Download High Premature Atrial Complex Loads Indicate a High Central Aortic

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Acta Cardiol Sin 2007;23:143-9
High Premature Atrial Complex Loads Indicate a
High Central Aortic Pressure Index in
Young Low-Risk Patients
Ju-Yi Chen, Wei-Chuan Tsai, Cheng-Han Lee, Yi-Heng Li, Liang-Miin Tsai, Jyh-Hong Chen and Li-Jen Lin
Objectives: To elucidate the relation between premature atrial complex (PAC) loads and aortic stiffness in the
low-risk young population.
Methods: We enrolled 200 consecutive patients (< 50 years old; 95 men; mean age, 36 ± 10 years) who received a
24-h ambulatory electrocardiography (ECG) examination for palpitation. Aortic stiffness and two aortic pressure
indices — augmentation (AG) and the augmentation index (AIx) — were measured, and atherosclerosis risk factors
were evaluated. Patients with < 2 risk factors were defined as the low-risk group.
Results: Twenty-three patients (12%) had high PAC loads. Age (p = 0.037), AG (p = 0.022), and AIx (p = 0.008)
were significantly higher in these patients. Gender, risk factors, and drug history were not associated with high PAC
loads. A multivariate analysis showed high PAC loads (p = 0.036, OR 1.09, 95% C.I. 1.01~1.18) was an independent
factor associated with AIx.
In the low-risk group, 19 (14%) patients had high PAC loads. Age (p = 0.042), AG (p = 0.012), and AIx (p = 0.002)
were significantly higher in patients with high PAC loads. A multivariate analysis showed high PAC loads (p =
0.021, OR 1.23, 95% C.I. 1.03~1.41) was an independent factor associated with AIx in low-risk patients.
Conclusion: High PAC loads were significantly associated with increased central aortic pressure indices in young
subjects, especially in the low-risk subgroup. High PAC loads might be a surrogate marker of central aortic stiffness
in a low-risk group.
Key Words:
Augmentation index · Arterial stiffness · Atrial tachyarrhythmias
INTRODUCTION
cholesterol, and diabetes mellitus. Still, a large proportion
of individuals are not identified before they develop cardiovascular disease.2 Non-invasive tests to detect individuals with atherosclerosis or arterial stiffness, preferably
before they develop cardiovascular disease, may improve
the selection of subjects for preventive treatments.
Pulse wave analysis, a non-invasive test and expressed as a central augmentation index, suggests that
atherosclerosis of the aorta and peripheral arteries may
be detected as increased arterial stiffness, even before
patients develop cardiovascular disease.3 High premature
atrial contraction (PAC) loads might be the precursor of
paroxysmal atrial fibrillation (AF), which is the most
frequent cardiac arrhythmia and associated with almost
all cardiac diseases.4,5 We also know that, in the general
Many risk models for cardiovascular disease, like
the Framingham coronary risk model, have been used in
an attempt to identify those who derive the highest benefit from preventive treatment.1 Such models are based
primarily on age, gender, blood pressure, smoking status,
Received: June 19, 2007
Accepted: September 10, 2007
Division of Cardiology, Department of Internal Medicine, National
Cheng Kung University Hospital, Tainan, Taiwan.
Address correspondence and reprint requests to: Dr. Li-Jen Lin,
Division of Cardiology, Department of Internal Medicine, National
Cheng Kung University Hospital, No. 138 Sheng-Li Rd., Tainan 704,
Taiwan. Tel: 886-6-235-3535 ext. 2382; Fax: 886-6-275-3834; E-mail:
[email protected]
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Acta Cardiol Sin 2007;23:143-9
Ju-Yi Chen et al.
patients gave written informed consent for this study,
and the study protocol was approved by the Human Research Committee of our hospital.
population, AF is associated with aortic atherosclerosis
and stiffness. This association is related to age since
both atrial fibrillation and aortic atherosclerosis are more
frequent in the elderly.6 We hypothesized that high PAC
loads might be associated with aortic stiffness in lowrisk young subjects. To test this hypothesis, we studied
200 outpatients from whom we took 24-hour Holter electrocardiogram (ECG) recordings from Feb. 2005 through
Dec. 2005.
