Download Responses of cardiac natriuretic peptides after paroxysmal

Articles in PresS. Am J Physiol Heart Circ Physiol (January 22, 2016). doi:10.1152/ajpheart.00668.2015
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Responses of cardiac natriuretic peptides after paroxysmal supraventricular
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tachycardia: ANP surges faster than BNP and CNP
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Jen-Yuan Kuo1,4, An-Mei Wang2, Sheng-Hsiung Chang1,3, Chung-Lieh Hung1,3,4,
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Chun-Yen Chen1,4, Bing-Fu Shih2, Hung-I Yeh1,3,4,*
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Running title: Natriuretic peptides and PSVT
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Medicine, MacKay Memorial Hospital, 3Mackay Medicine, Nursing, and
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Management College, and 4Mackay Medical College, Taipei, Taiwan
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AUTHOR CONTRIBUTIONS
Division of Cardiology, Department of Internal Medicine, 2Department of Nuclear
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Kuo JY and Yeh HI conception and design of research; Kuo JY, Chang SH, and Hung
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CL performed clinical studies; Wang AM measured plasma levels of natriuretic
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peptides; Kuo JY and Chen CY analyzed data; Kuo JY, Shih BF, and Yeh HI
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interpreted results of experiments; Kuo JY drafted manuscript; Yeh HI revised
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manuscript.
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*Corresponding author
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Hung-I Yeh
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Division of Cardiology
Tel: 886-2-2543-3535 ext. 2456
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MacKay Memorial Hospital
E-mail: [email protected] mailto:
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92, Sec 2, Chung Shan North Road, Taipei 10449, Taiwan
Fax: 886-2-2543-3642
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Copyright © 2016 by the American Physiological Society.
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Abstract
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Aims: Atrial natriuretic peptide (ANP) secretion increases after a 30-minute of
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paroxysmal supraventricular tachycardia (PSVT). Whether this phenomenon also
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applies to brain or C-type natriuretic peptides (BNP or CNP) remains unknown.
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Methods and Results: Blood samples of 18 patients (41±11 years old; 4 males) with
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symptomatic PSVT and normal left ventricular systolic function (ejection fraction
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65±6 %) were collected from the coronary sinus (CS) and the femoral artery (FA)
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before and 30 minutes after the induction, and 30 minutes after the termination of
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PSVT. The results showed that the ANP levels rose steeply after the PSVT and then
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reduced at 30 minutes after the termination (baseline vs. post PSVT vs. post
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termination, CS: 34.0±29.6 vs. 74.1±42.3 vs. 46.1±32.9; FA: 5.9±3.24 vs. 28.2±20.7
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vs. 10.0±4.6 pg/ml; all P < 0.05). In contrast, compared to ANP, the increases of BNP
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and CNP in CS after the PSVT were less sharp, but continued to rise after the
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termination of tachycardia (BNP, 10.2±6.4 vs. 11.3±7.1 vs. 11.8 ± 7.9; CNP, 4.5±1.2
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vs. 4.9±1.4 vs. 5.0±1.4 pg/ml; all P < 0.05). The rise of BNP and CNP in FA was
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similarly less sharp after the PSVT and remained stationary after the termination.
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Conclusion: PSVT exerted differential effects on cardiac natriuretic peptides levels.
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ANP increased greater after a 30-minute induced PSVT but dropped faster after
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termination of PSVT, as compared to BNP and CNP.
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Keywords: ANP; BNP; CNP; Natriuretic peptide; Paroxysmal supraventricular
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tachycardia
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New & Noteworthy
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This research article showed for the first time that PSVT exerted differential
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effects on cardiac natriuretic peptides levels. ANP increased greater after a 30-minute
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induced PSVT, but dropped faster after termination of PSVT, as compared to BNP
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and CNP.
