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Your search keyword '"Zwinderman, A. H."' showing total 37 results
Start Over Author "Zwinderman, A. H." Journal journal of the american college of cardiology
37 results on '"Zwinderman, A. H."'

1. Identifying Pathophysiological Mechanisms in Heart Failure With Reduced Versus Preserved Ejection Fraction

Author

Tromp, Jasper, Westenbrink, B. Daan, Ouwerkerk, Wouter, van Veldhuisen, Dirk J., Samani, Nilesh J., Ponikowski, Piotr, Metra, Marco, Anker, Stefan D., Cleland, John G., Dickstein, Kenneth, Filippatos, Gerasimos, van der Harst, Pim, Lang, Chim C., Ng, Leong L., Zannad, Faiez, Zwinderman, Aelko H., Hillege, Hans L., van der Meer, Peter, and Voors, Adriaan A.

Published
2018
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2. Biomarker-Guided Versus Guideline-Based Treatment of Patients With Heart Failure: Results From BIOSTAT-CHF

Author

Ouwerkerk, Wouter, Zwinderman, Aeilko H., Ng, Leong L., Demissei, Biniyam, Hillege, Hans L., Zannad, Faiez, van Veldhuisen, Dirk J., Samani, Nilesh J., Ponikowski, Piotr, Metra, Marco, ter Maaten, Jozine M., Lang, Chim C., van der Harst, Pim, Filippatos, Gerasimos, Dickstein, Kenneth, Cleland, John G., Anker, Stefan D., and Voors, Adriaan A.

Published
2018
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6. The cholesteryl ester transfer protein (CETP) TaqIB polymorphism in the cholesterol and recurrent events study: no interaction with the response to pravastatin therapy and no effects on cardiovascular outcome: A prospective analysis of the CETP TaqIB polymorphism on cardiovascular outcome and interaction with cholesterol-lowering therapy

Author

de Grooth, Greetje J., Zerba, Kim E., Huang, Shu-Pang, Tsuchihashi, Zenta, Kirchgessner, Todd, Belder, René, Vishnupad, Priya, Hu, Beihong, Klerkx, Anke H.E.M., Zwinderman, Aeilko H., Jukema, J.Wouter, Sacks, Frank M., Kastelein, John J.P., and Kuivenhoven, Jan Albert

Published
2004
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7. The PCSK9-LDL Receptor Axis and Outcomes in Heart Failure

Author

Bayes-Genis, Antoni, primary, Núñez, Julio, additional, Zannad, Faiez, additional, Ferreira, João Pedro, additional, Anker, Stefan D., additional, Cleland, John G., additional, Dickstein, Kenneth, additional, Filippatos, Gerasimos, additional, Lang, Chim C., additional, Ng, Leong L., additional, Ponikowski, Piotr, additional, Samani, Nilesh J., additional, van Veldhuisen, Dirk J., additional, Zwinderman, Aeilko H., additional, Metra, Marco, additional, Lupón, Josep, additional, and Voors, Adriaan A., additional

Published
2017
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9. Lifetime Risk of Pulmonary Hypertension for All Patients After Shunt Closure

Author

van Riel, Annelieke C.M.J., primary, Blok, Ilja M., additional, Zwinderman, Aeilko H., additional, Wajon, Elly M.C.J., additional, Sadee, Arthur S.J.M., additional, Bakker-de Boo, Mirjam, additional, van Dijk, Arie P.J., additional, Hoendermis, Elke S., additional, Riezebos, Robert K., additional, Mulder, Barbara J.M., additional, and Bouma, Berto J., additional

Published
2015
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11. Risk Factors for Malignant Ventricular Arrhythmias in Lamin A/C Mutation Carriers

