cardiovascular events in statin-naïve patients with acute STEMI, suggesting a potential link between furin cleavage process of PCSK9 and its effect on prognosis. (249 words)., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 The Authors.)

Published
2022
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46. Response to pre-dilatation with POBA can predict target lesion revascularization after DCB angioplasty for de novo small coronary artery lesions.

Author

Takamura TA, Kawai Y, Akita S, Oda M, Akao H, Nakagawa T, Takama S, Tsuchiya T, Kitayama M, and Kajinami K

Subjects
Dilatation, Humans, Paclitaxel, Retrospective Studies, Angioplasty, Balloon, Angioplasty, Balloon, Coronary, Coronary Artery Disease etiology, Coronary Artery Disease surgery
Abstract

Objective: To assess the determinants of target lesion revascularization (TLR) after drug-coated balloon (DCB) angioplasty for de novo small coronary artery lesions., Methods: This retrospective study enrolled consecutive lesions from patients that were in a stable condition and had undergone successful DCB treatment for de novo small coronary artery lesions. The study endpoint was TLR and major adverse cardiac events at 12 months., Results: A total of 68 patients with 83 lesions were enrolled in the study. Of these, 11 (13.3%) lesions required TLR. Mean ± SD pre-dilatation balloon diameters were similar in the non-TLR (2.33 ± 0.72 mm) and TLR (2.18 ± 0.36 mm) groups. A comparison of the two groups showed that post/pre-lumen area ratio during pre-dilatation (%) by plain old balloon angioplasty (POBA) was significantly and negatively associated with TLR and the optimal cut-off point was 170%. Cox proportional hazard and multivariate regression analyses showed that post/pre-lumen area ratio was the only independent predictor of TLR (hazard ratio 0.9318; 95% confidence interval 0.9001, 0.9645)., Conclusion: Greater pre-dilatation using POBA, assessed as the post/pre-lumen area ratio, may be independently associated with a lower 12-month TLR rate in patients undergoing DCB angioplasty for de novo small coronary lesions.

Published
2022
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47. Guidelines on the Clinical Evaluation of Medicinal Products for Treatment of Dyslipidemia.

Author

Yamashita S, Masuda D, Akishita M, Arai H, Asada Y, Dobashi K, Egashira K, Harada-Shiba M, Hirata K, Ishibashi S, Kajinami K, Kinoshita M, Kozaki K, Kuzuya M, Ogura M, Okamura T, Sato K, Shimano H, Tsukamoto K, Yokode M, Yokote K, and Yoshida M

Subjects
Aged, Anticholesteremic Agents pharmacology, Child, Cholesterol, LDL blood, Clinical Trials as Topic, Female, Humans, Japan, Male, Risk Factors, Triglycerides blood, Cardiology standards, Drug Evaluation, Preclinical, Dyslipidemias drug therapy, Dyslipidemias therapy
Published
2020
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48. Hokuriku-plus familial hypercholesterolaemia registry study: rationale and study design.

Author

Tada H, Okada H, Yoshida S, Shimojima M, Nomura A, Tsuda T, Mori M, Takashima SI, Kato T, Usui S, Sakata K, Hayashi K, Fujino N, Inazu A, Takahara S, Imai Y, Matsubara T, Nohara A, Miwa K, Namura M, Terai H, Yoshida T, Araki T, Minamoto M, Aburao T, Ito Y, Nakanishi C, Kawasaki S, Todo Y, Koizumi J, Kita Y, Matsumoto H, Shintaku H, Hodatsu A, Ino H, Higashikata T, Takata M, Misawa K, Yamaguchi M, Noji Y, Osato K, Mabuchi T, Ichise T, Kaku B, Katsuda S, Fujimoto M, Uchiyama K, Fujioka K, Nakahashi T, Nozue T, Michishita I, Usuda K, Otowa K, Okeie K, Hirota S, Aburadani I, Kurokawa K, Takatori O, Hondo S, Oda H, Takata S, Murai H, Kinoshita M, Nagai H, Sekiguchi Y, Sakagami S, Omi W, Fujita C, Katsuki T, Ootsuji H, Igarashi A, Nakano M, Okura S, Maeno K, Mitamura Y, Sugimoto N, Yamamoto M, Akao H, Kajinami K, Takamura M, and Kawashiri MA

Subjects
Cohort Studies, Humans, Japan epidemiology, Prospective Studies, Registries, Hyperlipoproteinemia Type II epidemiology, Hyperlipoproteinemia Type II genetics
Abstract