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Introduction
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Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type
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natriuretic peptide (CNP) are a family of structurally related peptides that participate
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in the integrated control of renal and cardiovascular function. ANP is a 28-amino acid
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peptide that is secreted from the atria and possesses natriuretic, vasoactive, and
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rennin-inhibiting actions (4, 6). BNP, also found in the heart, is a 32-amino acid
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peptide that shares structural and biological similarity to ANP (15). CNP, a
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vasorelaxant with a half-life of 2.6 minutes, is a 22-amino acid peptide that was first
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isolated from the porcine brain in 1990 (21). Although it shares structural and
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physiological properties with ANP and BNP, it appears to be secreted predominantly
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from the vascular endothelium (22, 25). In ventricular tissue, immunohistochemical
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staining confirmed the presence of all three peptides in normal hearts and was
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markedly enhanced in those with congestive heart failure (9, 26).
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Some studies have shown a marked increase of ANP secretion after PSVT
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sustains for 30 minutes (11, 24). Whether this phenomenon also occurs for BNP and
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CNP is unknown. We previously found that the myocardium regularly produced or
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released CNP in patients with normal LV systolic function. Brief periods of rapid right
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atrial pacing (with pacing cycle lengths starting from 750 ms, in 50 ms decrement, to
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a minimum of 400 ms, each for 2 minutes and rest for 2 minutes) or PSVT (sustained
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less than 2 minute) did not change the production and/or release (13). The aim of this
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study was to compare the response of the 3 peptides against a 30-minute induced
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PSVT.
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Methods
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Consecutive patients with clinically documented, symptomatic PSVT were
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referred to this laboratory for electrophysiological study (EPS) and radiofrequency
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(RF) ablation. The patients with age between 20 and 60 years old and relatively
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healthy were enrolled into the study. The patients who had chronic obstructive lung
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disease, abnormal renal function, impaired left ventricular systolic function, previous
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myocardial infarction, or coronary artery disease which may affect endothelial
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function were excluded from the study. Routine coronary angiography was performed
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in patients who were older than 45 years old. Twelve-lead electrocardiogram,
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treadmill exercise test, myocardial perfusion scan, and/or coronary angiography were
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used to exclude coronary artery disease if necessary. Ethical approval was granted by
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the Institute Review Board of our hospital. All patients had signed written consent
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forms.
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Electrophysiological test and radiofrequency ablation
Electrophysiological study was performed while the patient was fasting and not
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sedated. All antiarrhythmic medications were discontinued for at least 5 half-lives
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before study, and anti-diabetic agents were held on the day of study. Details of the
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electrophysiological study have been described previously (12). In brief, the
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diagnostic portion of the electrophysiological study included: (i) measurement of the
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electrical properties of the atrium, AV node, ventricle, and accessory pathways; (ii)
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induction of supraventricular tachycardia by programmed atrial and ventricular burst
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pacing or extrastimuli; and (iii) determination of the mechanism of tachycardia. If
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tachycardia could not be induced in the baseline state, isoproterenol (1 to 4 µg/min IV)
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was infused to facilitate its induction. AVNRT, AT and AVRT were diagnosed and
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differentiated from each other by previously described criteria.
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A 7F quadripolar electrode catheter with a 4-mm distal electrode and a
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thermistor-embedded tip (Daig, Bard, or EP Technologies, Inc.) was used for ablation.
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Radiofrequency energy was delivered from a generator (EPT 1000, USA). The
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maximal preset temperature was 70°C in every patient with AVRT, or 60°C in patients
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with AT or AVNRT. The ablation techniques used in various types of tachycardias
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have been described previously (12).
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Collection of blood sample and measurement of natriuretic peptides
Six samples, 2 ml for each, were collected from each patient. First, blood
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samples were collected from the CS and the FA immediately after four multipolar
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electrode catheters (Response CSL and Livewire, St. Jude Medical, Daig Division,
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Inc., Minnetonka, MN, USA) were positioned in the CS, the RA, the His-bundle area,
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and the right ventricle (RV) under fluoroscopy. The location of the CS mapping
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catheter in CS was confirmed by direct contrast medium injection via the catheter.
