Download PDF

Original Article
Acta Cardiol Sin 2014;30:259-265
Electrophysiology & Arrhythmia
Heart Rate Acceleration and Recovery Indices are
Not Related to the Development of Ventricular
Premature Beats During Exercise Test
Zafer Buyukterzi, Ozcan Ozeke, Mehmet Fatih Ozlu, Aytun Canga, Ozgul Malcok Gurel, Tumer Erdem Guler,
Veli Kaya, F1rat Ozcan, Serkan Cay, Serkan Topaloglu and Dursun Aras
Background: Changes in heart rate (HR) during exercise and recovery from exercise are mediated by the balance
between sympathetic and vagal activity. HR acceleration (HRA) and recovery (HRR) are important measures of
cardiac autonomic dysfunction and directly correlated with sympathetic and parasympathetic activity. It is not
known if the autonomic nervous system related to ventricular arrhythmias during exercise. The purpose was to
evaluate the HRA and HRR in patients with and without premature ventricular complex (PVC) during exercise, and
to examine the factors that might affect HRA and HRR.
Methods: The records of consecutive patients undergoing routine exercise test were reviewed. The characteristics
and the HRA and HRR were compared between patients with and without PVC during exercise.
Results: A total of 232 patients (145 men) were recruited; 156 (103 men) developed PVCs during the exercise. Max
HR was significantly lower in men with PVCs than in those without, which were not mirrored in women. There was
no difference in HRA and HRR between the patients with and without exercise-induced PVCs in both genders.
Compared to the men with PVCs, women had higher body mass index, shorter total exercise time, and higher HRA
indices after the 3 and 6 minutes exercise. In patients with PVCs, the HRA and HRR indices were similar regardless
of the presence of coronary artery disease and the phase of exercise test where PVC developed.
Conclusions: Although exercise performance may be different between the genders, the HRA or HRR indices were
not related to the development of PVC during exercise in both genders.
Key Words:
Exercise-induced arrhythmias · Heart rate acceleration · Heart rate recovery
INTRODUCTION
with heart disease and in all patients who have experienced sustained ventricular tachycardia.2,3 There is conflicting evidence about the relationship between exercise-induced PVCs and coronary artery disease (CAD) or
to cardiovascular risk, and the prognostic significance of
these ectopies is controversial. Recently, researches
focused on the possible mechanisms of exercise-induced PVCs.
The autonomic nervous system is suggested to play
an important role in the genesis of ventricular arrhythmias, and cardiovascular autonomic dysfunction is associated with significantly increased cardiovascular mortality.4 Heart rate (HR) responses in both the exercise
and recovery phase of EST have been used as markers of
Ventricular arrhythmias are a common finding during clinical exercise stress testing (EST). 1 Exercise-induced premature ventricular contractions (PVC) may be
found in up to 30% of healthy subjects, in 60% of those
Received: March 3, 2013
Accepted: June 7, 2013
Turkiye Yuksek Ihtisas Training and Research Hospital, Department of
Cardiology, Ankara, Turkey.
Address correspondence and reprint requests to: Dr. Ozcan Ozeke,
Turkiye Yuksek Ihtisas Hospital, Kardiyoloji Klinigi, Ankara, Turkiye.
Tel: 90 505 383 67 73; Fax: 222 224 44 00; E-mail: ozcanozeke@
gmail.com
Any relationship with industry: No.
259
Acta Cardiol Sin 2014;30:259-265
Zafer Buyukterzi et al.
groups and subgroups, HRA and HRR indices were compared.
Patients underwent EST using the Bruce protocol
after withdrawal of any drugs that might have affected
the EST. The predicted peak HR was calculated as (220age), with an aim to reach at least 85% of the age-predicted HR. The electrocardiography (ECG) was continuously recorded during the EST. Qualified exercise physiologists collected physiologic and hemodynamic data
during testing, including symptoms, HR, heart rhythm,
blood pressure, and estimated functional capacity in
metabolic equivalents. HRA indices were defined as the
increase in the HR at the 3rd and 6th minutes to pretest
HR (HRA3 and HRA6, respectively). Following peak exercise, patients walked for a 5-minute cool-down period
at 1.5 mph at a 2.5% grade. The HRR indices were defined as the reduction in the HR from the HR at peak
exercise to the HR at the first-, second, third and fifth
minute after the cessation of EST. These results were
expressed as HRR1, HRR2, HRR3, and HRR5, respectively.
