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1. Expanding the phenotype of LMNA mutations in dilated cardiomyopathy and functional consequences of these mutations

Author

Sebillon, P, Bouchier, C, Bidot, LD, Bonne, G, Ahamed, K, Charron, P, Drouin-Garraud, V, Millaire, A, Desrumeaux, G, Benaiche, A, Charniot, J-C, Schwartz, K, Villard, E, and Komajda, M

Subjects
Genetic aspects, Research, Atrial fibrillation -- Genetic aspects -- Research, Gene mutation -- Research -- Genetic aspects, Congestive cardiomyopathy -- Genetic aspects -- Research, Genetic disorders -- Research -- Genetic aspects, Gene mutations -- Research -- Genetic aspects, Cardiomyopathy, Dilated -- Genetic aspects -- Research
Abstract

Aims: Mutations in the lamin A/C gene (LMNA) have been reported to be involved in dilated cardiomyopathy (DCM) associated with conduction system disease and/or skeletal myopathy. The aim of this [...]

Published
2003

2. Genetic testing and genetic counselling in hypertrophic cardiomyopathy: the French experience. (Medical Genetics in Practice)

Author

Charron, P., Heron, D., Gargiulo, M., Richard, P., Dubourg, O., Desnos, M., Bouhour, J-B, Feingold, J., Carrier, L., Hainque, B., Schwartz, K., and Komajda, M.

Subjects
Psychological aspects, Standards, Social aspects, Physiological aspects, Usage, Research, Genetic aspects, Health aspects, Causes of, Sudden death -- Causes of -- Genetic aspects -- Research, Genetic testing -- Standards -- Usage -- Genetic aspects -- Physiological aspects -- Research -- Health aspects -- Social aspects -- Psychological aspects, Medical genetics -- Research -- Health aspects -- Physiological aspects -- Usage -- Social aspects -- Psychological aspects, Children -- Physiological aspects -- Social aspects -- Genetic aspects -- Psychological aspects -- Health aspects -- Research -- Usage, Amniocentesis -- Usage -- Health aspects -- Research -- Physiological aspects -- Psychological aspects -- Social aspects, Child health -- Health aspects -- Social aspects -- Usage -- Physiological aspects -- Psychological aspects -- Research, Familial diseases -- Research -- Genetic aspects, Hypertrophic cardiomyopathy -- Psychological aspects -- Genetic aspects -- Research, Gene mutation -- Health aspects -- Usage -- Social aspects -- Research -- Physiological aspects -- Genetic aspects -- Psychological aspects, Genetic counseling -- Usage -- Psychological aspects -- Research -- Physiological aspects -- Social aspects -- Health aspects, Molecular genetics -- Research -- Genetic aspects -- Social aspects -- Psychological aspects -- Physiological aspects -- Health aspects -- Usage, Gene mutations -- Health aspects -- Usage -- Social aspects -- Research -- Physiological aspects -- Genetic aspects -- Psychological aspects, Cardiomyopathy, Hypertrophic -- Psychological aspects -- Genetic aspects -- Research, Genetic screening -- Standards -- Usage -- Genetic aspects -- Physiological aspects -- Research -- Health aspects -- Social aspects -- Psychological aspects
Abstract

Aims: A major breakthrough in the molecular genetics of hypertrophic cardiomyopathy (HCM) has made genetic testing now available in clinical practice, raising new questions about its implications, potential benefits, and [...]

Published
2002

3. Relation between QT duration and maximal wall thickness in familial hypertrophic cardiomyopathy. (Cardiovascular Medicine)

Author

Jouven, X., Hagege, A., Charron, P., Carrier, L., Dubourg, O., Langlard, J.M., Aliaga, S., Bouhour, J.B., Schwartz, K., Desnos, M., and Komajda, M.

Subjects
Physiological aspects, Genetic aspects, Familial diseases -- Physiological aspects -- Genetic aspects, Hypertrophic cardiomyopathy -- Genetic aspects -- Physiological aspects, Cardiomyopathy, Hypertrophic -- Genetic aspects -- Physiological aspects
Abstract

Background: QT abnormalities have been reported in left ventricular hypertrophy and hypertrophic cardiomyopathy. Objective: To determine the relation between left ventricular hypertrophy and increased QT interval in familial hypertrophic cardiomyopathy. [...]

Published
2002

4. Empagliflozin in the treatment of heart failure with reduced ejection fraction in addition to background therapies and therapeutic combinations (EMPEROR-Reduced): a post-hoc analysis of a randomised, double-blind trial

