Relation between aging and circadian variation of paroxysmal atrial fibrillation

Yamashita, Takeshi; Murakawa, Yuji; Hayami, Noriyuki; Sezaki, Kazunori; Inoue, Masashi; Fukui, Ei-ichi; Omata, Masao

doi:10.1016/s0002-9149(98)00642-0

Cited by 43 publications

(24 citation statements)

References 13 publications

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“…Various types of circadian variation exist in the occurrence of many arrhythmias. [1][2][3][4][5] The distribution of ventricular tachyarrhythmias is known to have the first peak between morning and noon and the second peak in the evening. [1][2][3] Asystole is more evenly distributed but with the primary trough at night.…”

Section: Discussionmentioning

confidence: 99%

“…Most cardiac arrhythmias also follow this rule, showing characteristic circadian variations in their occurrences. [1][2][3][4][5] Ventricular tachyarrhythmias are known to occur more frequently in the daytime than at night. [1][2][3] On the contrary, we have reported that paroxysmal atrial fibrillation has a nocturnalpredominant circadian pattern in its existence.…”

mentioning

confidence: 99%

“…[1][2][3] On the contrary, we have reported that paroxysmal atrial fibrillation has a nocturnalpredominant circadian pattern in its existence. 4,5 Also, in patients with Brugada syndrome, syncope frequently occurs in the middle of the night. 6 These circadian fluctuations in the occurrences of arrhythmias have been thought to result from the physiological responses to autonomic nervous function.…”

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confidence: 99%

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Circadian Variation of Cardiac K ⁺ Channel Gene Expression

et al. 2003

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Background— Many cardiac arrhythmias have their own characteristic circadian variations. Because the expression of many genes, including clock genes, is regulated variably during a day, circadian variations of ion channel gene expression, if any, could contribute to the fluctuating alterations of cardiac electrophysiological characteristics and subsequent arrhythmogenesis. Methods and Results— To examine whether cardiac K + channel gene expression shows a circadian rhythm, we analyzed the mRNA levels of 8 Kv and 6 Kir channels in rat hearts every 3 hours throughout 1 day. Among these channels, Kv1.5 and Kv4.2 genes showed significant circadian variations in their transcripts: ≈2-fold increase of Kv1.5 mRNA from trough at Zeitgeber time (ZT) 6 to peak at ZT18 and a completely reverse pattern in Kv4.2 mRNA (≈2-fold increase from trough at ZT18 to peak at ZT6). Actually, along with the variations in the immunoreactive proteins, the density of the transient outward and steady-state currents in isolated myocytes and the responses of atrial and ventricular refractoriness to 4-aminopyridine in isolated-perfused hearts showed differences between ZT6 and ZT18, a circadian pattern comparable to that of Kv1.5 and Kv4.2 gene expression. Reversal of light stimulation almost inverted these circadian rhythms, although pharmacological autonomic blockade only partially attenuated the rhythm of Kv1.5 but not of Kv4.2 transcripts. Conclusions— Among all the cardiac K + channels, Kv1.5 and 4.2 channels are unique in showing characteristic circadian patterns in their gene expression, with Kv1.5 increase during the dark period partially dependent on β-adrenergic activities and Kv4.2 increase during the light period independent of the autonomic nervous function.

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Circadian Variation of Cardiac K ⁺ Channel Gene Expression

et al. 2003

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“…It occurred most frequently in the daytime with a single peak in elderly patients over 60 years old, while younger patients under 60 years of age showed a different pattern of circadian variation with 3 peaks after meals until midnight. 12) That is, they found that the relationship between paroxysmal AF and activity of the autonomic nervous system varies with age, and that sympathetic activity in elderly people and parasympathetic (vagal) activity in younger people are intimately related to the onset of paroxysmal AF. In the past, we have similarly reported that the preventive effect of AAD varies among patients with paroxysmal AF because the pharmacological blocking of channels is up-regulated by vagotonia as well as sympathicotonia.…”

Section: Discussionmentioning

confidence: 99%

Relationship Between the Long-Term Preventive Effect of Combined Treatment With Antiarrhythmic Drugs Plus Angiotensin-Converting Enzyme Inhibitors and Circadian Variation in the Onset of Paroxysmal Atrial Fibrillation