Patients with chronotropic incompetence during the
EST8 were excluded from the study, which was defined
accordingly to the following criteria: (a) peak HR 85% of
age-predicted peak HR and/or (b) failure to achieve 80%
of HR reserve (HR reserve = age-predicted peak HR resting HR).
The SPSS statistical software package (version 16.0;
SPSS Inc, Chicago, IL, USA) was used to perform all statistical calculations. Continuous variables were expressed
as mean ± SD. Categorical variables were expressed as
numbers and percentages, and compared using the
chi-squared test. Two group comparisons were performed
using an unpaired t-test or nonparametric Mann-Whitney U test according to normality test results, and an
analysis of variance (ANOVA) test with Tukey’s Honestly
Significant Difference (HSD) post-hoc test was used for
comparison of three groups. A p-value less than 0.05
was defined as statistically significant.
autonomic functions and shown to have prognostic values.4-6 The rise in HR during exercise is considered to be
due to the activation of the sympathetic nervous system
and the simultaneous suppression of the parasympathetic nervous system.
On the other hand, the fall in HR immediately after
exercise is regarded to be a function of the parasympathetic reactivation together with sympathetic withdrawal.1 It was suggested that alterations in the autonomic control of cardiac functions, characterized by
augmented sympathetic and reduced vagal activity, may
play a major role in cardiovascular mortality.1 Both abnormally elevated HR responses at the onset of an EST5
and impaired early4 or late6 heart rate recovery (HRR)
responses have emerged as important predictors of survival. Moreover, attenuated vagal reactivation during recovery might be associated with ventricular ectopy that
is not suppressed.7 It is not known whether patient age,
heart rate variability, turbulence or recovery, and other
markers of autonomic tone would contribute to the development of ventricular arrhythmia during routine exercise test. In the present study, we evaluated heart rate
acceleration (HRA) and HRR indices in patients with and
without PVCs during exercise test and examined the potential factors that might affect HRA and HRR in these
patients.
METHOD
We reviewed the records of consecutive patients
undergoing routine clinical EST at our institutions for
the presence or absence of pathologic arrhythmia during EST, and were diagnosed to have exercise-induced
PVC (Group 1). Members of Group 1 were analyzed and
compared to those without exercise-induced PVC (Group
2). In the second step, Group 1 was divided into two
groups: exercise-induced PVC in patients with and without CAD. Any CAD was defined as a > 50% luminal stenosis of the left main coronary artery or a > 70% stenosis
of any other major epicardial coronary artery or major
branch. In the third step, Group 1 was divided into three
subgroups: (a) patients with exercise-induced PVC during only exercise phase, (b) patients with exercise-induced PVC during only recovery phase and (c) patients
with exercise-induced PVC during both phases. In all
Acta Cardiol Sin 2014;30:259-265
RESULTS
The medical records of 232 patients (including 87
females and 145 males) undergoing exercise test were
reviewed. Among them, 156 patients (including 53 females and 103 males) developed PVCs during the exer260
Heart Rate Recovery Indices in Exercise-Induced PVC
Table 3 showed the comparison of the results of exercise testing indices in PVC patients with and without
CAD. For male PVC patients, both the maximal HR and
achieved age-predicted HR during exercise were significantly lower in those with CAD than in those without
CAD. There was no difference in other parameters including the HRA and HRR indices in male patients. There
was also no difference in all the parameters in female
PVC patients with and without CAD.
Table 4 showed the comparison of exercise testing
indices with regard to the phase of exercise test where
PVC occurred. In female patients, the HRA indices after
the 6th minute of the exercise period was significantly
higher when PVCs developed during the recovery phase
than those during exercise phase or during both phases.
There was no difference in other parameters during the
cise test. The maximal HR was significantly lower in male
patients, with 155.8 ± 12.2 bpm, than in those without
PVCs during exercise (161.4 ± 10.6 bpm, p = 0.01),
which was not seen in female patients. However, there
were no differences in baseline characteristics, other
parameters of exercise test, and both HRA and HRR
between the two groups (Table 1).
The characteristics and the exercise test performance of the patients with PVCs during exercise-based
test are further shown by gender in Table 2. For PVCs
patients, the BMI was greater, the total exercise time
was significantly shorter, and both HRA indices after the
3rd and 6th minutes of the exercise period were significantly higher in females than in males. However, there
was not any difference with regard to HRR indices between the genders.