Author

Verma, Subodh, Dhingra, Nitish K, Butler, Javed, Anker, Stefan D, Ferreira, Joao Pedro, Filippatos, Gerasimos, Januzzi, James L, Lam, Carolyn S P, Sattar, Naveed, Peil, Barbara, Nordaby, Matias, Brueckmann, Martina, Pocock, Stuart J, Zannad, Faiez, Packer, Milton, Packer, M, Anker, S, Butler, J, Filippatos, G, Pocock, S, Zannad, F, Ferreira, JP, Brueckmann, M, George, J, Jamal, W, Welty, FK, Palmer, M, Clayton, T, Parhofer, KG, Pedersen, TR, Greenberg, B, Konstam, MA, Lees, KR, Carson, P, Doehner, W, Miller, A, Haas, M, Pehrson, S, Komajda, M, Anand, I, Teerlink, J, Rabinstein, A, Steiner, T, Kamel, H, Tsivgoulis, G, Lewis, J, Freston, J, Kaplowitz, N, Mann, J, Petrie, J, Perrone, S, Nicholls, S, Janssens, S, Bocchi, E, Giannetti, N, Verma, S, Zhang, J, Spinar, J, Seronde, M-F, Boehm, M, Merkely, B, Chopra, V, Senni, M, Taddi, S, Tsutsui, H, Choi, D-J, Chuquiure, E, La Rocca, HPB, Ponikowski, P, Juanatey, JRG, Squire, I, Januzzi, J, Pina, I, Bernstein, R, Cheung, A, Green, J, Januzzi, J, Kaul, S, Lam, C, Lip, G, Marx, N, McCullough, P, Mehta, C, Ponikowski, P, Rosenstock, J, Sattar, N, Scirica, B, Shah, S, Tsutsui, H, Verma, S, Wanner, C, Aizenberg, D, Cartasegna, L, Colombo Berra, F, Colombo, H, Fernandez Moutin, M, Glenny, J, Alvarez Lorio, C, Anauch, D, Campos, R, Facta, A, Fernandez, A, Ahuad Guerrero, R, Lobo Márquez, L, Leon de la Fuente, RA, Mansilla, M, Hominal, M, Hasbani, E, Najenson, M, Moises Azize, G, Luquez, H, Guzman, L, Sessa, H, Amuchástegui, M, Salomone, O, Perna, E, Piskorz, D, Sicer, M, Perez de Arenaza, D, Zaidman, C, Nani, S, Poy, C, Resk, J, Villarreal, R, Majul, C, Smith Casabella, T, Sassone, S, Liberman, A, Carnero, G, Caccavo, A, Berli, M, Budassi, N, Bono, J, Alvarisqueta, A, Amerena, J, Kostner, K, Hamilton, A, Begg, A, Beltrame, J, Colquhoun, D, Gordon, G, Sverdlov, A, Vaddadi, G, Wong, J, Coller, J, Prior, D, Friart, A, Leone, A, Janssens, S, Vervoort, G, Timmermans, P, Troisfontaines, P, Franssen, C, Sarens, T, Vandekerckhove, H, Van De Borne, P, Chenot, F, De Sutter, J, De Vuyst, E, Debonnaire, P, Dupont, M, Pereira Dutra, O, Canani, LH, Vieira Moreira, MdC, de Souza, W, Backes, LM, Maia, L, De Souza Paolino, B, Manenti, ER, Saporito, W, Villaça Guimarães Filho, F, Franco Hirakawa, T, Saliba, LA, Neuenschwander, FC, de Freitas Zerbini, CA, Gonçalves, G, Gonçalves Mello, Y, Ascenção de Souza, J, Beck da Silva Neto, L, Bocchi, EA, Da Silveira, J, de Moura Xavier Moraes Junior, JB, de Souza Neto, JD, Hernandes, M, Finimundi, HC, Sampaio, CR, Vasconcellos, E, Neves Mancuso, FJ, Noya Rabelo, MM, Rodrigues Bacci, M, Santos, F, Vidotti, M, Simões, MV, Gomes, FL, Vieira Nascimento, C, Precoma, D, Helfenstein Fonseca, FA, Ribas Fortes, JA, Leães, PE, Campos de Albuquerque, D, Kerr Saraiva, JF, Rassi, S, Alves da Costa, FA, Reis, G, Zieroth, S, Dion, D, Savard, D, Bourgeois, R, Constance, C, Anderson, K, Verma, S, Leblanc, M-H, Yung, D, Swiggum, E, Pliamm, L, Pesant, Y, Tyrrell, B, Huynh, T, Spiegelman, J, Giannetti, N, Lavoie, J-P, Hartleib, M, Bhargava, R, Straatman, L, Virani, S, Costa-Vitali, A, Hill, L, Heffernan, M, Khaykin, Y, Ricci, J, Senaratne, M, Zhai, A, Lubelsky, B, Toma, M, Yao, L, McKelvie, R, Noronha, L, Babapulle, M, Pandey, A, Curnew, G, Lavoie, A, Berlingieri, J, Kouz, S, Lonn, E, Chehayeb, R, Zheng, Y, Sun, Y, Cui, H, Fan, Z, Han, X, Jiang, X, Tang, Q, Zhou, J, Zheng, Z, Zhang, X, Zhang, N, Zhang, J, Zhang, Y, Shen, A, Yu, J, Ye, J, Yao, Y, Yan, J, Xu, X, Wang, Z, Ma, J, Li, Y, Li, S, Lu, S, Kong, X, Song, Y, Yang, G, Yao, Z, Zhang, J, Zhang, Y, Pan, Y, Guo, X, Sun, Z, Dong, Y, Zhu, J, Peng, D, Yuan, Z, Lin, J, Yin, Y, Jerabek, O, Burianova, H, Fiala, T, Hubac, J, Ludka, O, Monhart, Z, Vodnansky, P, Zeman, K, Foldyna, D, Krupicka, J, Podpera, I, Busak, L, Radvan, M, Vomacka, Z, Prosecky, R, Cifkova, R, Durdil, V, Vesely, J, Vaclavik, J, Cervinka, P, Linhart, A, Brabec, T, Miklik, R, Bourhaial, H, Olbrich, H-G, Genth-Zotz, S, Kemala, E, Lemke, B, Böhm, M, Schellong, S, Rieker, W, Heitzer, T, Ince, H, Faghih, M, Birkenfeld, A, Begemann, A, Ghanem, A, Ujeyl, A, von Haehling, S, Dorsel, T, Bauersachs, J, Prull, M, Weidemann, F, Darius, H, Nickenig, G, Wilke, A, Sauter, J, Rauch-Kroehnert, U, Frey, N, Schulze, CP, König, W, Maier, L, Menzel, F, Proskynitopoulos, N, Ebert, H-H, Sarnighausen, H-E, Düngen, H-D, Licka, M, Marx, N, Stellbrink, C, Winkelmann, B, Menck, N, López-Sendón, JL, de la Fuente Galán, L, Delgado Jiménez, JF, Manito Lorite, N, Pérez de Juan Romero, M, Galve Basilio, E, Cereto Castro, F, González Juanatey, JR, Gómez, JJ, Sanmartín Fernández, M, Garcia-Moll Marimon, X, Pascual Figal, D, Bover Freire, R, Bonnefoy Cudraz, E, Jobbe