et al. 2010

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SummaryWe examined the relationship between the efficacy of combined treatment with antiarrhythmic drugs (AAD) plus enalapril for maintaining sinus rhythm and circadian variation in the onset of paroxysmal AF.Three hundred and forty-four patients with paroxysmal AF (239 men, mean age, 69 ± 11 years) who could be followed up ≥ 12 months were divided into 3 groups on the basis of circadian variation in the onset of AF: a diurnal group (7:00 AM-5:00 PM, n = 57), a nocturnal group (5:00 PM-7:00 AM, n = 108), and a mixed group (onset during both periods, n = 169). The maintenance rate of sinus rhythm during the follow-up period was compared between combined therapy (AAD plus enalapril) and AAD alone.In the diurnal group, the maintenance rates of sinus rhythm at 12, 36, 60, and 90 months were 100%, 100%, 100%, and 100%, respectively, for patients treated with AAD plus enalapril (n = 22) versus 97%, 91%, 89%, and 80% for patients treated with AAD alone (n = 35, P < 0.05). In the nocturnal group, the maintenance rates of sinus rhythm at 12, 36, 60, and 90 months were 96%, 96%, 96%, and 92%, respectively, in patients treated with AAD plus enalapril (n = 24) versus 100%, 100%, 100%, and 100% in patients treated with AAD alone (n = 84, P = NS). In the mixed group, maintenance rates of sinus rhythm at 12, 36, 60, and 90 months were 90%, 71%, 61%, and 57%, respectively, in patients treated with AAD plus enalapril (n = 49) versus 88%, 78%, 68%, and 61% in patients treated with AAD alone (n = 120, P = NS).Our findings suggest that the preventive efficacy of combined therapy with AAD plus enalapril is dependent on the timing of onset of paroxysmal AF, and this regimen seems to be most beneficial for the diurnal type of paroxysmal AF. The number of patients with AF in the United States exceeded 5 million in 2000 and is expected to increase two to threefold over the next 50 years.2) In Japan, the population is aging rapidly and the prevalence of AF among elderly persons aged 70 years or older is already around 3%. This is expected to increase to about 4.5% over the next 20 years.3) Antiarrhythmic drug (AAD) therapy for the maintenance of sinus rhythm in patients with AF has limitations. 4) Accordingly, attention has recently been paid to upstream treatment, in which AAD therapy is combined with renin-angiotensin-aldosterone system (RAAS) inhibitors 5,6) or statins 7) to modify the arrhythmic substrate of the atrial myocardium which is the underlying cause of AF. In a recent large clinical trial, however, additional treatment with angiotensin II-receptor blockers (ARB) to AAD was not associated with a reduction in the incidence of recurrent atrial fibrillation.8) It is still not clear which clinical profile of paroxysmal AF benefits from the addition of RAAS inhibitor therapy as an upstream treatment.We report on the results of our investigation into the longterm preventive effect of combined treatment with enalapril, an angiotensin-converting enzyme inhibitor (ACEI), plus AAD therapy in relation to circadian variation in the onse...

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“…6,19,20 Yue et al showed that atrial rapid pacing reduced transient outward currents (Ito) and L-type Ca 2+ currents (ICa), and that the reduced ICa abbreviated APD and decreased accommodation to changes in rate. 21 It is well known that vagal tone is one of the most important factors in the induction of AF [9][10][11][12][13][14][15] and this induction of AF by VS might be caused by nonuniform shortening of the atrial ERP; 9-11 it may also increase ERP dispersion. 11 Cardiac vagal tone declines with age, 22,23 the smaller tachycardiac response to isometric exercise in older humans is associated with an inability to decrease cardiac vagal tone below an already reduced baseline level.…”

Section: Discussionmentioning

confidence: 99%

Vagal Stimulation Prior to Atrial Rapid Pacing Protects the Atrium From Electrical Remodeling in Anesthetized Dogs.

et al. 2001

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Relation between aging and circadian variation of paroxysmal atrial fibrillation

Cited by 43 publications

References 13 publications

Circadian Variation of Cardiac K ⁺ Channel Gene Expression

Circadian Variation of Cardiac K ⁺ Channel Gene Expression

Relationship Between the Long-Term Preventive Effect of Combined Treatment With Antiarrhythmic Drugs Plus Angiotensin-Converting Enzyme Inhibitors and Circadian Variation in the Onset of Paroxysmal Atrial Fibrillation

Vagal Stimulation Prior to Atrial Rapid Pacing Protects the Atrium From Electrical Remodeling in Anesthetized Dogs.

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Relation between aging and circadian variation of paroxysmal atrial fibrillation

Cited by 43 publications

References 13 publications

Circadian Variation of Cardiac K + Channel Gene Expression

Circadian Variation of Cardiac K + Channel Gene Expression

Relationship Between the Long-Term Preventive Effect of Combined Treatment With Antiarrhythmic Drugs Plus Angiotensin-Converting Enzyme Inhibitors and Circadian Variation in the Onset of Paroxysmal Atrial Fibrillation

Vagal Stimulation Prior to Atrial Rapid Pacing Protects the Atrium From Electrical Remodeling in Anesthetized Dogs.

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Circadian Variation of Cardiac K ⁺ Channel Gene Expression

Circadian Variation of Cardiac K ⁺ Channel Gene Expression