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Articles in PresS. Am J Physiol Heart Circ Physiol (January 22, 2016). doi:10.1152/ajpheart.00668.2015 1 Responses of cardiac natriuretic peptides after paroxysmal supraventricular 2 tachycardia: ANP surges faster than BNP and CNP 3 Jen-Yuan Kuo1,4, An-Mei Wang2, Sheng-Hsiung Chang1,3, Chung-Lieh Hung1,3,4, 4 Chun-Yen Chen1,4, Bing-Fu Shih2, Hung-I Yeh1,3,4,* 5 Running title: Natriuretic peptides and PSVT 6 1 7 Medicine, MacKay Memorial Hospital, 3Mackay Medicine, Nursing, and 8 Management College, and 4Mackay Medical College, Taipei, Taiwan 9 AUTHOR CONTRIBUTIONS Division of Cardiology, Department of Internal Medicine, 2Department of Nuclear 10 Kuo JY and Yeh HI conception and design of research; Kuo JY, Chang SH, and Hung 11 CL performed clinical studies; Wang AM measured plasma levels of natriuretic 12 peptides; Kuo JY and Chen CY analyzed data; Kuo JY, Shih BF, and Yeh HI 13 interpreted results of experiments; Kuo JY drafted manuscript; Yeh HI revised 14 manuscript. 15 *Corresponding author 16 Hung-I Yeh 17 Division of Cardiology Tel: 886-2-2543-3535 ext. 2456 18 MacKay Memorial Hospital E-mail: [email protected] mailto: 19 92, Sec 2, Chung Shan North Road, Taipei 10449, Taiwan Fax: 886-2-2543-3642 20 Copyright © 2016 by the American Physiological Society. 21 Abstract 22 Aims: Atrial natriuretic peptide (ANP) secretion increases after a 30-minute of 23 paroxysmal supraventricular tachycardia (PSVT). Whether this phenomenon also 24 applies to brain or C-type natriuretic peptides (BNP or CNP) remains unknown. 25 Methods and Results: Blood samples of 18 patients (41±11 years old; 4 males) with 26 symptomatic PSVT and normal left ventricular systolic function (ejection fraction 27 65±6 %) were collected from the coronary sinus (CS) and the femoral artery (FA) 28 before and 30 minutes after the induction, and 30 minutes after the termination of 29 PSVT. The results showed that the ANP levels rose steeply after the PSVT and then 30 reduced at 30 minutes after the termination (baseline vs. post PSVT vs. post 31 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 32 vs. 10.0±4.6 pg/ml; all P < 0.05). In contrast, compared to ANP, the increases of BNP 33 and CNP in CS after the PSVT were less sharp, but continued to rise after the 34 termination of tachycardia (BNP, 10.2±6.4 vs. 11.3±7.1 vs. 11.8 ± 7.9; CNP, 4.5±1.2 35 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 36 similarly less sharp after the PSVT and remained stationary after the termination. 37 Conclusion: PSVT exerted differential effects on cardiac natriuretic peptides levels. 38 ANP increased greater after a 30-minute induced PSVT but dropped faster after 39 termination of PSVT, as compared to BNP and CNP. 2 40 Keywords: ANP; BNP; CNP; Natriuretic peptide; Paroxysmal supraventricular 41 tachycardia 3 42 43 New & Noteworthy 44 This research article showed for the first time that PSVT exerted differential 45 effects on cardiac natriuretic peptides levels. ANP increased greater after a 30-minute 46 induced PSVT, but dropped faster after termination of PSVT, as compared to BNP 47 and CNP. 48 4 49 50 51 Introduction 52 53 Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type 54 natriuretic peptide (CNP) are a family of structurally related peptides that participate 55 in the integrated control of renal and cardiovascular function. ANP is a 28-amino acid 56 peptide that is secreted from the atria and possesses natriuretic, vasoactive, and 57 rennin-inhibiting actions (4, 6). BNP, also found in the heart, is a 32-amino acid 58 peptide that shares structural and biological similarity to ANP (15). CNP, a 59 vasorelaxant with a half-life of 2.6 minutes, is a 22-amino acid peptide that was first 60 isolated from the porcine brain in 1990 (21). Although it shares structural and 61 physiological properties with ANP and BNP, it appears to be secreted predominantly 62 from the vascular endothelium (22, 25). In ventricular tissue, immunohistochemical 63 staining confirmed the presence of all three peptides in normal hearts and was 64 markedly enhanced in those with congestive heart failure (9, 26). 