Measurement of pulse wave analysis by
applanation tonometry
Before any testing, all measurements (including blood pressure and heart rate) were made with the patient
supine for 20 min in a quiet, temperature-controlled laboratory at 26 ± 1 °C.
The right radial and carotid pulse waves were detected directly using a piezo-resistive pressure transducer
(Millar SPT 301; Millar Instruments, Houston, TX) coupled to an electronic sphygmometer (SphygmoCor Px
Aortic BP Waveform Analysis System; AtCor Medical
Pty. Ltd., West Ryde, NSW, Australia). The timing of
these waveforms was compared to that of the R wave on
a simultaneously recorded ECG. The carotid-to-radial
pulse wave velocity (PWV) was calculated by dividing
the transit time by the distance between these two pulses.
The principle of this non-invasive method consists in the
registration of a pulse waveform at the radial artery and
its derivation at the ascending aorta using a mathematical transformation expressed as the central augmentation
index. The systolic part of the central arterial waveform
is characterized by two pressure peaks. The first peak is
caused by left ventricular ejection, and the second peak
by wave reflection. Two aortic pressure indices measured were augmentation (AG) and augmentation index
(AIx). AG represents the difference between the second
and first systolic peaks of the central pressure waveform
(Figure 1). AIx is defined as the percentage of the central pulse pressure attributed to the reflected pulse wave;
it reflects the degree to which central arterial pressure is
augmented by wave reflection (Figure 1).3
METHODS
Study population
We recruited 200 consecutive young outpatients (all
less than 50 years old, 95 men, mean age 36 ± 10 years),
all of whom were given a 24-hour ambulatory ECG examination for palpitation. Patients with peripheral vascular occlusion diseases, finger deformities, critical valvular heart diseases, or chronic atrial fibrillation were
excluded. Traditional risk factors for atherosclerosis —
diabetes mellitus, hypertension, hypercholesterolemia,
current smoking, or a family history of premature coronary artery disease — were all carefully evaluated in
each patient. Diabetes mellitus was diagnosed if the fasting plasma glucose concentration was > 125 mg/dL on
two separate occasions or if the patient was being treated
with insulin or oral hypoglycemic agents. Hypertension
was diagnosed if blood pressure was > 140/90 mm Hg
on three occasions or if the patient was taking any antihypertensive medication. Hypercholesterolemia was
defined as a total serum cholesterol concentration of 200
mg/dL or if the subject patient was receiving lipidlowering therapy. Smokers were defined as those who
habitually smoked cigarettes (³ 20 cigarettes/day) at the
start of this study. A family history of premature coronary artery disease (CAD) was defined as patients whose
parents, siblings, or grandparents were with CAD before
the age of 55 years in men and 65 years in women. Patients with fewer than two risk factors were defined as
the low-risk group. Each patient’s anti-hypertension drug
use history — angiotensin-converting enzyme inhibitors,
angiotensin II receptor blockers, statins, b-adrenergic
blockers, and calcium channel blockers — was also carefully reviewed. All patients were asked to refrain from
taking their medications for one day before each test. All
Acta Cardiol Sin 2007;23:143-9
24-hour holter ECG
Twenty-four-hour Holter recordings were taken using a standard 3-channel flash card recorder (RZ153;
Rozinn Electronics, Glendale, NY). The ECG signal was
digitized and stored using a commercially available personal computer-based system. All recordings were visually scanned and analyzed using the RZ153 Holter Analysis System. High and low PAC loads were defined as
> or £ 24 beats of PAC per day, respectively, detected using an ambulatory ECG.
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Aortic Stiffness and Premature Atrial Complexes
tinuous variables, or the Pearson c2 or Fisher’s exact test
for categorical variables. Multiple logistic regression analysis was used to assess the independent factor for high
PAC load. All data are presented as the mean ± standard
deviation. Statistical significance was set at p < 0.05. All
analysis was performed using SPSS 11.5 for Windows
(SPSS Inc., Chicago, IL).
RESULTS
Correlation between high PAC loads and
central aortic stiffness
We divided the patients with PAC loads as low and
high PAC loads. We took the median number of 200 patients whose PAC loads (24 beats/day) as a cut-off point.