Author

van Rijsingen, Ingrid A.W., primary, Arbustini, Eloisa, additional, Elliott, Perry M., additional, Mogensen, Jens, additional, Hermans-van Ast, Johanna F., additional, van der Kooi, Anneke J., additional, van Tintelen, J. Peter, additional, van den Berg, Maarten P., additional, Pilotto, Andrea, additional, Pasotti, Michele, additional, Jenkins, Sharon, additional, Rowland, Camilla, additional, Aslam, Uzma, additional, Wilde, Arthur A.M., additional, Perrot, Andreas, additional, Pankuweit, Sabine, additional, Zwinderman, Aeilko H., additional, Charron, Philippe, additional, and Pinto, Yigal M., additional

Published
2012
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12. CRITICAL APPRAISAL OF THE REVISED MARFAN NOSOLOGY IN CARDIOLOGICAL PRACTICE

Author

De Witte, Piet, primary, Radonic, Teodora, additional, Groenink, Maarten, additional, de Bruin -Bon, Rianne A., additional, Timmermans, Janneke, additional, Scholte, Arthur J., additional, van den Berg, Maarten P., additional, Baars, Marieke J., additional, van Tintelen, Peter J., additional, Kempers, Marlies, additional, Zwinderman, Aeilko H., additional, and Mulder, Barbara J., additional

Published
2011
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15. Lipoprotein Lipase Gene Polymorphisms and the Risk of Target Vessel Revascularization After Percutaneous Coronary Intervention

Author

Monraats, Pascalle S., primary, Rana, Jamal S., additional, Nierman, Melchior C., additional, Pires, Nuno M.M., additional, Zwinderman, Aeilko H., additional, Kastelein, John J.P., additional, Kuivenhoven, Jan Albert, additional, de Maat, Moniek P.M., additional, Rittersma, Saskia Z.H., additional, Schepers, Abbey, additional, Doevendans, Pieter A.F., additional, de Winter, Robbert J., additional, Tio, René A., additional, Frants, Rune R., additional, Quax, Paul H.A., additional, van Der Laarse, Arnoud, additional, van Der Wall, Ernst E., additional, and Jukema, J. Wouter, additional

Published
2005
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20. B-Mode Ultrasound Assessment of Pravastatin Treatment Effect on Carotid and Femoral Artery Walls and Its Correlations With Coronary Arteriographic Findings: A Report of the Regression Growth Evaluation Statin Study (REGRESS)

Author

de Groot, Eric, primary, Jukema, J.Wouter, additional, Montauban van Swijndregt, Alexander D., additional, Zwinderman, Aeilko H., additional, Ackerstaff, Rob G.A., additional, van der Steen, Anton F.W., additional, Bom, Nicolaas, additional, Lie, Kong I., additional, and Bruschke, Albert V.G., additional

Published
1998
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21. Modulation of Lipoprotein(a) Atherogenicity by High Density Lipoprotein Cholesterol Levels in Middle-Aged Men With Symptomatic Coronary Artery Disease and Normal to Moderately Elevated Serum Cholesterol fn1fn1This study was supported by Bristol-Myers Squibb Co., Princeton, New Jersey (REGRESS main study) and by Grant 94.032 from the Dutch Heart Foundation, Den Haag, The Netherlands [lipoprotein(a) substudy].

Author

Cobbaert, Christa, primary, Jukema, J.Wouter, additional, Zwinderman, Aeilko H., additional, Withagen, Adrie J.A.M., additional, Lindemans, Jan, additional, and Bruschke, Albert V.G., additional

Published
1997
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27. Paraoxonase Variants Relate to 10-Year Risk in Coronary Artery Disease Impact of a High-Density Lipoprotein–Bound Antioxidant in Secondary Prevention

Author

Regieli, Jakub J., Jukema, J. Wouter, Doevendans, Pieter A., Zwinderman, Aeilko H., Kastelein, John J., Grobbee, Diederick E., van der Graaf, Yolanda, Amsterdam Public Health, Epidemiology and Data Science, Amsterdam Cardiovascular Sciences, and Vascular Medicine

