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115 results on '"Wiesfeld, Ans C.P."'

1. Linking the heart and the brain: Neurodevelopmental disorders in patients with catecholaminergic polymorphic ventricular tachycardia

Author

Lieve, Krystien V.V., Verhagen, Judith M.A., Wei, Jinhong, Bos, J. Martijn, van der Werf, Christian, Rosés i Noguer, Ferran, Mancini, Grazia M.S., Guo, Wenting, Wang, Ruiwu, van den Heuvel, Freek, Frohn-Mulder, Ingrid M.E., Shimizu, Wataru, Nogami, Akihiko, Horigome, Hitoshi, Roberts, Jason D., Leenhardt, Antoine, Crijns, Harry J.G., Blank, Andreas C., Aiba, Takeshi, Wiesfeld, Ans C.P., Blom, Nico A., Sumitomo, Naokata, Till, Jan, Ackerman, Michael J., Chen, S.R. Wayne, van de Laar, Ingrid M.B.H., and Wilde, Arthur A.M.

Published
2019
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2. A randomized controlled trial of eplerenone in asymptomatic phospholamban p.Arg14del carriers

Author

de Brouwer, Remco, te Rijdt, Wouter P., Hoorntje, Edgar T., Amin, Ahmad, Asselbergs, Folkert W., Cox, Moniek G.P.J., van der Heijden, Jeroen F., Hillege, Hans, Karper, Jacco C., Mahmoud, Belend, van der Meer, Peter, Oomen, Anton, te Riele, Anneline S.J.M., Silljé, Herman H.W., Tan, Hanno L., van Tintelen, Jan Peter, van Veldhuisen, Dirk J., Westenbrink, Berend Daan, Wiesfeld, Ans C.P., Willems, Tineke P., van der Zwaag, Paul A., Wilde, Arthur A.M., de Boer, Rudolf A., van den Berg, Maarten P., de Brouwer, Remco, te Rijdt, Wouter P., Hoorntje, Edgar T., Amin, Ahmad, Asselbergs, Folkert W., Cox, Moniek G.P.J., van der Heijden, Jeroen F., Hillege, Hans, Karper, Jacco C., Mahmoud, Belend, van der Meer, Peter, Oomen, Anton, te Riele, Anneline S.J.M., Silljé, Herman H.W., Tan, Hanno L., van Tintelen, Jan Peter, van Veldhuisen, Dirk J., Westenbrink, Berend Daan, Wiesfeld, Ans C.P., Willems, Tineke P., van der Zwaag, Paul A., Wilde, Arthur A.M., de Boer, Rudolf A., and van den Berg, Maarten P.

Abstract

Phospholamban (PLN; p.Arg14del) cardiomyopathy is an inherited disease caused by the pathogenic p.Arg14del variant in the PLN gene. Clinically, it is characterized by malignant ventricular arrhythmias and progressive heart failure.1,2 Cardiac fibrotic tissue remodelling occurs early on in PLN p.Arg14del carriers.3,4 Eplerenone was deemed a treatment candidate because of its beneficial effects on ventricular remodelling and antifibrotic properties.5,6 We conducted the multicentre randomized trial ‘intervention in PHOspholamban RElated CArdiomyopathy STudy’ (i-PHORECAST) to assess whether treatment with eplerenone of asymptomatic PLN p.Arg14del carriers attenuates disease onset and progression.

Published
2023

3. A randomized controlled trial of eplerenone in asymptomatic phospholamban p.Arg14del carriers

Author

Cardiologie, Team Medisch, Team Onderzoek, Circulatory Health, Onderzoek Device, Genetica, Genetica Groep Van Tintelen, Child Health, de Brouwer, Remco, te Rijdt, Wouter P., Hoorntje, Edgar T., Amin, Ahmad, Asselbergs, Folkert W., Cox, Moniek G.P.J., van der Heijden, Jeroen F., Hillege, Hans, Karper, Jacco C., Mahmoud, Belend, van der Meer, Peter, Oomen, Anton, te Riele, Anneline S.J.M., Silljé, Herman H.W., Tan, Hanno L., van Tintelen, Jan Peter, van Veldhuisen, Dirk J., Westenbrink, Berend Daan, Wiesfeld, Ans C.P., Willems, Tineke P., van der Zwaag, Paul A., Wilde, Arthur A.M., de Boer, Rudolf A., van den Berg, Maarten P., Cardiologie, Team Medisch, Team Onderzoek, Circulatory Health, Onderzoek Device, Genetica, Genetica Groep Van Tintelen, Child Health, de Brouwer, Remco, te Rijdt, Wouter P., Hoorntje, Edgar T., Amin, Ahmad, Asselbergs, Folkert W., Cox, Moniek G.P.J., van der Heijden, Jeroen F., Hillege, Hans, Karper, Jacco C., Mahmoud, Belend, van der Meer, Peter, Oomen, Anton, te Riele, Anneline S.J.M., Silljé, Herman H.W., Tan, Hanno L., van Tintelen, Jan Peter, van Veldhuisen, Dirk J., Westenbrink, Berend Daan, Wiesfeld, Ans C.P., Willems, Tineke P., van der Zwaag, Paul A., Wilde, Arthur A.M., de Boer, Rudolf A., and van den Berg, Maarten P.

