Download Circadian Variation of Paroxysmal Supraventricular Tachycardia*

Circadian Variation of Paroxysmal
Supraventricular Tachycardia*
Shih-Huang Lee, MD; Pan-Chen Chang, MD; Huei-Fong Hung, MD;
Peiliang Kuan, MD; Jun-Jack Cheng, MD; and Chi-Ren Hung MD
Background: Various clinical manifestations of cardiovascular diseases have a pattern of circadian
variation. In this study, we investigated whether the onset and duration of paroxysmal supraventricular tachycardia (PSVT) has a circadian variation.
Methods and results: In our analysis, we included 105 patients with 498 PSVT episodes. In this
study, the onset of PSVT did not have a uniform distribution throughout the 24-h period. There
were nearly equal peaks in the time periods from 8:00 to 9:00 AM, 12:00 to 1:00 PM, and 5:00 to
6:00 PM, with a trough at night. The duration of PSVT also did not show a uniform distribution
throughout the 24-h period; it increased significantly during the daytime, with a peak between
1:00 and 2:00 PM, another peak between 6:00 and 7:00 PM, and a significant reduction at night.
Conclusions: The onset and duration of PSVT showed a circadian variation. However, the
time-oriented antiarrhythmic therapy for preventing PSVT needs further study.
(CHEST 1999; 115:674 – 678)
Key words: circadian variation; supraventricular; tachycardia
Abbreviation: PSVT 5 paroxysmal supraventricular tachycardia
distribution has been noted in some
C ircadian
cardiovascular phenomena, including heart rate,
BP, transient myocardial ischemia, acute myocardial
infarction, thrombotic stroke, and sudden cardiac
death,1–10 showing a prominent clustering of events
in the morning and another peak in the evening. This
provided a clue to the recognition of rhythmic
processes triggering these events, such as changes in
catecholamine levels, and supported the importance
of time-oriented therapy.11–13
Paroxysmal supraventricular tachycardia (PSVT) is
a common arrhythmia, and it occurs sporadically in
the affected patients. The distribution of the onset of
PSVT has not been studied extensively,14 –16 and it is
not known whether the duration of PSVT has a
circadian distribution. Therefore, the purpose of this
study was to determine whether the onset and
duration of PSVT showed a circadian distribution.
Materials and Methods
Study Population
Our study population was drawn from 2,689 consecutive patients
who underwent 24-h Holter monitor recordings in our hospital from
January 1996 to December 1997. Of this group, 105 patients had a
total of 498 recorded PSVT episodes. None of the patients received
antiarrhythmic drugs or any drugs with chronotropic effects, such as
calcium channel blockers, digoxin, and b-blockers. The PSVT was
defined by the following ECG criteria: (1) an episodic occurrence,
(2) a ventricular rate . 120 beats/min, (3) a narrow QRS interval
(, 0.08 s), functional right or left bundle branch block, and (4) a
, 0.02-s variation in successive R-R intervals.14,17
Statistical Analysis
The distributions of the onset and duration of PSVT by 1- and 6-h
intervals (1:00 to 7:00 am, 7:00 am to 1:00 pm, 1:00 to 7:00 pm, and 7:00
pm to 1:00 am) were tested for uniformity by the x2 for goodness of fit.
A p value of , 0.05 was considered statistically significant.
Results
*From the Division of Cardiology, Department of Medicine (Drs.
Lee, H.-F. Hung, Kuan, Cheng, and C.-R. Hung), Shin-Kong
Wu Ho-Su Memorial Hospital, Taipei; and the Mennonite
Christian Hospital (Dr. Chang), Hualien, Taiwan.
Manuscript received March 30, 1998; revision accepted July 28,
1998.
Correspondence to: Shih-Huang Lee, MD, Division of Cardiology, Shin Kong Wu Ho-Su Memorial Hospital, 95 Wen Chang
Road, Shih Lin, Taipei, Taiwan
Study Population
Of the 105 patients (mean [6 SD] age, 53 6 22
years), 47 were men. Of the 31 patients with associated cardiovascular diseases, 23 patients had hypertension, 5 had valvular heart disease, 7 had coronary
artery disease, and 1 patient had congenital heart
disease. Eleven patients were referred to receive
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Clinical Investigations
invasive electrophysiological study and radiofrequency catheter ablation because their PSVT was
refractory to antiarrhythmic drugs.