Subjects
lipoproteins, epidemiology, prognosis, genes, ischemic heart disease
Abstract

ObjectivesWe investigated the effects of paraoxonase (PON)-1 variants on long-term clinical outcome in patients with coronary artery disease (CAD).BackgroundPON-1 is a potential therapeutic target to further reduce cardiovascular risk because it is a detoxifying esterase with antioxidant properties. The PON-1 knockout models result in higher susceptibility to atherosclerosis, and PON activity contributes to cardiovascular risk in humans. Human gene variants determine PON activity; however, the impact of these variants on recurrent cardiovascular events in vascular disease is as of yet unknown.MethodsWe conducted a 10-year follow-up study of 793 CAD patients in the REGRESS (REgression GRowth Evaluation Statin Study) trial cohort, using nationwide registries. Genotypes were obtained of 2 PON-1 isotypes (L55M, rs854560, and Q192R, rs662), which were previously associated with PON activity. Absolute and relative risks by genotype were estimated using Kaplan-Meier and proportional hazards analyses.ResultsCarriership of the PON-1 glutamine isotype at codon 192 and methionine at codon 55 was associated with a higher risk of death due to ischemic heart disease. Hazard ratios per allele copy were 1.71 (95% confidence interval: 1.0 to 2.8, p = 0.03) for the glutamine isotype at codon 192 and 1.56 (95% confidence interval: 1.1 to 2.3, p = 0.03) for methionine at codon 55. Both isotypes had previously been related to lower PON activity. No effect was observed on all-cause mortality.ConclusionsPON-1 gene variants influence the 10-year risk of fatal complications from CAD in male patients, despite no effect on all-cause mortality. These long-term findings confirm functional data on PON-1 activity, emphasize the relevance of this pathway in vascular disease, and enforce its putative role as a target to modify and estimate cardiovascular risk.

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28. The cholesteryl ester transfer protein (CETP) TaqIB polymorphism in the cholesterol and recurrent events study: no interaction with the response to pravastatin therapy and no effects on cardiovascular outcome A prospective analysis of the CETP TaqIB polymorphism on cardiovascular outcome and interaction with cholesterol-lowering therapy

Author

de Grooth, Greetje J., Zerba, Kim E., Huang, Shu-Pang, Tsuchihashi, Zenta, Kirchgessner, Todd, Belder, René, Vishnupad, Priya, Hu, Beihong, Klerkx, Anke H. E. M., Zwinderman, Aeilko H., Jukema, J. Wouter, Sacks, Frank M., Kastelein, John J. P., Kuivenhoven, Jan Albert, Epidemiology and Data Science, Amsterdam Cardiovascular Sciences, Vascular Medicine, and Experimental Vascular Medicine

Subjects
lipids (amino acids, peptides, and proteins)
Abstract

OBJECTIVES On the basis of quantitative coronary angiography data, the cholesteryl ester transfer protein (CETP) TaqIB gene polymorphism has been postulated to predict the progression of coronary atherosclerosis and response to cholesterol-lowering therapy. BACKGROUND Cholesteryl ester transfer protein mediates the exchange of lipids between anti-atherogenic high-density lipoprotein (HDL) and atherogenic apolipoprotein B containing lipoproteins and therefore plays a key role in human lipid metabolism. Hence, CETP gene polymorphisms may alter susceptibility to atherosclerosis. METHODS To investigate the significance of the CETP TaqIB gene polymorphism with respect to clinical end points, we used the Cholesterol And Recurrent Events (CARE) cohort. The CARE study was designed to investigate the effect of five years of pravastatin therapy on coronary events. RESULTS We found that the odds ratios for the primary end point were not significantly different from unity for the three genetic subgroups after five years of placebo treatment. Furthermore, pravastatin induced similar changes in total cholesterol, low-density lipoprotein cholesterol, and HDL cholesterol among TaqIB genotypes, and both nonfatal myocardial infarction and deaths from coronary heart disease were reduced to the same extent in all three genotypes. CONCLUSIONS In the CARE cohort, the CETP TaqIB polymorphism does not predict cardiovascular events or discriminate between those who will or will not benefit from pravastatin treatment. (C) 2004 by the American College of Cardiology Foundation