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Second, PSVT was induced and allowed to continue for 30 minutes, while the RA, RV,
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and His mapping catheters were withdrawn to the inferior vena cava in the meantime
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for safety reason. Then, PSVT was terminated by ventricular or atrial rapid pacing
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immediately and blood samples were collected from the CS and the FA. Third, blood
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samples were collected from the CS and the FA at 30 minutes after the termination of
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PSVT. Heart rate, blood pressure, and RA pressure were recorded before PSVT, 30
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minutes after the induction of PSVT, and 30 minutes after the termination of PSVT.
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Details of the quantification of plasma natriuretic peptides in this laboratory have
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been described previously (8, 13). In brief, blood samples were collected into chilled
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test tubes containing ethylene diamine tetraacetic acid (EDTA) and aprotinin (0.6 TIU
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per ml blood; Phoenix Pharmaceuticals, California, USA). Samples were immediately
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centrifuged and plasma stored at -80℃ until measurement. The plasma levels of
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naturiuretic peptides were determined by a blinded operator (Wang AM) using RIA
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method with commercially available kits (Phoenix Pharmaceuticals, California, USA ),
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conducted according to the manufacturer’s manual. The intra-assay co-efficient of
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variation was 7.5% for ANP, 6.5% for BNP, and 6.9% for CNP. The lower limit of
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detection was 1 pg/ml.
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Determination of LV function by echocardiography
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Cardiac function was evaluated using echocardiography. An ejection fraction of
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LV > 50% without regional wall motion abnormality was considered as normal LV
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systolic function. The LV ejection fraction was measured by (LV diastolic volume –
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LV systolic volume) / LV diastolic volume.
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Statistical analysis
Quantitative data were expressed as mean ± standard deviation. Parametric data
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were compared by ANOVA or t test, and categorical data were analyzed by the
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Chi-square test with Yates’ correction or Fisher’s exact test. P<0.05 was considered
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statistically significant.
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Result
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Eighteen patients (4 men and 14 women, mean age 41±11 years old) were
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enrolled into the study. The baseline characteristics of patients were listed in table 1.
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Two had diabetes mellitus with well-controlled blood sugar, two had hypertension
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with well-controlled blood pressure, and one had mild left ventricular hypertrophy.
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Twelve-lead electrocardiogram of all the patients showed no myocardial ischemia. No
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patient had angina symptoms. Routine coronary angiography was performed in 7
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patients who were older than 45 years old. No patient had chronic obstructive lung
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disease, previous myocardial infarction, coronary artery disease, or angina. No patient
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underwent study within 1 week of the last PSVT. All patients had normal renal
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function (serum creatinine 0.7±0.2 mg/dl) and left ventricular (LV) systolic function
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(LV ejection fraction 65±6 %). All of the 18 patients had successful RF ablation for
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their PSVT, and did not have recurrence during two-year follow-up. Two additional
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patients were excluded from analysis because they did not complete the blood test due
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to no inducible PSVT in the electrophysiological laboratory.
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The ANP levels at 30 minutes after the induction of PSVT were significantly
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higher than those before the induction of PSVT (CS, 74.1±42.3 vs. 34.0±29.6; FA,
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28.2± 20.7vs 5.9±3.24 pg/ml; both P < 0.001). The ANP levels at 30 minutes after the
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termination of PSVT were also significantly higher than those before the induction
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(CS, 46.1±32.9 vs. 34.0±29.6; FA, 10.0±4.6 vs. 5.9±3.24 pg/ml; both P < 0.05).
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Moreover, the ANP levels at 30 minutes after the induction of tachycardia were
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significantly higher than those at 30 minutes after the termination of PSVT (CS,
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74.1±42.3 vs. 46.1±32.9, P< 0.05; FA, 28.2±20.7 vs. 10.0±4.6, P< 0.001) (Figure 1).