65 Some studies have shown a marked increase of ANP secretion after PSVT 66 sustains for 30 minutes (11, 24). Whether this phenomenon also occurs for BNP and 67 CNP is unknown. We previously found that the myocardium regularly produced or 68 released CNP in patients with normal LV systolic function. Brief periods of rapid right 5 69 atrial pacing (with pacing cycle lengths starting from 750 ms, in 50 ms decrement, to 70 a minimum of 400 ms, each for 2 minutes and rest for 2 minutes) or PSVT (sustained 71 less than 2 minute) did not change the production and/or release (13). The aim of this 72 study was to compare the response of the 3 peptides against a 30-minute induced 73 PSVT. 74 6 75 Methods 76 77 Consecutive patients with clinically documented, symptomatic PSVT were 78 referred to this laboratory for electrophysiological study (EPS) and radiofrequency 79 (RF) ablation. The patients with age between 20 and 60 years old and relatively 80 healthy were enrolled into the study. The patients who had chronic obstructive lung 81 disease, abnormal renal function, impaired left ventricular systolic function, previous 82 myocardial infarction, or coronary artery disease which may affect endothelial 83 function were excluded from the study. Routine coronary angiography was performed 84 in patients who were older than 45 years old. Twelve-lead electrocardiogram, 85 treadmill exercise test, myocardial perfusion scan, and/or coronary angiography were 86 used to exclude coronary artery disease if necessary. Ethical approval was granted by 87 the Institute Review Board of our hospital. All patients had signed written consent 88 forms. 89 90 91 Electrophysiological test and radiofrequency ablation Electrophysiological study was performed while the patient was fasting and not 92 sedated. All antiarrhythmic medications were discontinued for at least 5 half-lives 93 before study, and anti-diabetic agents were held on the day of study. Details of the 7 94 electrophysiological study have been described previously (12). In brief, the 95 diagnostic portion of the electrophysiological study included: (i) measurement of the 96 electrical properties of the atrium, AV node, ventricle, and accessory pathways; (ii) 97 induction of supraventricular tachycardia by programmed atrial and ventricular burst 98 pacing or extrastimuli; and (iii) determination of the mechanism of tachycardia. If 99 tachycardia could not be induced in the baseline state, isoproterenol (1 to 4 µg/min IV) 100 was infused to facilitate its induction. AVNRT, AT and AVRT were diagnosed and 101 differentiated from each other by previously described criteria. 102 A 7F quadripolar electrode catheter with a 4-mm distal electrode and a 103 thermistor-embedded tip (Daig, Bard, or EP Technologies, Inc.) was used for ablation. 104 Radiofrequency energy was delivered from a generator (EPT 1000, USA). The 105 maximal preset temperature was 70°C in every patient with AVRT, or 60°C in patients 106 with AT or AVNRT. The ablation techniques used in various types of tachycardias 107 have been described previously (12). 108 109 110 Collection of blood sample and measurement of natriuretic peptides Six samples, 2 ml for each, were collected from each patient. First, blood 111 samples were collected from the CS and the FA immediately after four multipolar 112 electrode catheters (Response CSL and Livewire, St. Jude Medical, Daig Division, 8 113 Inc., Minnetonka, MN, USA) were positioned in the CS, the RA, the His-bundle area, 114 and the right ventricle (RV) under fluoroscopy. The location of the CS mapping 115 catheter in CS was confirmed by direct contrast medium injection via the catheter. 