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29. American College of Cardiology/ European Society of Cardiology international study of angiographic data compression phase II The effects of varying JPEG data compression levels on the quantitative assessment of the degree of stenosis in digital coronary angiography

Author

Tuinenburg, Joan C, Koning, Gerhard, Hekking, Ellen, Zwinderman, Aeilko H, Becker, Tim, Simon, Rüdiger, and Reiber, Johan H.C

Abstract

OBJECTIVESThis report describes whether lossy Joint Photographic Experts Group (JPEG) image compression/decompression has an effect on the quantitative assessment of vessel sizes by state-of-the-art quantitative coronary arteriography (QCA).BACKGROUNDThe Digital Imaging and Communications in Medicine (DICOM) digital exchange standard for angiocardiography prescribes that images must be stored loss free, thereby limiting JPEG compression to a maximum ratio of 2:1. For practical purposes it would be desirable to increase the compression ratio (CR), which would lead to lossy image compression.METHODSA series of 48 obstructed coronary segments were compressed/decompressed at CR 1:1 (uncompressed), 6:1, 10:1 and 16:1 and analyzed blindly and in random order using the QCA-CMS analytical software. Similar catheter and vessel start- and end-points were used within each image quartet, respectively. All measurements were repeated after several weeks using newly selected start- and end-points. Three different sub-analyses were carried out: the intra-observer, fixed inter-compression and variable inter-compression analyses, with increasing potential error sources, respectively.RESULTSThe intra-observer analysis showed significant systematic and random errors in the calibration factor at JPEG CR 10:1. The fixed inter-compression analysis demonstrated systematic errors in the calibration factor and recalculated vessel parameter results at CR 16:1 and for the random errors at CR 10:1 and 16:1. The variable inter-compression analysis presented systematic and random errors in the calibration factor and recalculated parameter results at CR 10:1 and 16:1. Any negative effect at CR 6:1 was found only for the calibration factor of the variable inter-compression analysis, which did not show up in the final vessel measurements.CONCLUSIONSCompression ratios of 10:1 and 16:1 affected the QCA results negatively and therefore should not be used in clinical research studies.

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36. American College of Cardiology/European Society of Cardiolgoy International Study of Angiographic Data Compression Phase II: the effects of varying JPEG data compression levels on the quantitative assessment of the degree of stenosis in digital coronary angiography. Joint Photographic Experts Group.

Author

Tuinenburg JC, Koning G, Hekking E, Zwinderman AH, Becker T, Simon R, and Reiber JH

Subjects
Adult, Aged, Analysis of Variance, Bias, Calibration, Cardiology, Europe, Humans, Middle Aged, Reproducibility of Results, Sensitivity and Specificity, Single-Blind Method, Societies, Medical, United States, Coronary Angiography methods, Coronary Angiography standards, Coronary Disease classification, Coronary Disease diagnostic imaging, Image Processing, Computer-Assisted methods, Image Processing, Computer-Assisted standards, Severity of Illness Index
Abstract

