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1. Ritmestoornissen

Author

Loh, K. P., Clappers, N., Klöpping, C., editor, Jansen, R., editor, and van der Meer, M. G., editor

Published
2025
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7. The C50T polymorphism of the cyclooxygenase-1 gene and the risk of thrombotic events during low-dose therapy with acetyl salicylic acid

Author

Clappers, N., Oijen, M.G.H. van, Sundaresan, S., Brouwer, M.A., Morsche, R.H.M. te, Keuper, W., Peters, W.H.M., Drenth, J.P.H., and Verheugt, F.W.A.

Subjects
Cardiovascular diseases [NCEBP 14], Genetic defects of metabolism [UMCN 5.1], Translational research [ONCOL 3], Membrane transport and intracellular motility [NCMLS 5], Aetiology, screening and detection [ONCOL 5], Molecular gastro-enterology and hepatology [IGMD 2], Heart, lung and circulation [UMCN 2.1]
Abstract

Contains fulltext : 70838.pdf (Publisher’s version ) (Closed access) Aspirin prevents thrombotic events by inhibiting platelet cyclooxygenase-1 (COX-1), thus reducing thromboxane A2 formation and platelet aggregation. The C50T polymorphism of COX-1 is associated with an impaired inhibition of both thromboxane production and in-vitro platelet aggregation by aspirin. We studied whether this polymorphism is also associated with the risk of clinical thrombotic events in patients using aspirin. We included 496 patients admitted to our Coronary Care Unit for various indications treated with aspirin 80 mg daily. Genotyping for the C50T polymorphism demonstrated that 86.7% of the patients had the common genotype, and 13.3% had the variant (12.5% heterozygous, 0.8% homozygous). Baseline variables were well balanced, except that patients with the common genotype more frequently used aspirin prior to admission compared to those patients with the variant genotype. The composite primary endpoint of myocardial infarction, stroke, and/or cardiovascular death occurred in 98 patients (19.8%). Myocardial infarction occurred in 9.6% of patients, stroke in 1.6%, and cardiovascular death in 12.1%. The unadjusted hazard ratio (95% CI) for the primary endpoint for patients with the variant versus the common genotype was 1.07 (0.62-1.85), p = 0.8. The adjusted hazard ratio was 0.86 (0.49-1.50), p = 0.6. In prior laboratory studies the COX-1 C50T polymorphism was associated with an impaired inhibitory effect of aspirin on thromboxane production and platelet function. However, in this cohort of patients using low-dose aspirin for secondary prevention the polymorphism was not associated with a higher risk of atherothrombotic events.

Published
2008
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8. How to react to high platelet reactivity?

Author

Clappers, N., Brouwer, M.A., and Verheugt, F.W.A.

Subjects
Cardiovascular diseases [NCEBP 14], Heart, lung and circulation [UMCN 2.1]
Abstract

Contains fulltext : 69957.pdf (Publisher’s version ) (Closed access)

Published
2008

9. Assessment of plasma aminothiol levels and the association with recurrent atherothrombotic events in patients hospitalized for an acute coronary syndrome: a prospective study

Author

Jaspers Focks, J., Schaik, A. van, Clappers, N., Dijk, E.G.J.A. van, Oijen, M.G.H. van, Verheugt, F.W.A., Peters, W.H.M., Jaspers Focks, J., Schaik, A. van, Clappers, N., Dijk, E.G.J.A. van, Oijen, M.G.H. van, Verheugt, F.W.A., and Peters, W.H.M.

Abstract

Item does not contain fulltext, Background: The aminothiols homocysteine and, to a lesser extent, cysteine have been associated with adverse cardiovascular outcome, whereas glutathione, as an antioxidant, may protect against atherosclerosis and thrombosis. Potentially, the combined assessment of these aminothiols may provide a more accurate association with future cardiovascular outcome. We evaluated the association between recurrent atherothrombotic events and the concentration of total plasma cysteine, homocysteine, and glutathione and their combination. Methods: Respective aminothiols were measured by high-performance liquid chromatography in blood plasma of consecutive first-day survivors admitted for an acute coronary syndrome between April 2002 and January 2004. The combined score was calculated using the combination of the individual aminothiols. The end point was the composite of cardiovascular death, myocardial infarction, and/or stroke. Results: A cohort of 375 consecutive patients (median age 66 years, 66% male) were followed for a median duration of 2.7 years. The end point occurred in 82 patients (22%). In univariate analyses, all aminothiols were significantly associated with the composite end point. After correction for possible confounders, only cysteine and glutathione remained significantly associated. The strongest association with the end point was observed for the combined score (adjusted hazard ratio, 1.40 per standard deviation increase; p=0.005). Conclusions: Although homocysteine is generally considered the aminothiol of interest with respect to cardiovascular disease, in our prospective study, only cysteine and glutathione appeared independently associated with recurrent atherothrombotic events. Moreover, we showed that an imbalance in the combination of aminothiols could be of more importance than investigating the individual metabolites.