Table 1. The comparison of the results of exercise testing indices in patients with and without EIPVC
Female
Patient number
Age (year)
BMI (kg/m2)
Pretest HR (bpm)
Maximal HR (bpm)
Exercise time (min)
Achieved age-predicted HR
HRA3 (bpm)
HRA6 (bpm)
HRR1 (bpm)
HRR2 (bpm)
HRR3 (bpm)
HRR5 (bpm)
Male
Patient number
Age (year)
BMI (kg/m2)
Pretest HR (bpm)
Maximal HR (bpm)
Exercise time (min)
Achieved age-predicted HR
HRA3 (bpm)
HRA6 (bpm)
HRR1 (bpm)
HRR2 (bpm)
HRR3 (bpm)
HRR5 (bpm)
EIPVC (+) (n = 156)
EIPVC (-) (n = 76)
p value
53
58.0 ± 7.9
28.7 ± 4.0
81.4 ± 11.5
157.6 ± 9.1
7.97 ± 2.69
96.9 ± 3.4
38.5 ± 14.5
56.5 ± 17.5
28.5 ± 10.7
43.4 ± 12.2
58.0 ± 10.0
64.6 ± 9.50
34
56.3 ± 6.0
29.7 ± 5.1
81.7 ± 9.9
157.7 ± 7.20
8.54 ± 2.11
95.7 ± 4.4
35.9 ± 12.2
53.5 ± 13.2
27.5 ± 9.7
44.5 ± 12.3
61.2 ± 10.7
66.6 ± 9.6
0.301
0.322
0.901
0.960
0.767
0.294
0.403
0.505
0.642
0.663
0.170
0.354
103
57.6 ± 10.3
27.1 ± 3.80
81.6 ± 13.1
155.8 ± 12.20
10.23 ± 2.590
95.4 ± 5.30
29.0 ± 12.1
43.1 ± 13.1
27.0 ± 12.4
40.5 ± 13.8
56.2 ± 15.3
62.0 ± 13.6
42
54.8 ± 7.6
27.3 ± 3.6
082.4 ± 11.4
161.4 ± 10.6
10.64 ± 2.21
97.0 ± 4.1
029.8 ± 10.1
044.1 ± 13.1
27.9 ± 9.2
042.7 ± 10.4
056.9 ± 10.7
064.6 ± 10.3
0.151
0.773
0.746
0.010
0.369
0.081
0.722
0.660
0.655
0.364
0.790
0.270
BMI, body mass index; bpm, beats per minute; EIPVC, exercise-induced premature ventricular complex; HR, heart rate; HRA, heart
rate acceleration; HRR, heart rate recovery.
261
Acta Cardiol Sin 2014;30:259-265
Zafer Buyukterzi et al.
Table 2. The comparison of the results of exercise testing indices for both sexes
EIPVC (+)
Age (year)
BMI (kg/m2)
CAD (yes/no)
Pretest HR (bpm)
Maximal HR (bpm)
Exercise time (min)
Achieved age-predicted HR
EIPVC at only-recovery phase (%)
EIPVC at only-exercise phase (%)
EIPVC at both phase (%)
HRA3 (bpm)
HRA6 (bpm)
HRR1 (bpm)
HRR2 (bpm)
HRR3 (bpm)
HRR5 (bpm)
Female (n = 53)
Male (n = 103)
p value
58.0 ± 7.90
28.7 ± 4.00
21/32
81.4 ± 11.5
157.6 ± 9.100
7.97 ± 2.69
96.9 ± 3.40
35.6
25.4
39.0
38.5 ± 14.5
56.5 ± 17.5
28.5 ± 10.7
43.4 ± 12.2
58.0 ± 10.0
64.6 ± 9.50
57.6 ± 10.3
27.1 ± 3.80
54/49
81.6 ± 13.1
155.8 ± 12.20
10.23 ± 2.590
95.4 ± 5.30
24.3
27.2
49.5
29.0 ± 12.1
43.1 ± 13.1
27.0 ± 12.4
40.5 ± 13.8
56.2 ± 15.3
62.0 ± 13.6
0.599
0.017
0.890
0.905
0.617
< 0.001 <
0.176
0.807
0.124
0.195
< 0.001 <
< 0.001 <
0.441
0.210
0.439
0.235
BMI, body mass index; bpm, beats per minute; CAD, coronary artery disease; EIPVC, exercise-induced premature ventricular
complex; HR, heart rate; HRA, heart rate acceleration; HRR, heart rate recovery.