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The BNP levels at 30 minutes after the induction of PSVT were significantly higher
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than those before the induction of PSVT (CS, 11.3±7.1 vs. 10.2±6.4; FA, 9.6±6 vs.
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8.7±5.6 pg/ml; both P < 0.05). The BNP levels in CS at 30 minutes after the
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termination of PSVT were also significantly higher than those before the induction of
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PSVT (11.8±7.9 vs. 10.2±6.4 pg/ml; P < 0.05). However, there was no significant
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difference between baseline and 30 minutes after the termination of PSVT in FA.
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(9.1±6.3 vs. 8.7±5.6 pg/ml; P = 0.29) There was also no significant difference
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between the BNP levels at 30 minutes after the induction of PSVT and those at 30
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minutes after the termination (Figure 2). The CNP levels at 30 minutes after the
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induction of PSVT were significantly higher than those before the induction of PSVT
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(CS, 4.9±1.4 vs. 4.5±1.2; FA, 4.3±1.1 vs. 3.9±0.9 pg/ml; both P < 0.005). The CNP
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levels in CS at 30 minutes after the termination of PSVT were also significantly
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higher than those before the induction of PSVT (5±1.4 vs. 4.5±1.2 pg/ml; P = 0.005).
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However, there was no significant difference between baseline and 30 minutes after
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the termination of PSVT in FA (4.1±0.9 vs. 3.9±0.9 pg/ml; P = 0.07). There was also
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no significant difference between the CNP levels at 30 minutes after the induction of
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PSVT and those at 30 minutes after the termination (Figure 3). In 150 of 162 (92.6%)
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pairs of natriuretic peptide values, the natriuretic peptide levels in the CS were higher
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than those in the femoral artery. The ANP, BNP, and CNP levels in the CS at each
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time point were significantly higher than those in the femoral artery (Figure 4, all
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P<0.001). However, the transcardiac net production or release of natriuretic peptides
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did not correlate with the heart rate, tachycardia rate, RA pressure, or blood pressure.
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The mean RA pressure at 30 minutes after the induction of PSVT was
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significantly higher than that before the induction of PSVT (6±4 vs. 4±2 mmHg; P <
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0.01) (Figure 5). However, the change did not correlate with any of the natriuretic
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peptide levels (all P > 0.05). Baseline heart rate, tachycardia rate, or blood pressure
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also did not correlate with the natriuretic peptide levels.
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Discussion
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Major findings
This study showed that ANP, BNP, and CNP levels in the CS at baseline and each
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time point after PSVT were significantly higher than those in the FA in individuals
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with PSVT and normal LV systolic function, indicating that, in the body, the heart is a
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major source of natriuretic peptides, including ANP, BNP, and CNP, at rest and post
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PSVT. In addition, sustained PSVT for 30 minutes could enhance the heart to release
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ANP, BNP, and CNP. The increase of ANP to PSVT was to a greater degree but
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dropped faster, as compared to BNP and CNP.
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Previous reports regarding production or release of natriuretic peptides during
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PSVT
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Several previous studies showed that induction or spontaneous initiation of PSVT
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resulted in a marked elevation of plasma ANP levels (11, 17, 20, 23, 24). However,
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the effects of PSVT on the ANP levels remained discrepant. Tsai et al. showed that
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immediately after the induction of PSVT, plasma ANP levels began to increase,
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peaked at 32 minutes (734% increment on average), and then gradually decreased in 5
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patients. The ANP levels significantly increased at 15 minutes, 30 minutes after the
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induction of PSVT, and 5 minutes after the termination of PSVT, compared to those
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of control, but showed no significant increase at 5 minutes after the induction of
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PSVT, 15 or 30 minutes after the termination of PSVT (24). Kojima et al. found that
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plasma ANP levels in 10 patients with PSVT significant increased from 37±11 pg/ml
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during the control period to 110 pg/ml at 30 minutes, 160±54 pg/ml at 60 minutes
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after the induction of PSVT, and to 90 pg/ml at 30 minutes after the termination of
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PSVT (11). Anderson et al. showed that induction of AVRT in 3 patients produced an
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acute and marked rise in plasma ANP concentrations, which returned to normal at 30
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minutes after restoration of the sinus rhythm (1). In that study, the PSVT was allowed
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to sustain for 10.5 minutes, 30 minutes, and 42 minutes, respectively. In the present
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study, we found that the plasma ANP levels significantly increased at 30 minutes after
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the induction of PSVT, compared to those before PSVT. The ANP levels significantly
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fell at 30 minutes after the termination of PSVT, but still significantly higher than
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those before PSVT. These findings were consistent with Kojima and their coworker’s
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findings. However, the response of the ANP to PSVT in FA was greater in this study
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(+378% VS +197%). In the study of Tsai et al., the ANP levels at 30 minutes after
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termination of PSVT remained high than those of control, but showed no significant
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difference (9). Small patient numbers (N=5) might be one of the reasons. Taken
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together, with more patients and a strict protocol, the present study unequivocally
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showed that the release of ANP continued for at least 30 minutes after termination of
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PSVT.