Published
2013

10. Prognostic value of free plasma homocysteine levels in patients hospitalized with acute coronary syndrome.

Author

Oijen, M.G.H. van, Claessen, B.E., Clappers, N., Schaik, A. van, Laheij, R.J.F., Jansen, J.B.M.J., Peters, W.H.M., Verheugt, F.W.A., Oijen, M.G.H. van, Claessen, B.E., Clappers, N., Schaik, A. van, Laheij, R.J.F., Jansen, J.B.M.J., Peters, W.H.M., and Verheugt, F.W.A.

Abstract

Contains fulltext : 71329.pdf (publisher's version ) (Closed access), Elevated total plasma homocysteine is an established risk factor for cardiovascular disease. Experimental evidence suggests that non-protein-bound free homocysteine is particularly hazardous to the vascular endothelium. This study evaluates the predictive role of free plasma homocysteine levels on cardiovascular endpoints in patients with acute coronary syndrome (ACS). In a cohort of 379 hospitalized patients with a diagnosis of myocardial infarction or unstable angina pectoris, total and free plasma homocysteine levels were measured by high performance liquid chromatography. The patients were followed for a median 2.7 years. The primary endpoint was a composite of cardiovascular death, myocardial infarction and stroke during follow-up. Stepwise Cox regression was used for multivariate analysis. Primary outcome events occurred in 82 patients (22%) with a median time to event of 6 months. The unadjusted hazard ratio for a free homocysteine level >4.11 micromol/L was 2.16 (95% confidence intervals [CI] 1.36 to 3.42) compared with the 4 lower quintiles. After adjusting for the covariates the hazard ratio was 2.25 (95% CI 1.41 to 3.58, p = 0.01). Compared with the lower 4 quintiles, patients with a total homocysteine level >22.4 micromol/L had a 2.09-fold higher risk (95% CI 1.31 to 3.35) for an event during follow-up. Adjusted for age, discharge diagnosis, serum creatinine, history of atherothrombotic events, and diabetes mellitus, the adjusted hazard ratio was 1.37 (95% CI 0.83 to 2.25, p = 0.22). In conclusion, plasma free homocysteine levels >4.11 micromol/L are a significant and independent risk factor for recurrent cardiovascular events in patients hospitalized for ACS, although total plasma homocysteine levels have no predictive value.

Published
2008

11. Antiplatelet treatment for coronary heart disease.

Author

Clappers, N., Brouwer, M.A., Verheugt, F.W.A., Clappers, N., Brouwer, M.A., and Verheugt, F.W.A.

Abstract

Contains fulltext : 52327.pdf (publisher's version ) (Closed access)