Published
2023

4. Familial Atrial Fibrillation and Standstill

Author

Schoonderwoerd, Bas A., van Tintelen, J. Peter, Wiesfeld, Ans C.P., van Gelder, sabelle C., Gussak, Ihor, editor, Antzelevitch, Charles, editor, Wilde, Arthur A. M., editor, Friedman, Paul A., editor, Ackerman, Michael J., editor, and Shen, Win-Kuang, editor

Published
2008
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5. Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy According to Revised 2010 Task Force Criteria With Inclusion of Non-Desmosomal Phospholamban Mutation Carriers

Author

Groeneweg, Judith A., van der Zwaag, Paul A., Olde Nordkamp, Louise R.A., Bikker, Hennie, Jongbloed, Jan D.H., Jongbloed, Roselie, Wiesfeld, Ans C.P., Cox, Moniek G.P.J., van der Heijden, Jeroen F., Atsma, Douwe E., de Boer, Karin, Doevendans, Pieter A., Vink, Aryan, van Veen, Toon A.B., Dooijes, Dennis, van den Berg, Maarten P., Wilde, Arthur A.M., van Tintelen, J. Peter, and Hauer, Richard N.

Published
2013
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6. Severe cardiac phenotype with right ventricular predominance in a large cohort of patients with a single missense mutation in the DES gene

Author

van Tintelen, J. Peter, Van Gelder, Isabelle C., Asimaki, Angeliki, Suurmeijer, Albert J.H., Wiesfeld, Ans C.P., Jongbloed, Jan D.H., van den Wijngaard, Arthur, Kuks, Jan B.M., van Spaendonck-Zwarts, Karin Y., Notermans, Nicolette, Boven, Ludolf, van den Heuvel, Freek, Veenstra-Knol, Hermine E., Saffitz, Jeffrey E., Hofstra, Robert M.W., and van den Berg, Maarten P.

Published
2009
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7. Continuous vs episodic prophylactic treatment with amiodarone for the prevention of atrial fibrillation: a randomized trial

Author

Ahmed, Sheba, Rienstra, Michiel, Crijns, Harry J.G.M., Links, Thera P., Wiesfeld, Ans C.P., Hillege, Hans L., Bosker, Hans A., Lok, Dirk J.A., Van Gelder, Isabelle C., and Van Veldhuisen, Dirk J.

Subjects
Atrial fibrillation -- Care and treatment, Antibiotics -- Usage, Antibiotics -- Health aspects
Abstract

A study was conducted to compare major events among patients who received continuous against those who received episodic amiodarone treatment in order to prevent atrial fibrillation. Results indicated that outcome of adverse events in both groups were the same but episodic treatment had a higher recurrence of atrial fibrillation and mortality.

Published
2008

8. Sodium channel [beta]1 subunit mutations associated with Brugada syndrome and cardiac conduction disease in humans

Author

Watanabe, Hiroshi, Koopmann, Tamara T., Le Scouarnec, Solena, Yang, Tao, Ingram, Christiana R., Schott, Jean-Jacques, Demolombe, Sophie, Probst, Vincent, Anselme, Frederic, Escande, Denis, Wiesfeld, Ans C.P., Pfeufer, Arne, Kaab, Stefan, Wichmann, H.-Erich, Hasdemir, Can, Aizawa, Yoshifusa, Wilde, Arthur A.M., Roden, Dan M., and Bezzina, Connie R.