Introduction: Familial hypercholesterolaemia (FH) is an autosomal-dominant inherited genetic disease. It carries an extremely high cardiovascular risk associated with significantly elevated low-density lipoprotein (LDL) cholesterol. The diagnostic rate of this disease in some European nations is quite high, due to the presence of multiple prospective registries. On the other hand, few data-and in particular multicentre data-exist regarding this issue among Japanese subjects. Therefore, this study intends to assemble a multicentre registry that aims to comprehensively assess cardiovascular risk among Japanese FH patients while taking into account their genetic backgrounds., Methods and Analysis: The Hokuriku-plus FH registry is a prospective, observational, multicentre cohort study, enrolling consecutive FH patients who fulfil the clinical criteria of FH in Japan from 37 participating hospitals mostly in Hokuriku region of Japan from April 2020 to March 2024. A total of 1000 patients will be enrolled into the study, and we plan to follow-up participants over 5 years. We will collect clinical parameters, including lipids, physical findings, genetic backgrounds and clinical events covering atherosclerotic and other important events, such as malignancies. The primary endpoint of this study is new atherosclerotic cardiovascular disease (ASCVD) events. The secondary endpoints are as follows: LDL cholesterol, secondary ASCVD events and the occurrence of other diseases including hypertension, diabetes and malignancies., Ethics and Dissemination: This study is being conducted in compliance with the Declaration of Helsinki, the Ethical Guidelines for Medical and Health Research Involving Human Subjects, and all other applicable laws and guidelines in Japan. This study protocol has been approved by the Institutional Review Board at Kanazawa University. We will disseminate the final results at international conferences and in a peer-reviewed journal., Trial Registration Number: UMIN000038210., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Published
2020
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49. Monitoring the roles of prothrombin activation fragment 1 and 2 (F1 + 2) in patients with atrial fibrillation receiving rivaroxaban and apixaban.

Author

Ueno EI, Fujibayashi K, Sawaguchi J, Yasuda Y, Takano S, Fujioka N, Kawai Y, Fujita H, Tanaka Y, and Kajinami K

Subjects
Aged, Aged, 80 and over, Atrial Fibrillation blood, Atrial Fibrillation diagnosis, Atrial Fibrillation surgery, Biomarkers blood, Catheter Ablation, Factor Xa Inhibitors adverse effects, Female, Humans, Male, Prothrombin, Pyrazoles adverse effects, Pyridones adverse effects, Rivaroxaban adverse effects, Time Factors, Treatment Outcome, Atrial Fibrillation drug therapy, Drug Monitoring, Factor Xa Inhibitors therapeutic use, Peptide Fragments blood, Pyrazoles therapeutic use, Pyridones therapeutic use, Rivaroxaban therapeutic use
Abstract

Factor Xa (FXa) inhibitors are recommended for use in fixed doses without laboratory monitoring. However, prior studies reported the importance of establishing biomarkers representing anticoagulation intensity related to bleeding or thrombotic events. To test the hypothesis that prothrombin activation fragment 1 and 2 (F1 + 2), a non-specific marker of thrombin generation, could be altered during FXa inhibitor treatment in patients with atrial fibrillation. We conducted the study in two different clinical settings. First, the interrelations among biomarkers representing coagulation/fibrinolysis were investigated in 80 patients in an outpatient clinic. Second, these biomarkers were evaluated in 75 patients who underwent radiofrequency catheter ablation. Plasma concentration of FXa inhibitors was evaluated using an anti-FXa chromogenic assay (C-Xa). In the outpatient study, only F1 + 2 exhibited a significant and negative association with C-Xa (rS =  - 0.315, p = 0.026), and 37% of the variance could be explained by C-Xa levels. F1 + 2 levels above the reference range (> 229 pmol/L) could be considered as a cut-off to identify poor patient compliance or under-dosing. In the peri-ablation study, increased F1 + 2 levels were associated with decline of C-Xa levels after periprocedural discontinuation of FXa inhibitors, which was greater in the rivaroxaban group than in the apixaban group. F1 + 2 showed modest and inverse association with plasma concentration of rivaroxaban and apixaban in patients with atrial fibrillation. Larger study to test the hypothesis that continued thrombin generation despite anticoagulation is associated with a heightened risk of clinical events is required.

Published
2020
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50. Possible effect of direct oral anti-coagulant for preventing long stenting lesion from in-stent restenosis in femoropopliteal segment: Case report with angioscopy findings.

Author

Tsuchiya T, Akita S, Oda M, Takamura T, Kitagawa K, Kajinami K, and Kitayama M

Abstract

A 64-year-old female underwent a successful first percutaneous intervention using MISAGO stents for a de novo femoropopliteal lesion. Subsequently, three more effective procedures were done using balloon catheters for in-stent restenosis. In May 2016, a fourth procedure using Zilver PTX stent for in-stent restenosis was carried out. For this final procedure, we added direct oral anti-coagulant as she had additional problem of popliteal vein thrombosis and her femoropopliteal segment remained clear. A Zilver PTX stent, a drug-eluting stent for a peripheral artery, was expected to bring superior outcomes compared to conventional bare nitinol stents (i.e. MISAGO stent). But subsequent studies reported that Zilver PTX stent was not more effective than conventional bare nitinol stents. In our above mentioned case, her angioscopy findings suggest that her successful outcome appears to be related to the added direct oral anti-coagulant., Competing Interests: Declaration of conflicting interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2020.)

Published
2020
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