Published
2007

16. Comparison of fondaparinux and enoxaparin in acute coronary syndromes

Author

Yusuf, S., Mehta, S. R., Bassand, J. P., Budaj, A., Chrolavicius, S., Fox, K. A. A., Granger, C. B., Joyner, C., Peters, R. J. G., Wallentin, L., Avezum, A., Boden, W., Cardona, E., Ceremuzynski, L., Col, J., Commerford, P. J., Diaz, R., Faxon, D., Flather, M., Fodor, G., Franzosi, M. G., Granger, C., Halon, D., Hunt, D., Karatzas, N., Keltai, M., Kenda, M., Kim, J. H., Lanas, F., Lau, C. P., Lewis, B. S., Morais, J., Moccetti, T., Pais, P., Paolasso, E., Parkhomenko, A., Petrauskiene, B., Piegas, L., Pipilis, A., Robaayah, D., Ruda, M., Rumboldt, Z., Rupprecht, H. J., Sitkei, E., Steg, P. G., Swahn, E., Theroux, P., Valentin, V., Varigos, J., Weitz, J., White, H., Widimsky, P., Xavier, D., Zhu, J. R., Ameriso, S., Bonilla, C., Braekken, S., Chan, Y. K., Chen, W., Chenniappan, M., Cohen, E., Cottin, Y., Csiba, L., Czepiel, A., Raedt, H., Finet, G., Gardinale, E., Gaxiola, E., Gorecki, A., Gregor, P., Happola, O., Heras, M., Himbert, D., Irkin, O., Isaaz, K., Iyengar, S. S., Kalvach, P., Kevers, L., Klosiewicz-Wasek, B., Laine, M., Leys, D., Lundstrom, E., Lusic, I., Lutay, Y., Maggioni, A., Massaro, A., Mayosi, B. M., Moulin, T., Narendra, J., Naslund, U., Peeters, A., Penicka, M., Perakis, A., Petersen, P., Polic, S., Radhakrishnan, S., Renkin, J., Stockins, B., Sundararajan, R., Thygesen, K., Turazza, F., Belle, E., Vik-Mo, H., Zaborski, J., Sleight, P., Anderson, J. L., Johnstone, D. E., Hirsh, J., Demets, D., Holmes, D. R., Meeks, B., Afzal, R., Pogue, J., Boccalon, S., Chrysler, K., Cracknell, B., Horsman, C., Hoskin, T., Jedrzejowski, B., Johnson, J., Kotlan, S., Lawrence, M., Smiley, M., Stevens, C., Yallup, R., Connolly, S., Demers, C., Devereaux, P. J., Healey, J., Lonn, E., Magloire, P., Mckelvie, R., Morillo, C., Natarajan, M., Rokoss, M., Teo, K., Valettas, N., Velianou, J., Albisu, J. P., Amuchastegui, M., Bello, F. A., Bluguermann, J. J., Bono, J. O., Caccavo, A., Carlevaro, O. O., Cassettari, A., Cuneo, C., Farras, H. A., Fuselli, J., Garrido, M., Guerrero, R., Hasbani, E., Hominal, M. A., Hrabar, A., Marquez, L. L., Luciardi, H. L., Riera, L. M., Marzetti, E. M., Memoli, R., Nordaby, R., Orlandini, A. D., Perez, M., Piasentin, J. A., Ramos, H. R., Risolo, A. M., Sala, J., Salomone, O., Schygiel, P. O., Ubaldini, J., Vico, M., Amerena, J., Arnolda, L., Aroney, G., Boyd, P., Cahill, P., Chew, D., Counsell, J. T., Cross, D., Edington, J., Fitzpatrick, D., Hicks, P., Horowitz, J. D., Horrigan, M. C. G., New, G., Owensby, D., Schoeman, M., Thompson, P., Tulloch, G., Waites, J., Whelan, A., Ziffer, R., Huber, K., Jordanova, N., Al Shawafi, K., Convens, C., Coussement, P., Meester, A., El Allaf, D., Janssens, L., Marcovitch, O., Muyldermans, L., Roosen, J., Soeur, F., Lierde, J., Vrolix, M., Leaes, P., Carvalho, A. C., Schramm, E. C., Mora, R. D., Amino, J. D., Dutra, O., Manenti, E. R. F., Gun, C., Saraiva, J. F. K., Hayashi, E. K., Lichter, A., Lima, A., Marin-Neto, J. A., Teixeira, S. P. M., Abrantes, J. A. M., Baracioli, L. M., Nicolau, J. C., Maia, L. N., Jaeger, C. P., Esteves, J. P., Rabelo, A., Ramos, R. F., Reis, G., Rossi, P., Dos