Duval, A, Tomasevic, D, Habib, G, Isnard, R, Picard, F, Khanoyan, P, Dubois-Rande, J-L, Galinier, M, Roubille, F, Alexandre, J, Babuty, D, Delarche, N, Seronde, M-F, Berneau, J-B, Girerd, N, Saxena, M, Rosano, G, Yousef, Z, Clifford, C, Arden, C, Bakhai, A, Squire, I, Boos, C, Jenkins, G, Travill, C, Price, D, Koenyves, L, Lakatos, F, Matoltsy, A, Noori, E, Zilahi, Z, Andrassy, P, Kancz, S, Simon, G, Sydo, T, Vorobcsuk, A, Merkely, B, Kiss, RG, Toth, K, Szakal, I, Nagy, L, Barany, T, Nagy, A, Szolnoki, E, Chopra, VK, Mandal, S, Rastogi, V, Shah, B, Mullasari, A, Shankar, J, Mehta, V, Oomman, A, Kaul, U, Komarlu, S, Kahali, D, Bhagwat, A, Vijan, V, Ghaisas, NK, Mehta, A, Kashyap, J, Kothari, Y, TaddeI, S, Scherillo, M, Zacà, V, Genovese, S, Salvioni, A, Fucili, A, Fedele, F, Cosmi, F, Volpe, M, Senni, M, Mazzone, C, Esposito, G, Doi, M, Yamamoto, H, Sakagami, S, Oishi, S, Yasaka, Y, Tsuboi, H, Fujino, Y, Matsuoka, S, Watanabe, Y, Himi, T, Ide, T, Ichikawa, M, Kijima, Y, Koga, T, Yuda, S, Fukui, K, Kubota, T, Manita, M, Fujinaga, H, Matsumura, T, Fukumoto, Y, Kato, R, Kawai, Y, Hiasa, G, Kazatani, Y, Mori, M, Ogimoto, A, Inoko, M, Oguri, M, Kinoshita, M, Okuhara, K, Watanabe, N, Ono, Y, Otomo, K, Sato, Y, Matsunaga, T, Takaishi, A, Miyagi, N, Uehara, H, Takaishi, H, Urata, H, Kataoka, T, Matsubara, H, Matsumoto, T, Suzuki, T, Takahashi, N, Imamaki, M, Watanabe, N, Yoshitama, T, Saito, T, Sekino, H, Furutani, Y, Koda, M, Matsuoka, S, Shinozaki, T, Hirabayashi, K, Tsunoda, R, Yonezawa, K, Hori, H, Yagi, M, Arikawa, M, Hashizume, T, Ishiki, R, Koizumi, T, Nakayama, K, Taguchi, S, Nanasato, M, Yoshida, Y, Tsujiyama, S, Nakamura, T, Oku, K, Shimizu, M, Suwa, M, Momiyama, Y, Sugiyama, H, Kobayashi, K, Inoue, S, Kadokami, T, Maeno, K, Kawamitsu, K, Maruyama, Y, Nakata, A, Shibata, T, Wada, A, Cho, H-J, Na, JO, Yoo, B-S, Choi, J-O, Hong, SK, Shin, J-H, Cho, M-C, Han, SH, Jeong, J-O, Kim, J-J, Kang, SM, Kim, D-S, Kim, MH, Llamas Esperon, G, Illescas Díaz, J, Fajardo Campos, P, Almeida Alvarado, J, Bazzoni Ruiz, A, Echeverri Rico, J, Lopez Alcocer, I, Valle Molina, L, Hernandez Herrera, C, Calvo Vargas, C, Padilla Padilla, FG, Rodriguez Briones, I, Chuquiure Valenzuela, EJJR, Aguilera Real, ME, Carrillo Calvillo, J, Alpizar Salazar, M, Cervantes Escárcega, JL, Velasco Sanchez, R, Al - Windy, N, van Heerebeek, L, Bellersen, L, Brunner-La Rocca, H-P, Post, J, Linssen, GCM, van de Wetering, M, Peters, R, van Stralen, R, Groutars, R, Smits, P, Yilmaz, A, Kok, WEM, Van der Meer, P, Dijkmans, P, Troquay, R, van Alem, AP, Van de Wal, R, Handoko, L, Westendorp, ICD, van Bergen, PFMM, Rensing, BJWM, Hoogslag, P, Kietselaer, B, Kragten, JA, den Hartog, FR, Alings, A, Danilowicz-Szymanowicz, L, Raczak, G, Piesiewicz, W, Zmuda, W, Kus, W, Podolec, P, Musial, W, Drelich, G, Kania, G, Miekus, P, Mazur, S, Janik, A, Spyra, J, Peruga, J, Balsam, P, Krakowiak, B, Szachniewicz, J, Ginel, M, Grzybowski, J, Chrustowski, W, Wojewoda, P, Kalinka, A, Zurakowski, A, Koc, R, Debinski, M, Fil, W, Kujawiak, M, Forys, J, Kasprzak, M, Krol, M, Michalski, P, Mirek-Bryniarska, E, Radwan, K, Skonieczny, G, Stania, K, Skoczylas, G, Madej, A, Jurowiecki, J, Firek, B, Wozakowska-Kaplon, B, Cymerman, K, Neutel, J, Adams, K, Balfour, P, Deswal, A, Djamson, A, Duncan, P, Hong, M, Murray, C, Rinde-Hoffman, D, Woodhouse, S, MacNevin, R, Rama, B, Anderson, K, Broome-Webster, C, Kindsvater, S, Abramov, D, Barettella, M, Pinney, S, Herre, J, Cohen, A, Vora, K, Challappa, K, West, S, Baum, S, Cox, J, Jani, S, Karim, A, Akhtar, A, Quintana, O, Paukman, L, Goldberg, R, Bhatti, Z, Budoff, M, Bush, E, Potler, A, Delgado, R, Ellis, B, Dy, J, Fialkow, J, Sangrigoli, R, Ferdinand, K, East, C, Falkowski, S, Donahoe, S, Ebrahimi, R, Kline, G, Harris, B, Khouzam, R, Jaffrani, N, Jarmukli, N, Kazemi, N, Koren, M, Friedman, K, Herzog, W, Greenberg, B, Silva Enciso, J, Cheung, D, Grover-McKay, M, Hauptman, P, Mikhalkova, D, Hegde, V, Hodsden, J, Khouri, S, McGrew, F, McCullough, P, Littlefield, R, Bradley, P, McLaurin, B, Lupovitch, S, Labin, I, Rao, V, Leithe, M, Lesko, M, Lewis, N, Lombardo, D, Mahal, S, Malhotra, V, Mehta, V, Dauber, I, Banerjee, A, Needell, J, Miller, G, Paladino, L, Munuswamy, K, Nanna, M, McMillan, E, Mumma, M, Napoli, M, Nelson, W, O'Brien, T, Adlakha, A, Onwuanyi, A, Serota, H, Schmedtje, J, Paraschos, A, Potu, R, Sai-Sudhakar, C, Saltzberg, M, Sauer, A, Shah, P, Skopicki, H, Bui, H, Carr, K, Stevens, G, Tahirkheli, N, Tallaj, J, Yousuf, K, Trichon, B, Welker, J, Tolerico, P, Vest, A, Vivo, R, Wang, X, Abadier, R, Dunlap, S, Weintraub, N, Malik, A, Kotha, P, Zaha, V, Kim, G, Uriel, N, Greene, T, Salacata, A, Arora, R, Gazmuri, R, Kobayashi, J, Iteld, B, Vijayakrishnan, R, Dab, R, Mirza, Z, Marques, V, Nallasivan, M, Bensimhon, D, Peart, B, Saint-Jacques, H, Barringhaus, K, Contreras, J, Gupta, A, Koneru, S, and Nguyen, V