Subjects
Arrhythmia -- Risk factors, Arrhythmia -- Diagnosis, Arrhythmia -- Research, Gene mutations -- Complications and side effects, Long QT syndrome -- Risk factors, Long QT syndrome -- Diagnosis, Long QT syndrome -- Research
Abstract

Brugada syndrome is a genetic disease associated with sudden cardiac death that is characterized by ventricular fibrillation and right precordial ST segment elevation on ECG. Loss-of-function mutations in SCN5A, which encodes the predominant cardiac sodium channel [alpha] subunit [Na.sub.V]1.5, can cause Brugada syndrome and cardiac conduction disease. However, SCN5A mutations are not detected in the majority of patients with these syndromes, suggesting that other genes can cause or modify presentation of these disorders. Here, we investigated SCN1B, which encodes the function-modifying sodium channel [beta]1 subunit, in 282 probands with Brugada syndrome and in 44 patients with conduction disease, none of whom had SCN5A mutations. We identified 3 mutations segregating with arrhythmia in 3 kindreds. Two of these mutations were located in a newly described alternately processed transcript, [beta]1B. Both the canonical and alternately processed transcripts were expressed in the human heart and were expressed to a greater degree in Purkinje fibers than in heart muscle, consistent with the clinical presentation of conduction disease. Sodium current was lower when [Na.sub.V]1.5 was coexpressed with mutant [beta]1 or [beta]1B subunits than when it was coexpressed with WT subunits. These findings implicate SCN1B as a disease gene for human arrhythmia susceptibility., Introduction Voltage-gated sodium channels are critical for the generation and propagation of the cardiac action potential, and mutations in SCN5A, the gene encoding the major pore-forming sodium channel [alpha] subunit [...]

Published
2008

9. High yield of LMNA mutations in patients with dilated cardiomyopathy and/or conduction disease referred to cardiogenetics outpatient clinics

Author

van Tintelen, J. Peter, Hofstra, Robert M.W., Katerberg, Hilga, Rossenbacker, Tom, Wiesfeld, Ans C.P., du Marchie Sarvaas, Gideon J., Wilde, Arthur A.M., van Langen, Irene M., Nannenberg, Eline A., van der Kooi, Anneke J., Kraak, Marian, van Gelder, Isabelle C., van Veldhuisen, Dirk Jan, Vos, Yvonne, and van den Berg, Maarten P.

Published
2007
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10. Persistent atrial fibrillation is associated with appropriate shocks and heart failure in patients with left ventricular dysfunction treated with an implantable cardioverter defibrillator

Author

Rienstra, Michiel, Smith, Marcelle D., Nieuwland, Wybe, Tan, Eng S., Wiesfeld, Ans C.P., Anthonio, Rutger L., van den Berg, Maarten P., Van Veldhuisen, Dirk J., and Van Gelder, Isabelle C.

Subjects
Atrial fibrillation -- Development and progression, Atrial fibrillation -- Research, Cardiogenic shock -- Risk factors, Cardiogenic shock -- Research, Heart failure -- Risk factors, Heart failure -- Research, Heart ventricle, Left -- Diseases, Implantable cardioverter-defibrillators -- Patient outcomes, Implantable cardioverter-defibrillators -- Research, Health
Published
2007

14. Phospholamban R14del mutation in patients diagnosed with dilated cardiomyopathy or arrhythmogenic right ventricular cardiomyopathy: evidence supporting the concept of arrhythmogenic cardiomyopathy

Author

van der Zwaag, Paul A., van Rijsingen, Ingrid A.W., Asimaki, Angeliki, Jongbloed, Jan D.H., van Veldhuisen, Dirk J., Wiesfeld, Ans C.P., Cox, Moniek G.P.J., van Lochem, Laura T., de Boer, Rudolf A., Hofstra, Robert M.W., Christiaans, Imke, van Spaendonck-Zwarts, Karin Y., Lekanne dit Deprez, Ronald H., Judge, Daniel P., Calkins, Hugh, Suurmeijer, Albert J.H., Hauer, Richard N.W., Saffitz, Jeffrey E., Wilde, Arthur A.M., van den Berg, Maarten P., and van Tintelen, J. Peter

Published
2012
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27. Low-dose amiodarone for maintenance of sinus rhythm after cardioversion of atrial fibrillation or flutter

Author

Gosselink, A.T. Marcel, Crijns, Harry J.G.M., Gelder, Isabelle C. van, Hillige, Hans, Wiesfeld, Ans C.P., and Lie, Kong I.