Santos, F. R., Teixeira, M. S., Silveira, D. S., Lemos, Mabt, Timerman, A., Greque, G. V., Vaz, R., Bhargava, R., Brons, S., Colclough, M., Constance, C., Costi, P., Dacyk, A., Davies, T., Diodati, J., Dupuis, R., Elliott, H., Fell, D. A., Fung, A. Y., Gladstone, P. J. S., Gosselin, G., Grondin, F., Huynh, T., Janzen, I., Kalaparambath, T., Kornder, J., Kouz, S., Kuritzky, R., Labelle-Stimac, S., Lamothe, M., Lauzon, C., Lemay, M., Ma, P., Maccallum, G. C., Mccallum, A., Mitchell, D., Montigny, M., Nguyen, N., Pearce, M., Pistawka, K. J., Rebane, T., Roy, M., Senaratne, M., Smith, J., Stimac, J., Traboulsi, M., Vizel, S., Weeks, A., Zadra, R., Zimmerman, R. H., Alcaino, M. E., Castro, P., Chen, J., Chen, J. L., Fan, W., Ge, J., Hu, D., Huang, J., Jingxuan, G., Ke, Y., Ma, H., Wu, Y., Yingxian, S., Yu, B., Zhu, W., Bakula, M., Bergovec, M., Lukin, A., Milicevic, G., Padovan, M., Raguz, M., Aschermann, M., Belohlavek, J., Bocek, P., Branny, M., Budesinsky, T., Groch, L., Holm, F., Jansky, P., Jelinek, P., Jirka, V., Kaislerova, M., Konecny, P., Lisa, L., Maly, M., Marcinek, G., Oscipovsky, M., Stumar, J., Vacha, M., Nielsen, T., Vigholt, E., Laanmets, P., Soopold, U., Voitk, J., Naveri, H., Niemela, M., Peuhkurinen, K., Tuomainen, P., Ylitalo, A., Py, A., Amat, G., Bessede, G., Boschat, J., Carrie, D., Charbonnier, B., Coliet, J. P., Dambrine, P., Dubois-Rande, J. L., Ferrari, E., Fouche, R., Grollier, G., Jaboureck, O., Ketelers, R., Khalife, K., Leroy, F., Lognone, T., Macquin-Mavier, I., Montalescot, G., Pacouret, G., Poulard, J. E., Puel, J., Richard, M., Schiele, F., Bischoff, K. O., Buerke, M., Buerke, U., Dominick, K., Drexler, H., Feiler, A., Guelker, H., Haltern, G., Katus, H. A., Klauss, V., Klutmann, M., Koeth, O., Meinhardt, G., Muenzel, T. M., Nitschke, T., Offterdinger, M., Rieber, J., Schieffer, B., Stangl, K., Stangl, V., Vom Dahl, J., Witzenbichler, B., Zeymer, U., Alexopoulos, D., Blassopoulou, N., Christon, A., Fotiadis, I., Foussas, S., Grapsas, N., Moschos, N., Papasteriadis, E., Symeonidis, D., Tyrologos, A., Leung, W. S., Li, S. K., Arabadzisz, H., Csikazs, J., Dancs, T., Davidovits, Z., Edes, I., Farkas, E., Herczeg, B., Janos, S., Janosi, A., Kadar, A., Kis, E., Kristof, E., Lupkovics, G., Mark, L., Nagy, A., Nagy, L., Poor, F., Regos, L., Sebo, J., Tomcsanyi, J., Toth, K., Bharani, A., Chidambaram, N., Haridas, K. K., Jain, A., Jain, P. R. K., Jaison, T. M., Kerkar, P. G., Naik, S., Nambiar, A., Panwar, R. B., Parikh, K., Puri, V. K., Rajesh, T., Ramesh, M., Singh, B., Thanikachalam, S., Tongia, R. K., Varma, S., Barbiero, M., Bardelli, G., Bernardi, D., Bolognese, L., Capponi, L., Ferrari, G., Fanelli, R., Frediani, L., Galli, M., Izzo, A., Lombardi, A., Maresta, A., Martinoni, A., Melloni, C., Meneghetti, P., Mennuni, M., Moretti, L., Orlandi, M., Pancaldi, L. G., Petronzelli, S., Piovaccari, G., Salvioni, A., Severini, D., Terrosu, P., Zanini, R., Erglis, A., Kalnins, U., Verboenko, J., Zakke, I., Kugiene, R., Zaliunas, R., Bin Othman, A., Chee, K. H., Hian, S. K., Gutierrez, A. C., Diaz, A. C., Garcia-Castillo, A., Guerrero, M. C., Morales, C. L., Ramos-Lopez, G., Baldew, S. C., Basart, D. C. G., Clappers, N., Daniels, M. C. G., Weerd, G. J., Den