Abstract

It is important to evaluate whether a new treatment for heart failure with reduced ejection fraction (HFrEF) provides additive benefit to background foundational treatments. As such, we aimed to evaluate the efficacy and safety of empagliflozin in patients with HFrEF in addition to baseline treatment with specific doses and combinations of disease-modifying therapies.

Published
2022
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5. Rapport 20-05 – La transplantation cardiaque chez l’adulte

Author

Komajda, M., Gandjbakhch, I., Dorent, R., Leprince, P., Trochu, J.-N., and Welty, C.

Abstract

La transplantation cardiaque est le traitement de référence de l’insuffisance cardiaque terminale réfractaire au traitement médical optimal, avec une médiane de vie post greffe de 12 ans. Pourtant, l’accès à la transplantation tend actuellement à diminuer et il existe une inadéquation entre le nombre de receveurs et celui des donneurs. Ce rapport revoit les indications, les contre-indications de la transplantation cardiaque et les complications survenant lors du suivi. Les conditions d’une meilleure prise en charge de l’insuffisance cardiaque sévère dans l’ensemble du territoire national et d’une optimisation de l’offre de transplantation cardiaque sont examinées et le recours aux greffons prélevés chez des patients décédés après un arrêt circulatoire est discuté.

Published
2021
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6. Relation between severity of left ventricular systolic dysfunction and repolarisation abnormalities on the surface ECG: a report from the Euro heart failure survey

Author

Velavan, P., Khan, N.K., Rigby, A.S., Goode, K., Komajda, M., Follath, F., Swedberg, K., Madeira, H., Clark, A.L., and Cleland, J.G.F.

Subjects
Heart ventricle, Left -- Physiological aspects, Heart ventricle, Left -- Research, Heart failure -- Risk factors, Electrocardiogram -- Analysis, Electrocardiography -- Analysis, Health
Published
2006

7. Are angiotensin II receptor blockers indicated in chronic heart failure?

Author

Komajda, M.

Subjects
Drug therapy, Evaluation, Heart failure -- Drug therapy, Angiotensin II receptor blockers -- Evaluation
Abstract

Have the theoretical advantages of the angiotensin II receptor blockers become reality for the treatment of chronic heart failure? Chronic heart failure is one of the most serious cardiac problems [...]

Published
2002

9. Prevalence of anemia in patients with chronic heart failure and their clinical characteristics

Author

Komajda, M.

Abstract

Anemia is commonly seen in patients with chronic heart failure, but there is no literature consensus regarding the prevalence of anemia in these patients. Analysis of the results of clinical surveys and trials suggests that individual definitions of anemia and choice of the study population have a major influence on estimating the prevalence of anemia in patients with chronic heart failure. Examination of a number of large, contemporary databases shows that in patients with chronic heart failure anemia is an independent prognostic factor and is associated with older age, more severe symptoms and signs, and a greater likelihood of hospitalization.

Published
2004
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11. Double heterozygosity for mutations in the β-myosin heavy chain and in the cardiac myosin binding protein C genes in a family with hypertrophic cardiomyopathy

Author

Dubourg, O., Richard, P., Donatien, Y., Mathieu, B., Gary, F., Hainque, B., Hagege, A., Isnard, R., Charron, P., Komajda, M., Carrier, L., Bonne, G., and Schwartz, K.

Abstract

Familial hypertrophic cardiomyopathy is a genetically heterogeneous autosomal dominant disease, caused by mutations in several sarcomeric protein genes. So far, seven genes have been shown to be associated with the disease with the β-myosin heavy chain (MYH7) and the cardiac myosin binding protein C (MYBPC3) genes being the most frequently involved. We performed electrocardiography (ECG) and echocardiography in 15 subjects with hypertrophic cardiomyopathy from a French Caribbean family. Genetic analyses were performed on genomic DNA by haplotype analysis with microsatellite markers at each locus involved and mutation screening by single strand conformation polymorphism analysis. Based on ECG and echocardiography, eight subjects were affected and presented a classical phenotype of hypertrophic cardiomyopathy. Two new mutations cosegregating with the disease were found, one located in the MYH7 gene exon 15 (Glu483Lys) and the other in the MYBPC3 gene exon 30 (Glu1096 termination codon). Four affected subjects carried the MYH7 gene mutation, two the MYBPC3 gene mutation, and two were doubly heterozygous for the two mutations. The doubly heterozygous patients exhibited marked left ventricular hypertrophy, which was significantly greater than in the other affected subjects.We report for the first time the simultaneous presence of two pathological mutations in two different genes in the context of familial hypertrophic cardiomyopathy. This double heterozygosity is not lethal but is associated with a more severe phenotype.

Published
1999

12. Plasma levels and molecular forms of proatrial natriuretic peptides in healthy subjects and in patients with congestive heart failure

Author

Azizi, C, Maistre, G, Kalotka, H, Isnard, R, Barthélemy, C, Masson, F, Pham, P, Pousset, F, Eurin, J, Lechat, P, Komajda, M, and Carayon, A

Abstract

A specific and sensitive radioimmunoassay (RIA) for the N-terminal fragment of proatrial natriuretic peptide (NproANP) was developed. Antiserum raised in rabbits against a mixture enriched with prohormone was 100% cross-reactive with human proANP(1–30). Plasma concentrations of proANP(1–30) and ANP immunoreactivities (ir-) were simultaneously measured in healthy subjects and patients with congestive heart failure (CHF; 26 dilated cardiomyopathy and 5 ischemic heart disease). High plasma levels of both ir-proANP(1–30) and ir-ANP were detected in CHF patients. Circulating ir-ANP levels were elevated in New York Heart Association functional Classes II and III patients but not in Class I patients. However, plasma levels of ir-proANP(1–30) were higher in asymptomatic patients than in healthy subjects, and markedly increased in patients of Classes II and III. Analysis of ir-proANP(1–30) by gel filtration chromatography or reverse-phase high pressure liquid chromatography revealed a 10 kDa peptide circulating as a distinct entity.These findings indicate that: (i) the most probable form of NproANP in human plasma is a 10 kDa peptide and (ii) in CHF patients the rise in plasma ir-proANP(1–30) levels is more pronounced than the variation in plasma ir-ANP. Thus, NproANP plasma levels may prove to be a more sensitive marker of left ventricular dysfunction than ANP.Journal of Endocrinology(1996) 148,51–57

Published
1996
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13. Hemodynamic and neurohormonal effects of flosequinan in patients with heart failure

Author

Isnard, R., Lechat, P., Pousset, F., Carayon, A., Kalotka, H., Chikr, H., Salloum, J., Thomas, D., and Komajda, M.