Twenty-three (12%; 10 men) of the 200 patients had high
PAC loads. These patients were older (40 ± 10 years vs.
35 ± 10 years, p = 0.037) and had higher AG (7.5 ± 5.8
mmHg vs. 4.5 ± 5.8 mmHg, p = 0.022) and AIx (22.7% ±
17.0% vs. 13.6% ± 14.8%, p = 0.008) levels (Table 1).
Figure 1. Aortic pressure wave synthesized from the measured radial
artery pressure wave (applanation tonometry) using a generalized
transfer function. Ps, peak systolic pressure; Pi, an inflection point that
indicates the beginning upstroke of the reflected pressure wave; Pd,
minimum diastolic pressure; AIx = (Ps - Pi)/(Ps - Pd).
Statistical analysis
Differences between patients with or without high
PAC loads were compared using Student’s t-test for con-
Table 1. Clinical characteristics of patients with high and low PAC loads compared
PAC loads:
Characteristic
High (n = 23)
Numbers (%)
Low (n = 177)
Numbers (%)
p value
Male
10 (43.5)
85 (48.0)
0.681
Age, years
40 ± 10
35 ± 10
0.037
Body weight, kg
60 ± 10
63 ± 13
0.345
Systolic blood pressure, mmHG
117 ± 180
117 ± 180
0.955
Diastolic blood pressure, mmHG
72 ± 12
70 ± 11
0.345
Mean blood pressure, mmHG
87 ± 13
86 ± 11
0.568
Heart rate, bpm
68 ± 11
71 ± 11
0.239
Background
Diabetes mellitus
1 (4.5)
4 (2.3)
0.546
Hypertension
2 (8.7)
27 (15.3)
0.091
Hyperlipidemia
05 (21.7)
34 (19.2)
0.773
Current smoker
04 (17.4)
54 (30.5)
0.192
Chronic renal failure
0 (0.0)
2 (1.1)
0.608
Hyperthyroidism
1 (4.3)
8 (4.5)
0.970
Family history of CAD
1 (4.5)
5 (2.8)
0.881
Angiotensin-converting enzyme inhibitors
2 (8.6)
12 (6.7)0
0.685
Angiotensin receptor blockers
0 (0.0)
4 (2.2)
0.586
Statins
0 (0.0)
0 (0.0)
1.000
b-adrenergic blockers
2 (8.6)
10 (5.6)0
0.571
Calcium channel blockers
1 (4.3)
11 (6.2)0
0.634
Applanation tonometry
Pulse wave velocity
8.2 ± 1.0
8.5 ± 1.1
0.211
Augmentation (mmHG)
7.5 ± 5.8
4.5 ± 5.8
0.022
Augmentation index (%)*
22.7 ± 17.0
13.6 ± 14.8
00.008*
*The independent factor associated with PAC loads after a multivariate analysis adjusted for age and mean blood pressure; p = 0.036;
OR = 1.09; 95% C.I. = 1.01~1.18. CAD = coronary artery disease.
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Ju-Yi Chen et al.
two separate measurements of PWV and AIx were high
(r = 0.959, p < 0.01 and r = 0.978, p < 0.01). There were
no significant differences between the two measurements (6.37 ± 1.05 vs. 6.29 ± 1.00 m/sec, p = 0.276;
mean difference 0.09 ± 0.35 m/sec and 14.20% ± 10.22%
vs. 14.40% ± 11.08%, p = 0.396; mean difference 0.12%
± 0.08%). The coefficient of variation was 5.8% as calculated by using a method reported in a previous study.7
There were no differences in gender, risk factors, or drug
history between patients with and without high PAC
loads. After multivariate analysis adjusted for age and
mean blood pressure, high PAC loads (p = 0.036, OR
1.09, 95% C.I. 1.01~1.18) was an independent factor associated with AIx (Table 1).
In the low-risk group (134 patients), 19 patients
(14%) had high PAC loads. Age (38 ± 10 years vs. 34 ±
10 years; p = 0.042), AG (6.8 ± 6.0 mmHg vs. 3.5 ± 5.1
mmHg, p = 0.012), and AIx (21.8% ± 18.5% vs. 11.9% ±
15.0%, p = 0.002) were significantly higher in patients
with high PAC loads (Table 2). After a multivariate analysis adjusted for age and mean blood pressure, high PAC
loads (p = 0.021; OR 1.23; 95% C.I. 1.03~1.41) was an
independent factor associated with AIx in low-risk patients (Table 2).