Hartog, F. R., Hendriks, Ihgm, Herrman, J. P. R., Kofflard, M., Krasznai, K., Michels, H. R., Stoel, I., Ten Berg, J. M., Umans, Vawn, Beek, G. J., Daele, Merm, Den Berg, B. J., Hessen, M. W. J., Kalmthout, P. M., Rossum, P., Verheugt, F. W. A., Viergever, E. P., Withagen, Ajam, Achremczyk, P., Arasimowicz, P., Baranowska, T., Biegayto, J., Bronisz, M., Buszman, P., Dalkowski, M., Dluzniewski, M., Gessek, J., Goch, J. H., Janik, K., Janion, M., Kawecki, D., Kleinrok, A., Komorowski, P., Krasowski, W., Krauze-Wielicka, M., Malinowski, S., Nowak, T., Nowakowski, P., Ogorek, M., Piepiorka, M., Pluta, W., Puzio, E., Puzniak, M., Rekosz, J., Rybka, P., Sendrowski, D., Siminiak, T., Skura, M., Stopinski, M., Szetemej, R., Szolkiewicz, M., Szpajer, M., Trusz-Gluza, M., Waszyrowski, T., Wita, K., Wodniecki, J., Wojewoda, P., Zambrzycki, J., Zielinski, Z., Cardoso, P., Carrageta, D. M., Ferreira, D., Gomes, M. V., Santos, L., Arkhipov, M., Belousov, Y., Charchoglyan, R., Gordeev, I. G., Gratsiansky, N. A., Grinshtein, Y., Khrustalev, O., Kokorin, V. A., Komarov, A., Kozulin, V., Minushkina, L. O., Panchenko, E., Panov, A., Petrik, E. S., Shakhnovich, R. M., Shalaev, S. V., Sukhinina, T. S., Trifonov, I. R., Zateyshchikov, D. A., Khoo, B. C. H., Tan, H. C., Tan, R. S., Hricak, V., Motovska, Z., Poliacik, P., Kanic, V., Kovacic, D., Kranjec, I., Voga, G., Bayat, J., Essop, M. R., Maritz, F., Marx, J. D., Ntsekhe, M., Pretorius, M. P., Ranjith, N., Theron, H., Chae, I. H., Chae, S. C., Choe, K. H., Chung, N. S., Jeong, M. H., Kim, C. J., Kim, H. S., Kim, W., Rhim, C. Y., Shin, E. K., Shin, G. J., Alameda, M., Alonso-Orcajo, N., Bethencourt, A., Calvo, F., Avellaneda, J. L. C., Delgado, V., Diaz-Castro, O., Esplugas, E., Faus, R., Antonio Fernandez-Ortiz, Frutos, A., Goirena, P., Iglesias, F. C., Llorian, A. R., Macaya, C., Mancisidor, X., Melgares, R., Pascual, C., Ruiz-Nodar, J. M., Simon, J. M., Agewall, S., Ahlstrom, P., Ali, M., Andersson, L., Bandh, S., Digerfeldt, C., Ericsson, H., Forsgren, M., Jabro, J., Janzon, M., Joborn, H., Johnston, N., Karlsson, J. E., Larsson, L. E., Linderfalk, C., Lonnberg, I., Mooe, T., Oldgren, J., Pihl, E., Risenfors, M., Sjolund, E., Soderberg, I., Stjerna, A., Svennberg, L., Wodlin, P., Pagnamenta, A., Pieper, M., Rossi, M. G., Weber, K., Peng, M. C., Cheng, J. J., Chiang, F. T., Kuo, C. T., Tseng, C. D., Andreyeshcheva, I., Dzyak, G. V., Fedtchouk, L., Gontar, A., Karpenko, O., Kononenko, L., Koval, E. A., Kovalsky, I., Kraitz, I., Netiazhenko, V., Polyvoda, S., Prokopenko, Y., Prudkiy, I., Rudenko, L., Serediuk, N., Zolotaykina, V., Adgey, J., Ahsan, A., Brack, M., Bridges, A. B., Burton, J., Findlay, I., Fluck, D. S., Radford, L., Robson, R. H., Senior, R., Starkey, I. R., Alexander, J., Baber, Z., Campbell, M., Caputo, R., Chandna, H., Chandrashekhar, Y., Chu, A., Deraad, R. E., Druken, B., Goyal, A., Holly, D., Kemp, A., Kotlaba, D., Levine, M. J., Miller, G. P., Nygaard, T., Parikh, D. K., Ramos, C., Rivera, E., Rodriguez, R., Sangani, B., Walder, J. S., and Oasis