Abstract

Summary—In a double‐blind, placebo‐controlled study, the central and peripheral hemodynamic effects of 100 mg oral flosequinan and the impact of this drug on neurohormonal activation were noninvasively evaluated in 18 patients with congestive heart failure, after the first administration and after 10 days of treatment. No significant hemodynamic and neurohormonal changes were observed after acute admistration. After 10 days, flosequinan produced central and peripheral hemodynamic improvement characterized by an increase in left ventricular circumferential fiber shortening velocity (+12%), a decrease in total systemic resistance (‐36%), and an increase in leg blood flow (+37%). No significant changes were observed in heart rate and arterial pressure in patients receiving flosequinan, though a slight increase in heart rate (+17%) was recorded. Despite these favorable hemodynamic effects, flosequinan significantly increased plasma norepinephrine (+38%) and plasma renin activity (+13%) after 10 days of treatment. Thus, the beneficial central and peripheral hemodynamic effects of flosequinan are accompanied by activation of the sympathetic and renin‐angiotensin systems. This might be related to the unfavorable effects of the drug on survival in patients with heart failure.

Published
1997
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14. Captopril does not acutely modulate plasma endothelin-1 concentration in human congestive heart failure

Author

Grenier, O., Pousset, F., Isnard, R., Kalotka, H., Carayon, A., Maistre, G., Lechat, P., Guerot, C., Thomas, D., and Komajda, M.

Abstract

Congestive heart failure (CHF) is a syndrome characterized by increased levels of angiotensin II (Ang II) and endothelin-1 (ET-1). In vitro, Ang II stimulates ET-1 release. The purpose of this study was to assess the effect of a single dose of an angiotensin-converting enzyme inhibitor (ACEI) captopril versus placebo on plasma endothelin concentration in human congestive heart failure. Captopril (25 mg, given orally) was compared with placebo in a group of 20 patients with systolic dysfunction in a double-blind randomized study. Plasma irET concentration was significantly increased in CHF patients compared with normal subjects (5.59 pg/ml±0.35 vs. 3.58 pg/ml±0.99, p<0.0002). Despite the decrease in systolic blood pressure and the increase in plasma renin activity, suggesting a significant blockade of the renin-angiotensin system, no difference in plasma irET-1 was observed between captopril and placebo. Our results suggest that captopril does not acutely influence irET-1 plasma concentration in human CHF. These data do not support the hypothesis that the acute vasodilator effect of a single dose of 25 mg of captopril given orally involves modulation of the increased plasma concentration of endothelin observed in CHF.

Published
1996
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16. First description of germline mosaicism in familial hypertrophic cardiomyopathy

Author

Schwartz, K., Forissier, J-F., Komajda, M., Charbonnier, B., Dubourg, O., Richard, P., Ledeuil, C., Hainque, B., Briault, S., Moraine, C., Carrier, L., and Bonne, G.

Abstract

Familial hypertrophic cardiomyopathy is a genetically and phenotypically heterogeneous disease caused by mutations in seven sarcomeric protein genes. It is known to be transmitted as an autosomal dominant trait with rare de novo mutations.A French family in which two members are affected by hypertrophic cardiomyopathy was clinically screened with electrocardiography and echocardiography. Genetic analyses were performed on leucocyte DNA by haplotype analysis with microsatellite markers at the MYH7 locus and mutation screening by single strand conformation polymorphism analysis. Two subjects exhibited severe hypertrophic cardiomyopathy. A mutation in the MYH7 gene was found in exon 14 (Arg453Cys). The two affected patients were carriers of the mutation, which was not found in the circulating lymphocytes of their parents. Haplotype analysis at the MYH7 locus with two intragenic microsatellite markers (MYOI and MYOII) and the absence of the mutation in the father's sperm DNA suggested that the mutation had been inherited from the mother. However, it was not found in either her fibroblasts or hair.This is the first description of germline mosaicism shown by molecular genetic analysis in an autosomal dominant disorder and more especially in hypertrophic cardiomyopathy. This mosaicism had been inherited from the mother but did not affect her somatic cells. Such a phenomenon might account for some de novo mutations in familial hypertrophic cardiomyopathy.

Published
2000

17. Experience from clinical genetics in hypertrophic cardiomyopathy: proposal for new diagnostic criteria in adult members of affected families

Author

McKenna, W.J., Spirito, P., desnos, M., Dubourg, O., and Komajda, M.

Abstract

The diagnosis of hypertrophic cardiomyopathy has relied on echocardiographic demonstration of unexplained left ventricular hypertrophy. The prevalence of hypertrophic cardiomyopathy defined in this way has been estimated to be 1:500 and experience indicates that these criteria are relatively specific when other causes of left ventricular hypertrophy are absent. In recent years, however, the systematic evaluation of pedigrees performed in the context of molecular genetic studies revealed that in some families with hypertrophic cardiomyopathy up to 20% of adults who carry a disease causing gene defect do not fulfil conventional echocardiographic criteria. None the less, most of these individuals show symptoms, electrocardiographic alterations, and/or minor echocardiographic abnormalities. Revised diagnostic criteria in members of families with hypertrophic cardiomyopathy are proposed, including major and minor criteria based on symptoms, and electrocardiographic and echocardiographic abnormalities. Given that the chance of inheriting the gene defect is 1:2, the likelihood that symptoms plus electrocardiographic or echocardiographic abnormalities are the expression of a disease causing gene is high.

Published
1997

18. Mapping of a novel gene for familial hypertrophic cardiomyopathy to chromosome 11

Author

Carrier, L., Hengstenberg, C., Beckmann, J. S., Guicheney, P., Dufour, C., Bercovici, J., Dausse, E., Berebbi-Bertrand, I., Wisnewsky, C., Pulvenis, D., Fetler, L., Vignal, A., Weissenbach, J., Hillaire, D., Feingold, J., Bouhour, J.-B., Hagege, A., Desnos, M., Isnard, R., Dubourg, O., Komajda, M., and Schwartz, K.

Abstract

Familial hypertrophic cardiomyopathy (FHC) is a cardiac disorder transmitted as an autosomal dominant trait. FHC has been shown to be genetically heterogeneous with less than 50% of published pedigrees being associated with mutations in the p myosin heavy chain (β–MHC) gene on chromosome 14q11–q12. A second locus has recently been reported on chromosome 1. We examined the segregation of microsatellite markers in a French pedigree for which the disease is not linked to β–MHC gene. We found significant linkage of the disease locus to several (CA)nrepeats located on chromosome 11 (lod scores between +3.3 and +4.98). The data suggest the localization of the novel FHC gene in a region spanning 17 centiMorgans.