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Mechanisms of myocardial production or release of natriuretic peptides during
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PSVT
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In a rat study, Dietz showed that an increase in blood volume resulted in the
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release of an ANP via atrial stretch (7). Lang et al. also demonstrated that increased
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atrial stretch or ventricular stretch, such as volume overload led to increased secretion
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of ANP in atria and BNP in ventricles respectively (14). Increases in ANP were also
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found during both pacing-stimulated and spontaneously PSVT in the study of Nicklas
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et al (16). They speculated that the stimulus to ANP secretion during PSVT appears to
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be related to the rise in right atrial pressure rather than to the increase in heart rate.
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However, several studies showed that a significant positive correlation was found
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between plasma ANP levels and mean pulmonary capillary wedge pressure, while the
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correlation between plasma ANP levels and mean right atrial pressure was not
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significant (19, 24). In the present study, we found that there was no significant linear
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correlation between RA pressure and ANP levels, although the mean RA pressure at
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30 minutes after the induction of PSVT was significantly higher than that before
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PSVT and ANP levels did increase in the CS and FA. This might imply that the LA
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pressure plays more important role than the RA pressure in the production or release
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of ANP. However, the underlying mechanism remains unclear. Different effects of
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right and left atrial stretch by volume or pressure overload might partially explain the
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different results. Further studies are required to elucidate this issue.
The mechanisms regulating myocardial production or release of BNP and CNP
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in arrhythmias or tachycardias remain unclear. Kalra et al. suggested that elevated
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ventricular filling pressure may contribute to the increased production of CNP in
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patients with CHF (10). Borgeson et al. showed that acute intravascular volume
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overload in dogs resulted in the expected increase in right atrial pressure, PCWP,
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plasma ANP, and urinary CNP, but no change in plasma BNP and CNP levels (2).
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Rademaker et al. found that acute ventricular pacing for 1.5 hours in sheep increased
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plasma ANP and BNP levels by 8.6- and 3.6-fold, respectively, whereas chronic
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ventricular pacing for 4 days increased ANP and BNP by 7.8- and 9-fold, respectively
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(18). There was no study investigating whether a 30-minute induced PSVT in patients
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could affect the production or release of BNP or CNP in the past. In the present study
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we showed that plasma BNP and CNP levels significantly increased after a 30-minute
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of PSVT and remained raised at 30 minutes after the termination of PSVT. Enough
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loading of ventricular and/or atrial stretch during PSVT might enhance the release of
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BNP and CNP. Previously, we demonstrated that brief periods of rapid atrial pacing,
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short-term PSVT (less than 2 minutes), routine EPS or RF ablation procedure did not
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increase the production or release of CNP (13). The different baseline CNP values
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might be due to different clinical characteristics, such as LVEF, age, and baseline
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heart rate between these two groups. The different changes of CNP values in CS and
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FA might be due to different duration of PSVT. However, how long of PSVT is
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necessary to enhance the release of BNP and CNP remains unknown. The half-life of
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BNP was longer than that of ANP or CNP. This might partially explain why BNP
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remained raised while ANP fell at 30 minutes after the termination of PSVT in the CS.