DISCUSSION
In the present study, we showed that high PAC loads
might be a surrogate marker for central aortic stiffness in
low-risk young outpatients undergoing 24-hour ambulatory ECG recordings. We believe that this is the report of
a statistically significant association between PAC loads
and the aortic augmentation index derived from a noninvasive pulse wave analysis.
Reproducibility of PWV and AIx
The intra-class correlation coefficient between the
Table 2. Clinical characteristics of patients with high and low PAC loads in the low-risk subgroup compared
PAC loads:
Characteristic
Male
Age, years
Body weight, kg
Systolic blood pressure, mmHG
Diastolic blood pressure, mmHG
Mean blood pressure, mmHG
Heart rate, bpm
Background
Diabetes mellitus
Hypertension
Hyperlipidemia
Current smoker
Chronic renal failure
Hyperthyroidism
Family history of CAD
Angiotensin converting enzyme inhibitors
Angiotensin receptor blockers
Statins
b-adrenergic blockers
Calcium channel blockers
Applanation tonometry
Pulse wave velocity
Augmentation (mmHG)
Augmentation index (%)
High (n = 19)
Numbers (%)
Low (n = 115)
Numbers (%)
p value
7 (36.8)
38 ± 10
60 ± 12
117 ± 190
74 ± 11
88 ± 13
70 ± 11
40 (34.8)
34 ± 10
58 ± 80
113 ± 160
71 ± 11
85 ± 11
69 ± 11
0.688
0.042
0.397
0.333
0.554
0.250
0.966
0 (0)0.
02 (10.5)
02 (10.5)
1 (5.3)
0 (0.0)
1 (5.3)
03 (15.8)
1 (5.2)
0 (0.0)
0 (0.0)
1 (5.2)
1 (5.2)
4 (3.5)
10 (8.7)0
12 (10.4)
5 (4.3)
2 (1.7)
8 (7.0)
12 (10.4)
2 (1.7)
1 (0.8)
0 (0.0)
3 (2.6)
4 (3.4)
0.546
0.691
0.773
0.492
0.608
0.670
0.381
0.575
0.693
1.000
0.725
0.833
8.2 ± 1.0
6.8 ± 6.0
21.8 ± 18.5
8.2 ± 1.0
3.5 ± 5.1
11.9 ± 15.0
0.857
0.012
00.002*
*The independent factor associated with PAC loads after a multivariate analysis adjusted for age and mean blood pressure; p = 0.021;
OR = 1.23; 95% C.I. = 1.03~1.41. CAD = coronary artery disease.
Acta Cardiol Sin 2007;23:143-9
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Aortic Stiffness and Premature Atrial Complexes
We found that central aortic AIx rather than arterial
PWV was significantly correlated with high PAC loads
in low-risk young outpatients. Other studies have shown
that aortic stiffness is a risk factor for cardiovascular
events8,9 and an independent predictor of all-cause and
cardiovascular mortality in selected patient groups.10-13
Physiologically, the stiffness of the large arteries depends on three main factors: structural elements within
the arterial wall, such as elastin and collagen; distending
pressure; and vascular smooth muscle tone. Non-invasive tests to detect individuals with atherosclerosis or
arterial stiffness, preferably before they develop cardiovascular disease, may improve the selection of subjects
for preventive treatments. Arterial PWV provides a robust measure of arterial stiffness,14 and AIx provides a
composite measure of elastic plus muscular arterial stiffness and wave reflection.15 Aortic AIx is also a parameter
measured using pulse wave analysis; it is considered a
surrogate measure of aortic stiffness. Age, gender, and
blood pressure are known determinants of AIx.16,17 Central AIx is related to arterial properties via changes in
PWV. Increased arterial stiffness increases PWV and
causes an early return of the reflected wave from peripheral reflecting sites to the heart during systole when the
ventricle is still ejecting blood.18 This mechanism augments ascending aortic systolic and pulse pressures, an
effect that increases arterial wall stress and potentiates
the development of atherosclerosis.18
After a multivariate analysis adjusted for age and
blood pressure, we also found that high PAC loads were
significantly associated with aortic AIx in low-risk young
outpatients. This connoted that high PAC loads might be
a surrogate marker for aortic stiffness in the early stage
of atherosclerosis in the low-risk young population. Although patients with frequent PAC may be asymptomatic
or only mildly symptomatic, high PAC loads may be an
important marker for central aortic stiffness and, therefore, reflect a higher degree of atherosclerosis. It has
been proved that angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and statins effectively lower blood pressure and improve arterial stiffness.19-21 Vasodilator drugs decrease arterial stiffness and
PWV, thus reducing wave reflection via a delayed return
of the reflected wave from the periphery to the heart
while decreasing its amplitude and systolic duration.22-25
Morphologically, the reflected wave (second pressure
peak) on the radial pressure wave migrates rightward
and down. These modifications of reflected wave characteristics reduce central pulse pressure and AIx.26 badrenergic antagonists might also lower PAC loads. The
impact of drugs on PAC loads and arterial stiffness were
insignificantly different between high and low PAC-load
subgroups in our study.
