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Original 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] 143 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. 144 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. 145 Acta Cardiol Sin 2007;23:143-9 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;23:143-9 146 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. REFERENCES 1. Truett J, Cornfield J, Kannel W. A multivariate analysis of the risk of coronary heart disease in Framingham. J Chronic Dis 1967; 20:511-24. 2. Conroy RM, Pyorala K, Fitzgerald AP, et al. Estimation of ten-year risk of fatal cardiovascular disease in Europe: the SCORE Project. Eur Heart J 2003;24:987-1003. 3. O'Rourke MF, Gallagher DE. Pulse wave analysis. J Hypertens 147 Acta Cardiol Sin 2007;23:143-9 Ju-Yi Chen et al. Suppl 1996;14:S147-57. 4. Vincenti A, Brambilla R, Fumagalli MG, et al. Onset mechanism of paroxysmal atrial fibrillation detected by ambulatory Holter monitoring. Europace 2006;8:204-10. 5. Jensen TJ, Haarbo J, Pehrson SM, Thomsen B. Impact of premature atrial contractions in atrial fibrillation. PACE 2004; 27:447-52. 6. Agmon Y, Khandheria BK, Meissner I, et al. Association of atrial fibrillation and aortic atherosclerosis: a population-based study. Mayo Clin Proc 2001;76:252-9. 7. Tsai WC, Chen JY, Wang MC, et al. Association of risk factors with increased pulse wave velocity detected by a novel method using dual-channel photoplethysmography. Am J Hypertens 2005;18:1118-22. 8. Nurnberger J, Scheiber AK, Saez AMO, et al. Augmentation index is associated with cardiovascular risk. J Hypertens 2002; 20:2407-14. 9. O'Rourke M. Arterial stiffness, systolic blood pressure, and logical treatment of arterial hypertension. Hypertension 1990; 15:339-47. 10. Blacher J, Guerin AP, Pannier B, et al. Impact of aortic stiffness on survival in end-stage renal disease. Circulation 1999;99: 2434-9. 11. Laurent S, Boutouyrie P, Asmar R, et al. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients. Hypertension 2001;37:1236-41. 12. Meaume S, Benetos A, Henry OF, et al. Aortic pulse wave velocity predicts cardiovascular mortality in subjects > 70 years of age. Arterioscler Thromb Vasc Biol 2001;21:2046-50. 13. Cruickshank K, Riste L, Anderson SG, et al. Aortic pulse-wave velocity and its relationship to mortality in diabetes and glucose intolerance: An integrated index of vascular function? Circulation. 2002;106:2085-90. 14. Bramwell JC, Hill AV. Velocity of transmission of the pulse-wave and elasticity of the arteries. Lancet. 1922;i:891-2. 15. Safar ME, London GM. Therapeutic studies and arterial stiffness in hypertension: recommendations of the European Society of Hypertension. The Clinical Committee of Arterial Structure and Function. Working Group on Vascular Structure and Function of the European Society of Hypertension. J Hypertens. 2000;18: 1527-35. 16. Hayward CS, Kelly RP. Gender-related differences in the central Acta Cardiol Sin 2007;23:143-9 arterial pressure waveform. J Am Coll Cardiol 1997;30:1863-71. 17. Cameron JD, McGrath BP, Dart AM. Use of radial artery applanation tonometry and a generalized transfer function to determine aortic pressure augmentation in subjects with treated hypertension. J Am Coll Cardiol 1998;32:1214-20. 18. Nichols WW, Edwards DG. Arterial elastance and wave reflection augmentation of systolic blood pressure: deleterious effects and implications for therapy. J Cardiovasc Pharmacol Ther 2001;6:5-21. 19. Cuspidi C, Muiesan ML, Valagussa L. Comparative effects of candesartan and enalapril on left ventricular hypertrophy in patients with essential hypertension: the Candesartan Assessment in the Treatment of Cardiac Hypertrophy (CATCH) study. J Hypertens 2002;20:2293-300. 20. Rehman A, Rahman AR, Rasool AH. Effect of angiotensin II on pulse wave velocity in humans is mediated through angiotensin II type 1 (AT(1)) receptors. J Hum Hypertens 2002;16:261-6. 21. Matsuo T, Iwade K, Hirata N, et al. Improvement of arterial stiffness by the antioxidant and anti-inflammatory effects of short-term statin therapy in patients with hypercholesterolemia. Heart Vessels 2005;20:8-12. 22. Asmar RG, London GM, O'Rourke ME, Safar ME. Improvement in blood pressure, arterial stiffness and wave reflections with a very-low-dose perindopril/indapamide combination in hypertensive patient: a comparison with atenolol. Hypertension 2001; 38:922-6. 23. London GM, Asmar RG, O'Rourke MF, Safar ME. REASON Project Investigators. Mechanism(s) of selective systolic blood pressure reduction after a low-dose combination of perindopril/ indapamide in hypertensive subjects: comparison with atenolol. J Am Coll Cardiol 2004;43:92-9. 24. O'Rourke MF, Pauca AL. Augmentation of the aortic and central arterial pressure waveform. Blood Press Monit 2004;9:179-85. 25. Nichols WW, Singh BM. Augmentation index as a measure of peripheral vascular disease state. Curr Opin Cardiol 2002;17: 543-51. 26. Lonn E, Shaikholeslami R, Yi Q, et al. Effects of ramipril on left ventricular mass and function in cardiovascular patients with controlled blood pressure and with preserved left ventricular ejection fraction: a substudy of the Heart Outcomes Prevention Evaluation (HOPE) Trial. J Am Coll Cardiol 2004; 43:2200-6. 148 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