natriuretic-peptide--c-type and Tachycardia--Supraventricular

Topics: Atrial Natriuretic Factor; Biomarkers; Diagnostic Techniques, Endocrine; Heart Failure; Humans; Hypertension; Hyperthyroidism; Immunoradiometric Assay; Kidney Failure, Chronic; Natriuretic Peptide, Brain; Natriuretic Peptide, C-Type; Reference Values; Specimen Handling; Tachycardia, Supraventricular

The objective of this study was to evaluate production or release of CNP in individuals without CHF.. Nineteen patients with symptomatic paroxysmal supraventricular tachycardia (PSVT) and normal left ventricular systolic function were enrolled into the study. Blood samples were collected from the coronary sinus (CS), the femoral artery (FA), and the peripheral vein (PV) before pacing, after rapid RA pacing, and post electrophysiological study (EPS) and/or radiofrequency (RF) ablation.. The CNP level in the CS, compared to FA and PV, was significantly higher before pacing (CS, 3.2+/-0.8; FA, 2.6+/-0.7; PV, 2.5+/-0.5 pg/ml; CS vs. either FA or PV, both p<0.001), after the pacing (CS, 3.2+/-1.3; FA, 2.4+/-0.6 pg/ml; p=0.004), and post the EPS and/or RF ablation (CS, 3.1+/-0.7; FA, 2.6+/-0.9; PV, 2.5+/-0.8 pg/ml; CS vs. either FA or PV, both p<0.01).. The myocardium regularly produces or releases CNP in patients with normal LV systolic function. Brief periods of rapid RA pacing, PSVT, or EPS does not change the production and/or release.

Topics: Adult; Biomarkers; Catheter Ablation; Electrophysiologic Techniques, Cardiac; Female; Femoral Artery; Humans; Male; Middle Aged; Myocardium; Natriuretic Peptide, C-Type; Systole; Tachycardia, Paroxysmal; Tachycardia, Supraventricular; Veins; Ventricular Function, Left

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.

Topics: Adult; Atrial Natriuretic Factor; Biomarkers; Coronary Sinus; Disease Progression; Female; Femoral Artery; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Natriuretic Peptide, C-Type; Tachycardia, Paroxysmal; Tachycardia, Supraventricular; Time Factors