Study limitations
First, our study was limited by its cross-sectional
rather than a longitudinal design. However, after a careful multivariate analysis that considered all possible
factors, high PAC loads were still significantly associated with increased arterial stiffness in patients undergoing a 24-hour ambulatory ECG. Second, the sympathetic and parasympathetic imbalance is clinically related
to the occurrence of PAC, and an increased sympathetic
tone is also related to an increased aortic stiffness. The
parameters of heart rate variability should be recorded.
Finally, we did not measure the left ventricular systolic
(by ejection fraction) and diastolic performances (by
tissue Doppler) using echocardiography. The measurements might rationalize that increased aortic stiffness
leads to abnormal left ventricular systolic or diastolic performance which in turn increases left atrial pressure or
size, leading to high PAC loads in this study population.
CONCLUSION
High PAC loads were significantly associated with
increased central aortic pressure indices in young lowrisk outpatients. High PAC loads were a surrogate marker of central aortic stiffness in this study population,
which may further indicate the progression of atherosclerosis.
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Original
Acta Cardiol Sin 2007;23:143−9
在年輕低危險族群中，高的早發性心房收縮數
意味著有高的大動脈硬度指數
陳儒逸
背景
係。
蔡惟全 李政翰 李貽恆 蔡良敏 陳志鴻
台南市 成大醫學院附設醫院 心臟內科
林立人
本研究目的在檢驗在年輕低危險族群中，早發性心房收縮數與大動脈硬度指數之關
方法 本計畫包括 200 位病患因為心悸而接受二十四小時心電圖檢查並同時測量兩個大動
脈硬度指標 − 動脈反射波增強 (Augmentation: AG) 及動脈反射波增強指數 (Augmentation
index: AIx)。我們同時紀錄病患之血管粥狀硬化危險因子。少於兩個危險因子的為低危險
族群。
結果 在本研究的 200 位病患中，有 23 位病患 (12%) 有高的早發性心房收縮數。他們有
比較高的年紀 (p = 0.037)、動脈反射波增強 (p = 0.022)、及動脈反射波增強指數 (p =
0.008)。而性別、危險因子、及藥物史並無差異。在多變數分析中，高的早發性心房收縮
數 (p = 0.036) 是與動脈反射波增強指數相關之獨立因子。在本研究的 200 位病患中，有 134
位屬於低危險族群。其中 19 位病患 (14%) 有高的早發性心房收縮數。他們有比較高的年
紀 (p = 0.042)、動脈反射波增強 (p = 0.012)、及動脈反射波增強指數 (p = 0.002)。在多變
數分析中，高的早發性心房收縮數 (p = 0.021) 是與動脈反射波增強指數相關之獨立因子。
結論 我們認為在年輕低危險族群中，高的早發性心房收縮數與高的大動脈硬度指數具有
有意義之相關。高的早發性心房收縮數可能是大動脈硬度的預測因子。
關鍵詞：動脈反射波增強指數、動脈硬度、心房性心搏過速心律不整。
149