Regional, age-dependent, and genotype-dependent differences in ventricular action potential duration and activation time in 410 Langendorff-perfused mouse hearts View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2009-03-14

AUTHORS

Christoph Waldeyer, Larissa Fabritz, Lisa Fortmueller, Joachim Gerss, Dierk Damke, Andreas Blana, Sandra Laakmann, Nina Kreienkamp, Daniela Volkery, Günter Breithardt, Paulus Kirchhof

ABSTRACT

Although numerous studies have reported the effects of genetic alterations on murine electrophysiology, the range of normal values for ventricular activation, repolarization, and arrhythmias in mouse hearts is not known. We analyzed right ventricular (RV), left ventricular (LV), and septal activation times, monophasic action potential durations (APD), and right ventricular effective refractory periods during spontaneous rhythm, induced AV nodal block, right ventricular pacing (100–300 ms paced cycle length), and programmed stimulation in 410 beating, Langendorff-perfused, wild-type mouse hearts of CD1, DBAC3H, FVBN, C57/Bl6, and hybrid backgrounds (age 203 ± 132 days). Action potential duration was longer at longer cycle lengths. LV-APD prolonged more than RV-APD, resulting in an increased heterogeneity of APD at longer pacing cycle lengths. Higher heart weight/body weight ratio and DBAC3H and FVB/N backgrounds were associated with long APD, C57Bl/6 background was associated with short APD. Activation times were longer in older hearts. There were no clear-cut sex-dependent APD differences. Sustained spontaneous arrhythmias occurred in 1% of hearts, non-sustained arrhythmias in 18%. Induction of AV block and C57Bl/6 genetic background were associated with spontaneous arrhythmias. Programmed stimulation induced arrhythmias in 51% of hearts. Inducible arrhythmias were associated with advanced age and shorter refractory periods. Ventricular APD in beating mouse hearts show rate- and site-dependent changes comparable to man and large animals. Bradycardia provokes spontaneous arrhythmias in mouse heart, while age-dependent conduction slowing and short refractory periods predispose to induced arrhythmias. Genetic background influences repolarization and arrhythmogenesis. These findings provide systematic data for the design and interpretation of arrhythmia studies in murine disease models. More... »

PAGES

523-533

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00395-009-0019-1

DOI

http://dx.doi.org/10.1007/s00395-009-0019-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1045147712

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19288151


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32 schema:description Although numerous studies have reported the effects of genetic alterations on murine electrophysiology, the range of normal values for ventricular activation, repolarization, and arrhythmias in mouse hearts is not known. We analyzed right ventricular (RV), left ventricular (LV), and septal activation times, monophasic action potential durations (APD), and right ventricular effective refractory periods during spontaneous rhythm, induced AV nodal block, right ventricular pacing (100–300 ms paced cycle length), and programmed stimulation in 410 beating, Langendorff-perfused, wild-type mouse hearts of CD1, DBAC3H, FVBN, C57/Bl6, and hybrid backgrounds (age 203 ± 132 days). Action potential duration was longer at longer cycle lengths. LV-APD prolonged more than RV-APD, resulting in an increased heterogeneity of APD at longer pacing cycle lengths. Higher heart weight/body weight ratio and DBAC3H and FVB/N backgrounds were associated with long APD, C57Bl/6 background was associated with short APD. Activation times were longer in older hearts. There were no clear-cut sex-dependent APD differences. Sustained spontaneous arrhythmias occurred in 1% of hearts, non-sustained arrhythmias in 18%. Induction of AV block and C57Bl/6 genetic background were associated with spontaneous arrhythmias. Programmed stimulation induced arrhythmias in 51% of hearts. Inducible arrhythmias were associated with advanced age and shorter refractory periods. Ventricular APD in beating mouse hearts show rate- and site-dependent changes comparable to man and large animals. Bradycardia provokes spontaneous arrhythmias in mouse heart, while age-dependent conduction slowing and short refractory periods predispose to induced arrhythmias. Genetic background influences repolarization and arrhythmogenesis. These findings provide systematic data for the design and interpretation of arrhythmia studies in murine disease models.
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39 AV block
40 AV nodal block
41 BL6
42 C57/BL6
43 CD1
44 FVB/N background
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46 Langendorff
47 N background
48 Programmed stimulation
49 action potential duration
50 activation
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52 advanced age
53 age
54 alterations
55 animals
56 arrhythmia studies
57 arrhythmias
58 arrhythmogenesis
59 background
60 beating
61 block
62 body weight ratio
63 bradycardia
64 changes
65 conduction slowing
66 cycle length
67 data
68 design
69 differences
70 disease models
71 duration
72 effect
73 effective refractory period
74 electrophysiology
75 findings
76 genetic alterations
77 genetic background
78 genotype-dependent differences
79 heart
80 heart weight/body weight ratio
81 heterogeneity
82 higher heart weight/body weight ratio
83 hybrid background
84 induced arrhythmias
85 inducible arrhythmias
86 induction
87 interpretation
88 large animals
89 length
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91 longer cycle length
92 men
93 model
94 monophasic action potential duration
95 mouse hearts
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97 nodal block
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99 normal values
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101 old hearts
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105 range
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111 right ventricular
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116 site-dependent changes
117 slowing
118 spontaneous arrhythmias
119 spontaneous rhythm
120 stimulation
121 study
122 systematic data
123 time
124 values
125 ventricular
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127 ventricular activation
128 ventricular effective refractory period
129 ventricular pacing
130 weight ratio
131 weight/body weight ratio
132 wild-type mouse hearts
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