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Am J Physiol Heart Circ Physiol. 2016 Mar 15;310(6):H725-31. doi: 10.1152/ajpheart.00668.2015. Epub 2016 Jan 22.

Responses of cardiac natriuretic peptides after paroxysmal supraventricular tachycardia: ANP surges faster than BNP and CNP.

Author information

1
Division of Cardiology, Department of Internal Medicine, MacKay Memorial Hospital, Taipei, Taiwan; Mackay Medical College, Taipei, Taiwan.
2
Department of Nuclear Medicine, MacKay Memorial Hospital, Taipei, Taiwan;
3
Division of Cardiology, Department of Internal Medicine, MacKay Memorial Hospital, Taipei, Taiwan; Mackay Medicine, Nursing, and Management College, Taipei, Taiwan; and.
4
Division of Cardiology, Department of Internal Medicine, MacKay Memorial Hospital, Taipei, Taiwan; Mackay Medicine, Nursing, and Management College, Taipei, Taiwan; and Mackay Medical College, Taipei, Taiwan.
5
Division of Cardiology, Department of Internal Medicine, MacKay Memorial Hospital, Taipei, Taiwan; Mackay Medicine, Nursing, and Management College, Taipei, Taiwan; and Mackay Medical College, Taipei, Taiwan hungi.yeh@msa.hinet.net.

Abstract

Atrial natriuretic peptide (ANP) secretion increases after 30 min of paroxysmal supraventricular tachycardia (PSVT). Whether this phenomenon also applies to brain or C-type natriuretic peptides (BNP or CNP) remains unknown. Blood samples of 18 patients (41 ± 11 yr old; 4 men) with symptomatic PSVT and normal left ventricular systolic function (ejection fraction 65 ± 6%) were collected from the coronary sinus (CS) and the femoral artery (FA) before and 30 min after the induction, and 30 min after the termination of PSVT. The results showed that the ANP levels rose steeply after the PSVT and then reduced at 30 min after the termination (baseline vs. post-PSVT vs. posttermination: 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 vs. 10.0 ± 4.6 pg/ml; all P < 0.05). In contrast, compared with ANP, the increases of BNP and CNP in CS after the PSVT were less sharp, but continued to rise after the termination of tachycardia (BNP, 10.2 ± 6.4 vs. 11.3 ± 7.1 vs. 11.8 ± 7.9; CNP, 4.5 ± 1.2 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 similarly less sharp after the PSVT and remained stationary after the termination. PSVT exerted differential effects on cardiac natriuretic peptide levels. ANP increased greater after a 30-min induced PSVT, but dropped faster after termination of PSVT, compared with BNP and CNP.

KEYWORDS:

ANP; BNP; CNP; natriuretic peptide; paroxysmal supraventricular tachycardia

PMID:
26801306
DOI:
10.1152/ajpheart.00668.2015
[Indexed for MEDLINE]
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