116 Second, PSVT was induced and allowed to continue for 30 minutes, while the RA, RV, 117 and His mapping catheters were withdrawn to the inferior vena cava in the meantime 118 for safety reason. Then, PSVT was terminated by ventricular or atrial rapid pacing 119 immediately and blood samples were collected from the CS and the FA. Third, blood 120 samples were collected from the CS and the FA at 30 minutes after the termination of 121 PSVT. Heart rate, blood pressure, and RA pressure were recorded before PSVT, 30 122 minutes after the induction of PSVT, and 30 minutes after the termination of PSVT. 123 Details of the quantification of plasma natriuretic peptides in this laboratory have 124 been described previously (8, 13). In brief, blood samples were collected into chilled 125 test tubes containing ethylene diamine tetraacetic acid (EDTA) and aprotinin (0.6 TIU 126 per ml blood; Phoenix Pharmaceuticals, California, USA). Samples were immediately 127 centrifuged and plasma stored at -80℃ until measurement. The plasma levels of 128 naturiuretic peptides were determined by a blinded operator (Wang AM) using RIA 129 method with commercially available kits (Phoenix Pharmaceuticals, California, USA ), 130 conducted according to the manufacturer’s manual. The intra-assay co-efficient of 131 variation was 7.5% for ANP, 6.5% for BNP, and 6.9% for CNP. The lower limit of 132 detection was 1 pg/ml. 133 134 Determination of LV function by echocardiography 9 135 Cardiac function was evaluated using echocardiography. An ejection fraction of 136 LV > 50% without regional wall motion abnormality was considered as normal LV 137 systolic function. The LV ejection fraction was measured by (LV diastolic volume – 138 LV systolic volume) / LV diastolic volume. 139 140 141 Statistical analysis Quantitative data were expressed as mean ± standard deviation. Parametric data 142 were compared by ANOVA or t test, and categorical data were analyzed by the 143 Chi-square test with Yates’ correction or Fisher’s exact test. P<0.05 was considered 144 statistically significant. 145 146 10 147 Result 148 Eighteen patients (4 men and 14 women, mean age 41±11 years old) were 149 enrolled into the study. The baseline characteristics of patients were listed in table 1. 150 Two had diabetes mellitus with well-controlled blood sugar, two had hypertension 151 with well-controlled blood pressure, and one had mild left ventricular hypertrophy. 152 Twelve-lead electrocardiogram of all the patients showed no myocardial ischemia. No 153 patient had angina symptoms. Routine coronary angiography was performed in 7 154 patients who were older than 45 years old. No patient had chronic obstructive lung 155 disease, previous myocardial infarction, coronary artery disease, or angina. No patient 156 underwent study within 1 week of the last PSVT. All patients had normal renal 157 function (serum creatinine 0.7±0.2 mg/dl) and left ventricular (LV) systolic function 158 (LV ejection fraction 65±6 %). All of the 18 patients had successful RF ablation for 159 their PSVT, and did not have recurrence during two-year follow-up. Two additional 160 patients were excluded from analysis because they did not complete the blood test due 161 to no inducible PSVT in the electrophysiological laboratory. 162 The ANP levels at 30 minutes after the induction of PSVT were significantly 163 higher than those before the induction of PSVT (CS, 74.1±42.3 vs. 34.0±29.6; FA, 164 28.2± 20.7vs 5.9±3.24 pg/ml; both P < 0.001). The ANP levels at 30 minutes after the 165 termination of PSVT were also significantly higher than those before the induction 11 166 (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). 167 Moreover, the ANP levels at 30 minutes after the induction of tachycardia were 168 significantly higher than those at 30 minutes after the termination of PSVT (CS, 169 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). 170 The BNP levels at 30 minutes after the induction of PSVT were significantly higher 171 than those before the induction of PSVT (CS, 11.3±7.1 vs. 10.2±6.4; FA, 9.6±6 vs. 172 8.7±5.6 pg/ml; both P < 0.05). The BNP levels in CS at 30 minutes after the 173 termination of PSVT were also significantly higher than those before the induction of 174 PSVT (11.8±7.9 vs. 10.2±6.4 pg/ml; P < 0.05). However, there was no significant 175 difference between baseline and 30 minutes after the termination of PSVT in FA. 176 (9.1±6.3 vs. 8.7±5.6 pg/ml; P = 0.29) There was also no significant difference 177 between the BNP levels at 30 minutes after the induction of PSVT and those at 30 178 minutes after the termination (Figure 2). The CNP levels at 30 minutes after the 179 induction of PSVT were significantly higher than those before the induction of PSVT 180 (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 181 levels in CS at 30 minutes after the termination of PSVT were also significantly 182 higher than those before the induction of PSVT (5±1.4 vs. 4.5±1.2 pg/ml; P = 0.005). 