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However, it could not explain why CNP also remained raised at 30 minutes after the
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termination of PSVT. There might be other factors affecting the production or release
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of CNP. Another possible explanation was that the start of production or release of
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BNP and CNP could last longer than that of ANP after the stimulation of 30-minute
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PSVT. Again, further studies are required to elucidate the underlying mechanism.
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Study limitations
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This study has several limitations. First, the sample size of the study is small. If
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more patients could be enrolled into the study, there would be more power to draw the
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current conclusion. However, it’s the largest patient group to test the effects of
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paroxysmal supraventricular tachycardia on cardiac natriuretic peptide levels in the
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literature so far. Second, we might suspect that the length and the frequency of
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previous PSVT could affect the production of natriuretic peptide at baseline or the
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response to the PSVT. In this study, the length of previous PSVT ranged from
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several-decade minutes to several hours and the frequency of previous PSVT ranged
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from several times a month to several times a year in these patients. These might have
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chance to affect the production of natriuretic peptide at baseline although we did not
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know how much the influence was. However, no patient underwent study within 1
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week of the last PSVT. We speculated that the influence might be tiny. Third, to
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record heart rate, blood pressure, and urine amount, and to check the plasma renin
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activity, serum aldosterone level, and urine sodium value may help to understand the
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pathophysiology of myocardial release and/or production of natriuretic peptides.
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However, in this study, we only recorded blood pressure and heart rate, and found that
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they did not correlate with any of the natriuretic peptide levels. Fourth, to measure
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right atrial pressure, pulmonary arterial pressure, ventricular pressure, and pulmonary
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capillary wedge pressure of patients may help understand the mechanisms of
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increment of natriuretic peptides after an induced PSVT sustaining for 30 minutes.
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However, because it was not the routine procedure during the mapping and ablation of
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PSVT, we did not attempt to measure all of them. In this study, we only recorded right
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atrial pressure, and found that they did not correlate with any of the natriuretic peptide
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levels. Fifth, radiofrequency ablation may have its own acute and chronic effects on
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natriuretic peptides. Previously, we found that the production or release of CNP did
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not change at the end of EPS and/or radiofrequency ablation (13). In the literature,
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only two previous studies investigated the effect of radiofrequency ablation on plasma
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natriuretic peptide in patients with paroxysmal supraventricular tachycardia. One
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study showed that increment of plasma BNP level 3 and 24 hours after radiofrequency
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ablation, but no increment of plasma BNP level 30 minutes after radiofrequency
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ablation (5). The other study showed that levels of NT-proANP were significantly
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higher before RF ablation as compared to day one and day 120 after RF ablation.
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However, that study had no data regarding the level of natriuretic peptides within 3
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hours after RF ablation (3). The blood samples were collected within 30 minutes after
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radiofrequency ablation in all of our patients. Whether plasma levels of ANP or CNP
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would increase 30 minutes after RF ablation remained unknown before.
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Clinical implications
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To assay the plasma levels of ANP, BNP and CNP might have diagnostic
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significance for differentiating PSVT from non-PSVT palpitations. Other more
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serious cardiac diseases, such as congestive heart failure resulting from different
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cardiac etiologies, have more atrial and/or ventricular pressure or volume overload.
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Whether differential responses of ANP, BNP, and CNP have more values of diagnosis
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or evaluation of treatment or not deserve further investigation.
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Conclusions
PSVT exerted differential effects on cardiac natriuretic peptides levels in persons
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with PSVT and normal LV systolic function. ANP increased greater after a 30-minute
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induced PSVT, but dropped faster after termination of PSVT, as compared to BNP
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and CNP.
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Acknowledgments
We thank Hsin-Yu Chiu for the assistance of data collection, and Nikida Huang
for the assistance of figure preparation.