Published
1993
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21. Poster session 1

Author

Haberka, M, Banska, K, Gasior, Z, Garcia Martin, A, Moya-Mur, JL, Carbonell-San Roman, S-A, Rodriguez-Munoz, D, Garcia-Lledo, A, Casas-Rojo, E, Hinojar, R, Jimenez-Nacher, JJ, Fernandez-Golfin, C, Zamorano-Gomez, JL, Barbier, P, Ravani, A, Cefalu, C, Maltagliati, A, Frigerio, B, Sansaro, D, Amato, M, Baldassarre, D, Pellegrino, M, Bandera, F, Generati, G, Labate, V, Alfonzetti, E, Guazzi, M, Angelis, A, Aggeli, K, Ioakeimidis, N, Abdelrasoul, M, Felekos, I, Gourgouli, I, Aznaouridis, K, Rousakis, G, Vlachopoulos, C, Tousoulis, D, Howlett, PJ, Darasz, K, Mahmoudi, M, Shah, N, Jabr, RI, Hickman, M, Leatham, EW, Fry, CH, PREDICT-PAF, Madeira, M, Teixeira, R, Almeida, I, Caetano, F, Fernandes, A, Cassandra, M, Reis, L, Costa, M, Goncalves, L, Carrero, PJ, Nielsen, AJ, Carrero, MC, Saubidet, GL, Peralta, SP, Argentina, Aorta Abdominal, Hansen, KL, Moeller-Soerensen, H, Kjaergaard, J, Jensen, MB, Lund, JT, Pedersen, MM, Olesen, JB, Jensen, JA, Nielsen, MB, Trunina, I, Sharykin, AS, Karelina, EV, Telezhnikova, ND, Basar, C, Ozhan, H, Kayapinar, O, Albayrak, ES, Lie, OH, Saberniak, J, Dejgaard, L, Nestaas, E, Edvardsen, T, Haugaa, KH, Sade, LE, Bal, U, Eroglu, S, Pirat, B, Muderrisoglu, H, Gopal, A S, Muthukumar, L, Saha, SK, Toole, RS, Klug, G, Reinstadler, S, Feistritzer, HJ, Pernter, B, Mayr, A, Franz, WM, Mueller, S, Metzler, B, Rodriguez Gonzalez, E, Mingo Santos, S, Palomero Monivas, V, Gonzalez Mirelis, J, Goirigolzarri Artaza, J, Zorita Gil, B, Fernandez Diaz, JA, Goicolea Ruigomez, J, Restrepo Cordoba, MA, Alonso Pulpon, L, Ferrara, F, Gargani, L, D'alto, M, Ghio, S, Acri, E, Carannante, L, Argiento, P, D'andrea, A, Vriz, O, Bossone, E, Moustafa, S, Ho, TH, Shah, P, Murphy, K, Nelluri, BK, Lee, H, Wilansky, S, Mookadam, F, Naksuk, N, Peeraphatdit, T, Chaiteerakij, R, Klarich, KW, Cantinotti, M, Scalese, M, Melo, M, Assanta, N, Marotta, M, Crocetti, M, Spadoni, I, Giordano, R, Kutty, S, Iervasi, I, Michelsen, MM, Mygind, ND, Pena, A, Frestad, D, Hoest, N, Prescott, E, Fernandes, JMG, Romao, BO, Rivera, IR, Mendonca, MA, Carvalho, AC, Campos, O, Amato, A, Moises, VA, Demir, OM, Bashir, A, Marshall, K, Douglas, M, Wasan, B, Plein, S, Alfakih, K, Cano Carrizal, R, Casanova Rodriguez, C, Cadenas Chamorro, R, Iglesias Del Valle, D, Martin-Penato Molina, A, De Juan Baguda, J, Prieto Moriche, E, Garcia Garcia, A, De La Cruz Berlanga, E, Plaza Perez, I, Bouzas-Mosquera, A, Peteiro, J, Broullon, FJ, Alvarez-Garcia, N, Barbeito-Caamano, C, Larranaga-Moreira, JM, Maneiro-Melon, N, Martinez-Ruiz, D, Yanez, JC, Vazquez-Rodriguez, JM, Leao, S, Cordeiro, F, Magalhaes, P, Moz, M, Trigo, J, Mateus, P, Fontes, P, Moreira, I, Kuznetsov, VA, Krinochkin, DV, Plusnin, AV, Soldatova, AM, Nazir, S A, Shetye, A, Khan, JN, Singh, A, Kanagala, P, Swarbrick, DJ, Graham-Brown, M, Mccann, GP, Trifunovic, D, Krljanac, G, Savic, L, Asanin, M, Aleksandric, S, Lasica, R, Srdic, M, Zlatic, N, Petrovic, M, Mrdovic, I, Rodriguez Gonzalez, E, Mingo Santos, S, Monivas Palomero, V, Gonzalez Mirelis, J, Zorita Gil, B, Fernandez Diaz, JA, Restrepo Cordoba, MA, Goirigolzarri Artaza, J, Rivero Arribas, B, Goicolea Ruigomez, J, Spampinato, RA, Dobrovie, M, Da Rocha E Silva, JG, Bonamigo Thome, F, Kluttig, R, Schloma, V, Dmitrieva, Y, Strotdrees, E, Mohr, FW, Antonini-Canterin, F, Luzza, G, Caruso, R, Belfiore, R, Della Mattia, A, Poli, S, Vriz, O, Zito, C, La Carrubba, S, Carerj, S, Ribeiro, JM, Teixeira, R, Goncalves, L, Morgado, GJ, Carvalho, JF, Gomes, AC, Caldeira, D, Cruz, IR, Stuart, B, Maia, R, Fazendas, P, Pereira, H, Trifunovic, D, Rakocevic, I, Tutos, V, Petrovic, O, Petrovic, M, Boricic-Kostic, M, Stepanovic, J, Jovanovic, I, Banovic, M, Vujisic-Tesic, B, Reis, L, Teixeira, R, Leite, L, Fernandes, A, Cassandra, M, Madeira, M, Botelho, A, Santos, M, Nascimento, J, Goncalves, L, Naratrekoon, B, Yingchoncharoen, T, Vathesatogkit, P, Yamwong, S, Sritara, P, Soto-Ruiz, RM, Bonaque Gonzalez, J C, Abellan-Huerta, J, Rubio-Paton, R, Soria, F, Ramos, JL, Egea, S, Garcia-Gomez, J, Martinez Diaz, JJ, Castillo, JA, Penicka, M, Vecera, J, Mirica, C, Kotrc, M, Kockova, R, Zilberszac, R, Gabriel, H, Maurer, G, Rosenhek, R, De Chiara, B, Botta, L, Musca, F, Belli, O, Costetti, A, Trolese, I, Spano, F, Russo, C, Giannattasio, C, Moreo, A, Rifai, R, Berthelot, E, Le, MT, Hilpert, L, Montani, D, Sitbon, O, Jais, X, Humbert, M, Assayag, P, Gunduz, S, Yesin, M, Kalcik, M, Gursoy, MO, Cersit, S, Astarcioglu, MA, Karakoyun, S, Aykan, AC, Ozkan, M, Cersit, S, Gunduz, S, Tabakci, M, Kalcik, M, Yesin, M, Bayam, E, Ozkan, M, Devecchi, C, Degiovanni, A, Di Ruocco, MV, Marino, P, Ancona, F, Rosa, I, Stella, S, Barletta, M, Marini, C, Latib, A, Montorfano, M, Colombo, A, Margonato, A, Agricola, E, Smith, D, Ray, R, Gallagher, M, Nazir, M, Perreso, V, Sharma, R, Gargani, L, Pang, PS, Miglioranza, M, Landi, P, Dini, FL, Picano, E, Asmarats Serra, L, Pons Llinares, J, Macaya Ten, F, Pericas Ramis, P, Caldes Llull, O, Grau Sepulveda, A, Frontera, G, Bethencourt, A, Abreu, A, Santa Clara, H, Santos, V, Oliveira, M, Cunha, P, Portugal, G, Rio, P, Branco, L, Ferreira, R, Mota