17. Time matters: adenosine testing immediately after pulmonary vein isolation does not substitute a waiting period.

Author

Teunissen C, Clappers N, Kassenberg W, Hassink RJ, van der Heijden JF, and Loh P

Subjects
Action Potentials, Aged, Atrial Fibrillation diagnosis, Atrial Fibrillation physiopathology, Female, Heart Rate, Humans, Male, Middle Aged, Predictive Value of Tests, Prospective Studies, Pulmonary Veins physiopathology, Recurrence, Reproducibility of Results, Risk Factors, Time Factors, Treatment Outcome, Adenosine administration & dosage, Atrial Fibrillation surgery, Catheter Ablation adverse effects, Electrophysiologic Techniques, Cardiac, Pulmonary Veins surgery
Abstract

Aims: Adenosine testing can reveal dormant pulmonary vein (PV) conduction after PV antrum isolation (PVAI). However, the optimal timing for adenosine administration is unknown. We hypothesized that adenosine testing immediately after PVAI reliably reveals PV reconnection and thereby eliminates the need for an observation period., Methods and Results: Fifty patients underwent PVAI. Immediately after isolation of a PV pair, adenosine was administered. Both PV pairs were separately tested. If adenosine restored PV conduction, PVs were re-isolated. During a ≥30 min observation period after immediate adenosine-guided isolation, spontaneous reconnection was assessed and reconnected PVs were re-isolated. After the observation period, adenosine testing was repeated. Immediate adenosine testing revealed dormant conduction in 10.4% of the left PVs and 16.3% of the right PVs. All PVs were successfully re-isolated. During a mean observation period of 36 ± 10 min, spontaneous reconnection occurred in 8.2% of the left and 16.3% of the right PVs. None of these PVs had shown reconnection during immediate testing. Late adenosine testing revealed dormant conduction in 12.5% of the left and 16.3% of the right PVs. In patients without reconnection during immediate adenosine testing, 14.6% of the left PVs and 30.6% of the right PVs showed either spontaneous reconnection or restored PV conduction during late adenosine testing., Conclusion: Adenosine testing immediately after PVAI does not reliably exclude later spontaneous or adenosine-induced PV reconnection. Adenosine testing should be performed after an appropriate observation period to reduce risk of PV reconnection., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2016. For permissions please email: journals.permissions@oup.com.)

Published
2017
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18. Incidence of Pulmonary Vein Stenosis After Radiofrequency Catheter Ablation of Atrial Fibrillation.

Author

Teunissen C, Velthuis BK, Hassink RJ, van der Heijden JF, Vonken EPA, Clappers N, Doevendans PA, and Loh P

Subjects
Computed Tomography Angiography, Female, Humans, Incidence, Male, Middle Aged, Pulmonary Veins diagnostic imaging, Pulmonary Veins surgery, Stenosis, Pulmonary Vein diagnostic imaging, Stenosis, Pulmonary Vein etiology, Atrial Fibrillation surgery, Radiofrequency Ablation adverse effects, Stenosis, Pulmonary Vein epidemiology
Abstract

Objectives: This study aimed to determine incidence of pulmonary vein stenosis (PVS) and evaluate PVS-related symptoms., Background: The real-life incidence of PVS after radiofrequency catheter ablation (RFCA) of atrial fibrillation (AF) is unknown., Methods: All patients who underwent RFCA of AF from 2005 to 2016 with routine pre- and post-ablation screening by magnetic resonance imaging or computed tomography were included. Primary ablation strategy was PV antrum isolation alone in all patients. PVS, defined as a significant reduction in the superoinferior or anteroposterior PV diameter, was classified as mild (30% to 50%), moderate (50% to 70%), or severe (>70%)., Results: Sufficient quality imaging of the PV anatomy before ablation and during follow-up (mean 6 ± 4 months) was performed in 976 patients (76.4% men, 59.1% paroxysmal AF). Of these patients, 306 (31.4%) showed mild stenosis, 42 (4.3%) revealed moderate stenosis, and 7 (0.7%) had a severe stenosis in at least 1 PV. Incidence of PVS fluctuated over the past decade. All severe PVS cases were likely caused by ablations being performed inside the PVs. Only 1 (0.1%) patient reported PVS-related symptoms of severe dyspnea during follow-up. Computed tomography revealed a subtotal occlusion of the left inferior PV and a severe stenosis of the left superior PV, requiring stenting., Conclusions: Although mild PVS was frequently observed after RFCA in this large cohort, incidence of severe PVS was <1% and incidence of symptomatic PVS necessitating intervention was negligible. Based on these findings, it seems appropriate to only screen for PVS in patients with suggestive symptoms., (Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Published
2017
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19. Assessment of plasma aminothiol levels and the association with recurrent atherothrombotic events in patients hospitalized for an acute coronary syndrome: a prospective study.