Grants
This study was supported by grants MMH-9585 from the Department of Medical
Research, MacKay Memorial Hospital, Taipei, Taiwan.
Disclosures
No conflicts of interest, financial or otherwise, are declared by the authors.
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27
430
Figure Legends
431
432
Figure 1. Changes in plasma atrial natriuretic peptide level in CS (A) and FA (B)
433
before, during, and after paroxysmal supraventricular tachycardia. P < 0.001, CS vs.
434
FA at each time point; CS= coronary sinus, FA= femoral artery, PSVT= paroxysmal
435
supraventricular tachycardia.
436
437
Figure 2. Changes in plasma brain natriuretic peptide level in CS (A) and FA (B)
438
before, during, and after paroxysmal supraventricular tachycardia. P < 0.001, CS vs.
439
FA at each time point; CS= coronary sinus, FA= femoral artery, PSVT= paroxysmal
440
supraventricular tachycardia.
441
442
Figure 3. Changes in plasma C-type natriuretic peptide level in CS (A) and FA (B)
443
before, during, and after paroxysmal supraventricular tachycardia. P < 0.001, CS vs.
444
FA at each time point; CS= coronary sinus, FA= femoral artery, PSVT= paroxysmal
445
supraventricular tachycardia.
446
447
Figure 4. Natriuretic peptide levels in the coronary sinus and femoral artery at each
448
time point. (A) Plasma atrial natriuretic peptide level in CS and FA. (B) Plasma brain
449
natriuretic peptide level in CS and FA. (C) Plasma C-type natriuretic peptide level in
450
CS and FA. CS= coronary sinus, FA= femoral artery.
451
452
Figure 5. Mean right atrial pressure at each time point of paroxysmal supraventricular
453
tachycardia.＊P < 0.001, after PSVT-30 vs. before PSVT; †P < 0.01, PSVT-15 or
454
PSVT-30 vs. before PSVT; ‡P < 0.05, PSVT-0 vs. before PSVT; RAP= mean right
455
atrial pressure, PSVT= paroxysmal supraventricular tachycardia.
28
456
Table legend
457
458
459
460
461
AVNRT= atrioventricular reentrant tachycardia; B-BP= baseline blood pressure;
B-HR= baseline heart rate; BMI= body mass index; BSCL= baseline sinus cycle
length; CAD= coronary artery disease; Cr= serum creatinine; DM= diabetes mellitus;
HF= heart failure; HTN= hypertension; LVEF= left ventricular ejection fraction;
462
463
464
465
LVH= left ventricular hypertrophy; OAVRT= orthodromic atrioventricular
reciprocating tachycardia; PSVT= paroxysmal supraventricular tachycardia;
PSVT-HR= heart rate of paroxysmal supraventricular tachycardia; TCL= tachycardia
cycle length.