Subjects
Amiodarone -- Health aspects, Atrial fibrillation -- Drug therapy
Abstract

The anti-arrhythmic drug amiodarone may be effective in maintaining a normal heartbeat in patients with atrial fibrillation who do not respond to other anti-arrhythmic drugs. Eighty-nine patients with persistent atrial fibrillation took 600 milligrams (mg) of amiodarone for four weeks. Those who did not convert to a normal rhythm were defibrillated, and switched to approximately 200 mg of amiodarone a day. Fifteen patients converted to a normal rhythm on the drug alone and 74 had to be defibrillated. Normal rhythm was restored in 90% of the patients. Only three patients had a severe reaction to the drug and none developed a secondary arrhythmia. One patient died of end-stage heart failure, but this was not attributed to the drug. More than half the patients still had a normal rhythm three years later., Objective.--To study efficacy and safety of low-dose amiodarone for maintenance of sinus rhythm after electrical cardioversion of atrial fibrillation or flutter. Design.--Nonramdomized trial; mean duration of follow-up, 20.7 months. Setting.--Referral center; institutional practice; both hospitalized and ambulatory care. Patients.--Eighty-nine consecutive patients having chronic atrial fibrillation or flutter and eligible for cardioversion. Patients had failed previous treatment aimed at maintaining sinus rhythm. During follow-up one patient was withdrawn because of side effects; all patients were available for follow-up. Intervention.--Before cardioversion, patients received 600 mg of amiodarone daily during a 4-week loading period. After conversion, the daily maintenance dose was 204[+ or -]66 mg (mean[+ or -]SD). Main Outcome Measures.--Arrhythmia recurrence and adverse effects causing drug discontinuation. Results.--During loading, 15 patients (16%) converted, and after electrical cardioconversion, 90% of all patients had sinus rhythm. Actuarially, 53% of these patients were still in sinus rhythm after 3 years. In patients with compromised left ventricular function, 93% maintained sinus rhythm after 6 months. One patient died due to congestive heart failure. Intolerable side effects occurred in one patient. No proarrhythmia was observed. Logistic regression analysis revealed that amiodarone was ineffective in patients with mitral stenosis or chronic arrhythmia. Conclusions.--Low-dose amiodarone is effective for maintaining sinus rhythm in patients with difficult to treat chronic atrial fibrillation or flutter and is associated with a low incidence of serious side effects.

Published
1992

28. Linking the Heart and the Brain: Neurodevelopmental Disorders In Patients With Catecholaminergic Polymorphic Ventricular Tachycardia

Author

Cardiologie patientenzorg, Child Health, Lieve, Krystien V.V., Verhagen, Judith M.A., Wei, Jinhong, Bos, J. Martijn, van der Werf, Christian, Rosés i Noguer, Ferran, Mancini, Grazia M.S., Guo, Wenting, Wang, Ruiwu, van den Heuvel, Freek, Frohn-Mulder, Ingrid M.E., Shimizu, Wataru, Nogami, Akihiko, Horigome, Hitoshi, Roberts, Jason D., Leenhardt, Antoine, Crijns, Harry J.G., Blank, Andreas C., Aiba, Takeshi, Wiesfeld, Ans C.P., Blom, Nico A., Sumitomo, Naokata, Till, Jan, Ackerman, Michael J., Chen, S. R.Wayne, van de Laar, Ingrid M.B.H., Wilde, Arthur A.M., Cardiologie patientenzorg, Child Health, Lieve, Krystien V.V., Verhagen, Judith M.A., Wei, Jinhong, Bos, J. Martijn, van der Werf, Christian, Rosés i Noguer, Ferran, Mancini, Grazia M.S., Guo, Wenting, Wang, Ruiwu, van den Heuvel, Freek, Frohn-Mulder, Ingrid M.E., Shimizu, Wataru, Nogami, Akihiko, Horigome, Hitoshi, Roberts, Jason D., Leenhardt, Antoine, Crijns, Harry J.G., Blank, Andreas C., Aiba, Takeshi, Wiesfeld, Ans C.P., Blom, Nico A., Sumitomo, Naokata, Till, Jan, Ackerman, Michael J., Chen, S. R.Wayne, van de Laar, Ingrid M.B.H., and Wilde, Arthur A.M.

