Heart rhythm · 2024
Arrhythmogenic atrial remodeling during pregnancy in mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Long Valérie, Motok Beatrice, Leblanc Élisabeth, Tannous Georges, Pyle W Glen, Fiset Céline
Аннотация
BACKGROUND: Pregnancy is associated with greater vulnerability to supraventricular tachyarrhythmias.
OBJECTIVE: As the underlying mechanisms remain to be elucidated, we investigated whether pregnancy induces atrial remodeling that might contribute to this.
METHODS: Atrial electrophysiological and contractile properties were examined in nonpregnant and pregnant (P) mice. Cell shortening and Ca2+ imaging were measured on atrial myocytes. Atrial action potential and ionic currents were recorded using the patch-clamp technique. Atrial messenger RNA and protein expression were analyzed using quantitative polymerase chain reaction and Western blot.
RESULTS: The P-wave area on the electrocardiogram increased by 50% during pregnancy, suggesting atrial enlargement, confirmed by echocardiography. The atrial myocytes were longer in P mice, adding further evidence to the physiological hypertrophy associated with pregnancy. Echocardiography showed a 50% increase in atrial fractional area change during pregnancy, indicating much stronger contraction. A similar increase in cell shortening was observed in P mice and was associated with a decrease in sarcomere length and changes in myofilament protein phosphorylation. However, pregnancy did not affect L-type Ca2+ current, Ca2+ transients, and SR Ca2+ load. Myocytes from P mice showed twice as many spontaneous contractions and spontaneous diastolic Ca2+ releases. Moreover, pregnancy was associated with a 50% increase in action potential duration, linked to a reduction in the density of the Ca2+-independent transient outward K+ current and the underlying KV4.3 channel.
CONCLUSION: During pregnancy, atrial tissues undergo substantial remodeling, potentially contributing to the development of supraventricular tachyarrhythmias.
OBJECTIVE: As the underlying mechanisms remain to be elucidated, we investigated whether pregnancy induces atrial remodeling that might contribute to this.
METHODS: Atrial electrophysiological and contractile properties were examined in nonpregnant and pregnant (P) mice. Cell shortening and Ca2+ imaging were measured on atrial myocytes. Atrial action potential and ionic currents were recorded using the patch-clamp technique. Atrial messenger RNA and protein expression were analyzed using quantitative polymerase chain reaction and Western blot.
RESULTS: The P-wave area on the electrocardiogram increased by 50% during pregnancy, suggesting atrial enlargement, confirmed by echocardiography. The atrial myocytes were longer in P mice, adding further evidence to the physiological hypertrophy associated with pregnancy. Echocardiography showed a 50% increase in atrial fractional area change during pregnancy, indicating much stronger contraction. A similar increase in cell shortening was observed in P mice and was associated with a decrease in sarcomere length and changes in myofilament protein phosphorylation. However, pregnancy did not affect L-type Ca2+ current, Ca2+ transients, and SR Ca2+ load. Myocytes from P mice showed twice as many spontaneous contractions and spontaneous diastolic Ca2+ releases. Moreover, pregnancy was associated with a 50% increase in action potential duration, linked to a reduction in the density of the Ca2+-independent transient outward K+ current and the underlying KV4.3 channel.
CONCLUSION: During pregnancy, atrial tissues undergo substantial remodeling, potentially contributing to the development of supraventricular tachyarrhythmias.