183 However, there was no significant difference between baseline and 30 minutes after 184 the termination of PSVT in FA (4.1±0.9 vs. 3.9±0.9 pg/ml; P = 0.07). There was also 12 185 no significant difference between the CNP levels at 30 minutes after the induction of 186 PSVT and those at 30 minutes after the termination (Figure 3). In 150 of 162 (92.6%) 187 pairs of natriuretic peptide values, the natriuretic peptide levels in the CS were higher 188 than those in the femoral artery. The ANP, BNP, and CNP levels in the CS at each 189 time point were significantly higher than those in the femoral artery (Figure 4, all 190 P<0.001). However, the transcardiac net production or release of natriuretic peptides 191 did not correlate with the heart rate, tachycardia rate, RA pressure, or blood pressure. 192 The mean RA pressure at 30 minutes after the induction of PSVT was 193 significantly higher than that before the induction of PSVT (6±4 vs. 4±2 mmHg; P < 194 0.01) (Figure 5). However, the change did not correlate with any of the natriuretic 195 peptide levels (all P > 0.05). Baseline heart rate, tachycardia rate, or blood pressure 196 also did not correlate with the natriuretic peptide levels. 197 198 13 199 Discussion 200 201 202 Major findings This study showed that ANP, BNP, and CNP levels in the CS at baseline and each 203 time point after PSVT were significantly higher than those in the FA in individuals 204 with PSVT and normal LV systolic function, indicating that, in the body, the heart is a 205 major source of natriuretic peptides, including ANP, BNP, and CNP, at rest and post 206 PSVT. In addition, sustained PSVT for 30 minutes could enhance the heart to release 207 ANP, BNP, and CNP. The increase of ANP to PSVT was to a greater degree but 208 dropped faster, as compared to BNP and CNP. 209 Previous reports regarding production or release of natriuretic peptides during 210 PSVT 211 Several previous studies showed that induction or spontaneous initiation of PSVT 212 resulted in a marked elevation of plasma ANP levels (11, 17, 20, 23, 24). However, 213 the effects of PSVT on the ANP levels remained discrepant. Tsai et al. showed that 214 immediately after the induction of PSVT, plasma ANP levels began to increase, 215 peaked at 32 minutes (734% increment on average), and then gradually decreased in 5 216 patients. The ANP levels significantly increased at 15 minutes, 30 minutes after the 217 induction of PSVT, and 5 minutes after the termination of PSVT, compared to those 218 of control, but showed no significant increase at 5 minutes after the induction of 14 219 PSVT, 15 or 30 minutes after the termination of PSVT (24). Kojima et al. found that 220 plasma ANP levels in 10 patients with PSVT significant increased from 37±11 pg/ml 221 during the control period to 110 pg/ml at 30 minutes, 160±54 pg/ml at 60 minutes 222 after the induction of PSVT, and to 90 pg/ml at 30 minutes after the termination of 223 PSVT (11). Anderson et al. showed that induction of AVRT in 3 patients produced an 224 acute and marked rise in plasma ANP concentrations, which returned to normal at 30 225 minutes after restoration of the sinus rhythm (1). In that study, the PSVT was allowed 226 to sustain for 10.5 minutes, 30 minutes, and 42 minutes, respectively. In the present 227 study, we found that the plasma ANP levels significantly increased at 30 minutes after 228 the induction of PSVT, compared to those before PSVT. The ANP levels significantly 229 fell at 30 minutes after the termination of PSVT, but still significantly higher than 230 those before PSVT. These findings were consistent with Kojima and their coworker’s 231 findings. However, the response of the ANP to PSVT in FA was greater in this study 232 (+378% VS +197%). In the study of Tsai et al., the ANP levels at 30 minutes after 233 termination of