Table 3. The comparison of the results of exercise testing indices in EIPVC patients with and without CAD
EIPVC(+)
Female
Age (year)
BMI (kg/m2)
Pretest HR (bpm)
Maximal HR (bpm)
Exercise time (min)
Achieved age-predicted HR
HRA3 (bpm)
HRA6 (bpm)
HRR1(bpm)
HRR2 (bpm)
HRR3 (bpm)
HRR5 (bpm)
Male
Age (year)
BMI (kg/m2)
Pretest HR (bpm)
Maximal HR (bpm)
Exercise time (min)
Achieved age-predicted HR
HRA3 (bpm)
HRA6 (bpm)
HRR1 (bpm)
HRR2 (bpm)
HRR3 (bpm)
HRR5 (bpm)
CAD (+)
CAD (-)
n = 21
58.8 ± 7.6
28.6 ± 4.2
82.7 ± 11.6
156.2 ± 12.3
7.98 ± 2.36
97.0 ± 3.5
37.7 ± 13.7
54.5 ± 16.0
28.3 ± 11.0
42.7 ± 12.0
57.7 ± 10.4
64.2 ± 9.8
n = 54
58.9 ± 9.70
27.4 ± 3.70
81.0 ± 13.3
153.2 ± 13.00
9.90 ± 2.55
94.3 ± 5.80
28.0 ± 11.4
43.9 ± 13.7
27.0 ± 13.8
40.5 ± 14.2
55.4 ± 15.6
61.1 ± 13.8
n = 32
52.4 ± 7.80
29.3 ± 4.90
82.7 ± 10.4
166.4 ± 12.30
8.54 ± 2.11
95.9 ± 4.10
35.2 ± 11.0
52.8 ± 12.7
29.3 ± 11.2
46.6 ± 12.0
64.3 ± 11.1
70.0 ± 10.4
n = 49
56.1 ± 10.6
26.8 ± 4.00
82.3 ± 13.0
158.8 ± 10.50
10.59 ± 2.610
96.6 ± 4.40
30.1 ± 13.0
42.2 ± 12.5
26.9 ± 10.8
40.6 ± 13.5
57.1 ± 15.2
62.9 ± 13.3
p value
0.711
0.804
0.127
0.554
0.598
0.870
0.931
0.081
0.435
0.530
0.217
0.298
0.170
0.430
0.630
0.019
0.178
0.029
0.378
0.536
0.962
0.957
0.560
0.502
BMI, body mass index; bpm, beats per minute; CAD, coronary artery disease; EIPVC, exercise-induced premature ventricular
complex; HR, heart rate; HRA, heart rate acceleration; HRR, heart rate recovery.
Acta Cardiol Sin 2014;30:259-265
262
Heart Rate Recovery Indices in Exercise-Induced PVC
Table 4. A comparison of the results of exercise testing indices with regard to phase of EIPVC occurred
EIPVC (+)
Female
Age (year)
BMI (kg/m2)
Pretest HR (bpm)
Maximal HR (bpm)
Exercise time (min)
Achieved age-predicted HR
HRA3 (bpm)
HRA6 (bpm)
HRR1 (bpm)
HRR2 (bpm)
HRR3 (bpm)
HRR5 (bpm)
Male
Age (year)
BMI (kg/m2)
Pretest HR ( bpm)
Maximal HR (bpm)
Exercise time (min)
Achieved age-predicted HR
HRA3 (bpm)
HRA6 (bpm)
HRR1 (bpm)
HRR2 (bpm)
HRR3 (bpm)
HRR5 (bpm)
Only in exercise phase
Only in recovery phase
In both phases
n = 23
59.5 ± 9.90
28.1 ± 4.00
82.1 ± 9.90
156.0 ± 9.400
8.07 ± 2.98
97.5 ± 3.20
35.1 ± 11.3
51.3 ± 13.0
26.4 ± 11.4
40.6 ± 14.2
55.7 ± 9.30
62.2 ± 6.50
n = 25
57.9 ± 11.2
27.5 ± 3.50
82.3 ± 11.2
155.2 ± 12.9
10.03 ± 2.17
95.5 ± 4.6
28.3 ± 10.5
42.9 ± 11.6
25.1 ± 9.7
40.1 ± 11.4
55.7 ± 14.4
61.5 ± 14.5
n = 12
54.5 ± 10.1
30.8 ± 4.40
83.9 ± 13.0
161.1 ± 11.60
6.82 ± 1.29
95.4 ± 3.80
43.0 ± 16.0
67.3 ± 14.7
29.8 ± 12.3
46.7 ± 15.7
57.4 ± 11.4
65.4 ± 12.8
n = 22
61.1 ± 7.70
26.7 ± 4.30
81.2 ± 11.6
151.6 ± 12.6
9.44 ± 3.18
94.5 ± 6.3
30.0 ± 11.4
43.1 ± 13.0
24.7 ± 14.5
36.8 ± 16.0
52.0 ± 18.0
58.2 ± 14.1
n = 18
59.0 ± 6.50
28.0 ± 3.60
78.8 ± 12.6
157.4 ± 6.500
8.62 ± 2.85
97.2 ± 3.30
39.7 ± 16.6
55.9 ± 21.3
30.4 ± 8.60
44.7 ± 9.00
61.4 ± 9.60
67.1 ± 10.1
n = 56
56.1 ± 10.5
27.1 ± 3.80
81.5 ± 14.5
157.7 ± 11.40
10.62 ± 2.490
95.7 ± 5.20
29.0 ± 13.2
43.2 ± 14.0
28.7 ± 12.5
42.2 ± 13.8
58.1 ± 14.5
63.7 ± 12.9
p value
0.080
0.133
0.462
0.303
0.195
0.224
0.281
0.032
0.449
0.318
0.193