Onset of PSVT
The onset of PSVT by 1-h intervals did not
demonstrate a uniform distribution throughout the
24-h period (Fig 1, Top, A; p , 0.01). The frequency
of onset showed nearly equal peaks in three hourly
distributions (8:00 to 9:00 am, 12:00 to 1:00 pm, and
5:00 to 6:00 pm) and a trough at night. Otherwise,
the distribution of onset of PSVT was 56 episodes
(11%) from 1:00 to 7:00 am, 181 episodes (36%)
from 7:00 am to 1:00 pm, 178 episodes (36%) from
Figure 1. Top, A: the hourly frequency of the onset of PSVT. The peaks existed between 8:00 and 9:00
am, 12:00 and 1:00 pm, and 5:00 and 6:00 pm. The onset of PSVT did not show a uniform distribution
by 1-h intervals (p , 0.01). Bottom, B: the cumulative percentage of onset of PSVT by 6-h intervals.
The onset of PSVT also did not show a uniform distribution by 6-h intervals (p , 0.01).
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675
1:00 pm to 7:00 pm, and 83 episodes (17%) from 7:00
pm to 1:00 am (Fig 1, Bottom, B; p , 0.01).
Duration of PSVT
The duration of PSVT by 1-h intervals did not
show a uniform distribution throughout the 24-h
period (Fig 2, Top, A; p , 0.01). The duration of
PSVT increased during the daytime, with a peaks
between 1:00 and 2:00 pm and between 6:00 and
7:00 pm, and decreased at night. The distribution of
duration of PSVT was 142 min (11%) from 1:00 to
7:00 am, 389 min (29%) from 7:00 am to 1:00 pm,
Figure 2. Top, A: the hourly duration of PSVT. The peaks existed between 1:00 and 2:00 pm, and 6:00
and 7:00 pm. The duration of PSVT did not show a uniform distribution by 1-h intervals (p , 0.01).
Bottom, B: the cumulative percentage of duration of PSVT by 6-h intervals. The duration of PSVT also
did not show a uniform distribution by 6-h intervals (p , 0.01).
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Clinical Investigations
680 min (51%) from 1:00 to 7:00 pm, and 125 min
(9%) from 7:00 pm to 1:00 am (Fig 2, Bottom, B;
p , 0.01).
Discussion
Major Findings
This study demonstrated the circadian periodicity
of the onset and duration of PSVT. The onset and
duration of PSVT increased significantly during the
daytime.
Comparisons With Previous Studies
Previous studies have shown that the onset of
PSVT increased during the daytime and decreased at
night.14,16 However, Kupari et al15 showed no morning peak in the onset of PSVT. In these studies,
researchers investigated the distribution of the onset
of symptomatic PSVT episodes causing admission to
the emergency department or telephone transmission of electrocardiography; they did not include
asymptomatic PSVT episodes. In this study, we
demonstrated that the onset and duration of PSVT,
including symptomatic and asymptomatic episodes,
showed a circadian variation.
Onset of PSVT
This circadian pattern of the onset of PSVT was
similar to the pattern in some cardiovascular diseases,3–10 suggesting that PSVT and some cardiovascular
diseases share common mechanisms, such as an
increase in physical or mental stress, and changes in
autonomic nervous tone. A morning onset could
result from the augmented sympathetic tone and the
increased secretion of epinephrine that occurs as a
consequence of awakening and of morning activities.18 The increased catecholamines might increase
the likelihood of starting the reentrant tachycardia.19,20 The reasons for the evening peak in the
onset of PSVT were less obvious. It was possible that
late working shifts, heavy evening meals, or physical
recreation activities resulted in the evening peak.3,15
Our results suggest that it might be reasonable to
keep a high drug level during the daytime and a low
drug level at night. However, the time-oriented
antiarrhythmic therapy for preventing PSVT needs
further study.
Duration of PSVT
In this study, the total duration of PSVT was
longer from 1:00 to 7:00 pm than from 7:00 am to
1:00 pm, although the incidence of the onset of PSVT
was similar in the two periods. When compared to
the 1:00 to 7:00 pm time period, the PSVT was easier
to terminate spontaneously between 7:00 am and
1:00 pm; however, the exact mechanisms for this are
unclear.
Study Limitations
First, in this study, the data were analyzed on the
basis of Holter monitor recordings. Whether other
episodes of PSVT that were not recorded followed a
similar circadian pattern is unknown. However, prospective PSVT studies are difficult and unrealistic
because of the relatively long periods between recurrences. Furthermore, there might be some bias to
determine the time distribution of onset and duration according to the memory of the patients. Second, most of the patients had no symptoms after
receiving antiarrhythmic drugs, and they did not
receive electrophysiologic study and radiofrequency
catheter ablation. The exact mechanisms of PSVT in
these patients were unknown. However, our results
clearly demonstrated the circadian distribution of
the onset and duration of PSVT.
Conclusion
This study demonstrated that the onset and duration of PSVT showed a circadian variation. However,
the time-oriented antiarrhythmic therapy for preventing PSVT needs further investigation.
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