Objectives: This report describes whether lossy Joint Photographic Experts Group (UPEG) image compression/decompression has an effect on the quantitative assessment of vessel sizes by state-of-the-art quantitative coronary arteriography (QCA)., Background: The Digital Imaging and Communications in Medicine (DICOM) digital exchange standard for angiocardiography prescribes that images must be stored loss free, thereby limiting JPEG compression to a maximum ratio of 2:1. For practical purposes it would be desirable to increase the compression ratio (CR), which would lead to lossy image compression., Methods: A series of 48 obstructed coronary segments were compressed/decompressed at CR 1:1 (uncompressed), 6:1, 10:1 and 16:1 and analyzed blindly and in random order using the QCA-CMS analytical software. Similar catheter and vessel start- and end-points were used within each image quartet, respectively. All measurements were repeated after several weeks using newly selected start- and end-points. Three different sub-analyses were carried out: the intra-observer, fixed inter-compression and variable inter-compression analyses, with increasing potential error sources, respectively., Results: The intra-observer analysis showed significant systematic and random errors in the calibration factor at JPEG CR 10:1. The fixed inter-compression analysis demonstrated systematic errors in the calibration factor and recalculated vessel parameter results at CR 16:1 and for the random errors at CR 10:1 and 16:1. The variable inter-compression analysis presented systematic and random errors in the calibration factor and recalculated parameter results at CR 10:1 and 16:1. Any negative effect at CR 6:1 was found only for the calibration factor of the variable inter-compression analysis, which did not show up in the final vessel measurements., Conclusions: Compression ratios of 10:1 and 16:1 affected the QCA results negatively and therefore should not be used in clinical research studies.

Published
2000
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37. Modulation of lipoprotein(a) atherogenicity by high density lipoprotein cholesterol levels in middle-aged men with symptomatic coronary artery disease and normal to moderately elevated serum cholesterol. Regression Growth Evaluation Statin Study (REGRESS) Study Group.

Author

Cobbaert C, Jukema JW, Zwinderman AH, Withagen AJ, Lindemans J, and Bruschke AV

Subjects
Anticholesteremic Agents therapeutic use, Coronary Angiography, Coronary Artery Disease complications, Disease Progression, Double-Blind Method, Humans, Hypercholesterolemia complications, Hypercholesterolemia drug therapy, Male, Middle Aged, Multivariate Analysis, Pravastatin therapeutic use, Prospective Studies, Reference Values, Cholesterol blood, Cholesterol, HDL blood, Coronary Artery Disease blood, Lipoprotein(a) blood
Abstract

Objectives: This study sought to examine whether lipoprotein(a) levels predict coronary artery lumen changes in patients with symptomatic coronary artery disease (CAD) and normal to moderate hypercholesterolemia., Background: Recent conflicting reports have confirmed or refuted the association of lipoprotein(a) with clinical events or angiographically verified disease progression., Methods: The association between serum lipoprotein(a) and changes in coronary artery lumen was studied in 704 men entered into the Regression Growth Evaluation Statin Study (REGRESS), a double-blind, placebo-controlled, quantitative angiographic study that assessed the effect of 2 years of pravastatin treatment. The primary end points were changes in average mean segment diameter (MSD) and average minimal obstruction diameter (MOD). Pravastatin- and placebo-treated patients were classified as having progressing, regressing or stable CAD, and median lipoprotein(a) concentrations were compared. Bivariate and multivariate regression analyses were performed in the overall patient group and in high risk subgroups., Results: Pravastatin treatment did not affect serum apolipoprotein(a) levels. Median in-trial (sampled at 24 months) apolipoprotein(a) levels for regressing, stable and progressing CAD were, respectively, 130, 162 and 251 U/liter in placebo-treated patients and 143, 224 and 306 U/liter in pravastatin-treated patients. Predictors of MSD and MOD changes were baseline MSD and MOD, in-trial apolipoprotein(a), in-trial high density lipoprotein (HDL) cholesterol and baseline use of long-acting nitrates. The multivariate models predicted 14% of MSD changes and 12% of MOD changes; apolipoprotein(a) predicted only 2.6% and 4.8%, respectively. However, in patients with in-trial HDL cholesterol levels <0.7 mmol/liter, apolipoprotein(a) predicted up to 37% of the arteriographic changes., Conclusions: Serum lipoprotein(a) levels predict coronary artery lumen changes in normal to moderately hypercholesterolemic white men with CAD; its atherogenicity is marked in the presence of concomitant hypoalphalipoproteinemia.

Published
1997
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