PSVT remained high than those of control, but showed no significant 234 difference (9). Small patient numbers (N=5) might be one of the reasons. Taken 235 together, with more patients and a strict protocol, the present study unequivocally 236 showed that the release of ANP continued for at least 30 minutes after termination of 237 PSVT. 15 238 Mechanisms of myocardial production or release of natriuretic peptides during 239 PSVT 240 In a rat study, Dietz showed that an increase in blood volume resulted in the 241 release of an ANP via atrial stretch (7). Lang et al. also demonstrated that increased 242 atrial stretch or ventricular stretch, such as volume overload led to increased secretion 243 of ANP in atria and BNP in ventricles respectively (14). Increases in ANP were also 244 found during both pacing-stimulated and spontaneously PSVT in the study of Nicklas 245 et al (16). They speculated that the stimulus to ANP secretion during PSVT appears to 246 be related to the rise in right atrial pressure rather than to the increase in heart rate. 247 However, several studies showed that a significant positive correlation was found 248 between plasma ANP levels and mean pulmonary capillary wedge pressure, while the 249 correlation between plasma ANP levels and mean right atrial pressure was not 250 significant (19, 24). In the present study, we found that there was no significant linear 251 correlation between RA pressure and ANP levels, although the mean RA pressure at 252 30 minutes after the induction of PSVT was significantly higher than that before 253 PSVT and ANP levels did increase in the CS and FA. This might imply that the LA 254 pressure plays more important role than the RA pressure in the production or release 255 of ANP. However, the underlying mechanism remains unclear. Different effects of 256 right and left atrial stretch by volume or pressure overload might partially explain the 16 257 258 different results. Further studies are required to elucidate this issue. The mechanisms regulating myocardial production or release of BNP and CNP 259 in arrhythmias or tachycardias remain unclear. Kalra et al. suggested that elevated 260 ventricular filling pressure may contribute to the increased production of CNP in 261 patients with CHF (10). Borgeson et al. showed that acute intravascular volume 262 overload in dogs resulted in the expected increase in right atrial pressure, PCWP, 263 plasma ANP, and urinary CNP, but no change in plasma BNP and CNP levels (2). 264 Rademaker et al. found that acute ventricular pacing for 1.5 hours in sheep increased 265 plasma ANP and BNP levels by 8.6- and 3.6-fold, respectively, whereas chronic 266 ventricular pacing for 4 days increased ANP and BNP by 7.8- and 9-fold, respectively 267 (18). There was no study investigating whether a 30-minute induced PSVT in patients 268 could affect the production or release of BNP or CNP in the past. In the present study 269 we showed that plasma BNP and CNP levels significantly increased after a 30-minute 270 of PSVT and remained raised at 30 minutes after the termination of PSVT. Enough 271 loading of ventricular and/or atrial stretch during PSVT might enhance the release of 272 BNP and CNP. Previously, we demonstrated that brief periods of rapid atrial pacing, 273 short-term PSVT (less than 2 minutes), routine EPS or RF ablation procedure did not 274 increase the production or release of CNP (13). The different baseline CNP values 275 might be due to different clinical characteristics, such as LVEF, age, and baseline 17 276 heart rate between these two groups. The different changes of CNP values in CS and 277 FA might be due to different duration of PSVT. However, how long of PSVT is 278 necessary to enhance the release of BNP and CNP remains unknown. The half-life of 279 BNP was longer than that of ANP or CNP. This might partially explain why BNP 280 remained raised while ANP fell at 30 minutes after the termination of PSVT in the CS. 281 However, it could not explain why CNP also remained raised at 30 minutes after the 282 termination of PSVT. There might be other factors affecting the production or release 283 of CNP. Another possible explanation was that the start of production or release of 284 BNP and CNP could last longer than that of ANP after the stimulation of 30-minute 285 PSVT. Again, further studies are required to elucidate the underlying mechanism. 