0.255
0.158
0.768
0.958
0.127
0.186
0.663
0.894
0.997
0.301
0.294
0.285
0.273
BMI, body mass index; bpm, beats per minute; EIPVC, exercise-induced premature ventricular complex; HR, heart rate; HRA, heart
rate acceleration; HRR, heart rate recovery.
different phase in females and neither in any parameters during the difference phase in males.
shorter total exercise time, and higher HRA indices after
the 3rd and 6th minutes of the exercise period. However, there was no difference in HRA and HRR indices
between the patients with and without exercise-induced PVC in both genders. Furthermore, in patients
with PVCs, the HRA and HRR indices were similar, regardless of the presence or absence of coronary artery
disease or the phase of exercise test where PVC developed (exercise phase, recovery phase, or both). Accordingly, the causes of the development of PVCs are
still not known.
Changes in heart rate during exercise and recovery
from exercise are mediated by the balance between
sympathetic and vagal activity. Parasympathetic reactivation is thought to be the underlying mechanism of
HRR during recovery phase 9,10 and abnormalities in
parasympathetic activation have been suggested as the
link to arrhythmogenesis and mortality.4 In the absence
DISCUSSIONS
Although it is well-known that the autonomic nervous system plays an important role in the genesis of
ventricular arrhythmias, and there are numerous studies about HRA/HRR indices and cardiac mortality and
arrhythmogenesis in the literature,4 we did not detect
any association between the HRA or HRR indices and
the development of PVCs during exercise test in both
genders.
In the current study, max HR was significantly lower
in male patients with PVCs than in those without, which
was not seen in females. Compared to the male patients
with PVCs, the female ones had higher body mass index,
263
Acta Cardiol Sin 2014;30:259-265
Zafer Buyukterzi et al.
clear. While some have found that recovery exerciseinduced PVC is more robustly associated with adverse
prognosis than exercise period exercise-induced PVC,7
other results suggest a different connection.19 Dewey et
al. reported that whereas exercise-induced PVCs were
related to the HR increase with exercise, recovery PVCs
were related to CAD and ST-segment depression.20 They
demonstrated that “recovery-only” exercise-induced
PVCs also have prognostic significance that augments
established risk factors, whereas “exercise-only” exercise-induced PVCs have limited prognostic significance.
We could not detect HRA and HRR indices with regard to
phase of occurrence of exercise-induced PVC in current
study.
Although an association between the occurrence of
exercise-induced PVCs and CAD has been described, a
consensus has not arisen regarding the relationship between exercise-induced PVC to CAD or to cardiovascular
risk because of the conflicting results from the available
studies.21-23 There was not any difference in HRA and
HRR indices in exercise-induced PVC patients with and
without CAD in the present study.