Published
2019

29. Effects of streptokinase during acute myocardial infarction on the signal-averaged electrocardiogram and on the frequency of late arrhythmias

Author

Tobe, Tom J.M., Langen, Cees D.J. de, Crijns, Harry J.G.M., Wiesfeld, Ans C.P., Gilst, Wiek H. van, Faber, Karin G., Lie, Kong I., and Wesseling, Harry

Subjects
Heart attack -- Physiological aspects, Streptokinase -- Physiological aspects, Arrhythmia, Health
Abstract

Although a number of studies have shown that the incidence of late potentials is lower after thrombolytic therapy, it is not known whether this is paralleled by fewer arrhythmic events during long-term follow-up. In patients with first acute myocardial infarction, filtered QRS duration was significantly shorter when treated with streptokinase (95 [+ or -] 11 ms, n = 53) than when treated with conventional therapy (99 [+ or -] 12 ms, n = 77, p

Published
1993

33. Clinical Presentation, Long-Term Follow-Up, and Outcomes of 1001 Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy Patients and Family Members

Author

Groeneweg, Judith A., primary, Bhonsale, Aditya, additional, James, Cynthia A., additional, te Riele, Anneline S., additional, Dooijes, Dennis, additional, Tichnell, Crystal, additional, Murray, Brittney, additional, Wiesfeld, Ans C.P., additional, Sawant, Abhishek C., additional, Kassamali, Bina, additional, Atsma, Douwe E., additional, Volders, Paul G., additional, de Groot, Natasja M., additional, de Boer, Karin, additional, Zimmerman, Stefan L., additional, Kamel, Ihab R., additional, van der Heijden, Jeroen F., additional, Russell, Stuart D., additional, Jan Cramer, Maarten, additional, Tedford, Ryan J., additional, Doevendans, Pieter A., additional, van Veen, Toon A., additional, Tandri, Harikrishna, additional, Wilde, Arthur A., additional, Judge, Daniel P., additional, van Tintelen, J. Peter, additional, Hauer, Richard N., additional, and Calkins, Hugh, additional

Published
2015
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34. Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy

Author

Cox, Moniek G.P.J., primary, van der Zwaag, Paul A., additional, van der Werf, Christian, additional, van der Smagt, Jasper J., additional, Noorman, Maartje, additional, Bhuiyan, Zahir A., additional, Wiesfeld, Ans C.P., additional, Volders, Paul G.A., additional, van Langen, Irene M., additional, Atsma, Douwe E., additional, Dooijes, Dennis, additional, van den Wijngaard, Arthur, additional, Houweling, Arjan C., additional, Jongbloed, Jan D.H., additional, Jordaens, Luc, additional, Cramer, Maarten J., additional, Doevendans, Pieter A., additional, de Bakker, Jacques M.T., additional, Wilde, Arthur A.M., additional, van Tintelen, J. Peter, additional, and Hauer, Richard N.W., additional

Published
2011
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35. Distinguishing Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia–Associated Mutations From Background Genetic Noise

Author

Kapplinger, Jamie D., primary, Landstrom, Andrew P., additional, Salisbury, Benjamin A., additional, Callis, Thomas E., additional, Pollevick, Guido D., additional, Tester, David J., additional, Cox, Moniek G.P.J., additional, Bhuiyan, Zahir, additional, Bikker, Hennie, additional, Wiesfeld, Ans C.P., additional, Hauer, Richard N.W., additional, van Tintelen, J. Peter, additional, Jongbloed, Jan D.H., additional, Calkins, Hugh, additional, Judge, Daniel P., additional, Wilde, Arthur A.M., additional, and Ackerman, Michael J., additional

Published
2011
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36. Genotype-Phenotype Analysis in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy: Follow-Up of a Large Series of Dutch Index-Patients and Family Members

Author

Cox, Moniek G.P.J., primary, van der Zwaag, Paul A., additional, van der Werf, Christian, additional, van der Smagt, Jasper J., additional, Noorman, Maartje, additional, Bhuiyan, Zahir A., additional, Wiesfeld, Ans C.P., additional, Volders, Paul G.A., additional, van Langen, Irene M., additional, Atsma, Douwe E., additional, Dooijes, Dennis, additional, van de Wijngaard, Arthur, additional, Houweling, Arjan C., additional, Jongbloed, Jan D.H., additional, Jordaens, Luc, additional, Cramer, Maarten J., additional, Doevendans, Pieter A., additional, de Bakker, Jacques M.T., additional, Wilde, Arthur A.M., additional, van Tintelen, J. Peter, additional, and Hauer, Richard N.W., additional