Author

Focks JJ, van Schaik A, Clappers N, van Dijk EG, van Oijen MG, Verheugt FW, and Peters WH

Subjects
Aged, Coronary Thrombosis complications, Coronary Thrombosis diagnosis, Female, Humans, Male, Middle Aged, Prognosis, Prospective Studies, Recurrence, Acute Coronary Syndrome complications, Acute Coronary Syndrome therapy, Coronary Thrombosis blood, Cysteine blood, Glutathione blood, Homocysteine blood, Hospitalization
Abstract

Background: The aminothiols homocysteine and, to a lesser extent, cysteine have been associated with adverse cardiovascular outcome, whereas glutathione, as an antioxidant, may protect against atherosclerosis and thrombosis. Potentially, the combined assessment of these aminothiols may provide a more accurate association with future cardiovascular outcome. We evaluated the association between recurrent atherothrombotic events and the concentration of total plasma cysteine, homocysteine, and glutathione and their combination., Methods: Respective aminothiols were measured by high-performance liquid chromatography in blood plasma of consecutive first-day survivors admitted for an acute coronary syndrome between April 2002 and January 2004. The combined score was calculated using the combination of the individual aminothiols. The end point was the composite of cardiovascular death, myocardial infarction, and/or stroke., Results: A cohort of 375 consecutive patients (median age 66 years, 66% male) were followed for a median duration of 2.7 years. The end point occurred in 82 patients (22%). In univariate analyses, all aminothiols were significantly associated with the composite end point. After correction for possible confounders, only cysteine and glutathione remained significantly associated. The strongest association with the end point was observed for the combined score (adjusted hazard ratio, 1.40 per standard deviation increase; p=0.005)., Conclusions: Although homocysteine is generally considered the aminothiol of interest with respect to cardiovascular disease, in our prospective study, only cysteine and glutathione appeared independently associated with recurrent atherothrombotic events. Moreover, we showed that an imbalance in the combination of aminothiols could be of more importance than investigating the individual metabolites.

Published
2013
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20. Prognostic value of free plasma homocysteine levels in patients hospitalized with acute coronary syndrome.

Author

van Oijen MG, Claessen BE, Clappers N, van Schaik A, Laheij RJ, Jansen JB, Peters WH, and Verheugt FW

Subjects
Aged, Chromatography, High Pressure Liquid, Female, Hospitalization, Humans, Male, Middle Aged, Multivariate Analysis, Myocardial Infarction blood, Odds Ratio, Predictive Value of Tests, Prognosis, Proportional Hazards Models, Prospective Studies, Risk Factors, Stroke blood, Acute Coronary Syndrome blood, Homocysteine blood
Abstract

Elevated total plasma homocysteine is an established risk factor for cardiovascular disease. Experimental evidence suggests that non-protein-bound free homocysteine is particularly hazardous to the vascular endothelium. This study evaluates the predictive role of free plasma homocysteine levels on cardiovascular endpoints in patients with acute coronary syndrome (ACS). In a cohort of 379 hospitalized patients with a diagnosis of myocardial infarction or unstable angina pectoris, total and free plasma homocysteine levels were measured by high performance liquid chromatography. The patients were followed for a median 2.7 years. The primary endpoint was a composite of cardiovascular death, myocardial infarction and stroke during follow-up. Stepwise Cox regression was used for multivariate analysis. Primary outcome events occurred in 82 patients (22%) with a median time to event of 6 months. The unadjusted hazard ratio for a free homocysteine level >4.11 micromol/L was 2.16 (95% confidence intervals [CI] 1.36 to 3.42) compared with the 4 lower quintiles. After adjusting for the covariates the hazard ratio was 2.25 (95% CI 1.41 to 3.58, p = 0.01). Compared with the lower 4 quintiles, patients with a total homocysteine level >22.4 micromol/L had a 2.09-fold higher risk (95% CI 1.31 to 3.35) for an event during follow-up. Adjusted for age, discharge diagnosis, serum creatinine, history of atherothrombotic events, and diabetes mellitus, the adjusted hazard ratio was 1.37 (95% CI 0.83 to 2.25, p = 0.22). In conclusion, plasma free homocysteine levels >4.11 micromol/L are a significant and independent risk factor for recurrent cardiovascular events in patients hospitalized for ACS, although total plasma homocysteine levels have no predictive value.

Published
2008
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