There were some limitations of the study. The main
limitation of the present study was its retrospective
design. Second, there was a relatively small sample size
in the female group. Third, HRR was strongly dependent
on the type of recovery protocol used (e.g., complete
cessation of exercise or cool-down in recovery and its
position such as supine, sitting, standing).24 The first reports of HRR were based on patients who underwent an
upright cool-down protocol with a slow walk during the
first 2 minutes after exercise. A HRR value of £ 12 bpm
at 1 minute was identified as a best-value cut point for
upright position in recovery phase, and an abnormal
HRR was defined as failure of the HR to fall by more
than 12 beats during the first minute after exercise.4,11
However, in patients undergoing different kinds of protocols, such as those undergoing stress echocardiography 14 or those sitting down after exercise, 12 HRR
values tend to be higher. Thus, for patients undergoing
stress echocardiography, an abnormal value of £ 18 bpm
has been reported for supine position,14 whereas in patients undergoing a more classic type of recovery protocol, the abnormal reported value has been < 22 bpm
over 2 minutes of recovery for sitting position.12,19 However, we could not use a specific cut-off point for HRR.
of normal vagal reactivation, HRR is attenuated, with an
associated increase in mortality.11-15 Jouven et al. demonstrated that an HRR of < 25 beats/min after the
first minute of exercise recovery was associated with an
increased relative risk of 2.2 for sudden cardiac death as
compared with a cohort that had > 40 beats/min drop.15
Nishime et al. reported that when HRR decreases to less
than 12 beats/min, risk of death increases markedly.11 In
fact, the mechanisms of adverse outcome associated
with abnormal HRR are unclear, and a major challenge
in the use of HRR in routine clinical exercise testing has
been how best to characterize it.12,13 One-minute HR recovery (HRR1) first emerged as an important predictor
of survival more than a decade ago and is directly associated with parasympathetic activity. Dramatic physiologic changes occur during this time and HRR1 predominantly reflects early parasympathetic reactivation
after exercise, with elevated HRR indicating greater
parasympathetic reactivation.4 Recently, there has been
an increased focus on the prognostic significance of late
HR recovery (HRR2 and HRR5), which is an index of persistent sympathetic tone and/or late vagal withdrawal
immediately preceding sympathetic activation.6 In fact,
it has been shown that parasympathetic effects reach a
peak approximately 2 minutes into recovery from exercise; sympathetic effects dissipate more slowly, with significant increases in plasma catecholamines and HR.16
Whereas Imai et al. reported that the initial HRR within
30 s is mediated primarily by vagal reactivation,10 Savin
et al. suggested that “sympathetic withdrawal” contributes more to HRR soon after peak exercise cessation, with “parasympathetic activation” playing a greater
role later in recovery at lower heart rates.17 Kannankeril
et al.18 evaluated heart rates in 10 healthy subjects at
maximal exercise and recovery under normal physiologic conditions as well as during selective parasympathetic blockade with atropine. These data indicated that
parasympathetic effects persist during high-intensity exercise, and a large parasympathetic effect on the heart
rate was noted in 1 min, increased until 4 min, and then
remained stable until 10 min into the recovery period.
In the present study, we did not detect any difference in
early or late HRR indices between patients with and
without exercise-induced PVC.
The relative prognostic significance of exercise and
recovery-period exercise-induced PVC also remains unActa Cardiol Sin 2014;30:259-265
264
Heart Rate Recovery Indices in Exercise-Induced PVC
CONCLUSIONS
10.
In this study, while exercise performance may be
different between the genders, the HRA or HRR indices
were not related to the development of PVC during the
exercise test in both genders. The presence of CAD and
the exercise phase of PVC development did not modify
the HRA or HRR indices in patients with PVC during
exercise test. There is still no optimal risk stratification
strategy for the development of PVC during exercise.
Future experiments are required to clarify this issue.
11.
12.
13.
14.
ACKNOWLEDGEMENT
The abstract section of the current study has been
already presented at the 29th Annual Congress of the
Turkish Society of Cardiology [26-29 October 2013
Antalya-Turkey; 821].
15.
REFERENCES
17.
16.
1. Beckerman J, Wu T, Jones S, Froelicher VF. Exercise test-induced
arrhythmias. Prog Cardiovasc Dis 2005;47:285-305.
2. Candinas RA, Podrid PJ. Evaluation of cardiac arrhythmias by
exercise testing. Herz 1990;15:21-7.