Carmo, M, Ikonomidis, I, Paraskevaidis, I, Papadopoulos, C, Stasinos, V, Parissis, J, Lekakis, J, Biernacka, B, Rubis, P, Gackowski, A, Wisniowska-Smialek, S, Lesniak-Sobelga, A, Kostkiewicz, M, Gomes, AC, Bento, D, Correia, E, Teles, L, Picarra, B, Lourenco, C, Faria, R, Magalhaes, P, Domingues, K, Azevedo, O, Caballero, L, Climent Paya, V, Martinez Moreno, M, Gimeno, JR, Oliva, MJ, Saura, D, Sanchez Quinones, J, Garcia Honrubia, A, Valdes, M, De La Morena, G, Mansencal, N, Richard, P, Guerard, S, Brion, R, Paul, P, Dubourg, O, Komajda, M, Isnard, R, Arslan, M, Charron, P, Venturini, C, Avegliano, G, Andres, S, Costabel, JP, Kuschnir, P, Sciancalepore, A, Mendoza, O, Perea, G, Ronderos, R, Zaroui, A, Ben Said, RYM, EL Chalbia, TEJ, Wali, SANA, Mourali, MS, Mechmeche, RACHID, Leren, I S, Saberniak, J, Haland, TF, Edvardsen, T, Haugaa, KH, Astrom Aneq, M, Svetlichnaya, J S, Shikha, SS, Scheinmann, MS, Klein, LK, Nucifora, G, Prati, G, Vitrella, G, Allocca, G, Cukon Buttignoni, S, Muser, D, Morocutti, G, Pinamonti, B, Sinagra, G, Proclemer, A, Rocon, CRLA, Melo, MDTM, Bocchi, EAB, Araujo, JABAF, Demarchi, LMMFD, Mady, CM, Biselli, BB, Kalil, RKF, Salemi, VMCS, Tuma, RT, Cho, J Y, Kim, K H, Yoon, H J, Lee, K J, Park, H, Kim, J H, Ahn, Y, Jeong, M H, Cho, J G, Park, J C, Cho, J Y, Kim, K H, Yoon, H J, Park, H J, Kim, J H, Ahn, Y, Jeong, M H, Cho, J G, Park, J C, Sade, LE, Kozan, H, Eroglu, S, Pirat, B, Sezgin, A, Aydinalp, A, Muderrisoglu, H, Stampfli, S F, Oezkartal, T, Bernhart, S, Flammer, AJ, Vecchiati, A, Froehlich, GM, Ruschitzka, F, Tanner, FC, Cho, EJ, Choi, KY, Kim, DB, Jang, SW, Cho, JS, Park, CS, Jung, HO, Jeon, HK, Youn, HJ, Stevanovic, A, Dekleva, M, Pena, J L, Fortes, PRL, Passos, BR, Rodrigues, AB, Sampaio, IH, Oliveira, MCN, Silva, MG, Cardoso, RAF, Tofani, FA, Moreira, MCV, Ognibeni, F, Cioffi, G, Viapiana, O, Dalbeni, A, Fracassi, E, Di Nora, C, Cherubini, A, Mazzone, C, Di Lenarda, A, Rossini, M, Colunga, S, Corros, C, Garcia-Campos, A, Martin, M, Rodriguez-Suarez, M, Leon, V, Fidalgo, A, Lopez-Iglesias, F, Moris, C, De La Hera, JM, Borowiec, A, Dabrowski, R, Wozniak, J, Jasek, S, Chwyczko, T, Kowalik, I, Musiej-Nowakowska, E, Szwed, H, Hristova, K, Marinov, R, Stamenov, G, Mihova, M, Chacheva, K, Persenska, S, Racheva, A, Kosmala, W, Przewlocka-Kosmala, M, Rojek, A, Karolko, B, Mysiak, A, Marwick, TH, Lesniak-Sobelga, A M, Kostkiewicz, M, Wisniowska-Smialek, S, Biernacka, B, Rubis, P, Kaldararova, M, Tittel, P, Kardos, M, Vrsanska, V, Ondriska, M, Hraska, V, Nosal, M, Masura, J, Simkova, I, Stanojevic, D, Apostolovic, S, Salinger-Martinovic, S, Jankovic-Tomasevic, R, Djordjevic-Radojkovic, D, Stanojlovic, T, Atanaskovic, V, Pavlovic, M, Tahirovic, E, Dungen, HD, Carbonell San Roman, A, Moya Mur, JL, Rodriguez-Munoz, D, Lozano Granero, C, Jimenez Nacher, JJ, Gonzalez Gomez, A, Fraile Sanz, C, Segura De La Cal, T, Fernandez-Golfin, C, Zamorano Gomez, JL, Hoetink, A, Jansen Klomp, WW, Van 'T Hof, AWJ, Brandon Bravo Bruinsma, GJ, Spanjersberg, AJ, Grandjean, J, Nierich, AP, Ferreira, R, Ferreira, J, Lazaro Mendes, S, Martins, R, Monteiro, S, Pego, M, Rohani, A, Khamene Bagheri, R, Wierzbowska-Drabik, K, Peruga, JZ, Sobczak, M, Plewka, M, Wcislo, T, Krecki, R, Kasprzak, JD, Carvalho, J F, Morgado, G, Cruz, I, Caldeira, D, Almeida, AR, Joao, I, Lopes, L, Fazendas, P, Cotrim, C, Pereira, H, Cherubini, A, Cioffi, G, Mazzone, C, Faganello, G, Pandullo, C, Russo, G, Stefenelli, C, Furlanello, F, Tarantini, L, Di Lenarda, A, Teramoto, K, Suzuki, K, Satoh, Y, Minami, K, Mizukoshi, K, Kamijima, R, Kou, S, Takai, M, Izumo, M, Akashi, YJ, May, CJH, Ayuk, J, Geh, I, Shah, T, Edwards, NC, Steeds, RP, Wejner-Mik, P, Sobczak, M, Miskowiec, D, Wdowiak-Okrojek, K, Kasprzak, JD, Lipiec, P, Gurzun, M M, Rosca, M, Calin, A, Beladan, C, Serban, M, Ginghina, C, Popescu, BA, Perea, GO, Lombardero, M, Henquin, R, Corneli, M, Tinetti, M, Laveau, F, Hekimian, G, Achkar, M, Isnard, R, Combes, A, Hammoudi, N, Mahmoud, HM, Al-Ghamdi, M, Ghabashi, A, Ezzat, M H, Al-Amin, A, Sanz, M, Giraldeau, G, Sarvari, SI, Marin, J, Brambila, C, Gabrielli, L, Bijnens, B, Sitges, M, Sanchez-Martinez, S, Duchateau, N, Erdei, T, Fraser, A, Bijnens, B H, Piella, G, Montserrat, S, Sanchis, L, Borras, R, Vidal, B, Prat, S, Azqueta, M, Pare, C, Grazioli, G, Sanz, M, Sitges, M, Kowalczyk, E, Kasprzak, JD, Wejner-Mik, P, Wdowiak-Okrojek, K, Lipiec, P, Park, CS, Jung, MH, Ahn, HS, Kim, JH, Cho, JS, Jeon, HK, Youn, HJ, Hinojar, R, Fernandez-Golfin, C, Megias, A, Alonso, GL, Gonzalez-Gomez, A, Rincon, LM, Esteban, A, Fernandez Mendez, MA, Barrios, V, Zamorano, JL, Van Berendoncks, A M, Van Gaal, L, De Block, C, Salgado, R, Vrints, C, Shivalkar, B, Guedes, H, Pereira, A, Santos, R, Marques, L, Moreno, N, Carvalho, R, Pires, M, Sousa, R, Andrade, A, Pinto, P, Nestaas, E, Stoylen, A, Fugelseth, D, Onut, R, Tautu, O, Onciul, S, Marinescu, C, Zamfir, D, Dorobantu, M, Moran, L, Sanchez Sanchez, V, Navas, P, Garcia-Cosio, D, Diaz, B, Carballo-Alzola, L, Lombera, F, Delgado, J, Kisko, A, Babcak, M, Kishko, N, Agmon, Y, Eitan, A, Mutlak, D, Kehat, I, Corneli, M, Meretta, AH, Perea, GO, Belcastro, F, Aguirre, E, Rosa, D, Zaefferer, P, Masoli, O, Peovska Mitevska, IPM, Srbinovska, ES, Bosevski, MB, Antova, EA, Pop Gorceva, DPG, Barreiro Perez, M, Martin Fernandez, M, Costilla Garcia, SM, Diaz Pelaez, E, and Moris De La Tassa, C

