Genetic susceptibility to adverse drug effects - Epidemiology ...

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Common NOS1AP variants potentiate digoxin induced QT-shortening and risk of sudden cardiac death 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. Drugs that Prolong the QT Interval and/or Induce Torsades de Pointes Ventricular Arrhythmia. The University of Arizona Center for Education and Research on Therapeutics, Arizona Health Sciences Center. (Accessed 14 September, 2006, at http://www.qtdrugs.org/medical-pros/drug-lists/drug-lists.htm.) Myerburg RJ, Castellanos A. Cardiac arrest and sudden cardiac death. In: Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Heart Disease: A Text Book of Cardiovascular Medicine. seventh ed. Philadelphia: Elsevier Saunders Company; 2004:865-908. Priori SG, Aliot E, Blomstrom-Lundqvist C, et al. Task Force on Sudden Cardiac Death of the European Society of Cardiology. Eur Heart J 2001;22(16):1374-450. Post W, Shen H, Damcott C, et al. Associations between genetic variants in the NOS1AP (CAPON) gene and cardiac repolarization in the old order Amish. Hum Hered 2007;64(4):214-9. Hauptman PJ, Kelly RA. Digitalis. Circulation 1999;99(9):1265-70. Santana LF, Gomez AM, Lederer WJ. Ca2+ flux through promiscuous cardiac Na+ channels: slip-mode conductance. Science 1998;279(5353):1027-33. Jaffrey SR, Snowman AM, Eliasson MJ, et al. CAPON: a protein associated with neuronal nitric oxide synthase that regulates its interactions with PSD95. Neuron 1998;20(1):115-24. Bai CX, Namekata I, Kurokawa J, et al. Role of nitric oxide in Ca2+ sensitivity of the slowly activating delayed rectifier K+ current in cardiac myocytes. Circ Res 2005;96(1):64-72. Burkard N, Rokita AG, Kaufmann SG, et al. Conditional neuronal nitric oxide synthase overexpression impairs myocardial contractility. Circ Res 2007;100(3):e32-44. Antzelevitch C, Pollevick GD, Cordeiro JM, et al. Loss-of-function mutations in the cardiac calcium channel underlie a new clinical entity characterized by ST-segment elevation, short QT intervals, and sudden cardiac death. Circulation 2007;115(4):442-9. Splawski I, Timothy KW, Decher N, et al. Severe arrhythmia disorder caused by cardiac L-type calcium channel mutations. Proc Natl Acad Sci U S A 2005;102(23):8089-96; discussion 6-8. Cerrone M, Noujaim S, Jalife J. The short QT syndrome as a paradigm to understand the role of potassium channels in ventricular fibrillation. J Intern Med 2006;259(1):24-38. 101
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Genetic susceptibility to adverse d
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The work presented in this thesis w
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Promotiecommissie Promotoren: Prof.
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1 General Introduction
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Chapter 1 genome. Every SNP represe
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Chapter 1 References 1. 2. 3. 4. 5.
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2 Quantifying the risk of adverse d
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Chapter 2 Introduction The cardiac
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Chapter 2 Table 1 Characteristics o
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Chapter 2 digoxin treatment appears
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3 Common variants in the ABCB1 gene
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Chapter 3.1 Introduction The ATP-Bi
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Chapter 3.1 Co-variables. Covariate
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Chapter 3.1 Table 3 Frequencies of
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Chapter 3.1 Table 5 Risk of serum d
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Chapter 3.1 Table 6 Other studies o
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Chapter 3.1 References 1. 2. 3. 4.
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3.2 Common ABCB1 variants increase
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Common ABCB1 variants increase QTc
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Common ABCB1 variants increase QTc
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Page 61 and 62: Chapter 3.3 Introduction The quinol
Page 63 and 64: Chapter 3.3 In addition to the diar
Page 65 and 66: Chapter 3.3 Table 1 General charact
Page 67 and 68: Chapter 3.3 confounding by contrain
Page 69 and 70: Chapter 3.3 adverse effects of mefl
Page 71 and 72: Chapter 3.3 References 1. 2. 3. 4.
Page 74: 4 Common variants in the NOS1AP gen
Page 77 and 78: Chapter 4.1 Introduction Sudden car
Page 79 and 80: Chapter 4.1 Assessment of QTc inter
Page 81 and 82: Chapter 4.1 Table 1 Baseline charac
Page 83 and 84: Chapter 4.1 Table 3 Number of indiv
Page 85 and 86: Chapter 4.1 ditional GG haplotype c
Page 87 and 88: Chapter 4.1 References 1. 2. 3. 4.
Page 90 and 91: 4.2 Common NOS1AP variants potentia
Page 92 and 93: Common NOS1AP variants potentiate d
Page 104 and 105: 4.3 Cardiovascular drugs, NOS1AP an
Page 106 and 107: Cardiovascular drugs, NOS1AP and QT
Page 118: Cardiovascular drugs, NOS1AP and QT
Page 121 and 122: Chapter 4.4 Introduction Sulfonylur
Page 123 and 124: Chapter 4.4 potentially affecting t
Page 125 and 126: Chapter 4.4 Table 2 Average change
Page 127 and 128: Chapter 4.4 had lower mortality rat
Page 129 and 130: Chapter 4.4 In population based stu
Page 131 and 132: Chapter 4.4 26. 27. 28. 29. 30. 31.
Page 134: 5 Effect of ABCB1 and NOS1AP genoty
Page 137 and 138: Chapter 5 Introduction Digoxin is o
Page 139 and 140: Chapter 5 Echocardiography. Our pri
Page 141 and 142: Chapter 5 Table 1 Population charac
Page 143 and 144: Chapter 5 Table 3 Association betwe
Page 145 and 146: Chapter 5 Table 5 Effect of digoxin
Page 147 and 148: Chapter 5 Discussion Digoxin is kno
Page 149 and 150: Chapter 5 References 1. 2. 3. 4. 5.
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6 General discussion
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Chapter 6 2 per 1000 person years o
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Chapter 6 cardial repolarization. B
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Chapter 6 ated with reduced mortali
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Chapter 6 selection bias. However,
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Chapter 6 of the main problems is t
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Chapter 6 49. 50. 51. 52. 53. 54. 5
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Chapter 6 2007;356(11):1094-7. 101.
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7 Summary 171
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Chapter 7.1 2677-3435 TTT-haplotype
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Samenvatting 7.2 Samenvatting Ondan
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Samenvatting gereerden de regressie
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Chapter 8 proefschrift. Verder spec
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9 About the author Albert-Jan Aarno
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Chapter 10 Aarnoudse ALHJ, Dieleman
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