286 Study limitations 287 This study has several limitations. First, the sample size of the study is small. If 288 more patients could be enrolled into the study, there would be more power to draw the 289 current conclusion. However, it’s the largest patient group to test the effects of 290 paroxysmal supraventricular tachycardia on cardiac natriuretic peptide levels in the 291 literature so far. Second, we might suspect that the length and the frequency of 292 previous PSVT could affect the production of natriuretic peptide at baseline or the 293 response to the PSVT. In this study, the length of previous PSVT ranged from 294 several-decade minutes to several hours and the frequency of previous PSVT ranged 18 295 from several times a month to several times a year in these patients. These might have 296 chance to affect the production of natriuretic peptide at baseline although we did not 297 know how much the influence was. However, no patient underwent study within 1 298 week of the last PSVT. We speculated that the influence might be tiny. Third, to 299 record heart rate, blood pressure, and urine amount, and to check the plasma renin 300 activity, serum aldosterone level, and urine sodium value may help to understand the 301 pathophysiology of myocardial release and/or production of natriuretic peptides. 302 However, in this study, we only recorded blood pressure and heart rate, and found that 303 they did not correlate with any of the natriuretic peptide levels. Fourth, to measure 304 right atrial pressure, pulmonary arterial pressure, ventricular pressure, and pulmonary 305 capillary wedge pressure of patients may help understand the mechanisms of 306 increment of natriuretic peptides after an induced PSVT sustaining for 30 minutes. 307 However, because it was not the routine procedure during the mapping and ablation of 308 PSVT, we did not attempt to measure all of them. In this study, we only recorded right 309 atrial pressure, and found that they did not correlate with any of the natriuretic peptide 310 levels. Fifth, radiofrequency ablation may have its own acute and chronic effects on 311 natriuretic peptides. Previously, we found that the production or release of CNP did 312 not change at the end of EPS and/or radiofrequency ablation (13). In the literature, 313 only two previous studies investigated the effect of radiofrequency ablation on plasma 19 314 natriuretic peptide in patients with paroxysmal supraventricular tachycardia. One 315 study showed that increment of plasma BNP level 3 and 24 hours after radiofrequency 316 ablation, but no increment of plasma BNP level 30 minutes after radiofrequency 317 ablation (5). The other study showed that levels of NT-proANP were significantly 318 higher before RF ablation as compared to day one and day 120 after RF ablation. 319 However, that study had no data regarding the level of natriuretic peptides within 3 320 hours after RF ablation (3). The blood samples were collected within 30 minutes after 321 radiofrequency ablation in all of our patients. Whether plasma levels of ANP or CNP 322 would increase 30 minutes after RF ablation remained unknown before. 323 Clinical implications 324 To assay the plasma levels of ANP, BNP and CNP might have diagnostic 325 significance for differentiating PSVT from non-PSVT palpitations. Other more 326 serious cardiac diseases, such as congestive heart failure resulting from different 327 cardiac etiologies, have more atrial and/or ventricular pressure or volume overload. 328 Whether differential responses of ANP, BNP, and CNP have more values of diagnosis 329 or evaluation of treatment or not deserve further investigation. 330 331 332 Conclusions PSVT exerted differential effects on cardiac natriuretic peptides levels in persons 20 333 with PSVT and normal LV systolic function. 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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