Abstract

Background: The attainment of the primary (low density lipoprotein cholesterol; LDL-C) and the secondary (non-high density lipoprotein cholesterol; non-HDL) lipid therapeutic targets may depend on several potential factors. Our aim was assess the associations between ultrasound fat indexes, lipid levels and the lipid goals attainment in high and very high cardiovascular (CV) risk patients. Methods: Four hundred twenty (n=420) patients (F/M=146/274; age=61 ± 7 y.o.) with high (43%) or very high (57%) cardiovascular risk and chronic statin treatment (³12 months) were enrolled into the study. Obesity measures (body-mass index, BMI; bioelectrical impedance body fat; BF, waist circumference, WC, body adiposity index; BAI), serum levels of lipids (total cholesterol–TC, LDL-C, HDL-C and triglycerides–TG) and goal lipid levels (LDL-C and non-HDL-C) according to the CV risk were determined in all patients. The following ultrasound fat parameters were used in the study: intraabdominal fat (IAT), preperitoneal fat thickness (PreFT), epicardial (EFT) and pericardial (PFT) fat thickness and were indexed to BMI. Results: Our study patients had 5.2 ± 1.7 CV risk factors (80% hypertension, 32% diabetes, 59% metabolic syndrome), 49% were obese, 63% had high BF% and 85% had increased waist circumference (F>80 or M>94cm). All the patients were on a long-term statin treatment (rosuvastatin, atorvastatin or simvastatin). The attainment of the target lipid levels in the study group was as follows: LDL-C–34%, non-HDL-C–39%, both LDL-C and non-HDL-C 31%. Mean fat parameters in the study group were as follows: IAT–76.4 ± 26mm, PreFT–23.3 ± 6.5mm, EFT–3.5 ± 1.5mm and PFT–8.6 ± 3.8mm. Patients with LDL-C goal attainment had significantly higher BAI (34.6 ± 33 vs 30.5 ± 7, p=0.04), but significantly lower IAT/BMI (2.35 ± 0.7 vs 2.51 ± 0.7, p<0.05) with no differences in other clinical (BMI, BF%, WC) and ultrasound (PreFT/BMI, EFT/BMI, PFT/BMI) indexes. The LDL-C goal achievement revealed inverse association with IAT/BMI (r=-0.15, p<0.05) and no associations with PreFT/BMI, EFT/BMI or PFT/BMI. Multivariable regression analysis revealed independent association between IAT/BMI and the LDL-C goal achievement. Conclusions: Intraabdominal fat thickness representing visceral adipose tissue is inversely associated with the LDL-C goal attainment independently from general obesity. It may help to identify individuals requiring more aggressive management of dylipidaemia.

Published
2015
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25. The heart of genomics.

Author

Komajda M and Charron P

Subjects
Genetic Counseling, Heart Diseases genetics, Humans, Pedigree, Pharmacogenetics, Heart Diseases diagnosis, Heart Diseases therapy, Human Genome Project
Published
2001
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