3. McHenry PL, Morris SN, Kavalier M, Jordan JW. Comparative
study of exercise-induced ventricular arrhythmias in normal
subjects and patients with documented coronary artery disease.
Am J Cardiol 1976;37:609-16.
4. Cole CR, Blackstone EH, Pashkow FJ, et al. Heart-rate recovery
immediately after exercise as a predictor of mortality. N Engl J
Med 1999;341:1351-7.
5. Falcone C, Buzzi MP, Klersy C, Schwartz PJ. Rapid heart rate increase at onset of exercise predicts adverse cardiac events in patients with coronary artery disease. Circulation 2005;112:195964.
6. Johnson NP, Goldberger JJ. Prognostic value of late heart rate
recovery after treadmill exercise. A J Cardiol 2012;110:45-9.
7. Frolkis JP, Pothier CE, Blackstone EH, Lauer MS. Frequent ventricular ectopy after exercise as a predictor of death. Am J
Cardiol 2003;348:781-90.
8. Lauer MS, Francis GS, Okin PM, et al. Impaired chronotropic response to exercise stress testing as a predictor of mortality. JAMA
1999;281:524-9.
9. Arai Y, Saul JP, Albrecht P, et al. Modulation of cardiac autonomic
18.
19.
20.
21.
22.
23.
24.
265
activity during and immediately after exercise. Am J Physiol
1989;256:H132-41.
Imai K, Sato H, Hori M, et al. Vagally mediated heart rate recovery
after exercise is accelerated in athletes but blunted in patients
with chronic heart failure. J Am Coll Cardiol 1994;24:1529-35.
Nishime EO, Cole CR, Blackstone EH, et al. Heart rate recovery
and treadmill exercise score as predictors of mortality in patients
referred for exercise ECG. JAMA 2000;284:1392-8.
Shetler K, Marcus R, Froelicher VF, et al. Heart rate recovery: validation and methodologic issues. J Am Coll Cardiol 2001;38:
1980-7.
Gibbons RJ. Abnormal heart-rate recovery after exercise. Lancet
2002;359:1536-7.
Watanabe J, Thamilarasan M, Blackstone EH, et al. Heart rate recovery immediately after treadmill exercise and left ventricular
systolic dysfunction as predictors of mortality: the case of stress
echocardiography. Circulation 2001;104:1911-6.
Jouven X, Empana JP, Schwartz PJ, et al. Heart-rate profile during
exercise as a predictor of sudden death. N Engl J Med 2005;
352:1951-8.
Wang NC, Chicos A, Banthia S, et al. Persistent sympathoexcitation long after submaximal exercise in subjects with and
without coronary artery disease. Am J Physiol Heart Cric Physiol
2011;301:H912-20.
Savin WM, Davidson DM, Haskell WL. Autonomic contribution to
heart rate recovery from exercise in humans. J Appl Physiol
Respir Environ Exerc Physiol 1982;53:1572-5.
Kannankeril PJ, Le FK, Kadish AH, Goldberger JJ. Parasympathetic
effects on heart rate recovery after exercise. J Investig Med
2004;52:394-401.
Morshedi-Meibodi A, Evans JC, Levy D, et al. Clinical correlates
and prognostic significance of exercise-induced ventricular premature beats in the community: the Framingham Heart Study.
Circulation 2004;109:2417-22.
Dewey FE, Kapoor JR, Williams RS, et al. Ventricular arrhythmias
during clinical treadmill testing and prognosis. Arch Intern Med
2008;168:225-34.
Sami M, Chaitman B, Fisher L, et al. Significance of exerciseinduced ventricular arrhythmia in stable coronary artery disease: a coronary artery surgery study project. Am J Cardiol
1984;54:1182-8.
Elhendy A, Chandrasekaran K, Gersh BJ, et al. Functional and
prognostic significance of exercise-induced ventricular arrhythmias in patients with suspected coronary artery disease. Am J
Cardiol 2002;90:95-100.
Marieb MA, Beller GA, Gibson RS, et al. Clinical relevance of
exercise-induced ventricular arrhythmias in suspected coronary
artery disease. Am J Cardiol 1990;66:172-8.
Kligfield P, Lauer MS. Exercise electrocardiogram testing: beyond
the ST segment. Circulation 2006;114:2070-82.
Acta Cardiol Sin 2014;30:259-265