466
29
p<0.05
(A)
p<0.001
p<0.05
180.0
160.0
ANP (pg/ml)
140.0
120.0
100.0
80.0
60.0
40.0
20.0
0.0
Before PSVT
PSVT-30
After PSVT-30
p<0.05
(B)
90.0
p<0.001
p<0.001
80.0
ANP (pg/ml)
70.0
60.0
50.0
40.0
30.0
20.0
10.0
0.0
0.0
Before PSVT
PSVT-30
After PSVT-30
(A)
p<0.05
p<0.05
p=NS
30.0
BNP (pg/ml)
25.0
20.0
15.0
10.0
5.0
0.0
Before PSVT
(B)
After PSVT-30
PSVT-30
p=NS
p<0.05
p=NS
25.0
BNP (pg/ml)
20.0
15.0
10.0
5.0
0.0
0.0
Before PSVT
PSVT-30
After PSVT-30
p<0.01
(A)
p<0.01
p=NS
9.0
8.0
CNP (pg/ml)
7.0
6.0
5.0
4.0
3.0
0.0
0.0
Before PSVT
PSVT-30
After PSVT-30
p=NS
(B)
7.0
p<0.005
p=NS
6.5
6.0
CNP (pg/ml)
5.5
5.0
4.5
4.0
3.5
3.0
2.5
0.0
0.0
Before PSVT
PSVT-30
After PSVT-30
p<0.001
p<0.001
Before PSVT
PSVT-30
After PSVT-30
p<0.001
p<0.001
p<0.001
Before PSVT
PSVT-30
After PSVT-30
p<0.001
p<0.001
p<0.001
PSVT-30
After PSVT-30
p<0.001
ANP (pg/ml)
(A)
180.0
160.0
140.0
120.0
100.0
80.0
60.0
40.0
20.0
0.0
(B)
30.0
BNP (pg/ml)
25.0
20.0
15.0
10.0
5.0
0.0
(C)
9.0
8.0
CNP (pg/ml)
7.0
6.0
5.0
4.0
3.0
2.0
0.0
Before PSVT
12
RAP (mmHg)
10
8
‡
†
6
†
4
点
2
0
Before
PSVT
PSVT-0
PSVT-15
PSVT-30
After
PSVT-15
After
PSVT-30
Table. Patient characteristics
Patient No.
Gender
Age
type of PSVT
LVEF(%)
Cr
BMI
B-BP
B-HR
BSCL (msec)
PSVT-HR
TCL (msec)
HF
HTN
CAD/Angina
LVH
DM
Medication
1
F
27
AVNRT
59
0.7
20.64
94/55
88
682
190
315
-
-
-
-
-
Verapamil, Fludiazepam
2
F
51
AVNRT
79
0.6
20.7
140/80
98
612
209
287
-
-
-
-
-
Propranolol, Fludiazepam
3
M
19
OAVRT
70
0.8
25.35
120/70
72
833
139
431
-
-
-
-
-
Propafenone
4
F
24
OAVRT
68
0.8
16.12
111/67
72
833
156
384
-
-
-
-
-
Verapamil
5
F
52
AVNRT
62
0.6
21.64
100/60
82
732
188
320
-
-
-
-
-
Verapamil, Propranolol
6
F
42
OAVRT
71
0.8
21.31
110/70
80
750
149
403
-
-
-
-
-
Verapamil
7
F
42
OAVRT
67
0.8
18.33
130/70
94
638
219
274
-
+
-
-
-
Procainamide, Valsartan, Bromazepam
8
F
46
AVNRT
64
0.7
31.64
116/73
97
619
125
480
-
-
-
-
-
Verapamil, Fludiazepam
9
F
26
AVNRT
66
0.5
18.93
99/53
85
706
233
257
-
-
-
-
-
Verapamil
10
F
39
OAVRT
65
0.6
25.28
133/70
66
909
149
402
-
-
-
-
+
Verapamil, Nateglinide, metformin
11
M
42
AVNRT
55
0.9
27.22
118/70
85
706
209
287
-
-
-
-
-
Verapamil, Fludiazepam
12
F
50
AVNRT
59
0.7
24.08
137/90
78
769
199
302
-
-
-
-
-
Propafenone, Glimepiride
13
F
52
AVNRT
66
0.8
26.71
120/70
84
714
178
337
-
+
-
-
-
Verpamil, Atenolol,Perindopril
14
F
48
AVNRT
64
0.6
27.51
122/60
66
909
166
362
-
-
-
-
+
Fludiazepam, Metformin, Gliclazide
15
F
41
AVNRT
73
0.7
22.48
110/70
78
769
155
386
-
-
-
-
-
Verapamil, Fludiazepam
16
M
42
OAVRT
57
0.8
20.2
113/68
84
714
141
426
-
-
-
-
-
Verapamil
17
F
42
AVNRT
66
0.7
19.76
98/67
82
732
120
502
-
-
-
-
-
Verapamil
18
M
58
OAVRT
60
1.2
28.66
110/66
62
968
148
406
-
-
-
+
-
Verapamil