Published
2010
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37. New ECG Criteria in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy

Author

Cox, Moniek G.P.J., primary, van der Smagt, Jasper J., additional, Wilde, Arthur A.M., additional, Wiesfeld, Ans C.P., additional, Atsma, Douwe E., additional, Nelen, Marcel R., additional, Rodriguez, Luz-Maria, additional, Loh, Peter, additional, Cramer, Maarten J., additional, Doevendans, Pieter A., additional, van Tintelen, J. Peter, additional, de Bakker, Jacques M.T., additional, and Hauer, Richard N.W., additional

Published
2009
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38. Desmoglein-2 and Desmocollin-2 Mutations in Dutch Arrhythmogenic Right Ventricular Dysplasia/Cardiomypathy Patients

Author

Bhuiyan, Zahurul A., primary, Jongbloed, Jan D.H., additional, van der Smagt, Jasper, additional, Lombardi, Paola M., additional, Wiesfeld, Ans C.P., additional, Nelen, Marcel, additional, Schouten, Meyke, additional, Jongbloed, Roselie, additional, Cox, Moniek G.P.J., additional, van Wolferen, Marleen, additional, Rodriguez, Luz M., additional, van Gelder, Isabelle C., additional, Bikker, Hennie, additional, Suurmeijer, Albert J.H., additional, van den Berg, Maarten P., additional, Mannens, Marcel M.A.M., additional, Hauer, Richard N.W., additional, Wilde, Arthur A.M., additional, and van Tintelen, J. Peter, additional

Published
2009
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39. Expanding Spectrum of Human RYR2 -Related Disease

Author

Bhuiyan, Zahurul A., primary, van den Berg, Maarten P., additional, van Tintelen, J. Peter, additional, Bink-Boelkens, Margreet T.E., additional, Wiesfeld, Ans C.P., additional, Alders, Marielle, additional, Postma, Alex V., additional, van Langen, Irene, additional, Mannens, Marcel M.A.M., additional, and Wilde, Arthur A.M., additional

Published
2007
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41. Verapamil Versus Digoxin and Acute Versus Routine Serial Cardioversion for the Improvement of Rhythm Control for Persistent Atrial Fibrillation

Author

Hemels, Martin E.W., primary, Van Noord, Trudeke, additional, Crijns, Harry J.G.M., additional, Van Veldhuisen, Dirk J., additional, Veeger, Nic J.G.M., additional, Bosker, Hans A., additional, Wiesfeld, Ans C.P., additional, Van den Berg, Maarten P., additional, Ranchor, Adelita V., additional, and Van Gelder, Isabelle C., additional

Published
2006
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42. Plakophilin-2 Mutations Are the Major Determinant of Familial Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy

Author

van Tintelen, J.Peter, primary, Entius, Mark M., additional, Bhuiyan, Zahurul A., additional, Jongbloed, Roselie, additional, Wiesfeld, Ans C.P., additional, Wilde, Arthur A.M., additional, van der Smagt, Jasper, additional, Boven, Ludolf G., additional, Mannens, Marcel M.A.M., additional, van Langen, Irene M., additional, Hofstra, Robert M.W., additional, Otterspoor, Luuk C., additional, Doevendans, Pieter A.F.M., additional, Rodriguez, Luz-Maria, additional, van Gelder, Isabelle C., additional, and Hauer, Richard N.W., additional

Published
2006
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49. Genetic aspects of atrial fibrillation

Author

Wiesfeld, Ans C.P., Hemels, Martin E.W., Van Tintelen, J. Peter, Van den Berg, Maarten P., Van Veldhuisen, Dirk J., and Van Gelder, Isabelle C.

Subjects
*ATRIAL fibrillation, *ATRIAL arrhythmias, *GENETIC polymorphisms, *HEART diseases
Abstract

Abstract: Atrial fibrillation (AF) occurs predominantly in the elderly and is commonly associated with underlying cardiac diseases. A significant number of patients, however, have early onset AF that is not associated with any underlying disease. At present, it is unknown how often this form of AF is familial and how frequently familial AF is due to genetic causes. Recent data suggest that familial AF occurs more frequently than previously recognized. Also, in AF in the setting of underlying diseases, it is suggested that some form of genetic control may be present. Understanding the molecular mechanisms underlying AF may provide insight into the pathogenesis of AF and eventually may lead to improved, patient-tailored rhythm control strategies. [Copyright &y& Elsevier]

Published
2005
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